Personal Skincare Information

Mornings can be difficult. Between hitting the snooze button, to taking care of the kids, to making sure you get to work on time, sometimes your skin is the last thing on your mind. A good skincare regimen, however, can be essential for helping to kick off your day and making sure your skin is ready to take on the day. These eight simple steps can help you improve your morning routine and help you turn healthy looking skin into a habit.

Have a Glass of Water

A great way to start your daily skin routine is to have a glass of water when you wake up in the morning. Cold water can help hydrate your body in the morning. Your skin slowly becomes dehydrated through the night and early morning fluids can help your skin rehydrate.

Take a Warm Shower… Not Hot

A great way to remove that dirt and keep your skin healthy is to take a shower in the morning to start your day off fresh and clean. Try to avoid long, hot showers, which can strip your skin of the essential oils it produces to naturally moisturize by preventing dehydration.

Cleanse Your Face

While you might wash your face before you go to sleep, your skin continues to produce oils while you sleep to naturally protect itself. Be sure to wash your face every morning with lukewarm water and use a mild skin cleanser for your skin type. Then, follow up with a gentle hypoallergenic and fragrance-free moisturizer to soothe, protect and hydrate your skin.

Soothe Chapped Lips

You might think that chapped lips can only occur in the winter. But your lips can get dry in hot or cold temperatures. Make sure you keep you and your family’s lips moisturized and pain free all year long by using a petrolatum-containing product, to protect your lips against harsh temperatures.

Moisturize From Head to Toe

Making sure your skin is moisturized throughout the day—especially after stripping it in the shower—is a very important step in a morning routine for you and your family’s skin health. Combat dry skin and seal in moisture for the day by using a rich ointment like Aquaphor Healing Ointment. It protects and soothes your skin.

Consider Using a Makeup Primer

When used correctly and in moderation, primers can provide a layer in between your skin and your makeup to allow pores to stay makeup-free.

Make Sure Your Makeup Application is Sanitary

It’s very important that the makeup tools you use and the makeup you put on every morning is clean because it will be sitting on your face all day. If you are using powder or pressed foundation make sure your brushes are washed on a weekly basis. If you use liquid foundation, you may want to toss the sponge and just use your hands to evenly apply foundation—just make sure you wash your hands before and after touching your face.

Wear Sunscreen

No matter what season it is, UV rays from the sun can damage your skin. It is important that sunscreen is a part of your daily skincare regimen before you put on your makeup. Apply a thin layer of a broad spectrum sunscreen (at least SPF 30 or higher) onto your face for to help protect from sunburn and damaging effects of sun exposure.

Nighttime skincare routines are essential for healthy looking skin. How you prep your skin before bed every night is important in order to let it rest, rejuvenate, and heal while you sleep. Find out some of the best things you can do at night to get on the road to better and more beautiful skin.

Wash Your Face First

A great first step when you get home from work — before preparing dinner or watching TV — is to wash your face. If you wait until right before bed to wash your face, you may skip this step in order to get to sleep faster. But letting your face sit with makeup and other pore-cloggers for eight hours while you sleep can be harmful to your skin and pores. Ensure healthy looking, breakout-free skin by washing your makeup off of your face before you’re too tired.

Take a Shower

Taking a shower is a great way to wash off dirt and pollution that has found its way into your hair and skin throughout the day. A nice warm nighttime shower is a great way to help you relax from your stressful day while also making sure your skin is clean before you go to sleep. Try not to have the temperature too high or your shower too long, since doing so can strip essential oils off of the skin that it normally produces to protect itself.

Use a Humidifier

During the winter months your skin can get dehydrated from the lack of moisture in the warm air inside. You can easily change that by using a humidifier in your room while you sleep. The steam from the humidifier releases humidity and adds moisture in the air while you sleep.

Moisturize Your Body

This is an important step in your nighttime routine, so try to make it a habit. After washing your face or showering you should apply a non-comedogenic moisturizer to help hydrate and protect your skin: cleansing the skin strips your body of water and essential oils that it needs to protect itself from damage and dehydration. Use a multi-purpose moisturizing ointment, like Aquaphor Healing Ointment, to moisturize and soothe your face, arms, legs, and feet before bed. For even better results, try wearing cotton socks on your feet to wake up with softer, smoother skin.

Change Your Pillowcase Frequently

If you are not a person that likes to shower at night, you may be transferring dirt and grime collected on your skin and hair to your pillowcase. That can then transfer to and affect your face when you use the same pillowcase night after night. Swap out your pillowcases on a weekly basis in order to guarantee that your skin is getting the best and cleanest nighttime protection.

Get Some Sleep

Getting a decent amount of sleep every night is essential for your whole body, including your skin. Make sure you are clocking in seven to nine hours a night in order to reduce dark circles, redness, puffy eyes and to give your skin time to restore itself. To help get to sleep quickly, try creating a routine by going to bed at the same time every night.

Your skin is affected by all of the seasons, weather conditions, and elements in the air. All of these environmental factors can cause damage, dryness, and signs of aging to your skin. Learn how to protect your skin properly by knowing what can affect it and the preventative measures you can take throughout the year.

Windy Days

The wind can dry out your face. Before you go outside, make sure you apply a moisturizer, like Aquaphor Healing Ointment, to protect and relieve chapped or cracked skin and lips from the drying effects of wind and cold weather. Take additional precaution by wearing gloves and covering most of your face with a scarf in harsh wind conditions.

Cold Winters

The cold air can damage the lipid layer that protects and moisturizes your skin, potentially leaving you and your family with dry, cracked, or chapped faces, lips, and hands. Protect everyone’s skin in your family from excessive damage this winter by applying a hydrating moisturizer every morning and night to protect and help heal skin throughout the season.

Sweltering Heat

Hot days bring lots of sunshine and sweat. Your skin can actually dry out when it’s hot outside because your skin becomes dehydrated from excessive heat. On hot and humid days make sure to drink a lot of water to help keep your body, and skin, well-hydrated and wear sunscreen to protect your skin from the sun’s harmful UV rays.

Pollution in Urban Environments

Cigarettes, fossil fuels, and other elements that pollute the air in big cities can be harmful to your skin. These chemicals can enter your bloodstream through the air you breathe, damaging many of the organs of your body including your skin. Certain chemicals in heavily polluted air may cling to your skin and affect skin health. Be sure to cleanse your skin regularly to help wash off dirt and pollution.

Everyday Sunlight

Regardless of what season it is, the UV rays in sunlight can be harmful to your skin. People can and do frequently get sunburns during the winter months, even on cold days. Make sure that wearing a sunscreen with an SPF of 30 or higher is part of your daily skincare routine. For an added bonus, use a multi-purpose moisturizer with SPF to hydrate your skin and combat the seasonal elements.

Soothe Scaly Sunburn

Everyone loves the extra dose of vitamin D that comes with summer but all that fun in the sun can lead to painful sunburn. To treat inflamed skin, take a cool bath or use a cool water compress followed with skin-soothing gels and oils like aloe vera, which help calm inflammation. Next time, stay cool and sunburn-free by using a broad spectrum SPF 30, sunglasses, and a floppy hat.

Cool Off Oily Skin

If you have oily skin, you know the havoc that summer heat, humidity, and smog can cause on your skin. Control enlarged pores, excess shine, and acne by using a gel cleanser, SPF, and moisturizer every day. Believe it or not, oily skin needs moisture to keep it from overproducing oil and clogging pores. Reduce redness, breakouts, and inflammation with this plan.

Relieve Itchy Red Skin

More time spent outside means more time for pesky bug bites and rashes! Try using over the counter 1% hydrocortisone cream to help treat insect bites. You can use this treatment also if you think you’ve come in contact with poison ivy but wash your skin first and your clothes thoroughly. If the rash covers a large area of the body, call your doctor for a prescription cream.

Stop Folliculitis In Its Tracks

Folliculitis happens when common bacteria that live on the skin get into hair follicles, triggering inflamed red bumps and pimples, and can occur more in the summer thanks to sweaty exercise sessions outside. You can prevent folliculitis by changing out of your sweaty clothes quickly once you’re done with your workout. Also, try a topical medication, body wash, or soap with the active ingredient benzoyl peroxide, which may help kill the bacteria that cause folliculitis.

Shave, Wax or Laser?

When we get down to the nitty-gritty, who wants to be hairy scary? Not me and obviously not you; none of us do! The options for hair removal can be endless but finding the one that works best for you and your budget can be a bit challenging. Some of our options include razors, over-the-counter hair removal products, waxing and lasers. So, what is a girl to use when it comes to the least amount of pain, cost and hair regrowth?

When we get down to the nitty-gritty, who wants to be hairy scary? Not me and obviously not you; none of us do! The options for hair removal can be endless but finding the one that works best for you and your budget can be a bit challenging. Some of our options include razors, over-the-counter hair removal products, waxing and lasers. So, what is a girl to use when it comes to the least amount of pain, cost and hair regrowth?

Let’s face it, we’ve all shaved and waxed our legs, underarms and bikini area for years, and although today’s razors and over-the-counter hair removal products can be great, we still have to deal with the side effects like nicks, cuts, bleeding, razor burn, rashes and those infamous ingrown hairs, medically referred to as folliculitis.

So, let’s talk lasers. To give you some background, laser hair removal began about 20 years ago when it was experimentally used and tested. In 1997, the FDA approved certain lasers for hair removal. Laser hair removal works through a process called photothermolysis or SPTL. This proven procedure selectively targets dark matter or melanin which is what gives our skin and hair its color and darkness; it is also the area of hair growth. Lasers heat the hair follicle and not the skin. In addition, they deliver a specific wavelength of light and pulse duration where the light is absorbed by the dark areas/hair follicles on our skin.

Laser hair removal has been proven to significantly reduce or remove hair long-term or permanently. A lot of men and woman use laser hair removal to get baby-smooth skin and there’s no worry about scraggly hairs sticking out in the wrong places at the wrong time. The good news is that it’s also less painful and causes less skin irritation when compared to waxing. Yes, there can be side effects like itching, redness and swelling, but if you’re a chicken to the waxing, like me, then this option is a winner!

I know you’re wondering how much laser hair removal will set you back. Well, if you think about the cost of waxing, plus the number of times you have to go to the salon month after month, year after year, it can add up.

Yes, laser hair removal can cost more up front, but over the long run, it can actually save you money, time and there’s less pain. Who wouldn’t want baby-smooth, hairless skin that you don’t have to shave or wax – or deal with any of the mishaps that can happen. It’s so freeing to wake up knowing you can throw on your shorts and tank top without worrying about scary, hairy, scraggly stubble.


Step 1: Morning Routine

Rinse with warm water, no soap or cleanser. Follow with SPF and no moisturizer.

Step 2: Nightly Routine

Use an oil-free, water-based gentle gel cleanser and moisturizer. The texture should feel slippery, not thick. Avoid hard scrubs or sodium lauryl sulfate. Drying up the skin doesn’t help, and all products should be fragrance-free so they’re not irritating. Products should be labeled “noncomedogenic,” which means it won’t clog pores. Follow with moisturizer at night only.

Step 3: Oily Skin Mask

Once a week, make a homemade mask of three crushed aspirin with a tablespoon of plain yogurt and a tablespoon of honey. The honey and yogurt moisturize, and aspirin may calm down oily skin, redness, breakouts and reduce inflammation. The acetylsalicylic acid in aspirin is a close relative of salicylic acid, which dermatologists recommend to treat acne and for exfoliation.

Skincare With Ayurveda

Ayurveda – The Science of Life

Ayurveda is a 5,000-year-old system of natural healing that has its origins in the Vedic culture of India. Although suppressed during years of foreign occupation, Ayurveda has been enjoying a major resurgence in both its native land and throughout the world. Tibetan medicine and Traditional Chinese Medicine both have their roots in Ayurveda. Early Greek medicine also embraced many concepts originally described in the classical ayurvedic medical texts dating back thousands of years.

More than a mere system of treating illness, Ayurveda is a science of life (Ayur = life,Veda = science or knowledge). It offers a body of wisdom designed to help people stay vital while realizing their full human potential. Providing guidelines on ideal daily and seasonal routines, diet, behavior and the proper use of our senses, Ayurveda reminds us that health is the balanced and dynamic integration between our environment, body, mind, and spirit.

Recognizing that human beings are part of nature, Ayurveda describes three fundamental energies that govern our inner and outer environments: movement, transformation, and structure. Known in Sanskrit as Vata (Wind), Pitta (Fire), and Kapha (Earth), these primary forces are responsible for the characteristics of our mind and body. Each of us has a unique proportion of these three forces that shapes our nature. If Vata is dominant in our system, we tend to be thin, light, enthusiastic, energetic, and changeable. If Pitta predominates in our nature, we tend to be intense, intelligent, and goal-oriented and we have a strong appetite for life. When Kapha prevails, we tend to be easy-going, methodical, and nurturing. Although each of us has all three forces, most people have one or two elements that predominate.

For each element, there is a balanced and imbalance expression. When Vata is balanced, a person is lively and creative, but when there is too much movement in the system, a person tends to experience anxiety, insomnia, dry skin, constipation, and difficulty focusing. When Pitta is functioning in a balanced manner, a person is warm, friendly, disciplined, a good leader, and a good speaker. When Pitta is out of balance, a person tends to be compulsive and irritable and may suffer from indigestion or an inflammatory condition. When Kapha is balanced, a person is sweet, supportive, and stable but when Kapha is out of balance, a person may experience sluggishness, weight gain, and sinus congestion.

An important goal of Ayurveda is to identify a person’s ideal state of balance, determine where they are out of balance, and offer interventions using diet, herbs, aromatherapy, massage treatments, music, and meditation to reestablish balance.



What it means—and why it’s essential to your beauty routine

The history of natural healing is often be traced back to Ancient China and Tibet. From meditation to yoga and massage, these countries are credited for developing the medicine and therapies we look to relieve everything from insomnia to chronic back pain.

But believe it or not, their approach is rooted in one that started five-thousand years ago in neighboring India. It’s called Ayurveda (pronounced eye-your-VAY-da), which translates to “the science of life”. And as it, Ayurveda “is designed to help people stay vital while realizing their full human potential. Providing guidelines on ideal daily and seasonal routines, diet, behavior and the proper use of our senses, Ayurveda reminds us that health is the balanced and dynamic integration between our environment, body, mind, and spirit.”

Ayurveda isn’t only to better our mind and body—it’s an up-and-coming beauty trend, too. Why? Research published in the Journal of Ayurvedic and Integrative Medicine finds that Ayurvedic cosmetics can smooth and hydrate a person’s skin, restoring the radiant and healthy look.


Ancient Indians believed there were three elements—or doshas—that governed the body: Wind, fire and earth. Or, in Sanskrit, Vata, Pitta, and Kapha. The proportion of each element varies from person to person but, says the Chopra Center, “if Vata is dominant, [those people] tend to be thin, light, enthusiastic, energetic, and changeable. If it’s Pitta, [those people] tend to be intense, intelligent, and goal-oriented, while Kapha [results in a person being more] easy-going, methodical, and nurturing.”

Our bodies thrive, in every respect, when each of these elements is balanced. But when there is an imbalance, it can cause distress, leading to conditions such as dry skin, anxiety, sluggishness and even weight gain. (Don’t know your dosha?

According to Ayurveda, each of us inherits a unique mix of three mind/body principles which creates our specific mental and physical characteristics. These three principles are called doshas.

Most of us have one or two doshas which are most lively in our nature, with the remaining one(s) less significant. The three doshas are known as Vata, Pitta, and Kapha.

The three doshas are known as Vata, Pitta, & Kapha

If we are predominantly Vata, we tend to be thin, light and quick in our thoughts and actions. Change is a constant part of our lives. When Vata is balanced, we are creative, enthusiastic and lively. But if Vata becomes excessive, we may develop anxiety, insomnia or irregular digestion.

If the Pitta dosha is most lively in our nature, we tend to be muscular, smart and determined. If balanced, we are warm, intelligent and a good leader. If out of balance, Pitta can make us critical, irritable and aggressive.

If we have mostly Kapha in our nature, we tend to have a heavier frame, think and move more leisurely and are stable. When balanced, it creates calmness, sweetness and loyalty. When excessive, Kapha can cause weight gain, congestion and resistance to healthy change.

Using the principles of Ayurveda, we can identify our mind/body nature and use this understanding to make the most nourishing choices in our lives. It is common for people to have a blend of characteristics and usually one will tend to be dominate

Just as our dosha can determine the type of person we are, it can also determine what kind of skin we have.  the Vata dosha is typically associated with dry skin; Pitta with sensitive; and Kapha with oily or combination skin.

While science hasn’t confirmed a dosha-driven beauty routine can definitely reverse aging, there’s evidence that Ayurvedic ingredients, such as turmeric, ginger, garlic, pepper and grape seed extract, can reduce wrinkles and damage from harmful UV rays.


However, Ayurvedic ingredients aren’t just limited to your spice cabinet. In that same study from the Journal of Ayurvedic and Integrative Medicine, researchers point to several herbs that solve skin problems.

For example, there’s Vayasthapana—an herb that balances all three doshas while nourishing the skin to “maintain youthfulness.” Another group of herbs known as Varnya (think sandalwood and Indian sarsaparilla) can restore a healthy glow, brightening your complexion. Supplement these herbs with natural sources of Vitamins A, C and E. can enhance their benefits. “Feeding the skin properly is very important to prevent it aging,” says researchers.

Since, again, doshas are different in every person, it’s best to mull your options over with a specialist. Just because 500 mg of an herb renders anti-aging results in one person doesn’t mean it’ll work similarly in someone else; in which case, check out The Ayurvedic Institute.

Yes, there are herbs and topical treatments that can help prevent aging. But what makes Ayurveda so successful is the fundamental idea that you need to be healthy on the inside in order to be healthy on the outside.

And according to neurologist and Ayurveda experts this includes food. They suggests a Vata dosha focus on eating whole grains and vegetables for better digestion and metabolism, which impacts skin hydration. A Pitta dosha wants anti-inflammatory fruits, like melons and pears, and a Kapha dosha should spice it up—literally. “The spicy food helps to stimulate their digestion and since Kapha individuals have the slowest metabolism, they need all the extra heat their food has to offer,” she tells Dr. Oz.


As for beauty products, says the Journal of Ayurvedic and Integrative Medicine, Vata doshas want to “nourish and rehydrate the skin with warm oil-self massage and all natural moisturizers; Pitta doshas want to invest in good sunscreen and a daily facial oil; while Kapha doshas want a daily warm oil massage and to gently exfoliate.” As if you needed an excuse to pamper yourself.

That said, don’t limit massage or exfoliating to just your face. In an interview with Yoga Journal, Ayurvedic counselor Melanie Sachs, the author ofAyurvedic Beauty Care, says “foot massage can relieve eye strain, relaxing and opening the face and allowing our beauty to shine through easily.” she says.

Oh, and of course, exercise and get plenty of rest. “We work very hard these days and this makes us stressed, depressed and exhausted,” says Red Mountain Resort’s fitness manager Kim Watters. “Our bodies are supposed to achieve balance again each night as we sleep.  Unfortunately few people get enough quality sleep to bring their body back in to balanced, ready to go again state.”

What’s the bottom line?

Those who practiced Ayurveda thousands of years ago knew how important it was to balance both mind and body. And incorporating an approach like this into your life will not just boost your skin—it will boost your overall well-being.

Healing cuts

Every child will, at some point, scrape a knee, cut a finger or break their skin open in some way. While more serious lacerations require medical attention, here are some basic tips for assisting in the healing of minor cuts and avoiding infection or irritation.

First aid for minor cuts and abrasions

  • Before treating a child’s injuries it is important to first wash your own hands, covering any breaks in the skin with bandages or gloves.
  • Generally speaking, shallow cuts and abrasions stop bleeding on their own. However, if bleeding persists, it may be necessary to physically stem the flow of blood by gently holding a sterile dressing to the wound and applying pressure.
  • Gently, but thoroughly, cleanse the cut with fresh water, dabbing lightly with a clean cloth to dry. Stubborn debris can be removed using a damp cloth or sterile tweezers.
  • Apply an antibiotic ointment (such as iodine) to kill any bacteria which may have gotten into the wound.
  • Cover the cut with a sterile bandage, this stops germs from getting in and also protects the wound from further irritation. Any dressings should be kept dry, clean and be changed regularly.
  • Monitor the injury to make sure it is healing properly. Redness, swelling, pus, pain or warmth may all be signs that the wound has become infected; this usually requires treatment with antibiotics by your doctor.

Severe injury

Deep lacerations or wounds may require more extensive treatment, including prolonged pressure, elevation of the affected body part and specialist medical attention. In the case of wide, deep or long wounds that will not stop bleeding, seek immediate medical assistance.

Closing wounds

It is important to properly clean a cut as soon as possibleIn the case of wounds that are particularly deep, open or have body tissue sticking out the doctor may be required to physically close the wound using a variety of methods. Adhesive butterfly strips are often sufficient to hold together small cuts. Gaping wounds may need cyanoacrylate glue, staples or stitches (sutures) to close them up properly.

Tetanus shots

Tetanus is a type of infection which causes severe, potentially fatal, muscle spasms; it is caused by the bacteria Clostridium tetani . The bacteria can infect deep cuts and wounds, thus it is recommended that a tetanus vaccination be given every 10 years. If a wound was caused by a dirty or rusty object (such as a nail or tin), gets dirty, or is particularly deep, and your last tetanus shot was not within the last 5 years, your doctor may suggest a booster.


Children’s Hospital Colorado 2011, ‘Checking Out Cuts, Scatches, and Abrasions’, retrieved 6 September 2011, <>.

Mayo Clinic 2009, ‘Cuts and scrapes: First aid’, retrieved 6 September 2011, <>.

St John Ambulance 2004, ‘FACT SHEET: First aid in and around the Home’, retrieved 6 September 2011, <>.


burns_introBurns are injuries to the skin caused by heat from flames, liquids, radiation, chemicals or electrical devices. The severity of a burn is determined by its depth, the age of the patient, the particular sites on the body burnt (hands, feet, face, genitals and joints are the most complicated) and the total surface area of the burns. While minor burns usually cause nothing more than temporary shock and mild discomfort, severe or widespread burns can be physically destructive, permanently debilitating and even fatal.

Types of burns

Burns can be classified by the depth of tissue they injure. The names for various types of burns have changed over the years.Superficial burn – previously known as first-degree burns, these are minor burns which affect only the outer layer of skin, the epidermis. They may become red, inflamed and painful, but generally heal within 10 days with no scarring.

Partial thickness – these burns (formerly second-degree) damage the middle layer of skin called the dermis. The dermis is much thicker than the epidermis so the severity of these burns can vary depending on their depth. Often red and/or white in colour with blisters, partial thickness burns can take several weeks to heal and often leave scarring.

Deep full thickness – burns which penetrate the entire width of the skin, down through the epidermis, dermis and hypodermis, are classified as full thickness, or third-degree. When the hypodermis is injured, other elements contained within this layer, such as hair follicles, sweat glands and nerve cells, are also destroyed. Skin which has incurred a full-thickness burn may be white or charred and surrounded with large blisters. These typically require skin grafts and usually leave considerable scarring.

Full thickness with injury to underlying tissue – sometimes this fourth classification (fourth-degree burn) is used to describe a burn which involves the loss of all three layers of the skin, plus underlying muscles, ligaments or bone. These types of burns are frequently life-threatening; they regularly cause permanent physical impairment or require amputation.

Basic first aid for minor burns

Basic first aid and at-home care is usually sufficient for treating children who receive a first degree burn on a small portion of their body.Basic first aid and at-home care is usually sufficient for treating children who receive a first degree burn on a small portion of their body:

  • Stop the child’s skin from burning. This could mean removing the source of the burns (chemical, electrical or putting out a fire) or taking the child out of the situation.
  • Soak the burnt area of skin or place it under cold running water immediately. Continue to cool the skin for 10-20 minutes; this stops the skin burning, minimises pain and reduces the resultant inflammation.
  • Remove clothing and jewelry from the burn area whilst you are cooling it with water.
  • Once cooled, cover gently with a dry, sterile bandage.
  • If necessary, a child-appropriate medicine containing paracetamol (i.e Panadol or Dymadon) will help to relieve pain from minor burns. Be sure to read the label before using.
  • If blisters form on the burnt skin, do not pop them, this will leave the wound susceptible to infection.
  • If pain persists beyond a few hours or the skin appears to be becoming infected (oozes or becomes inflamed) consult your family doctor.

Things to avoid when treating burns

  • Do not use ice as this can hinder the body’s repair of a burn.
  • Do not apply lotions, ointments, butter or powder; rather than improving the injury these make burns worse. By trapping heat in, these substances make the skin burn for longer.
  • Avoid rubbing burnt skin, since this makes it more likely to blister.

In an emergency: severe burns

In the event of a severe burn, call emergency services as soon as possibleIn the event of a severe burn (one which is third degree, encompasses more than 10% of the body or causes intense pain), call emergency services as soon as possible – 000 (Australia), 911 (US). While you await their attendance you can assist the child by taking the following measures:

  • Put the burnt areas of the body under cold running water as soon as possible (this is beneficial even if it cannot be applied immediately).
  • As you cool the skin, quickly remove clothing and jewelry from the burn. If material is stuck to the skin it is important to leave it in place.
  • To prevent hypothermia, do your best to keep the child warm – wrap unburned areas of the body in a blanket and increase the temperature in the room to between 28 and 30 degrees celsius (82-86 degrees fahrenheit).
  • Elevate the burnt body parts.

Medical treatment of severe burns

The amount of skin injured and the depth of a burn will affect how quickly it heals and whether infection or scarring is likely. Burns are usually treated with special dressings to encourage healing. Sometimes ‘wet dressings’ are used, these are slightly moist and contain silver – an antimicrobial agent – to reduce the risk of infection. It is vital that these dressings are kept clean, dry and in place. A medical professional will manage the checking or changing of dressings and provide the child with suitable pain relief.

It can take several days following a burn to ascertain the extent of the damage and for specialists to determine whether further treatment is necessary. Severe burns often require skin grafting, an operation which involves replacing burnt skin with healthy skin from another site on the body to help those areas heal better.

Long term care of burns

As burns heal, their scars can protrude, become red, sore or itchy and restrict movement. Physiotherapists are often employed to minimise the appearance of burn scars and manage their physical effects.

Along with plenty of fluids and rest, a nutritious, varied diet will help to optimise wound healing. A moisturising lotion, such as glycerine and sorbolene, should be applied to the burn scars a minimum of twice daily. This will enhance the healing process by nourishing the fresh skin, keeping it strong and supple.

Children should be discouraged from scratching their scars as this impairs the repair process and can inflict further damage. Your pharmacist or doctor may be able to recommend moisturisers or antihistamines to reduce the irritation of itchy skin. Sun exposure can further injure burns and burn scars, therefore it is important to keep them covered when spending time outdoors.

Preventing burns

Being aware of potential threats and discussing the risks of burns with your family will help with prevention.Ideally, we want to avoid children receiving burns in the first place. The following safety suggestions may help to prevent an incident from occurring:

  • Keep flammable chemicals out of reach of children (preferably in a locked cupboard) and away from flames, sparks and heat.
  • Do not allow young children to handle very hot food or drinks.
  • Teach children how to avoid the hazards of household appliances such as heaters, ovens and irons.
  • If older children are using hot appliances (i.e. sandwich press or hairdryer), show them how to do so safely.
  • Ensure your home is fitted with fire blankets, extinguishers and working smoke detectors.
  • Prepare a fire plan (including exit routes and meeting points) and practice a drill with your children.
  • Make sure that the stove top is never left on unsupervised.
  • Store matches and lighters in a safe place where children cannot access them.
  • Show children the method of “Stop, Drop and Roll” to put out fire on their own clothes or body.
  • Do not allow children near fireworks.
  • When cooking with your child, ensure that they only undertake tasks they are capable of performing safely.
  • Teach your child about the danger of scalds from hot water when bathing and cooking.
  • Decrease the thermostat on your hot water to less than 49 degrees celsius (120 degrees fahrenheit).


The Children’s Hospital at Westmead 2011, ‘Burns and Scalds – Burn Care Advice’, retrieved 7 September 2011, <>.

Healthy Children 2010, ‘Treating and Preventing Burns’, retrieved 7 September 2011, <>.

Healthy Children 2011, ‘First Aid for Burns’, retrieved 7 September 2011, <>.

The Royal Children’s Hospital Melbourne 2010, ‘Burns-general treatment’, retrieved 7 September 2011, <>.


bruises_introBruises are one of the most common and visible injuries, often caused by intense or repeated contact of the skin with another object. Bruises frequently result from falls, accidents or sports injuries, but they may also be indicative of an underlying medical condition. For this reason, parents of children who bruise easily or experience regular, severe or unexplained bruising should seek medical treatment.

What is a bruise?

A bruise is a form of internal bleeding, known medically as a contusion. It is caused when muscle fibres, capillaries and venules (small veins) under the skin are damaged but the skin itself remains intact, causing blood to seep into the surrounding tissue.

The skin around a bruise appears discoloured and is usually more sensitive to touch. Sometimes even light contact will cause pain due to increased pressure on nerve endings within the region, meaning that the body is more receptive to other forms of pressure applied to the area. Bruises typically resolve after approximately two weeks, though additional damage to the area may prolong the healing process.

Colour variation

One of the greatest fascinations with bruises is their change of colour, this is the result of chemical changes in the blood beneath the skin.

Initially bruises appear as red spots, reflecting new blood seeping into the area. As the hemoglobin (a key component in red blood cells) breaks down, it creates new colours in the skin. Firstly a black, blue or purple colour followed by green, yellow and then finally golden brown as the bruise heals. It is quite common for a bruise to have multiple colours at once as the hemoglobin breaks down at different rates in the skin.

Treatment of bruises

Most minor bruises will resolve by themselves over time (normally around two weeks), but it is best to avoid damaging (bumping or prodding) the area further to allow it to heal.A severely bruised elbow. Image: OakleyOriginals on Flickr

The application of a cold compress (ice or ice pack) and raising the affected area immediately following an injury – and for up to 48 hours thereafter – can help to reduce blood flow and thus reduce swelling and bruising. Painkillers, such as paracetamol or ibuprofen, can help to relieve pain caused by more serious bruising.

Extensive bruising could indicate that greater damage has been caused or that an underlying medical condition is contributing to the bruise. In these instances, it is best to seek medical assistance.

Causes of bruising

Certain regular use of medications which thin the blood, including aspirin, can contribute to increased blood flow and more severe bruising. Consult a medical professional if you’re unsure about the effects of a medication.

A number of diseases, including hemophilia, leukemia, thrombocytopenia (low blood platelets), autoimmune diseases (lupus and rheumatoid arthritis), infectious diseases (measles and meningitis) and rarer blood disorders can all cause children to bruise more easily.


American Academy of Orthopaedic Surgeons 2007, ‘Muscle Contusion (Bruise)’, retrieved 18 May 2011, <>.

Robin, S 2011, ‘Diseases That Cause Easy Bruising in Children’, LIVESTRONG.COM, retrieved 18 May 2011, <>.

Shiel, WC 2008, ‘Bumps and Bruises (Contusions and Ecchymoses)’, MedicineNet, retrieved 18 May 2011, <>.

MedlinePlus 2011, ‘Bruise’, retrieved 18 May 2011, <>.

Insect bites and stings

Mosquitoes, bees, wasps, fleas, spiders and ticks are the most common perpetrators of insect bites and stings in children. The symptoms and extent of the reaction your child experiences following a bite or sting will depend largely on how allergic they are, but most pain and irritation is only temporary.

Often there is only slight, transient inflammation (redness and irritation) of the skin in the spot where the insect has bitten or stung. The bite/sting may be sore, tender or itchy and usually resolves within a few days. More intense reactions involve redness and swelling over a larger area which can take a week or so to settle.

Very occasionally a child can have a severe allergic reaction to an insect bite or sting, known as anaphylaxis. Symptoms may include; dizziness, collapse, widespread hives or rashes, nausea or vomiting, swollen lips or tongue, wheezing, coughing and difficulty breathing or swallowing. Anaphylaxis is a medical emergency; seek immediate treatment for the child as these reactions can be fatal. Some people with known allergies carry an oral steroid drug, such as prednisolone, or an injection of epinephrine (“epi-pen”) to treat anaphylaxis. Ensure you know how to locate and administer these medications if you are caring for a child with acute allergy. A medical alert bracelet may also be useful for teenagers or children who are traveling with other guardians (such as teachers or sports coaches).

Treatment for minor insect bites

To care for mild insect bites at home:

  • Gently wash the affected area with clean water
  • Apply an ice/cold pack to minimize pain and swelling (be sure to wrap this in a cloth to prevent skin burn)
  • Apply calamine lotion several times each day to ease itchiness and try to stop your child from scratching when possible
  • Where necessary, oral antihistamines can be given to reduce the skin reaction. Over-the-counter antihistamine medications containing promethazine hydrochloride or cetirizine hydrochloride are usually effective. It is important to speak with your chemist about the particular medication and dose appropriate for your child, as these vary with age.
  • Application of topical steroid creams may also provide your child with some relief; however these often require a prescription from your doctor or discussion with your chemist.
  • Administration of a mild painkiller such as paracetamol or aspirin may help with painful bites.

If an extreme reaction occurs, symptoms persist for longer than a week or the skin becomes infected, seek professional medical advice.

Bee and wasp stings

A bee sting. Image: Waugsberg from Wikimedia commonsGetting stung by a wasp or bee is quite painful and can cause swelling, which may increase over the following 24 hours. Stings are usually sore for several hours and swollen or itchy skin may last for up to a week.

To treat a bee or wasp sting:

  • A bee leaves its stinger in the skin, remove this as quickly as possible. Stingers contain venom and the longer a stinger is in place, the more venom will be injected.
  • Press a wrapped ice pack onto the affected area to minimise the pain and swelling.
  • If the reaction persists for longer than a week or spreads over a large area, consult a medical professional.
  • You will need to take the child to hospital if they have been stung a number of times.

Bee and wasp stings can sometimes cause the extreme reaction, anaphylaxis, if the child is allergic to proteins in the venom. If a child’s lips or tongue begin to swell or they experience trouble breathing or swallowing, seek emergency medical assistance.

Preventing insect bites


Mosquito nets can help protect you from insect bites. Image: FlickrLickr from Wikimedia commonsInsect repellents are an effective way to prevent insect bites when outdoors, though should be applied in moderation. DEET (N,N-Diethyl-meta-toluamide) is the most commonly used active ingredient in insect repellant. Products with a concentration of less than 10 percent are safe for use on children’s skin, however the ingredient should not be used on infants less than two months.

Physical barriers such as mosquito nets are useful when sleeping outdoors or camping, netting can also be fitted to prams. It is a good idea to keep food and rubbish contained to avoid attracting insects (such as ants and wasps); heavily scented soaps, deodorants or perfumes may also entice them. Additionally, you can cover your child’s exposed skin with long pants and tops to protect their skin.


Close windows before turning on lights in a room (this attracts insects) and have screens fitted to open doors or windows. Aerosols containing insecticide can be used to deal with individual insects and automated units can be used to control insects in the home. These devices should be operated in open, ventilated spaces away from children’s regular activities.


The Royal Children’s Hospital Melbourne 2010, Insect bites and stings’, retrieved 14 March 2011, <>.

Sydney Children’s Hospital n.d., ‘Factsheet – Bites and stings’, retrieved 14 March 2011, <>.

Xeroderma Pigmentosum (XP)

Xeroderma Pigmentosum (XP) is a rare, hereditary disease where patients experience skin hypersensitivity to ultraviolet (UV) light. It is characterized by dry skin, increased freckling as well as patches of hypo pigmentation and signs of premature aging. Affected individuals are particularly susceptible to developing actinic keratoses and squamous and basal cell carcinomas due to a defect in or lack of nucleotide excision repair (NER). Eye and neurological problems are likely to occur over time but neurological defects only develop those with the greatest impairment of DNA repair.


Squamous cell carcinoma skin cancer. Patients with XP have an extreme risk of contracting skin cancer.

Squamous cell carcinoma skin cancer. Patients with XP have an extreme risk of contracting skin cancer.

Squamous cell carcinoma skin cancer. Patients with XP have an extreme risk of contracting skin cancer.

There are currently 8 known complementation groups (XPA through to XPG and XPV), all with corresponding defects in their gene products. These groups differ in frequencies, with XPC being fairly common and XPE being relatively rare and severity of the disease, with XPG being severe and XPF being mild.

XP occurs worldwide, with the prevalence of 1 in 250,000 in the general population. It appears to affect men and women equally across all races. However Japan has a higher frequency of the disease with 1 in 40,000 having XP with XPA being the most common variant. The prevalence in the U.S is also 1 in 250,000.

Being a genetic disease, familial history and consanguinity increases the chance of inherited. An estimated 80% of XP sufferers will develop eye abnormalities and 30% will develop neurological disorders.

Mutation prevalence

Whilst mutations occurring in any one of the XP genes can lead to the disease, splice mutations have been found to be more common in the XPA and XPC complementation groups. An estimated 1% of the Japanese population has a splice mutation in exon 3 of the XPA gene and on the other end of the scale; only 2 individuals have been reported to carry mutations in the XPE gene. XPC is the most common form of XP amongst Americans.


XP is an autosomal recessive disease, which means the individual with the disease has inherited two copies of the mutated gene (one from each parent) that causes XP. If only one XP gene is inherited then that person carries of the disease gene but is not affected by it. Having two XP genes causes skin cells to be hypersensitive to UV light, resulting in a range of symptoms.

Essentially, the symptoms are caused by faulty DNA repair mechanisms in the skin. A defect in nucleotide excision repair (NER) results in an inefficient DNA repair mechanism in XP. Sun exposure damages DNA. As the cells are unable to repair it, the DNA remains damaged, which leads to cell death or the development of cancerous cells.

XP can be separated into 8 different groups based on what and where the mutation is. Each can vary in symptoms and have different susceptibilities to developing certain symptoms. Neurological abnormalities have only been seen in XP patients with mutations in the complementation groups XPA, XPB, XPD and XPG.

DNA damage and NER in-depth

The majority of DNA damage is induced by UVB light but recently UVA rays have also been linked to the same mutations. The most common forms of DNA damage occurs via the cross linking of adjacent pyrimidines resulting in the formation of cyclobutane pyrimidine dimers (CPDs) and 6-pyrimidine-4-pyrimidone photoproducts. Mutations caused are almost always located at the interface of pyrimidine-pyrimidine interactions, characterized by C to T, C to C or T to T sequence.

The electromagnetic spectrum highlighting UV radiation which causes skin damage.

The electromagnetic spectrum highlighting UV radiation which causes skin damage.

NER repairs mutations caused by UV light. NER can be divided into two subtypes; global genome repair (GGR) that can function throughout the entire genome and transcription-coupled repair (TCR) that is restricted to the transcribed strand of active genes. 7 out of 8 groups of XP genes are involved with NER and if one or more of those genes are mutated, the repair process is disrupted. XPV is a variant of XP and does not affect NER. Instead, there is a defect in DNA polymerase ? which alters post replication repair. NER functions by removing and replacing damaged DNA with newly synthesized DNA. It begins with a detection phase, performed in GGR by a complex involving the product of the XPC gene and another factor. In addition, the XPA gene product has been reported to have an affinity for damaged DNA. Therefore, it is likely that XPA has a role in the damage detection phase. When DNA damage is detected, Transcription factor II H (TFIIH) helicases unwind the DNA. The XPG gene product forms an open complex called the ‘pre-incision complex’. XPB and XPD gene products are part of a 9-subunit protein complex (TFIIH) that is also needed for the open complex formation. After the assembly of the pre-incision complex, single strand incisions are made in the damaged strand by complexes involving the XPG and XPF genes which encode endonucleases. Subsequently the damaged DNA is removed and the resulting gap is filled in with new DNA by the DNA polymerases and DNA ligase.

The NER genes that encode XPB and XPD are a part of the TFIIH basal transcription factor and are essential to life.

Three stages of XP

Figure 1. Xeroderma Pigmentosum. (Warning: graphic medical content)

Figure 1. Xeroderma Pigmentosum. (Warning: graphic medical content)

At birth, the skin appears normal. Onset of the disease usually begins at around 6 months and generally progresses through 3 stages.

Stage 1 is usually demonstrated by about 6 months with the following signs:

  • Areas exposed to the sun show diffuse erythema and freckling;
  • Irregular dark spots may begin to appear;
  • Xerosis and scaling may follow.

Continuous sun exposure will lead to stage 2.

Stage 2 is presented as poikiloderma, which is a result of an accumulation of actinic changes. Often, it appears at the median age of 2 and is characterized by the following:

  • Solar lentigines;
  • Skin atrophy and thinning;
  • Telangiectasias;
  • Patches of hypopigmentation and hyperpigmentation.

Stage 3 is the development of actinic keratoses and skin cancer. This stage may occur as early as 4-5 years or as late as adolescence.


Figure 2. Xeroderma Pigmentosum. (Warning: graphic medical content)

Figure 2. Xeroderma Pigmentosum. (Warning: graphic medical content)


XP normally presents early after birth, with it extreme sun sensitivity being detected at the age of 1-2 years. Freckling from sun exposure typically occurs in young children with XP which rarely occurs in normal children. The accumulation of DNA damage results in many other symptoms including:

  • Diffuse redness
  • Sunburn from minimal sun exposure
  • Dry, scaly skin
  • Thin skin
  • Patches of discolored skin
  • Talangiectasias


Individuals with XP have a 1,000 fold risk of developing skin cancer then the normal population. It will typically manifest before the age of 20 and is common in XP. Skin cancers are more prevalent in sun exposed patches of skin such as the face, neck and forearms. There is also a 10 – 20 fold increase in the likelihood of developing cancer or tumors affecting internal organs.

Eye abnormalities

Any structure of the eye can develop abnormalities from UV exposure. Many individuals experience:

 XP Electromagnetic spectrum of UVA & UVB

XP Electromagnetic spectrum of UVA & UVB

  • Photophobia – pain/discomfort from light
  • Conjunctivitis
  • Loss of vision
  • Irritation
  • Loss of eyelashes
  • Blepharitis – inflammation of the eyelids
  • Keratits – inflammation of the cornea

Patients also have an increased risk of developing cancerous or non cancerous growths in the eye

Neurological Disorders

Neurological disorders mainly occur due to neuronal degeneration and are only seen in particular subsets of XP with symptoms varying in severity. The most common abnormality is a loss of high-frequency hearing. Other neurological defects include poor co-ordination, decreased reflex responses (hyporeflexia), progressive mental retardation, seizures and spasticity.

Differential Diagnoses

The NER pathway involves many genes including the XP genes. Because of this, other rare disorders that have defects in NER such as Trichothiodystrophy (TTD) and Cockayne syndrome (CS) can be mistaken for XP and vice versa. The clinical features of these patients have some similarities and but also have marked differences. While XP patients have 1000-fold increase in risk of developing to skin cancer, TTD and CS patients don’t. Several of the genes involved in NER also affect somatic growth and developments, meaning some patients have growth retardation and immature sexual development. Progressive loss of hearing is also a feature of XP and CS. Neurological abnormalities in XP are primarily due to neuronal degeneration. In contrast, CS and TTD patients have reduced myelination of the neurons in the brain which are unrelated to sun exposure but could be due to faulty DNA repair mechanisms.


Being a genetic disorder there is no curative treatment. Preventative therapy must begin immediately upon diagnosis, which is usually in childhood. This means minimal exposure to the sun where possible and using a combination of UV protection such as complete coverage from the sun with clothing and hats, UV-protective glasses and constant application of sunscreen (SPF30+ or above is recommended).

Skin treatment

Manifestations of the condition are treatable but there is no guarantee that the symptoms will not recur. Larger areas of sun damaged skin may be removed by dermabrasion to remove the superficial layers of skin. This allows for regeneration of the population of skin cells that were not affected by UV rays.

Avoidance of the sun is crucial in preventing the symptoms seen in the skin. However, XP progresses to skin cancer then standard anti-cancer therapies would be used such as topical 5-fluorouracil, freezing with liquid nitrogen or surgical excision of the cancerous cells. If other malignancies develop they would be treated in the same manner as cancer patients without XP. Physicians may also prescribe medications such as high-dose oral Isotretinoin to prevent new cancers from forming, but there are toxic side effects to this treatment.

It is also recommended that frequent skin examinations are performed in order for early detection of any new lesions and monitor any growths for changes in shape, color and size.

Ocular treatment

Corneal transplantation has been successful in restoring vision to those with corneal opacities and severe keratitis, however immunosuppressive therapy is necessary in order to prevent rejection and can increase the chance of infections. Abnormal growths in the eye and tissue surrounding the eye would be treated surgically.

Neurological treatment

Neurological treatment is restricted due to lack of known treatments as well as fact that many drugs cannot get into to brain or they would cause too many unwanted side effects. Drug use for these symptoms is limited to anticonvulsants such as Phenytoin to prevent seizures.

Experimental treatments

Recently novel enzyme and gene therapies have been developed based on the etiology of XP. T4N5, a bacteriophage T4 endonuclease 5 has been utilized for topical therapy in a liposomal lotion. It is able to diffuse into the nucleus without a nuclear localization sequence and enables NER to recognize and cleave CPDs using light energy. This lotion holds significant promise for those with XP, receiving a Fast Track designation from the FDA.

Gene therapy using recombinant retroviruses carrying additional DNA repair genes to correct damaged cells and restore the capacity of NER are still being developed with aims of validating the procedure.


Due to its genetic basis, XP cannot be prevented. Carriers of the disease are asymptomatic and need not worry. Preventative therapy can slow down the progression of the disease and must begin immediately upon diagnosis, which is usually in childhood by the age of 2. This means minimal exposure to the sun where possible and using a combination of UV protection such as complete coverage from the sun with clothing and hats, UV-protective glasses and constant application of sunscreen (SPF30+ or above is recommended).

As individuals with XP have cells that are hypersensitive to environmental mutagens, cigarette smoke and alcohol should be avoided. It has also been reported that some individuals with XPV are sensitive to caffeine and it increases the amount of defective DNA repair.


Many patients with XP die at an early age from skin cancers and less than 40% will live past the age of 20. However, if a person is diagnosed early, does not have severe neurological symptoms and takes all the precautionary measures to avoid exposure to UV light, they may survive beyond that age.


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  • Kramer, K H, (2008) ‘Xeroderma Pigmentosum’. [Online]. [Accessed 28/11/2008, no longer online].
  • Kramer, K H, et al. (2007) ‘Xeroderma Pigmentosum, Trichothiodystrophy and Cockrayne syndrome: a complex genotype-phenotype relationship’. Neuroscience, Vol 145, pp.1388-1396.
  • Lichon, V (2007) ‘Xeroderma Pigmentosum: beyond skin cancer’ Journal of Drugs in Dermatology, Vol 6, pp.281-288.
  • Sugasawa, K (2008) ‘Xeroderma Pigmentosum genes: functions inside and outside of DNA repair’ Carcinogensis, Vol 29, pp.455-465.
  • Zahid, S, Brownell, I (2008) ‘Repairing DNA damage in Xeroderma Pigmentosum: T4N5 lotion and gene therapy’. Journal of Drugs in Dermatology, Vol 7, pp.405-408.
  • Zeng, L, et al. (1997) ‘Retrovirus-mediated gene transfer corrects DNA repair defect of xeroderma pigmentosum cells of complementation groups A, B and C’. Gene Therapy, Vol 6, pp.1077-1084.
Urticaria Pigmentosa (UP)

Urticaria pigmentosa (UP) is a rare disease that affects the skin and occasionally other parts of the body. UP is a type of mastocytosis (also known as mastocytoma), which affects a sub-type of immune cells known as mast cells. UP is characterised by skin lesions and itching. Mast cells are formed in the bone marrow from pluripotent stem cells, under the influence of stem cell factor (SCF). SCF aids mast cell proliferation and survival. Mast cells are the primary effector cells in immunoglobulin E (IgE) mediated inflammatory reactions. They have been implicated both in innate and acquired immune responses. Mastocytosis is characterised by a pathological accumulation of mast cells and associated symptoms.

Hives may form if the skin lesions are rubbed or stroked. In addition to the skin, the bone marrow, liver, spleen, lymph nodes, or the gastrointestinal tract may be affected in rare cases of UP.


The exact number of affected individuals with urticaria pigmentosa is unknown, but the disease is rare. It has been estimated that mastocytosis, of which UP is the most common sub-type, is present in 1 in 1000 to 1 in 8000 individuals who attend a dermatology clinic. The disease is more common in children than in adults. About 75% of cases occur during infancy or early childhood. Incidence peaks again in mid-adulthood (30 to 49 years).

Childhood UP usually resolves or becomes less severe before adulthood. Conversely, adults with UP may develop a more aggressive form of the disease with a prolonged clinical course and systemic involvement. Men are slightly more frequently affected by UP than women. Also, UP is more common in Caucasians compared with other races.


Urticaria pigmentosa is caused by an excess of inflammatory mast cells, which are made in the bone marrow and help fight infections. Mast cells, when activated, release a compound called histamine, which causes swelling, itchiness and redness in the affected area. It is not known what causes the excess of mast cells that characterises UP, but environmental triggers have been identified that activate mast cells and cause symptoms associated with UP. These include:

  • Stress;
  • Physical stimuli, such as heat or cold, exercise and sunlight;
  • Venoms, such as bee stings;
  • Certain foods, such as lobster, crayfish, cheese, hot beverages and spicy foods;
  • Alcohol; and
  • Certain drugs, such as narcotics and quinine.

Cellular involvement in urticaria pigmentosa

The mechanisms involved in the pathogenesis of UP is not known. Increased mast cell growth factors in skin lesions of UP are thought to stimulate mast cell proliferation, melanocyte proliferation and the production of melanin pigment. The hyperpigmentation associated with UP can be attributed to melanocyte proliferation and melanin production. It has been hypothesized that BCL-2, a protein that prevents apoptosis, is upregulated in patients with UP and other forms of mastocytosis, leading to a reduction in mast cell apoptosis. Mutations in the proto-oncogene, KIT, which encodes a cytokine receptor that binds to stem cell factor and allows mast cell proliferation and survival, have been identified in patients with UP. The precise role of these mutations in the disease process is not clear. Interleukin-6 is elevated in patients with UP and is correlated with the severity of the condition. The systemic involvement of UP is thought to be mediated by mast cell-derived modulators, such as histamine and prostaglandins. Mast cell infiltration can also explain the development of extra-cutaneous symptoms.


Urticaria pigmentosa can affect any part of the skin, but usually involves the trunk. Urticaria pigmentosa usually appears as lesions (macules), yellow-tan to red-brown in colour, with the trunk almost selectively affected. Limbs and face may be affected, but rarely so. The size of the lesions can range from 1 mm to several centimeters. Once UP becomes widespread, the lesions become symmetrical.

On the skin, UP may appear as

  • Freckle like brown patches;
  • Nodules (lumps), papules or plaques
  • Itchy rashes;
  • Hives or welts may arise if the lesions are rubbed or scratched. This phenomenon is known as the Darier sign and the presence of Darier sign may aid in the diagnosis of mastocytosis;
  • Blister formation; and/or
  • Flushing of the face

Rarely, if other parts of the body are involved, UP can cause:

  • Diarrhea;
  • Fast heart rate;
  • Fainting due to low blood pressure; or
  • Rarely, some adults may develop telangiectasia eruptive macularis perstans (TEMP). TEMP is associated with red macules that overlie dilated capillaries (i.e. telangiectasia).

Systemic involvement

In adults UP can cause systemic involvement, severe allergic reaction and, rarely, death. About 85% of individuals with all forms of systemic mastocytosis have UP as a characteristic feature. About 15 – 30% of adults with skin lesions have extra-cutaneous symptoms. Headache and itching are common symptoms. Involvement of the vasculature can lead to palpitations, lightheadedness (due to hypotension) and syncope. If the gastrointestinal system is affected, nausea, vomiting, abdominal pain, diarrhoea, gastritis and peptic ulcers can occur. Hepatomegaly and splenomegaly with mast cell infiltration is often present. Lymphadenopathy is present in some cases. Involvement of the bone marrow can lead to fractures, anaemia and osteoporosis.

It should be noted that the systemic symptoms mentioned above are very rare in individuals diagnosed with UP, but may occur with other forms of mastocytosis, such as aggressive systemic mastocytosis.

Darier sign

When the lesions are rubbed or scratched, welt or hives formation can occur on the skin. This is known as the Darier sign and is useful in the diagnosis of UP and other mastocytotic disorders.


Diagnosis of UP is based on the appearance of the skin, the presence of the Darier sign, elevated levels of urine histamine and skin biopsy that confirms the presence of increased numbers of mast cells.


Identifying and avoiding the environmental triggers may be sufficient in preventing the symptoms of mild forms of urticaria pigmentosa. If treatment is required, as in the more severe cases, the following options are available:

  • Antihistamines, with H1 angtagonists used to relieve skin symptoms, itching and flushing and H2 antagonists used to treat hyperacidity that may occur in patients with UP. For anaphylaxis, both H1 and H2 antagonists need to be used. In the rare, but severe, possibility of anaphylaxis, a medical alert bracelet must be worn and an injectable adrenaline (epinephrine) solution should be carried at all times. A similar course of action is needed if circulatory collapse and shock occurs.
  • Mast cell stabilizers, such as Disodium cromoglicate, inhibit mast cell degranulation following exposure to specific antigens. These agents improve diarrhoea, abdominal pain, headaches and bone pain associated with UP. Several weeks of treatment may be needed before improvement in symptoms is noticed.
  • Low-dose aspirin may help, although in some cases, exacerbations can occur. Treatment with low-dose aspirin is usually restricted to patients with vascular collapse who are unresponsive to H1 and H2 antagonists, as aspirin has the potential to cause degranulation of mast cells and worsen the symptoms.
  • Photochemotherapy, or PUVA, utilizes long wave UVA radiation (340 – 400 nm) for the treatment of UP. Irradiated skin shows a reduction in mast cells. Two to three treatments are required each week for several months. PUVA reduces the severity of pruritis and improves the appearance of skin lesions. Recurrence is likely to occur within 12 months and further PUVA therapy may be necessary.Topical steroids;
  • High potency topical steroids may offer transient relief from symptoms, especially with pruritis. The lesions, however, invariably tend to recur. For severe UP with systemic involvement, systemic steroids may be necessary.


The precise causes of urticaria pigmentosa are unknown and, therefore, the disease cannot be prevented or cured. It is, however, possible to identify factors that may trigger UP and to circumvent them. Certain foods, physical exertion and stress are potential triggers in exacerbating UP and these should be avoided. Lesions should not be rubbed or scratched, as this may cause hives. In rare cases, where anaphylactic reactions can occur, patients need to be educated about symptoms and treatments, including the use of injectable adrenaline (also known as epinephrine), or EpiPen, where necessary. If extra-cutaneous (beyond the skin) involvement is present, it is important to regularly review the progress of the condition.


The prognosis of urticaria pigmentosa depends on the age of onset. UP generally begins during infancy or early childhood. The prognosis of childhood-onset UP is good, with resolution of the disease, or marked improvement in symptoms before adulthood. If UP begins in late-childhood or during adulthood, the prognosis is poor, as the disease tends to be persistent with systemic involvement. Haematological malignancies are a severe, but remote, possibility.


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  • Simon, J C, Pfieger, D & Schopf, E (2000). ‘Recent advances in phototherapy’. European Journal of Dermatology, Vol 10(8), pp. 642-645.
  • Slavkovic-Jovanovic, M, Jovanovic, D, Petrovic, A & Mihailovic, D (2008). ‘Utricaria Pigmentosa: a case report’. ACTA Dermatovenereologica APA, Vol 17(2), pp. 79-82.
Solar urticaria (SU)
Solar Urticaria reaction on skin

Solar Urticaria reaction on skin

Solar urticaria (SU) is a rare, sunlight or UV induced hypersensitivity (allergic) reaction that causes wheals (raised red skin welts) very soon after or during sun or light exposure. In solar urticaria, the reaction is triggered by exposure to UV or visible light. It may be severely disabling and can even be life threatening.


Solar urticaria is rare but occurs worldwide. 3.1 per 100,000 people are affected and females are more likely to be affected than males.


Following limited exposure to sunlight, sufferers may develop an itchy or burning redness on exposed skin. Initial presentation has also been reported after first solarium use.

Symptoms usually develop within five minutes of sun/UV exposure and often develop from an unpleasant sensation to itching, redness and swelling, followed by localized or widespread development of wheals (an urticarial flare). Gradual resolution then follows over 1-2 hours.

Rarely, a more prolonged exposure may be required for symptoms to develop, or the onset of symptoms may be delayed for several hours. With extensive whealing some patients also experience headache, nausea, bronchospasm (asthma-type respiratory symptoms) and syncope (dizziness) which may become life threatening (although this is rare). Conversely, in some people with mild disease, or in those who quickly recognize their onset and avoid further exposure, whealing may not be reported.

Sun-exposed areas are most commonly affected, although occasionally reactions are seen in dermal areas that are not exposed to the sun. Rarely sun-exposed sites are spared suggesting that tolerance may occur.


Solar urticaria may be primary or secondary.

Primary solar urticaria is an immediate hypersensitivity response (IgE mediated allergic reaction) towards an allergen (a compound produced in the body when UV light is absorbed by a cellular pre-cursor) induced in the body following sunlight exposure. The responsible allergen is not know but is termed a photoallergen. The allergic reaction that follows prolonged sunlight exposure leads to a widespread inflammatory response.

Mast cell degranulation and histamine release are important factors in SU but many other inflammatory cells, particularly neutrophils and eosinophils are involved in amplifying the whealing response.

Many wavelengths light may trigger the production of different photoallergens but SU is most commonly caused by UVA or visible light. There appears to be no genetic basis for this condition.

Very rarely, secondary solar urticaria occurs in association with other photosensitivity disorders, such as cutaneous porphyria or lupus, or with certain medications known to cause photosensitivity.


Complete potential action spectrum for Solar Urticaria

Complete potential action spectrum for Solar Urticaria

Phototesting confirms the diagnosis and reveals the wavelengths responsible for inducing an urticarial response. Phototesting may be performed with a monochromator (single wavelengths of light selected at a time), broad spectrum source or natural sunlight to estimate the minimal urticarial dose (MUD) of light required to induce symptoms. Screening tests to exclude lupus (ANA,eNA) and cutaneous porphyria (porphyrin studies) must be done to exclude these conditions. Medications must also be considered as a possible cause.

Differential diagnosis

  • Cutaneous lupus
  • Polymorphic light eruption (PLE)
  • Photo-exacerbated dermatoses i.e. eczema
  • Other physical urticarias


Treatment of solar urticaria is usually directed towards relief of symptoms and avoidance of their onset through behavioural change. High doses of H1-antihistamines taken an hour before sun exposure are very effective in one third of patients and give another third partial relief.

Avoidance of sunlight, photoprotective clothing and broad-spectrum sunscreens are necessary to prevent symptoms; however this may not always be useful in cases where visible light is responsible for the solar urticaria.

Desensitisation with phototherapy may be useful for some patients however therapy generally needs to be continued to maintain its benefit and so consequently carries a risk of long-term risks such as skin cancers. In severely affected individuals, this treatment also carries the risk of disease onset and anaphylaxis (severe, often life threatening allergic reaction) and so should be undertaken with extreme caution.

In extreme cases these patients need to be hospitalized to undergo plasmaphoresis (a procedure similar to dialysis where the plasma in their blood is removed and the blood cells are returned to the patient). Immunosuppressant medications such as Cyclosporin and intravenous immunoglobulins may also need to be considered in the most severe cases.


For the majority of patients symptoms will persist indefinitely. For a small proportion of patients solar urticaria will deteriorate however some do experience improvement with an estimated 26% chance of resolution at 10 years.


  • Dice, J P. (2004). ‘Physical Urticaria’, Immunology and Allergy Clinics of North America, 24, pp225-246.
  • Roelandts, R (2003). ‘Diagnosis and treatment of solar urticaria” Dermatologic Therapy, pp52-56.
  • Beattie, P E, Dawe, R S, Ibbotson, S H, & Ferguson, J. (2003) ‘Characteristics and prognosis of idiopathic solar urticaria: A cohort of 87 cases’, Archives of Dermatology. 139 (9), pp1149-1154.
  • Buxton, P K, (2003). ABC of Dermatology. London: BMJ Publishing Group Ltd.
  • Ng, J H C, Foley, P A, Crouch, R B, & Baker, C S. (2002). ‘Changes of Photosensitivity and Action Spectrum with Time in Solar Urticaria’, Photodermatology, Photoimmunology & Photomedicine, 18, pp191-195.
Porphyria Cutanea Tarda (PCT)

Porphyria cutanea tarda (PCT) is the most frequently seen disease of a group of disorders (the Porphyrias) that can be acquired or inherited. It is caused by low levels of an enzyme (uroporphyrinogen decarboxylase or UROD) involved in the production of haem (heme).

Haem is a component of hemoglobin in red blood cells and is vital as it needs it to carry oxygen around the body. These result in a build-up of chemicals called porphyrins. In PCT, porphyrins accumulate in the skin, causing the skin to be very sensitive to light (photosensitive).

In PCT, porphyrins accumulate in the skin, causing the skin to be very sensitive to light (photosensitive), causing blistering of the skin in areas that receive higher levels of exposure to sunlight.


Haem Synthesis Pathway

Haem Synthesis Pathway

Porphyria cutanea tarda is the most common of all the Porphyrias and occurs throughout the world, yet PCT is considered to be an uncommon condition, affecting about 1 in 25,000 of the population. All races are equally affected.

Before the widespread use of oestrogens in hormone replacement therapies and oral contraceptives, the disease developed predominantly in males but the incidence among sexes is approximately equal now. It should also be noted that males that are on oestrogen therapy have also developed PCT. Age of onset is usually around the ages of 30 – 40; to see the disorder before puberty it quite unusual.

An estimated 80% of porphyria cutanea tarda sufferers have sporadic PCT (Type I – acquired, not inherited) and the remaining 20% have familial PCT (Type II – inherited). Onset of the disease is usually in late adulthood between the ages of 30 – 40 years. It is unusual for the disease to manifest before puberty.


Porphyria cutanea tarda is caused by either an inherited or acquired deficiency of Uroporphyrin Decarboxylase (UROD), the enzyme involved in fifth step of haem synthesis. A decreased level of UROD causes accumulation of haem building-blocks (porphyrins) that have failed to be incorporated into haem. The porphyrins build up in the skin where they absorb both visible and ultraviolet light, causing the main symptoms of PCT. Porphyrin accumulation does not occur in normal people.

Not all family members that inherit the gene mutations associated with PCT will present with the disorder, therefore it is proposed that PCT requires other factors that increase the production of porphyrins to be present as well.

Most classifications of PCT separate it into two types, in which both are associated with low UROD activity.

  • Type I – Sporadic or acquired PCT. It encompasses around 80% of cases. The enzyme deficiency is restricted to the liver with an approximated 50% of UROD levels. Acquired PCT occurs most commonly in patients who also have haemochromatosis or chronic hepatitis C infection. This form most often occurs after use of alcohol, oestrogens, oral contraceptives, other drugs and certain environmental pollutants but sometimes no cause can be found. Most people who consume alcohol and take estrogens do not develop a porphyria; therefore, it is likely that genetic factors are of higher importance even though there is no family history of PCT.
  • Type II – Familial or hereditary. This type of PCT is an autosomal dominant disorder but inheritance of the mutated gene/s does not necessarily mean expression of skin disease nor can it predict the severity of the condition.The UROD gene has been mapped to chromosome 1p34. Mutations have been identified in the UROD gene, including DNA base substitutions and deletions. These mutations result in reduced activity of the enzyme. Some mutations result in PCT and others result in the recessively inherited HEP. HEP is the homozygous forms of familial PCT. Levels of UROD are also decreased to approximately to 50% in all tissues although porphyrins only accumulate in the liver. Many UROD mutations have been identified in patients with familial PCT and most carriers of mutant UROD alleles do not express a clinical phenotype unless additional factors are present.

Numerous precipitating factors are known to contribute to the development of both types of PCT. Each of these is discussed briefly in the following sections.


Ethanol has long been recognized to precipitate PCT. It has been shown to induce the hepatic enzyme ALA-synthase in patients along with diminished UROD activity after acute ingestion or in those who are chorinic alcoholics. Alcohol and cyclic hydrocarbons may also induce the ALA-synthetase gene, increasing Urogen, the precursor of UROD inhibitors thereby also decrease the activity of available UROD. Chronic alcoholism can also lead to the suppression of erythropoesis and increased absorption of dietary iron.


The important role of iron the in the pathogenesis of PCT is confirmed by elevated levels of ferritin and serum iron in individuals with PCT. Hepatic iron overload is almost present in all cases of PCT with total iron stores being approximately twice of normal levels. PCT is particularly common in those with alcoholism and iron overload together.

There are many complex hypotheses proposed about iron and its role in PCT pathogenesis:

  • It may directly inhibit UROD.
  • An ionic state of iron acts as a catalyst for the formation if reactive oxygen species that can cause lipid peroxidation and damage the lipid rich membranes of microsomes and mitochondria in the liver.
  • Increased mutations in the HFE gene (encodes a human leukocyte antigen class I-like protein) have been found in British patients with type I PCT. This hemochromatosis mutation appears to be responsible for iron overload in many populations.
  • Induction of the enzyme ALA-synthase by iron could also participate in the accumulation of porphyrins.

Reduction of iron levels has been shown to lead to the improvement or remission of many cutaneous lesions.

Viral infections

Research has found an association between human immunodeficiency virus (HIV) and hepatitis C virus (HCV). Their roles in the pathogenesis of PCT is unclear but it has been suggested that chronic viral hepatitis may cause increased deposition of iron in the liver, which has been observed in biopsy specimens from patients with chronic hepatitis C.


The role of oestrogens in PCT is also unclear but an association between the use of oral contraceptives containing oestrogen and hormone supplements for both males, as an adjunct therapy for prostatic cancer and females, as post-menopausal hormone replacement therapy, has been found.

From the known of the affects from the above factors, it is possible that all or any of these could contribute to the excessive porphyrinogenesis characteristic of PCT.


The main clinical manifestation is blistering of the skin of sun-exposed areas, such as the back of the hands, forearms, face, ears, and neck. The skin becomes increasingly sensitive and fragile and any minor trauma leads to lesions and ulcerations that can become crusty and result in scarring when they resolve. Numerous small milia (cysts commonly known as ‘milk spots’) can also develop and patients find that they become very sensitive to light. This photosensitivity is due to the overproduction of porphyrins in the liver, due to the enzyme deficiency. They then leak out into the blood and build up in the skin, absorbing both UV and visible light. Other skin changes that can be seen include hyper or hypopigmentation, particularly on the face in spotty of diffuse patterns. Sclerodermoid plaques can also develop on sun exposed areas. These come in the form of scattered, white to yellow waxy plaques.

Hypertrichosis is frequently observed on the cheeks, temples, eyebrows and, less frequently, arms, legs and trunk. The hair can vary from a fine or course texture, vary in length and differ in colour. The hair may continue to grow, darken or thicken and is more apparent in females. Males often complain about changes in growth pattern of their beards and difficulty in shaving.


There is no curative treatment for porphyria cutanea tarda but avoidance of trigger factors that may have caused exacerbation of the disease can result in improvement. The main focus of treatment is to remove or decrease any triggers for PCT, reduce iron levels and to remove the excess porphyrin that has accumulated in the body. Avoidance of sunlight, alcohol and oestrogens and paying attention to skin care is particularly helpful in PCT. The most widely recommended treatment is repeated phlebotomies (removal of blood, see below) to deplete excess iron levels in the liver, thereby effectively reducing iron stores in the body. Antimalarials, chloroquine or hydroxychloroquin, are another approach to treatment when phlebotomies are contraindicated in patients with other medical conditions, as these work to increase porphyrin excretion through the urine.

If there is an inadequate response to either treatment alone, a combination of both therapies is used. Any viral infections found to be present should be treated accordingly.


Phlebotomies are the treatment of choice for PCT. It is effective because it depletes the excessive stores of iron in the liver and reducing iron levels in the body. Phlemboomies are considered safe and are associated with minimum morbidity. The amount of blood removed varies but is repeated every 2nd or every 3rd week; shorter intervals unnecessarily risk causing anemia. When serum iron or ferritin levels fall slightly below normal, phlebotomy is stopped. Usually, only 5 to 6 sessions are needed. Urine and plasma porphyrins fall gradually with treatment and continue to fall even after therapy is stopped. The skin eventually returns to normal but this can take several months to several years. After remission, further phlebotomy is needed only if there is a recurrence.


Phlebotomies are contraindicated in some patients because of the presence of anemia and cardiovascular disorders. Instead, low dose antimalarials such as chloroquine and hydroxychloroquine as used. They work by removing excess porphyrins from the liver by increasing the excretion rate. The mechanism might relate to forming water solubledrug-porphyrin complexes that are easily excreted. Remission can be seen within 6-12 months. Originally, higher doses were used to treat the condition but are no longer recommended because of liver toxicity.


If a trigger factor has been identified to have set off the disease then effort should be taken to reduce or eliminate exposure to that factor. Patients should avoid sun exposure where possible. Typical sunscreens that block UV light are ineffective, but UVA-absorbing sunscreens may be more beneficial. Wearing a hat and protective clothing is also highly recommended and considered the best form of protection from the sun.

Alcohol ingestion should be avoided permanently, but oestrogen supplementation can usually be resumed safely after the disease undergoes remission.

These treatments are not suitable for PCT patients who have advance renal disease. This is because there is usually underlying anemia and since renal activity is already low, drug-porphyrin complexes are not filtered out by the kidneys. The use of human recombinant erythropoietin mobilizes and reduces excess iron. It resolves the anemia enough to permit successful low volume phlebotomy.


Porphyria cutanea tarda is an important medical condition because it can be disfiguring if skin lesions are not treated. Remission can be achieved through avoidance of trigger factors or treatment and any reoccurrences respond well to the same treatments.


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Hydroa Vacciniforme (HV)

Hydroa vacciniforme (HV) is a rare, chronic photosensitivity disorder which chiefly occurs in children. The disease is characterised by the eruption of inflamed bumps and fluid-filled blisters (vesicles) on the skin following exposure to sunlight. Commonly presenting on the face, ears and hands, these vesicles heal over time as pox-like or “vacciniform” scars. Ultraviolet A (UVA) radiation (320-400nm) is the main wavelength of light which has been demonstrated to induce symptoms.

Figure 1. Blisters/lesions in a HV patient

Figure 1. Blisters/lesions in a HV patient

HV was first described in 1862 in France by Antoine Pierre Ernest Bazin and Emile Baudot. The vast majority of cases begin in childhood and resolve spontaneously in adolescence or early adulthood. The disease is not fatal, however, due to its prevalence in pediatric patients, the level of discomfort suffered and the long-term scarring which results, HV is considered to have a high impact upon patient quality of life.


HV is a rare disease and prevalence data is limited, but in Scotland rates are reported as approximately one in 300,000. Occurring predominantly in children aged 3-15, one study indicates a median onset age of 7.9 years for HV. A few cases have also been reported in infants and elderly people up to 60 years of age. There is a higher incidence of HV in females and the disease also presents at a younger age in female patients than in males. It has been found, however, that there is a longer course of the disease in males.


The exact cause of HV is unknown, though the distribution of the lesions on sun exposed areas of skin tend to suggest a causal relationship with sunlight. Reproduction of HV papules following repeated exposure to artificial sources of UV light indicates that UVA is the wavelength responsible for the symptoms. While the precise pathologic mechanism is unknown, HV is believed to be caused by an auto-immune disorder. Hence, it is classified along with polymorphic light eruption, actinic prurigo, chronic actinic dermatitis and solar urticaria as an IMP or “immunologically mediated photodermatosis”. These are a group of immune-influenced diseases which elicit symptoms in the skin upon exposure to light, mainly that in the UVA spectrum.

Figure 2. Child with HV scars

Figure 2. Child with HV scars

There have been two familial cases of HV in siblings which have led to the notion of there being a genetic component to the disease, though further study is required to substantiate this theory. In addition, a single case has been reported following treatment with the immunosuppressant drug “cyclosporine”. Due to the inconsistent responses to a broad range of treatments and disparity in the ages of onset/remission, some also speculate that HV may be a disease arising from different origins that present as a similar clinical syndrome.


The first symptoms of HV generally appear on the cheeks and nose in the spring or summer months, though can occur on any sun-exposed skin. Initially patients will experience a mild burning or tingling sensation, this has also been described as stinging and itching. Erythema (redness of skin caused by inflammation) leads to the development of multiple small blisters, bumps or lesions within 30 minutes to 2 hours following sun exposure. These lesions are originally taut and swollen with accumulated fluid then slowly form necrotic, pox-like crusts and scabs (sometimes blackish in colour). They heal over several days, eventually becoming light or unpigmented scars which tend to be depressed or indented; these may last for a number of years. The vesicles, or blisters, recur upon subsequent exposure to solar radiation.

Figure 3. Child with HV blisters

Figure 3. Child with HV blisters

Some HV patients experience ocular problems – light sensitivity (photophobia), mild inflammation of the eyes (keratoconjunctivitis) and clouding/inflammation of the cornea (the front part of the eye), known as keratitis. Uncommon symptoms, described by only a couple of patients, include: bone and cartilage reabsorption, earlobe mutilation, separation of nails from their nail-beds and systemic (whole-body) effects.

A high rate of Epstein-Barr Virus (EBV) infection in HV patients has been reported in medical literature. The pathological association between the disease and the virus is unclear, though one theory is that the disease is mediated by the T-cells of the immune system which can become infected with EBV. One study revealed that individuals with severe HV had more chronic, active infections, whereas those with more subtle forms of the disease tended to have mild or latent infections.

Severe forms of HV-like eruptions have been linked with an aggressive type of T-cell lymphoma (EBV-associated) mainly found in children from Asia and Latin America. While some researchers claim that HV can evolve into T-cell lymphoma, most insist that this is a disease distinct from the classical HV.

Diagnosis and Treatment

HV diagnosis is difficult since the characteristic lesions are similar to those produced by other skin disorders such as porphyria and polymorphous light eruption. Repetitive UVA phototesting involves deliberately exposing a section of skin to an artificial source of UVA radiation to determine the cutaneous reaction generated. This is the best available method of diagnosis, though it is by no means definitive.

A range of preventative treatments have been employed with efficacy varying between patients. To date, no consistent therapy has been discovered. The mainstay of treatment remains photoprotection of skin; with UVA blocking sunscreens, tight-weave, sun-protective clothing (including wide brimmed hats) and avoidance of sunlight. When lesions occur they are usually treated with wet dressings and topical antibiotics.

The following treatments have been trialed with varying success:
Narrowband and broadband UVB phototherapy – The aim of UVB phototherapy is to harden the skin of HV patients against the lesion-inducing effects of UVA radiation without provoking symptoms. UVB radiation consists of wavelengths between 280 and 315 nanometres (nm), Traditional sources of UVB radiation give off wavelengths of light across the spectrum (broadband). It has been found that the shorter wavelengths are particular harmful and more carcinogenic than longer wavelengths. Moreover, it is the longer wavelengths which generally provide greater therapeutic effects for a range of skin disorders (commonly psoriasis). Thus, narrowband therapy was developed to utilize only those wavelengths which provided beneficial effects. Special tubes have been created which emit the wavelengths necessary to produce the therapeutic effect (305-315); for instance, the phosphor tube light (TL-01) emission is 311 to 312 nm. Narrowband is preferable to broadband therapy as it has remedial value while minimising potential damage. UVB phototherapy has been shown to reduce the severity of HV in several cases, but some consider it too dangerous due to the known deleterious effects of UV radiation. Furthermore, the treatments, which are administered several times over weeks or months, often involve the patient standing or lying in a booth with tube lights for a period of time; some children may find this experience intimidating.

Fish oil/Omega 3 oral supplements – A diet rich in omega-3 fatty acids (commonly obtained from fish oil) has traditionally been shown to reduce erythema in response to UV radiation in a range of patients, particularly those with polymorphic light eruption. It was therefore hoped to reduce the sensitivity of skin of patients with HV. One study of 3 boys resulted in significant improvement in one patient, moderate improvement in the second and no noticeable reduction in the third’s lesions at all. This is typical of the unpredictable and variable nature of HV treatments to date.

Pharmaceutical therapies – A few individuals treated with oral antimalarials such as chloroquine noted fewer, less severe lesions and increased resistance to UVA radiation, but overall these have been found widely insufficient. Some patients have been shown to benefit from carotenoids such as beta-carotene (an antioxidant) and canthaxanthin, with a few even claiming total resolution of symptoms. Immunosuppressant drugs, including cyclosporine A and azathioprine, can be given alone or intermittently with steroids, this option has also had some success.


Most cases of HV will remit by late adolescence or early adulthood, but a few have been reported to continue into adulthood. Lifelong HV symptoms have been encountered but are extremely rare. There has been the occasional report of late onset HV in the patients 20’s, with one as late as 58 years of age. As previously mentioned, boys tend to suffer longer than girls and the average duration of the disease from follow-up studies has been established as nine years.

Online associations

Hydroa Vacciniforme online support group, for those with a family member suffering from the condition.


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  • Kim, W.S et al., 1998, ‘A case of hydroa vacciniforme with unusual ear mutilation’, Clinical Experimental Dermatology, 23(2):70-72.
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Erythropoietic Protoporphyria (EPP)

Erythropoietic protoporphyria (EPP) is a rare inherited metabolic disorder of the haem (heme) pathway causing severe phototoxicity (toxic reactions to light) in skin due to the build up of a phototoxic chemical in the skin.

EPP belongs to a heterogenous group of disorders (porphyrias) that result from a dysfunction of specific enzymes involved in the haem biosynthesis. Haem serves many essential functions in the body one of which is oxygen transport via haemoglobin.


Erythropoietic Protoporphyria (EPP) reaction

Erythropoietic Protoporphyria (EPP) reaction

Erythropoietic protoporphyria is rare, and few studies have been done on its prevalence. Geographic location generally doesn’t seem to bias the incidence of EPP, although one study has suggested that the incidence in Slovenia is 1:58,000. Other studies include incidence that range from 1:75,000 to 1:200,000. Case reports suggest that EPP is prevalent globally.

It is estimated that between 5,000-10,000 individuals worldwide have EPP.


Typically, erythropoietic protoporphyria symptoms begin in childhood and are characterized by episodes of phototoxicity. The main symptoms are pain, which is often described as heat, prickling, itch or extreme sensitivity of skin exposed to light. The pain is often very severe, and swelling and blistering of the skin may result. Skin lesions resolve slowly often leaving waxy or pitted scars. Repeated exposure leads to scarring and waxy thickening of the skin on the backs of the knuckles and nose.

Erythropoietic Protoporphyria (EPP) reaction

Erythropoietic Protoporphyria (EPP) reaction

As little as a few minutes of sunlight (which may overcast or window transmitted) may be sufficient to evoke symptoms. Symptoms are due to visible light (at wavelength above 400 nanometers, part of the electromagnetic spectrum). In most affected individuals, skin involvement persists throughout life, although some people become less symptomatic with time. Symptoms can be seasonal, starting early in the spring, continuing through summer and diminishing in winter. Some patients report that wind may exacerbate their symptoms.

Erythropoietic protoporphyria patients will sometimes have a mild microcytic anaemia, presumably due to the inability or reduced ability to form haem. This should not be confused with iron deficiency anaemia and patients should not take iron replacement for this as it may actually exacerbate the porphyria. Gall stones, usually pigment stones, are more common at an earlier age in EPP.

Liver failure occurs in 5% of erythropoietic protoporphyria patients; this is thought to be related to the increased work of the liver to clear the excessive intermediate by-products from the defective haem pathway. If liver failure occurs it can be fatal.

This lack of permanent symptoms in erythropoietic protoporphyria leads to frequent misdiagnosis by doctors, much to the frustration of parents and their child.


Protoporphyrin IX molecule

Protoporphyrin IX molecule

Erythropoietic protoporphyria is inherited and can be autosomal dominant or recessive. This disorder causes a chemical known as protoporphyrin IX to accumulate in the skin. When the skin is exposed to the sun, these molecules undergo a chemical reaction that results in swelling, severe and intolerable pain and scarring, a condition known as phototoxicity.

The pain is sometimes described as like having hot needles stuck into the skin. The lifelong pain experienced by these patients typically resigns them to become socially isolated, due to the lack of an efficacious treatment and their need to continuously avoid sunlight.

Ferrochelatase deficiency

The specific defective enzyme in erythropoietic protoporphyria is ferrochelatase, the last of eight enzymes in the porphyrin-haem pathway. Consequently there is an inability to chelate iron with protoporphyrin IX to form haem. Intermediates from the pathway accumulate before this final step and cause toxic effects which are involved in the dermal symptoms of EPP.

The gene for the ferrochelatase enzyme, which shares the same name, is located on chromosome 18q21.3. Molecular studies on the gene indicate that more than 60 different mutations exist, most of which are insertions or deletions.


Diagnosis of erythropoietic protoporphyria is based on the detection of increased levels of free protoporphrin IX in red blood cells. Monitoring of liver function tests and red cell porphyrins are sometimes performed to pick up any early signs of liver failure.


Action spectrum of PPIX

Action spectrum of PPIX

Sun avoidance by remaining indoors or wearing sun protective clothing including cotton gloves and a wide brimmed hat is the first line in erythropoietic protoporphyria management. The remaining treatment is focused upon symptomatic relief, although no effective symptomatic treatments have been reported. Patients have reported immersing affected skin in water (both hot and cold) to try and relieve the phototoxicity.

Most commercially available sunscreens are of no value as a treatment, but a large particle size titanium dioxide sunscreen may be of some benefit if used with other forms of sun protection.

Drugs such as β-carotene, cysteine (an amino acid which has been shown to decrease photosensitivity) and cimitedine have been used with various disappointing results and because the disease is inherited, genetic counselling is recommended.

Hematin infusion may temporarily decrease the production of haem and may also result in a decrease of plasma and faecal porphyrins. Also, there is sporadic evidence that autologous blood cell transfusion with washed red blood cells may successfully induce clinical and biochemical remission for erythropoietic protoporphyria patients. Finally, narrow band UVB phototherapy as a treatment option may provide some protection, presumably through epidermal thickening and tanning.

Since sun avoidance is recommended, patients lead lives where they are in the sun for very limited time. This can prevent normal social activities and the intense pain that is experienced interferes with normal daily activities and can prevent adequate sleep.

Liver transplantation in EPP

Liver failure occurs in 2-5% of patients with erythropoietic protoporphyria; this is thought to be related to the increased workload of the liver to clear excessive intermediate by-products from the defective haem pathway. If liver failure occurs it can be fatal.

31 European liver transplants in EPP patients have been reported in medical literature from 1983 and 2008. A 2005 US study followed up 20 patients who had undergone the procedure.

When conducting transplants and other surgery in EPP patients, it has been recommended that yellow filters be fixed to surgical lights to remove light wavelengths below 470nm and prevent phototoxic reactions resulting from exposure.

Psychological and social impact

EPP has been widely recognised as having a serious impact on the quality of patients’ lives due to sun avoidance leading to social exclusion. Depression, anxiety due to fear of reactions and suicidal thoughts have been reported by EPP patients in the literature. A 2010 UK study has also shown that individuals with photosensitive disorders, including EPP, have a greater unemployment rate.

Misdiagnosis and ‘invisible’ reaction symptoms can compound these issues as patients also report accusations of hypochondria when experiencing reactions or avoiding situations which may cause the onset of symptoms.


Symptoms of erythropoietic protoporphyria are usually with patients for life; however a few people have described symptoms reducing over time.


  • Lecha, M et al., (2009). ‘Erythropoietic protoporphyria’, Orphanet Journal of Rare Diseases. 14(9) available online at
  • Marko PB et al., (2007). ‘Erythropoietic protoporphyria patients in Slovenia’, Acta Dermatoven. 16(3):99-104.
  • McGuire BM, et al, (2005). Liver transplantation for erythropoietic protoporphyria liver disease. Liver Transpl. 11(12):1590-6.
  • Murphy GM, (2003). ‘Diagnosis and Management of the Erythropoitetic Porphyrias’, Dermatologic Therapy. 16:57-64.
  • Rufener EA (1987). ‘Erythropoietic protoporphyria: a study of its psychosocial aspects’, British Journal of Dermatology. 116:703-708.
  • Schneider-Yin et al., (2000). “New insights into the pathogenesis of erythropoietic protoporphyria and their impact on patient care”, European Journal of Pediatrics. 125:719-725.
  • Stafford R, et al., (2010). ‘The impact of photosensitivity disorders on aspects of lifestyle.’ British Journal of Dermatology. 163(4):817-822.
  • Thunell S, Harper P & Brun A, (2000). ‘Porphyrins, Porphyrin Metabolism and Porphyrias, IV, Pathophysiology of Erythropoietic Protoporphyria – Dianosis, Care and Monitoring of the Patient’, Scandinavian Journal of Clinical and Laboratory Investigation. 60:581-604.
  • Todd DJ. ‘Clinical Implications of the Molecular Biology of Erythropoietic Protoporphyria’, Journal of European Academy of Dermatology Venereology. 11:207-213.
  • Wahlin S, et al, (2008). “Protection from phototoxic injury during surgery and endoscopy in erythropoietic protoporphyria.” Liver Transpl. 14(9):1340-6.
  • Wahlin S, et al, (2011). “Liver transplantation for erythropoietic protoporphyria in Europe.” Liver Transpl. epublished May 20.
Actinic Prurigo (AP)

Actinic Prurigo (AP) is a rare chronic, idiopathic skin condition, which is characterised by abnormal cutaneous responses to ultraviolet radiation (i.e. photosensitivity). AP is thought to be mediated by an abnormal immune response in the background of genetic predisposition. AP is a rare condition and is usually seen in certain populations of the Americas. Skin lesions can appear hours to days after sun exposure and rarely, non-exposed skin can be affected. AP is also known as Hutchinson prurigo. Although AP is not associated with mortality, it can cause significant morbidity in afflicted individuals.


Typically, AP first appears in the sunnier months and patients often report exacerbations in symptoms during summer and spring. Rarely, however, the symptoms are worse during winter and autumn, and immunological tolerance during summer is thought to be responsible for this phenomenon. AP tends to occur equally in both the sexes in children and adolescents. In adults, however, females are twice as frequently affected as males. A positive family history of AP or PLE is present in one-fifth of individuals with APThe prevalence of AP in the general population is not known, but is thought to be less than 5% in the above-mentioned populations. In Europe and the Asia-Pacific, where a pathogenetically similar but clinically distinct disease known as polymorphic light eruption (PLE) is more common, rare cases of AP have been reported.AP usually begins in childhood. In some individuals, it may resolve before adulthood. In others, however, it is chronic and tends to recur persistently. Rarely, the disease may arise in adults and the clinical course in these cases is usually chronic.Actinic prurigo can affect the skin of all races, although it is more commonly observed in Latin-American Mestizo and Native American populations. Sporadic cases have been reported in the United Kingdom, the United States, Europe, Australia and Japan.


Sun-exposure, i.e. exposure to ultraviolet A and B radiation, is the predominant cause of actinic prurigo, yet the reason for the abnormal response to sun exposure is not fully understood. AP is believed to be delayed-type hypersensitivity reaction to antigens exposed or changed following exposure of the skin to ultraviolet radiation. The exact nature of these antigens is not known. It is also believed that genetic predilection may play a role in the pathogenesis of AP, with up to 90% of patients with AP showing various human leukocyte antigen (HLA) variants. In particular, HLA type DRB1*0401 and HLA type DRB1*0407 have been associated with AP.

Cellular involvement in actinic prurigo

Langerhans cells (LC) are believed to play a role in the pathogenesis of AP. LC are antigen presenting cells that are involved in the induction of cell-mediated immune responses to antigens located in the skin. LCs in patients with AP show a reduced susceptibility to ultraviolet radiation. UV-resistant LCs in patients with AP activate immune responses via putative antigens. Because of the presence of UV-resistant LCs, the putative antigens may be delivered to lymphocytes in large amounts or in a chronic fashion, leading to inflammation seen in AP. Thus, a combination of altered expression of adhesion molecules and UV-resistant LCs may be involved in the pathogenesis of AP. Further studies are required to elucidate the identity of these putative antigens and to gain a better understanding of the disease process.Expression of cell adhesion and activation molecules has been shown to be increased in AP. This suggests that lymphocytes in skin lesions of AP are, therefore, activated and may play a role in the damage observed in this condition. An increased adhesiveness of lymphocytes, as a result of increased expression of adhesion molecules, enables them to migrate through the endothelium and extracellular matrix. Similarly, the activation molecules can act on their respective receptors to induce lymphocyte proliferation and activation. Ultraviolet radiation is thought to activate adhesion molecules, such as ICAM-1, via activated lymphocyte infiltrates in keratinocytes, leading to inflammation that is observed in AP.Skin lesions in AP have been shown to be infiltrated by CD4+ T cells. An abnormal immune sensitization occurs against epidermal antigens in AP. AP can be considered as an autoimmune disease, because lymphocyte activation occurs in response to patient’s own ultraviolet-irradiated keratinocytes.


The symptoms of actinic prurigo include:

  • Extremely itchy (pruritic) skin rash;
  • Red and inflamed bumps (papules);
  • Thickened patches (plaques); and/or
  • Lumps (nodules)

The symptoms of AP are often described as similar to those seen in atopic dermatitis (eczema).

In addition to the symptoms listed above, skin ulcerations, crusting and scaling can occur.

Although areas exposed to the sun, such as the cheeks, nose and hands, are more commonly affected, non-exposed areas can rarely occur in severe AP. Pseudo-alopecia of the eyebrows can occur if the face is constantly scratched. In severe cases, permanent mild scarring and hypopigmented lesions may develop.

In about 65% of the patients affected with AP, the lips are affected. Inflammation of the lip (cheilitis) and pruritis are commonly observed. Other features such as oedema, crusting, ulceration and scales may be present. Interestingly, in 10% of the patients with AP, the lips are the only sites that are affected.

In about 45% of AP patients conjunctivae of the eyes are affected. Hyperaemia, brown pigmentation, photophobia, epiphora (excess production of tears), and formation of pseudopterygium (where the conjunctiva adheres to the cornea) are potential symptoms associated with the involvement of conjunctivae.


Observational diagnosis of actinic prurigo

Nevertheless, blood tests may be performed to rule out systemic diseases with involvement of the skin. The presence of HLA type DRB1*0401, or DRB1*0407 in genetic testing is suggestive of AP. Histological studies may be helpful. As a skin disease that does not involve internal organs, no blood tests are available to diagnose AP.Histologically, mild acanthosis, exocytosis, and spongiosis of the epidermis are observed. Lymphocyte infiltration and lymphoid follicles may be present. Eosinophils are often present. With the conjunctival histology, the epithelium appears thinned and atrophied. The basal cells are vacuolised with lymphocytic infiltration in the sub-mucosal follicles. Eosinophils are conjunctival pigmentation are common findings. The presence of lymphoid follicles in the mucosal and conjunctival laminae is the most characteristic pathological finding in AP.AP is diagnosed based on clinical assessment and the pathological study of the mucosae of the lips, conjunctivae, or the skin.

Phototesting and actinic prurigo

Other laboratory tests are used to rule out other systemic diseases with a photosensitivity component, rather than to diagnose AP. The presence of anti-nuclear antibodies and extractable nuclear antibodies should be undertaken to rule out lupus. The highly contagious Scabies should always be ruled out prior to diagnosing AP. When the skin on the nose is not affected, the condition is more likely to be photosensitive atopic dermatitis than AP. Polymorphic light eruption and prurigo nodularis are other morphologically similar diseases that should be excluded during the diagnosis of AP.Phototesting may help with the diagnosis, but is non-specific and does not rule out other photosensitive disorders. The minimal erythema dose, the minimum dose of narrow-band ultraviolet (UVB) radiation that is required to produce redness 24 hours after exposure, is reduced in patients with AP. It should be noted that a negative cutaneous phototesting does not exclude the diagnosis of AP.


Actinic prurigo is seldom cured and so preventative measures are important in managing actinic prurigo. The disease may resolve before adulthood in some individuals. In others, however, it is persistent and seasonal outbreaks during summer and spring may occur. Rarely, AP may arise in adulthood and persist throughout life. Treatment is aimed at prevention and controlling symptoms. Avoiding UV exposure and appropriate sun protection measures may be beneficial.

Prophylactic phototherapy may be helpful in some cases. Other treatment options include:

  • Emollients to relieve itching.
  • Topical steroids as anti-inflammatories. Oral steroids may be necessary in more severe disease. Hypersensitivity and infections are possible side-effects of steroid use.
  • Anti-malarial drugs, such as chloroquine, may be effective in some cases. These drugs have anti-inflammatory and photoprotective effects. Also, topical calcineurin inhibitors, such as tacrolimus, may be used to treat relatively mild AP
  • Oral thalidomide, an immune suppressant, is usually effective in treating more resistant AP in all age groups. Adverse effects include drowsiness, headache and weight gain. Nerve conduction studies should be performed regularly to assess for peripheral neuropathy, another side-effect of thalidomine treatment. Thalidomide is teratogenic and pregnancy must be avoided.
  • Oral immunosuppressants, such as azathioprine or cyclosporine.
  • Prophylactic phototherapy with UVB or PVB in spring, when the symptoms usually worsen, may be effective in some patients.


Actinic prurigo is an idiopathic disease – i.e. the precise cause(s) of AP are unknown. As sun exposure is the primary trigger of the disease, prudent steps must be taken to reduce or avoid exposure to the sun. The use of sunglasses, wearing appropriate clothing, and the appropriate use of sunscreen may be beneficial. In case of excoriations, sunscreen should be used cautiously. Patients should be taught about the appropriate application of sunscreens. Patients should also be made aware that even minor exposure to ultraviolet radiation may result in outbreaks or exacerbations of symptoms. Annual prophylactic phototherapy may be of benefit in some patients.

Actinic prurigo usually arises in childhood, and persists into adulthood. In some individuals, AP can improve or resolve before adulthood. Rarely, it may arise in adulthood, and persist chronically. Although not a fatal disease, AP can lead to significant morbidity, with exacerbations during the sunnier months. Secondary infections and impetigo are potential complications. Irritant contact dermatitis can manifest with inappropriate use of sunscreens.


  • (2008) Actinic Prurigo. [Online]. Available online [Accessed 10/12/2008].
  • (2008) Actinic Prurigo. [Online]. Available online [Accessed 10/12/2008].
  • Hawk, J L & Ferguson, J (2008). ‘Chapter 90. Abnormal Responses to Ultraviolet Radiation: Idiopathic, Probably Immunologic, and Photo-Exacerbated’. In Wolff, K, Goldsmith, L A, Katz, S I, Gilchrest, B, Paller, A S & Leffell, D J: Fitzpatrick’s Dermatology in General Medicine, 7th Edition. Available online [Accessed 10/12/2008].
  • McGregor, J M, Grabczynska, S, Vaughan, R, Hawk, J L, Lewis, C L (2000). ‘Genetic Modeling of Abnormal Photosensitivity in Families with Polymorphic Light Eruption and Actinic Prurigo’. The Journal of Investigative Dermatology, Vol 115, pp. 471-476.
  • Ortiz-Castillo, J V, Boto-de Los-Bueis, A, de Lucas-Laguna, R, Pastor-Nieto, B, Pelaez-Restrepo, N, & Fonseca-Sandomingo, A (2006). ‘Topical cyclosporine in the treatment of ocular actinic prurigo’. Archivos de la Sociedad Espanola de Oftalmologia, Vol 81, pp. 661-664.
  • Torres-Alvarez, B, Baradana, L, Fuentes, C, Delgado, C, Santos-Martinez, L, Portales-Perez, D, Moncada, B & Gonzalez-Amaro, R (1998). ‘An immunohistochemical study of UV-induced skin lesions in actinic prurigo: Resistance of Langerhans cells to UV light’. European Journal of Dermatology, Vol 8(1), pp. 24-28.
Congenital Erythropoietic Porphyria (CEP)

Congenital erythropoietic porphyria, or CEP, is an extremely rare, inherited metabolic disorder. It is caused by genetic defects which lead to deficiency of the enzyme uroporphyrinogen III cosynthase (UROS). The disease is characterised by extreme photosensitivity (abnormal cutaneous reaction to sunlight) which can leave severe scarring, blister formation and the loss of digits or other features. Damaged skin can become infected, leading to further necrosis and deformities. The face, hands and arms are the most significantly affected as they are frequently exposed; sometimes presenting as severe disfiguration.


The incidence of CEP is not known, but it is exceedingly rare; as of 2006, there were approximately 150 cases reported worldwide. Onset is usually during the early years of life as the genetic defects are present from birth. A milder form with onset in adulthood has been described in a small number of patients; six individuals as of 1990.


Congenital erythropoietic porphryia belongs to a family of diseases known as porphyrias. These are characterised by the overproduction and accumulation of chemicals, known as porphyrins, in various tissues within the body. The porphyrias come about due to faults or deficiencies in the pathway which leads to the production of haem (a major component of the haemoglobin in red blood cells).

CEP is caused by a genetic defect, or mutation, in the UROS gene. This gene encodes an enzyme, uroporphyrinogen III cosynthase, which is essential to the step-wise progression of haem synthesis (see Figure 1). The effect of the mutation is that the enzyme is only marginally active. This means that not only is haem synthesis severely impeded, but also that the pathway takes an alternative route, leading to the build of porphyrins. In the case of CEP, the particular porphyrins in excess are uroporphyrin I and coproporphyrin I.
Haem Biosynthetic pathway

 Figure 1. The Haem Biosynthetic Pathway, illustrating the defect in CEP

Figure 1. The Haem Biosynthetic Pathway, illustrating the defect in CEP

While the enzyme’s activity is dramatically reduced in CEP patients, it is not entirely absent as this would likely result in the complete absence of red blood cells and therefore death. The porphyrins are partially excreted in the urine and faeces, though a large portion enters into circulation and is deposited in bodily tissues; primarily the bone marrow, skin, blood and teeth. Porphyrin accumulation has toxic effects on the cells in these organs. This accounts for many of the symptoms experienced by CEP patients, including their heightened photosensitivity.

CEP’s rarity is partially due to its pattern of inheritance as a recessive trait. This means that an individual needs to have two copies of the defective gene – one from their mother and one from their father – in order for the condition to be present. An individual with just one defective gene will be a carrier of the disease but will not exhibit any symptoms, since the properly functioning gene is able to produce intermediate levels of the enzyme. There is typically no family history of CEP and both parents are healthy.

A number of mutations in the UROS gene have been discovered in CEP patients, all cause dysfunction of the UROS enzyme. Of the 35 described, the C73R mutation is the most common, present in about a third of all cases. This particular mutation is associated with a severe form of the disease.


Symptoms of CEP are diverse and can range from mild to severe. Along with cutaneous damage due to enhanced photosensitivity, CEP patients commonly suffer anaemia due to the breakdown of red blood cells (hemolysis). The following symptoms may be present to differing extents in individual patients:


  • Blistering and rashes on light-exposed skin
  • Scarring
  • Increased skin fragility
  • Skin destruction and erosion
  • Abnormal hair growth (hypertrichosis/hirsutism)
  • Loss of eyebrows and eyelashes
  • Mutilation of cartilage structures, such as the ears and nose
  • Loss of digits and facial features
  • Bacterial infection of damaged skin, possibly leading to further necrosis and deformation

Blood and other tissues

  • Anaemia due to the breakdown of red blood cells
  • Excessive red blood cell production (erythrocyte hyperplasia)
  • Bone loss, fragility or hardening
  • Enlarged spleen (splenomegaly)
  • Brown, pink or red discolouration in urine, due to the presence of porphyrins
  • Teeth stained red (erythrodontia), also due to accumulation of porphyrins
  • Ocular (eye) lesions


  • Brownish colour to the amniotic fluid
  • Accumulation of fluid in the fetus whilst still in utero (hydrops fetalis)

In addition to the physical symptoms, CEP patients often suffer poor mental health. This is due to both the level of pain and discomfort experienced and the psychological impacts of their appearance. These individuals can be stigmatised and often avoid interaction with other people. Many struggle both socially and professionally, thus CEP has an extreme impact upon patient quality of life.


CEP is the only porphyria that can be diagnosed prenatally. It is indicated by raised levels of uroporphyrin I in the amniotic fluid as early as 16 weeks in utero. More commonly, diagnosis is in infancy or childhood through a combination of the following methods:

  • History of patient symptoms
  • Quantitative screening using spectrophotometry or fluorimetry is considered the most accurate method of diagnosis. When uroporphyrin I and coporphyrin I are present in blood a plasma spectrofluorimetry is seen at 615-620 nm.
  • Measurement of elevated levels of uroporphyrin I and coproporphyrin I in blood, urine or faecal analyses
  • Examination of the eyes or urine using a Wood’s lamp


Total avoidance of sunlight and other sources of visible/UV light (i.e. solariums) is vital to preventing skin damage in CEP. Sun-protective clothing and sunscreen containing the light-blocking compounds zinc oxide or titanium dioxide may offer some protection. Plastic window films and window tinting around the home and in the car can reduce damaging wavelengths of light penetrating the skin. In addition, incandescent light bulbs emit less phototoxic wavelengths of light than fluorescent lights. Physicians recommend CEP patients try to avoid physical injury which may worsen fragile or damaged skin.

CEP treatments can be radical and patient response is varied:
Bone marrow transplantation (BMT) – the only therapy to date that presents a potential cure for CEP. It has proved extremely successful in a handful of patients, however the long-term results of BMT are not yet known. This form of therapy also comes with significant risks, including infectious complications and a high mortality rate. In a few children, BMT has resulted in complete remission of CEP. Improvements included normal haemoglobin, considerably reduced uroporphyrin I in the urine and no skin lesions in spite of unrestricted sun exposure; this is evidence of the best case scenario. Stem cell cord blood transplantation has also been reported effective in a few CEP patients.

Blood transfusions – these decrease the production of red blood cells and hence porphyrins in CEP patients. Transfusions have successfully reduced disease symptoms in several patients, however there are complications associated with chronic transfusions (i.e. iron overload).

Splenectomy – a splenectomy is the surgical removal of the spleen. It can increase the lifespan of red blood cells, reducing anaemia.

Oral sorbent medications – these include activated charcoal and cholestyramine which act by binding the excess porphyrins and preventing their absorption. In several patients these have reduced porphyrins in the blood and urine, in one case leading to complete remission. In contrast, there are also several reports of no effect and one of exacerbated condition; thus, caution should be exercised. Further, this treatment may be accompanied by the mild complication of poor nutrient absorption.

Oral beta-carotene – may act as a mild photoprotectant to reduce the symptoms of photosensitivity, though treatment usually requires unreasonably large doses. It has been trialed in CEP with minimal efficacy.

Oxygen quenchers – these are oral medications, such as ascorbic acid and alpha-tocopherol, which mop up excess reactive oxygen species to lessen porphyrin-induced photodamage; also only marginally effective.


The prognosis for a CEP patient depends on both the clinical severity of the condition and their response to available treatment. Severity is mainly dependent on the amount of residual activity the UROS enzyme has. Into the future, potential therapies may exist in the form of stem cell transplantation and gene therapy to correct the mutation and produce a functional UROS enzyme.

During puberty, a child’s haemoglobin levels increase to that of an adult. Along with an increase in haem comes a rise in porphyrin levels in CEP patients, therefore increase in symptoms or relapse may occur during adolescence. Where treatment is ineffective, the life expectancy of CEP patients is shortened.


  • American Porphyria Foundation, n.d, Congenital Erythropoietic Porphyria (CEP), accessed 23rd August 2010, <>.
  • Canadian Association for Porphyria, n.d, Congenital Erythropoietic Porphyria, accessed 23rd August 2010, (no longer online).
  • Hebel, J.L, 2009, Congenital Erythropoietic Porphyria: Treatment & Medication, eMedicine Specialties, accessed 23rd August 2010, <>.
  • Hift, R.J, Meissner, P.N & Kirsch, R.E, 1993, ‘The effect of oral activated charcoal on the course of congenital erythropoietic porphyria’, The British Journal of Dermatology, 129(1):14-17.
  • National Organization for Rare Disorders, 2008, Porphyria, Congenital Erythropoietic, accessed 22nd December 2015,<>.
  • Singh, D.K & Rai, R, 2008, ‘Congenital Erythropoietic Porphyria’, Indian Pediatrics, 45:865.
  • Wiederholt, T, 2006, ‘Identification of mutations in the uroporphyrinogen III cosynthase gene in German patients with congenital erythropoietic porphyria’, Physiological Research, 55(suppl. 2):S85-S92.
Seborrheic dermatitis (SD)
Seborrheic Dermatitis

Seborrheic Dermatitis

Seborrheic dermatitis (SD) is a form of eczema and a common, inflammatory skin disorder that affects infants and adults and is usually associated with seborrhea (increased sebum production). It is characterized by reddish or pink patches of skin, accompanied by greasy, yellowish flakes or scales. It most commonly occurs in the scalp and on the face, especially at the creases of the nose, eyebrows, and forehead, where the skin is most oily and rich in sebaceous glands. It may also develop on the ears, chest, back or groin. The disease varies in severity, with the severe end of the spectrum involving large areas of the body.


Seborrheic dermatitis occurs approximately in 3-5% of the general population and affects all races. The condition mainly occurs at two age peaks, early on in infancy, during the first few months of life, or in adulthood between the ages of 30 and 60. SD appears to affect males more than females in both infantile and adult onset of the disease. SD is also one of the most common skin manifestations of patients with human immunodeficiency virus (HIV) infections or acquired immunodeficiency syndrome (AIDS), found in up to 85% of patients. Patients with central nervous system disorders such as epilepsy and Parkinson’s disease also appear to be prone to the development of SD.


Whilst the cause of seborrheic dermatitis is not entirely clear, many factors are thought to contribute to the disorder. These include:

  • Seborrhea – the symptoms of SD generally occur in regions of skin rich in sebaceous glands such as the scalp, face and upper body. Many patients appear to have greasy skin and active sebaceous glands seem to be necessary to the development of the disease. It might provide a predisposition to developing the disease but SD is not a disease of the sebaceous glands. Studies have shown that there is no marked increase in sebum production in those with SD despite that induced reduction of sebum production can improve SD.
  • Malassezia yeast (increased numbers of a common yeast that lives on human skin) – Malassezia furfur or its yeast form, Pityrosporum ovale may play a causative role in SD. This yeast is found in high abundance in normal skin and is lipophilic. The lipid composition of the skin in patients has been found to be different in that there is an increased proportion of cholesterol, triglycerides and paraffin. The abnormalities in surface lipids could lead to ineffective keratinization and/or the lipase activity of Pityrosporum ovale, which can generate inflammatory fatty acids. Research has also shown that Malassezia furfur or its metabolic by-products can cause inflammation via a cell-mediated immune response involving T cells, Langerhans cells and the complement cascade.
  • Oily skin – the sebaceous glands in the skin begin to produce too much oil (sebum)
  • Genetic Factors – a family history of eczema might predispose one to developing SD. The actual genes involved, if any, are not known.
  • Immune dysfunction/ deficiency – there is an increased incidence of SD in immunocompromised patients (HIV/AIDS), suggesting that they are unable to keep Malassezia numbers in check. Though antifungals may ‘clear’ the symptoms of the condition with a reduction in the number of the microbes, recolonization and relapse occur upon discontinuing treatment. This could be explained by an underlying immunological problem, indicating that being immunocompromised might be responsible for increased numbers of Malassezia furfur.
  • Neurological abnormalities – SD has been found to occur in high frequencies among patients with neurological disorders such as epilepsy and Parkinson’s disease. This suggests that the nervous system may be involved, though there is no hard evidence as yet to support this theory.

The following risk and environmental factors may also increase the likelihood of developing SD:

  • Cold, dry weather;
  • Stress;
  • Fatigue;
  • Skin injuries;
  • Obesity;
  • Nutritional deficiencies of zinc, riboflavin, niacin and pyridoxine;
  • Various drugs and medications such as cimetidine, ethionamide, gold, arsenic, interferon-a, lithium and methyldopa.


Seborrhoeic Dermatitis symptoms

Seborrhoeic Dermatitis symptoms

Signs and symptoms can vary from day to day and may depend on the severity of the disease. In general, they include:

  • Skin lesions and crusts;
  • Plaques over large area (rare);
  • Greasy, oily, waxy appearance of the skin;
  • Skin scales – white and flaking, or yellowish and oily;
  • Itching – may become more itchy if infected from scratching;
  • Mild redness and swelling;
  • Scalp scaling (dandruff).

SD in infants – cradle cap

SD in infants, also called cradle cap, is a harmless, temporary condition. It appears as thick, crusty, yellow or brown scales over the child’s scalp. Similar scales may also be found around the face and in the groin. Cradle cap may be seen in newborns and small children up to the age 3. Cradle cap is not contagious, nor is it caused by poor hygiene. It is not dangerous and is self-limited. It may or may not itch but excessive scratching of the area and breaks in the skin may cause inflammation, mild infections or bleeding.

SD in adults

The course and clinical features of seborrheic dermatitis are different in adults. The mild form of the disease is eczema-like and presents over the scalp, nasolabial folds, eyebrows and forehead. Often it can spread to the neck, shoulder blades and back. It is associated with seborrhea, erythema, scaling and itching of the lesions. Dandruff is also found at the mild end of the scale. The more classic and chronic form of the disease is patchy SD and involves recurrent lesions. The lesions are localized to the same places as the mild form and are characterized by yellow, oily, thick scaly crusts, inflammatory infiltrate and erythema. The lesions start off as small mounds of redness but progress and spread to form clearly outlined patches. Patients may also experience itching and burning sensations. Other manifestations of SD include blepharitis and dermatitis of the ear canal. In rare cases, the disease will progress into the extreme variant of SD, generalized seborrheic erythroderma, where large areas of the body are covered in erythromatous plaques.

The disease is chronic and continues in a cycle where the disease will subside over a period of time and then relapse.



Infantile seborrheic dermatitis (cradle cap) is benign and will generally clear itself within a few weeks or months. Treatment is not necessary, but parents often do so because they find it unsightly. Using a mild shampoo and gently massaging the scalp will help loosen and remove the scales. When SD extends beyond the scalp, dermatologists will usually prescribe a topical medication such as antifungal creams or mild corticosteroids.


The adult form of SD is chronic and tends to subside and flare up again. It cannot be cured, thus therapy is aimed at controlling the symptoms.

Due to the long course of the disease, rather than aggressive treatment, mild regimens are recommended.

  • Scalp – many cases of SD are effectively treated by shampooing daily with antidandruff shampoos containing selenium sulfide, pyrithione zinc, salicylic acid or coal tar. Alternatively, shampoos containing ketoconazole may also be effective. The doctor may prescribe a mild corticosteroid cream or lotion for more severe scalp symptoms, as well as flaking and scaling on the face, ears, and other parts of the body. Corticosteroids should be used sparingly because excessive use could lead to telangiectasias and skin atrophy.
  • Non Scalp – treatments for non scalp SD aim to reduce inflammation and the buildup of scaling on the skin. Topical antifungal agents, such as itraconazole, along with frequent application of coal tar or zinc containing shampoos or zinc soaps, may help control symptoms. Additionally, oral antifungal agents such as ketoconazole and/or a topical corticosteroid cream such as betamethasone valerate, could also be of value but may pose some long term side effects.

A class of medications called immunomodulators, such as tacrolimus and pimecrolimus, affect the immune system. These calcineurin inhibitors exert their anti-inflammatory effects by inhibiting T lymphocyte activation and proliferation. They also exhibit anti-fungal properties and might be an appropriate alternative to corticosteroids for SD as they lack the long term side effects.

Occasionally, a patient with severe SD can be unresponsive to the usual topical therapy. Isotretinoin is currently being used as an experimental therapy for the disease. It is not officially approved for this indication yet but there have been positive results. It has been shown to induce a reduction in sebaceous gland size, with a corresponding reduction in sebum production. Isotretinoin also possesses anti-inflammatory properties but also carries several potential side effects including; hyperlipidemia, neutropenia, anemia and hepatitis.


SD cannot be prevented but the severity of the disease can be decreased by controlling the risk factors and by maintaining skin care.


The prognosis for infantile seborrheic dermatitis is good as it is benign and usually clears up within a few weeks or months. There is no sign that infants with the disease are more likely to undergo the adult form of SD.
In adults, SD is chronic and tends to flare up in colder climates and subside in warmer conditions. It cannot be cured but there are effective treatments available to control the symptoms.


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Rosacea magnified

Rosacea magnified

Rosacea is a very common, chronic disease of the skin where facial veins become highly reactive. It is often characterised by frequent or persistent flushing in the central area of the face, swelling and/or acne like appearance. Erythema can also occur in peripheral areas such as the neck and chest. Telangiectasias, or the development of small punctual bleeding areas of the skin, can also contribute to the redness due to dilated or broken capillaries. Swelling, papules and pustules can also be associated with the various forms of rosacea and can often lead to edema or mimic acne. It is a common misconception that rosacea can be a form of acne due to the disease previously being named Acne Rosacea.

The disease is commonly overlooked and is not detrimental to one’s health; however it may have an impact on the patients’ psychosocial and emotional well being, similar to acne.


Studies of mild cases have shown that the prevalence of rosacea is roughly around 10% of the population, developing between the ages of 30 – 50. Women are more likely to develop it than men with a ratio of 1:3 but the odds could be different due to the disease being undiagnosed or under-reported. The exact prevalence isn’t known but it is considered most common within Caucasian populations in light/fair-skinned individuals. Although people of any race can be affected by rosacea, rarely do those of Asian or African descent develop rosacea.

Rosacea is most likely to first present between the ages of 30 – 50, however children and adolescents can also develop the disease.

Currently it is estimated that 14 million Americans have rosacea but this figure is likely to be substantially higher due to it frequently being undiagnosed by doctors and/or the disease being under-reported by patients. It is often mistaken for adult acne or sunburn.


The exact cause of rosacea is unknown and little is known about the inflammatory process that causes it. Since there are many subtypes, it is plausible that there are pathophysiological and etiological differences between them. It is suspected that facial vasculature is more superficial in roscea patients than others, suggesting possible abnormalities in the vasculature or vasculature homeostasis.

Rosacea has a variety of suspected causes; the most common being sun exposure. Other substances that are known to provoke rosacea include:

  • Hot and Spicy foods/drinks;
  • Alcohol;
  • Some facial creams and topical steroids;
  • Stress;
  • Exercise;
  • Other environmental factors (ie. wind, extreme hot or cold).

Suspected causes of rosacea

Epidemiological studies done have confirmed that patients with Papulopustular Rosacea (Stage 2) have a higher Demodex (common hair follicle mite) densities then those without rosacea and it appears that having the disease also seems to promote the proliferation of Demodex mites. The limit of this study is that causation can not be proven, only that changes in skin morphology and possibly lack of washing may lead to larger densities of mites on the skin. Sebaceous glands are also known to be involved, as with acne.

Other proposed causes include:

  • Matrix degeneration – degradation of the dermal matrix has be shown histologically in samples from rosacea patients. Rosacea may alter the vascular and lymphatic structure within the dermis.
  • Ingested agents – since many foods trigger rosacea, gastro intestinal tract diseases might influence exacerbations.

These mechanisms, along with trigger agents, all potentially have a link in causing rosacea but further studies are still required to determine them.


The main features rosacea patients present are:

  • Frequent or prolonged flushing/blushing particularly over the nose, cheeks, forehead and chin, but occasionally can be found to digress to the neck, back and chest;
  • Spider veins (talangiectasias; usually on the nose);
  • Papules and pustules (acne like appearance, but lacking comedones);
  • Facial burning and stinging;
  • Swelling of facial areas;
  • Enlargement of sebaceous glands giving the nose a bulbous appearance;
  • Dry and flaky facial skin;
  • Occasional burning/itching of the eye or conjunctivitis may arise.

Primarily for therapeutic reasons, rosacea has been categorized into sub-types pending on which symptoms present and what stage of the disease they are at. The disease is most likely to continue until it reaches its course but progression is very preventable.

Erythematotelangiectatic Rosacea (ETR) or Stage 1

ETR is characterised by persistent flushing, usually for hours or days, along with the presence of telangiectasias and/or facial swelling and edema. Flushing that only lasts for a few minutes is not considered to be an early stage of rosacea. Quite often the erythema is brought on by various stimuli including: spicy foods, hot drinks, stress and sun exposure, causing the patient to experience stinging and burning sensations but exacerbations occur just as often in absence of any stimuli.

As the disease develops, the telangiectasias progressively become more prominent, especially on the nose and cheeks, forming a spray like pattern as well as increased roughness and irritation of the skin.

Papulopustular Rosacea (PPR) or Stage 2

PPR consists of persistent erythema along with inflammatory papules and pustules. These lesions all originate from either sebaceous or hair follicles which can sometimes heal and scar. Burning and stinging may also occur in PPR but is less common when compared to ETR. The inflammation associated with the papulopustules can result in chronic edema which can manifest into solid facial edemas or lead to phymatous (Stage 3) changes.

Phymatous Rosacea or Stage 3

Not many patients proceed to this stage of the disease. It is characterized by inflammatory nodules, thickening of the skin, irregular contours, hypertrophy of connective tissue and hyperplasia of sebaceous glands. Phyma most frequently occurs in the nose (Rhinophyma) giving it either a shiny bulbous appearance or in severe cases, an irregular shape with skin resembling that of an orange surface. It is less frequent elsewhere on the face but can still occur. Women only experience the glandular features of stage 3. The exact reason is unknown but hormone may be a factor.

Ocular Rosacea

Ocular symptoms can present simultaneously, or develop after skin symptoms, but may not affect all patients. They can experience itching, stinging, burning, grittiness and erythema and swelling of the eyelids. It can commonly manifest as conjunctivitis and blepharitis in severe cases, keratitis, which can potentially lead to blindness. Pain and photophobia may also present.


Currently, there is no cure for rosacea but there are effective ways of managing the disease by treating the symptoms. If left untreated, the disease will progressively aggravate. Treatment of rosacea also depends on the sub-type present as each has its own symptoms.

Measures need to be taken to avoid stimuli that can trigger rosacea to minimize the frequency and severity of outbreaks. This includes avoiding hot and spicy foods, cosmetics/irritants and the sun or UV exposure. Symptomatic treatments are outlined below.

Topical treatments

In general topical agents such as Metronidazole and Azelaic acid have been used to improve skin condition and reduce lesions in PPR, but there is a lack of evidence that suggest that it improves the flushing reactions. Some people may experience burning and stinging side effects so use of topical treatments should be avoided in sensitive patients.

Oral treatments

Although there is little proof that microorganisms are involved in rosacea, the use of antibiotics has been approved by the FDA and have been shown to have beneficial effects, so clinicians are sometimes reluctant to exclude it as a form of therapy. Antibiotics tend to be used as a long term therapy due to the chronicity of the disease but prolonged use could lead to resistant strains of bacteria and irregular levels of natural flora, which raises several health issues.

Also approved by the FDA, tetracyclines such as doxycycline have been shown to be very effective in managing papulapustules and the inflammation associated with them. Its anti-inflammatory effects include down regulating the production of pro-inflammatory cytokines such as IL-1 and TNF-α and modulating the inflammatory pathway.

Other oral treatments currently used include β-blockers, calcineurin inhibitors, clonidine, selective serotonin re-uptake inhibitors, macrolides and anti-androgenic agents, most of which are used in reducing the severity of flushing.

Laser and light treatments

Intense pulsed light (IPL) therapy and vascular lasers are good alternatives to oral and topical treatments. They may be used in adjunct with them and seem to be the most successful form of treatment in reducing erythema and telangiectasias. They generally exert the same effect as each other, removing telangiectasias and some other blood vessels in the face associated with erythema but they differ simply by the wavelengths they are used at. It has also been reported that it can extend remission time. Scarring rarely occurs in these procedures but drawbacks such as cost might be a major issue for many patients.

Treatment of phyma

Due to phyma causing morphological changes in the skin structure, advanced cases generally require surgical approaches to eradicate lesions and/or to reshape the phyma. In early stages Isotretinoin appears to be efficient in reducing the size of enlarged sebaceous glands and halting the progression of the disease. Particular surgical techniques have excellent results with minimal scarring and low chance of reoccurrence.

Ocular treatment

As the eye is a vital organ and it is estimated that over 50% of rosacea sufferers will present with ocular symptoms, it is important that they are treated to prevent damage. Most ocular symptoms respond well to topical treatments and basic eyelid hygiene with regular washing using gentle cleansers. If they are inadequate then most antibiotics should be able to clear up symptoms.

In summary, to effectively treat rosacea, clinicians need to understand the broad symptoms that rosacea can present with and which of those apply to the patient. Treatment is considered to be successful if symptoms are minimized and controlled along with reducing the risk of relapsing in the long term.


As the pathology of rosacea is unknown, preventative measures might be very broad and restrict the patient unnecessarily. If the triggers for each individual can be identified, patients should be stressed to avoid those stimuli. Some people may have a genetic predisposition to develop veins so preventative measures might not be as useful.


Rosacea is not a fatal disease although severe cases can result in blindness and/or facial disfigurement which may have devastating effects on a person’s self-esteem, emotions and psychological well being.


  • 2004, Therapeutic Guidelines: Dermatology, North Melbourne, Therapeutic guidelines Limited.
  • Baldwin, H. E., (2007) ‘Systemic Therapy for Rosacea’, Vol 12. [Online] Available from [Accessed 25/11/08.
  • Berg M, Liden S., (1989) ‘An epidemiological study of Rosacea’. Acta Dermto-Venereologica, Vol 69, pp.419-423.
  • Crawford, G.H., Pelle, M.T., James, W. D., (2004) ‘Rosacea: I. Etiology, pathogenesis, and subtype classification’ Journal of the American Academy of Dermatology, Vol 51, pp.327-341.
  • Forton, F. et al., (2005) ‘Demodicosis and rosacea: Epidemiology and significance in daily dermatologic practice’. Journal of the American Academy of Dermatology, Vol 52, pp.74-87.
  • Jansen. T., Plewig, G., (1997) ‘Rosacea: classification and treatment’. Journal of the Royal Society of Medicine, Vol 90, pp.44-150.
  • Lount, B. W., and Pelletier, A. L., (2002) ‘Rosacea: A Common, Yet Commonly Overlooked, Condition.’ American Family Physician, Vol 66, pp.435-442.
  • Woolff, K., Goldsmith, L.A., Katz, S.I., Gilchrest, B.A., Paller, A.S., Leffer, D.J., (2003). Fitzpatrick’s Dermatology in General Medicine, 7e. Ch. 79. The McGraw Hill Companies.
Psoriasis symptoms

Psoriasis symptoms

Psoriasis is a chronic, inflammatory condition of the skin in which both genetic and environmental factors are thought to be an influence. There are five clinical subtypes, each with unique signs and symptoms, but is generally characterized by thick, red skin with overlying silver-white patches called scales, referred to as psoriatic plaques. The scaly patches are caused by excessive skin production and the accumulation of skin leads to the silvery-white appearance. Regardless of what subtype of psoriasis, patients can experience burning, itching or soreness at the affected site. Psoriasis frequently develops on the elbows, knees, scalp and back but can affect any part of the body.


Psoriasis is a very common condition. It affects an estimated 2-3 percent of the world’s population (with estimates around125 million people affected globally) and according to the National Institute of Health (NIH), between 5.8 and 7.5 million Americans have psoriasis. While it affects men and women equally, occurrence varies according to race, environmental factors and geography. There seems to be a higher occurrence rate among Caucasian populations but rare or absent among African-American, West-African and North American-Indian populations. Psoriasis seems to be an inherited disorder. Over a third of people with psoriasis also have an affected family member.

Psoriasis may develop at any age, but most commonly begins between ages 15 and 35. In 75% of cases, patients developed psoriasis before the age of 40. It can appear suddenly or slowly and in many cases, psoriasis subsides and then flares up again repeatedly over time.

Between 10 and 30 percent of people with psoriasis will also develop psoriatic arthritis. It can develop at any time but commonly occurs between the ages of 30 – 50.



Psoriasis seems to be inherited disorder, with over a third of people with psoriasis also having an affected family member. Nearly one-quarter of people with psoriasis have cases that are considered moderate to severe. Mild psoriasis is defined as affecting less than 3 percent of the body (according to The National Psoriasis Foundation); 3-10% is considered moderate; and more than 10% of the body is considered severe.

At least nine Psoriatic susceptibility loci have been identified (PSORS1-9). An association with the PSORS has been found with functional polymorphisms in modifier genes that mediate inflammation (i.e TNF-α) and vascular growth (i.e VEGF). These genes could determine how a person’s immune system would react. Research also indicates that a “trigger” is needed to set off psoriasis.

Cellular involvement – T cells and psoriasis

Psoriasis was first thought to be immune mediated when transplant patients with psoriasis experienced clearing of the plaques when taking cyclosporine, an immunosuppressant. Now it is known that T-cell activation is central to the inflammation and hyperproliferative nature of the skin found in psoriasis.

Psoriasis involves a complex interaction between keratinocytes (skin cells) and the immune system, mainly with a type of white blood cell called a T cell. Normally, skin cells take 28 days to mature, migrate to the skins surface and shed but in psoriasis, this process occurs in 3 – 6 days. The skin cells are immature and instead of shedding, they pile up causing psoriatic plaques.

T cells function to regulate all immune responses to protein antigens and serve as effector cells to eliminate any foreign particles or microbes, helping to protect the body from disease. In order to function, T cells need to be activated by binding to an antigen presenting cell (APC). In the skin the most efficient APC’s are Langerhans cells. Once bound, a naïve T cell is activated and converted to an antigen specific cell and can develop memory for long lasting immunity against that particular antigen. Upon activation, T cells then proceed to recruit inflammatory cells such as macrophages, dendritic cells and keratinocytes. Together these cells release a variety of chemical mediators, primarily cytokines, which induce inflammatory responses leading to the clinical features presented in psoriasis.

Cytokines involved in the development of psoriasis include: granulocyte-macrophage colony stimulating factor (GMCSF), some interleukins, epidermal growth factor (EGF), interferon-α and tumour necrosis factor-α. TNF-α has been strongly implicated in psoriasis and can lead to keratinocyte proliferation. This hyperproliferative response decreases the approximate time it takes for normal maturation of skin cells (epidermal transit time) from 28 days to 3-6 days. Instead of shedding, the immature keratinocytes layer up and produce the typical scaly plaques of psoriasis.

In short, it is thought that T cells are activated by mistake by faulty signals in the immune system. They become overactive and set off other immune responses, leading to a faster turnover of skin cells.

Environmental causes

Research has helped the understanding of the role of environmental factors and genetics in psoriasis. So far nine gene mutations have been discovered that could be associated with psoriasis, yet it can be activated or worsened by specific environmental factors. Common triggers include:

  • Infections
  • Trauma in the skin or sunburn
  • Stress
  • Smoking
  • Strep infection
  • Drugs
  • Some medications: anti-malarial drugs, beta-blockers (medication used to treat high blood pressure and heart failure) and lithium (anti-depressant)

Psoriasis is also associated with several co-morbidities, including depression, decreased quality of life, increased cardiovascular risk, metabolic syndrome and other immune-mediated conditions such as type 2 diabetes, Crohn’s disease, and psoriatic arthritis. TNF-? has also been implicated in Psoriatic arthritis. High TNF-α levels found in the synovium of psoriasis patients confirm this. The understanding of the involvement of TNF-? in the pathogenic mechanisms has led to the development of TNF-α blocking agents, termed ‘biologicals’, for therapeutic use.


Psoriasis is characterized by reoccurring outbreaks of distinct red areas of skin, covered by silvery-white flaky skin. It may affect any or all parts of the skin. There are five clinical subtypes of psoriasis, each associated in with different symptoms.

  • Plaque Psoriasis – This is the most common type of psoriasis, seen in over 80% of individuals with the disease. Thick, raised, red patches of skin are covered by flaky, silver-white scales. Lesions may be single or numerous and may coalesce into large areas. Common sites for lesions to develop are the elbows, knees, back and scalp but can occur all over the body.
  • Guttate Psoriasis – Small, pink-red scaly spots in the order of 2 -10 mm in size appear on the trunk and limbs. The number of lesions may range from 5 or 10 to over 100. Guttate psoriasis accounts for 2% of the total cases of psoriasis. It is typically seen in young adulthood and might be triggered by a streptococcal infection in the upper respiratory tract. Guttate psoriasis may persist despite clearance of the strep infection. In children, an acute episode is usually self limiting; in adults, flares may complicate chronic plaque disease.
  • Inverse Psoriasis – Skin redness and irritation occurs in the armpits, groin, breasts and skin folds around the genitals. It has a smooth red appearance and is more common in overweight people as the skin is aggravated by sweat and friction.
  • Pustular Psoriasis – Primarily seen in adults, it is characterized by white, non-infectious blisters that are surrounded by red, irritated skin. It may be localized to certain areas of the body or can be generalized, covering most of the body. Pustular psoriasis reportedly may be triggered by medications, irritating topical agents, overexposure to UV light, infections, emotional stress and sudden withdrawal of medications.
  • Erythrodermic Psoriasis – The least common form. Involvement of the entire skin surface may occur in a sudden burst or as a result from gradual extension of psoriatic plaques. The redness of the skin is very intense usually accompanied by severe itching and pain. Edema, especially around the ankles, may also develop along with infection. Erythroderma may also be a manifestation of unstable psoriasis, possibly precipitated by drugs, infection, tar, or withdrawal of corticosteroids. The body’s temperature regulation is often disrupted, producing shivering episodes. Infection, pneumonia and congestive heart failure brought on by erythrodermic psoriasis can be life threatening. People with severe cases of this condition often require hospitalization.

Up to 30% of patients will go on to develop psoriatic arthritis. Along with skin lesions, joints become painfully swollen and can potentially lead to compromised joint function.

Other variations of the disease include:

  • Nail Psoriasis – Psoriasis of the nail may present as lifting (onycholysis) or pitting of the nail. It often mimics fungal infections.
  • Scalp Psoriasis – At least half of all people who have psoriasis have it on their scalp. Scalp psoriasis can be very mild, with slight, fine scaling. It can also be very severe with thick, crusty plaques covering the entire scalp, which can cause hair loss. Occasionally it will extend beyond the hairline to the back of the neck and forehead.
  • Genital Psoriasis – Psoriasis may be confined only to the genital area without sign of it being anywhere else. It usually lacks the scaling associated with psoriasis on other parts of the body.


Depending on the type of psoriasis, its size, location and the patient’s previous medical history, different treatments will be recommended. The goal of treatment is to reduce symptoms and prevent secondary infections because it cannot be cured. They can include one or combinations of the following therapies. Generally, topical treatments are used as a first line of therapy before other types.

Topical treatments

Topical creams should be tailored to the patients need and take into account the extent of the disease, site involved, patient’s age and the likelihood of compliance with the treatment.

  • Corticosteroids – Anti-inflammatory effects by inhibiting cytokine production. More potent preparations are used to treat more severe cases of psoriasis. Adverse effects include skin atrophy, irritation and telangiectasias.
  • Tars – Anti-inflammatory agent with antipruritic effects. Compliance is often an issue due to their color and odour. Examples include coal tar and pine tar.
  • Emollients – Relieves irritation by soothing lesions.
  • Keratolytics – used to lift and soften thick scales in psoriasis.
  • Calipotriol/calcipotriene – a derivative of Vitamin D that helps regulate proliferation and differentiation of keratinocytes. Results often take a minimum of 6 weeks to show.
  • Tazarotene – a selective retinoid that affects keratinocyte differentiation.
  • Over the counter moisturizers and creams – sorbelene and vaseline are suitable preparations.

Systemic treatments

Often used when psoriasis is severe, widespread or causing disfigurement. Most drugs have immunosuppressive, anti-proliferative or anti-inflammatory effects.

  • Acitretin – affects proliferation and differentiation mechanisms as well as having anti-inflammatory properties. It also increases the efficacy of phototherapy.
  • Methotrexate – an immunosuppressant that slows epidermal cell proliferation. It is the most common prescribed oral antipsoriasis drug. Long term use could lead to liver or pulmonary fibrosis.
  • Cyclosporine – an immunosuppressant that inhibits activated T cells, reduces T cell proliferation and the production of cytokines. Long term use is not advised due to adverse effects. They include hypertension, decreased renal function and development of neoplasias.
  • Immunobiologics – proteins such as antibodies are created in living cells and are targeted at blocking specific proteins or pathways involved in the development of psoriasis. This innovation has showed great promise in working at specific immunological targets.


Ultraviolet light suppresses cell mediated immunity by inhibiting the function of epidermal Langerhan cells. Three forms of phototherapy are used in psoriasis and some come with adverse effects.

  • Narrowband UVB – used at a wavelength of 311nm. It has a lack of long term side effects and should be used as a first line of phototherapy.
  • Broadband UVB – used at a wavelength between 290 – 320 nm. Usually combined with tar therapy for added efficacy.
  • Psolaren + UVA (PUVA) – Psolaren sensitizes the skin to UV light. Adverse effects include photosensitivity and nausea. Long term use can lead to skin atrophy and increases the risk of developing skin cancer.

Differential Diagnosis

The different subtypes of psoriasis can commonly be mistaken for other diseases. Listed below are common diagnoses for particular subtypes.

  • Plaque Psoriasis – discoid eczema, cutaneous T cell lymphoma (CTCL) and tinea corporis
  • Guttate Psoriasis – pityriasis rosea, lichen planus and pityriasis lichenoides chronica
  • Erythrodermic Psoriasis – drug induced erythroderma, eczema, pityriasis rubra pilaris and CTCL
  • Pustular Psoriasis – impetigo, superficial candidiasis, reactive arthritis syndrome and superficial folliculitis


There is no way of preventing psoriasis, but people living with the disease can ease their discomfort and maximize the effectiveness of treatment by minimizing flare-ups. This can be done by avoiding certain stimuli that trigger psoriasis and overall maintenance of good health to help the body avoid stress and feel tired.


Psoriasis is a chronic, lifelong condition but can be controlled with treatment. There is no cure and it will usually have negative effect on the patient’s quality of life. It usually does not adversely affect general health, unless it is neglected or occurs in the elderly or very young. It is likely that psoriatic arthritis will develop so early diagnosis and treatment will be beneficial in prolonging the health and integrity of the joints.


  • Barker, J. (2007) ‘Psoriasis’. European Journal of Dermatology. Vol 17, pp.563-564.
  • Guenther, L C, Koo, J & Choi, J (2007) ‘Psoriasis Treatment’ [Online] Available online [Accessed on 5/12/2008].
  • Halder, R M (2006). Dermatology and Dermatological Therapy of Pigmented Skins. pp.93-99. Taylow & Francis Group.
  • Hann, S & Nordlund, J J (2000). Vitiligo: A Monograph on the Basic and Clinical Science, Ch.16. Blackwell Publishing.
  • Joshi, R (2004) ‘Immunopathogenisis of Psoriasis’. Indian Journal of Dermatology, Venereology and Leprology. Vol 70, pp.10-12.
  • Langley, R G B, Krueger, G G & Griffiths, C E M (2005) ‘Psoriasis: epidemiology, clinical features, and quality of life’. Annals of the Rheumatic Diseases, Vol 64, pp.18-23.
  • Park, R. (2007) ‘Psoriasis’ [Online] Available online [Accessed on 5/12/2008].
  • Pietrzak, A et al (2008) ‘Genes and structure of selected cytokines involved in pathogenesis of psoriasis’. FOLIA HISTOCHEMICA ET CYTOBIOLOGICA. Vol 46, pp.11-21.
  • Therapeutic Guidelines (2004). Therapeutic Guidelines: Dermatology, North Melbourne, Therapeutic guidelines Limited.
  • Traub, M & Marshall, K (2007) ‘Psoriasis – Pathophysiology, Conventional, and Alternative Approaches to Treatment’. Alternative Medicine Review. Vol 12, pp.319-330.
  • Woolff, K, Goldsmith, L A, Katz, S I, Gilchrest, B A, Paller, A S & Leffer, D J, (2003) ‘Fitzpatrick’s Dermatology in General Medicine’, 7e. Ch. 72. The McGraw Hill Companies.
Polymorphic Light Eruption (PLE)
Polymorphic Light Eruption symptoms

Polymorphic Light Eruption symptoms

Also known as PLE, PME or PMLE, Polymorphic Light Eruption is the most common skin disorder characterized by photosensitivity and, after sunburn, is the most common sun-related problem seen by doctors.

PLE is a recurrent abnormal reaction to sunlight (or artificial ultraviolet radiation). It occurs after a delay on areas of the skin not regularly exposed, such as cleavage, upper arms, and trunk following sun exposure.

The disease can present in many forms (hence polymorphic), with variants including papular, vesicular, papulovesicular, plaque, erythema multiforme-like, insect bite-like, purpuric and sine eruptione.

Although PLE is regarded to be severely debilitating, there is a common understanding that only a fraction of patients present to dermatologists for treatment of their symptoms. The main reason for this is the lack of currently available efficacious therapies other than the administration of high doses of corticosteroids. PLE has a considerable impact on the quality of life for many people because of the need to avoid sun exposure during the spring and summer months.


PLE is very common world wide affecting up to 20% of southern Scandinavians and 5% of southern Australians. It has only rarely been reported in Asian and African countries. Its prevalence decreases with decreasing latitude.

The incidence of PLE has been reported in literature to be approximately 5% in Australia, 10% in the United States, 15% in the United Kingdom and approximately 15% – 20% in the most northerly latitudes of Europe. While it occurs in people with all skin types, it is more common in fair-skinned individuals.

A positive family history is common occurring in about a fifth of cases. 15% of monozygotic twins compared with 5 % of dizygotic twin pairs were both considered to have PLE, helping to confirm an inherited component to the pre-disposition to develop PLE.

PLE usually starts before the age of 30 and is much more common in females than males.


Polymorphic Light Eruption symptoms on both legs

Polymorphic Light Eruption symptoms on both legs

PLE eruption typically occurs after the first substantial UV radiation exposure and is common in spring and early summer. It has also been reported to occur after solarium use and, rarely, to visible radiation. Continued exposure often leads to abatement of symptoms – the ‘hardening phenomenon’, and so PLE is often less troublesome towards the end of summer than in spring.

Symptoms include non-scarring, itching (pruritis) or burning, red papules, vesicles or plaques and appears on sun-exposed skin 30 minutes to several hours following exposure to sunlight.

The eruption always occurs on an exposed, but typically not regularly exposed, site of the body and is intensely itchy, the itch sometimes preceding development of the rash. PLE outbreaks always tend to recur at the same site within an individual and are usually symmetrical. Symptoms usually resolve within a few days to 2 weeks of onset and with subsequent light avoidance.

PLE has many possible morphologic forms as suggested by the name (polymorphic). Papular and vesicular morphologies are most common, followed by plaque and papular subtypes. PLE often looks similar each time it occurs within an individual (monomorphic) however some patients do have different morphologies on different sites, for example plaques on the face and a papular eruption on the forearms.


PLE is believed to be a delayed hypersensitivity (allergic) reaction to an allergen produced in the body following sun light exposure. Individual susceptibility differs, and the delay of disease onset after exposure is usually several hours to days. There is, however, an early onset PLE variant with symptoms as soon as 30 minutes after first exposure.

The aetiology (origin) of PLE is unknown. It is believed to be a delayed type hypersensitivity response to an ultraviolet-induced allergen (photoallergen). The clinical observation that a first time eruption occurs after particularly intense ultraviolet exposure (deliberate sunbathing or solarium use) could indicate that such an exposure leads to the development of autosensitisation thus lending support to an autoimmune role in the development of this disease.

Differential diagnosis

Differential diagnosis of Polymorphic Light Eruption include:

  • Solar Urticaria (SU)
  • Erthyropoietic Protoporphryria (EPP)
  • photo-exacerbated dermatoses such as atopic or seborrheic eczema or acne


Sun avoidance and protective measures alone are sufficient for most mild/moderately affected people and are the mainstays of treatment in those severely affected. Avoiding unnecessary environmental exposure, such as beach holidays, wearing appropriate clothing with tightly woven fabrics, using broad spectrum high factor sunscreens applied thickly and frequently and avoiding the midday sun are some integral. For those more severely affected, the use of UV absorbing film, and shielding from glass, car and house windows is often appropriate.

Patients who experience PLE infrequently usually respond to short courses of oral corticosteroids. Topical steroids may also be useful. There is evidence for the use of topical steroids applied prophylactically immediately after exposure and this can also be helpful preventing flares during desensitisation.

Severe PLE treatment

For those more severely affected by PLE, prophylactic photochemotherapy with narrow-band UVB or PUVA given in spring serves to desensitise the skin and is beneficial in the majority of patients. Such therapy can in itself induce a reaction. Various other therapies have also been tried but appear largely ineffective. These include hydroxycholoroquinine, beta-carotene, nicotinamide, omega-3-polyunsaturated fatty acids. Oral immunosuppressive therapy with Azathioprine or Cyclosporin has been shown to be effective for severe cases.


A large number of PLE sufferers experience resolution of their symptoms or have a milder form of the disease seen a mean of 32 years after initial diagnosis. Whether this is due to spontaneous resolution or whether it is a result of repeated treatment courses is unknown.


  • Hawk, J & Ferguson, J (2008). “Abnormal Repsonses to Ultraviolet Radiation: Idopathic, Probably Immunologic and Photoexacerbated”, in Fitzpatrick’s Dermatology in General Medicine 7th Edition. Ch 90, pp816-818.
  • Ferguson, J, (2006). “Polymorphic light eruption”, in: Introduction to Photodermatology Photodynamic therapy and laser therapy, Ninewells Hospital and Medical School, Dundee.
  • Hasan T, et al., (1998). “Disease associations in polymorphous light eruption. A long-term follow up study of 94 patients”, Archives of Dermatology Vol 134, pp1081-1085.
  • Ferguson, J (1996). “The management of the photodermatoses with phototherapy” in Honigsmann H, Jori G, Young AR (eds) The fundamental bases of phototherapy. OEMF spa, Milan, Italy, pp 171-179.
  • Gonzalez-Amaro R et al., (1991). “Immune sensitization against epidermal antigens in polymorphous light eruption”, Journal of American Academic Dermatology. Vol 24, pp70-73.
  • Frain -Bell, W (1985). “The idiopathis dermatoses”, in Cutaneous photobiology. Oxford University Press, Oxford. pp24-59.
Atopic Dermatitis
Atopic Dermatitis

Atopic Dermatitis

Atopic dermatitis (AD), also known as atopic eczema, is one of the most common chronic inflammatory skin diseases. It is characterised by itchiness (pruritis) and associated defects in the skin barrier. AD is a complex disease with significant genetic and environmental influences, but its precise mechanisms are poorly understood. Its prevalence is rising in developed countries and, although predominantly a childhood disease, a small proportion of adults do suffer AD. Over 80% of adult AD patients suffer from hayfever or asthma.

A majority of patients with AD have mild disease. A significant minority, however, have moderate to severe AD, which is difficult to manage and requires second-line therapies.


The prevalence of atopic dermatitis varies between different populations. If affects less than 2% of children in China and Iran, whilst the prevalence can be as high as 20% in northern and western Europe, Australia and the USA. The prevalence of adults with AD is as low as 0.9% in the USA and can be up to 10% in other countries. AD affects all races and affects both sexes, although females are slightly more frequently affected than males.

The prevalence of AD has increased dramatically in the past three decades. Some studies report that the incidence and prevalence of AD may have stabilized in recent years.

The increase in recent years can be attributed to environmental influences. A higher incidence in AD has been observed in industrialized and urban settings, higher socioeconomic status and a smaller family size. The “hygiene hypothesis” has been proposed to explain recent increases in AD. This hypothesis suggests that absence of infections early in life in the above-mentioned populations predisposes individuals to developing AD. The support for this hypothesis, however, has been equivocal. Also, the role of dietary factors in AD has been far from proven. A family history of AD, asthma or allergic rhinitis may increase susceptibility to developing AD.


The precise causes of atopic dermatitis are unknown, but AD considered to be caused by complex interactions of deficient innate and adaptive immune responses as well as a result of genetic predisposition. The following factors are thought to play a causal role in AD:

  • A family history of AD, asthma or hayfever is common, suggesting a role for genetic variants in the development of AD;
  • Defects in the immune system are thought to play in the hypersensitivity reaction that characterises AD;
  • Allergies may play a role in the exacerbation of AD. Although patients with AD develop allergies to food and environmental allergens, it is not clear if allergies cause or maintain AD;
  • Environmental irritants, such as detergents, may cause flare-ups of AD;
  • Itching may further damage the skin barrier and cause flare-ups of AD and secondary infections;
  • Overgrowth of Staphylococcus aureus (S aureus) may lead to recurrence of AD;
  • Dry skin, temperature changes, stress and exposure to water may worsen the symptoms of AD.

Genetic predisposition to atopic dermatitis

AD has a strong genetic component and linkage studies have identified chromosomal loci 1q21, 3q21, 3q24-22, 3q26-24 and 17q25 as possible regions of interest in AD. Specific regions that predispose to AE with increased allergen-specific IgE and concomitant asthma have also been identified. These loci are thought to contain genes or gene families that modulate immune reactions in the skin and mucosa. The genetic variants in these loci are thought to be involved in epidermal barrier dysfunction, via regulating epidermal differentiation, inflammation and atopy.

Impaired barrier defence

The epidermis of the skin functions as a physical barrier and an immunological organ. The barrier confers protection against allergens, microbes and irritants. In AD, a modified skin barrier with increased transepidermal water loss and dehydration of the skin is the hallmark feature. The dysfunctional barrier allows allergens, microbes and irritants to enter the skin and causes an immune response that characterises AD. Impaired epidermal differentiation is believed to be responsible for epidermal dysfunction in AE. During differentiation, keratinocytes move from a proliferative cell type in the basal layer of epidermis through the granular layer where the cornified envelope is formed, to an association of flattened, dead cell remnants (corneocytes) in the uppermost layer of the skin, the stratum corneum (SC). The cornified envelope prevents water loss and acts as a barrier against allergens and microbes. Altered enzymatic activities have been postulated to affect SC integrity, cohesion and permeability barrier function. Impaired barrier defences can also occur due to abnormal expression of structural proteins involved in the cornification process.

Innate immune responses are the first-line cellular and biochemical defence mechanisms that respond to microbial invasion via their recognition by pattern-recognition receptors (PRR). PRR plays a crucial role in activating innate immune response and trigger adaptive immune responses. Impaired PRR responses have been implicated in the pathogenesis of AD. Furthermore, impaired innate immune mechanisms with deficiency of antimicrobial proteins are believed to be responsible for the increased susceptibility to skin infections seen in patients with AD.

In addition to innate immunity, keratinocytes are crucial in mediating adaptive immunity via cytokines. In patients with AD, keratinocytes produce increased amounts of proinflammatory mediators. Because of the underlying barrier dysfunction and increased production of cytokines, minimal exogenous skin trauma (such as scratching) is sufficient to activate disease in hitherto clinically uninvolved skin. Memory and effector T cells migrate to the inflammed skin and cause atopy.

AD is a biphasic disease. Initially, T helper type 2 (Th2) cytokines predominate. As the disease progresses to a chronic phase, T helper type 1 (Th1) cytokines predominate. Immunoglobulins (IgE), produced by B lymphocytes, are under the support of Th2 cytokines. Marked Th2 production and the resultant increase in IgE levels characterise AD. Modified regulatory T cells, and altered levels of immune modulators such as Interferon predispose patients with AD to viral infections (e.g. herpes simplex virus) and allergic sensitizations.


Atopic Dermatitis

Atopic Dermatitis

Atopic dermatitis is characterised by the following symptoms:

  • Intense itching (pruritis);
  • Skin rash;
  • Papular rashes (more common in darker skinned individuals;
  • Oozing or crusting blisters;
  • Moist or ‘weeping’ skin;
  • Dry skin (xerosis);
  • Discharge or bleeding from the ears;
  • Altered skin tone;
  • Inflamed or red skin;
  • Thickened (lichenified) skin; and/or
  • Rough and flaky skin.

Although atopic dermatitis can occur anywhere, particular patterns are usually observed at different ages. Initially, the face is usually affected. In crawling infants, the forearms, extensor aspects of the knees and the ankle flexures are the most affected. In infants, the skin lesions are ill-defined, scaly and crusted patches.

In older children, the flexor aspects of the elbow and the knees are the most affected.

The clinical course of AD fluctuates with intermittent flare-ups, although the causes may not always be discernible.

In adults, lesions become diffuse and erythematous. Xerosis is common and skin thickening may occur. A brown macular ring, which is localized deposition of amyloid, around the neck may be present. About 80% of adults with AD suffer from allergic rhinitis or asthma.

Infective complications can occur, particularly due to Staphylococcus infections, which may present as bullous impetigo or as exacerbated eczema with redness and oozing. Occlusion can occur from wet dressings and cause staphylococcal folliculitis. Herpes simplex virus infections are also common in patients with AD.


Recurrent bacterial, viral and fungal infections often afflict patients with AD. In patients with AD, up to 90% of microbial flora on the skin is colonized by S aureus, compared to about 10% in healthy individuals. In addition to promoting pruritis, S aureus can cause glucocorticoid resistance in patients with AD. Other complications of AD include allergies to food and other air-borne allergens, due to IgE sensitization and specific T cell mediated immune responses. Autoreactivity of IgE has been postulated in the involvement of progression to chronic and severe AD.


Atopic dermatitis is diagnosed based on the appearance of the skin and on family history. Excluding other conditions such as scabies, contact dermatitis, psoriasis and other morphologically similar diseases enables a more accurate diagnosis of AD. It is also important to rule out other, often rare, condition that present with AD, such as Comel-Netherton syndrome. Clinicians often use the SCORAD index, developed by the European Taskforce on Dermatitis and validated in children and adults, to assess the severity of AD. The SCORAD index can be used to derive a score, based on the severity and distribution of symptoms. This score can then be used to ascertain the progression and severity of AD. In patients with moderate to severe AD, where required, a validated stepwise allergy test (using food, contact allergens and atopens) may be helpful.


A range of treatments exist for atopic dermatitis, depending on the severity of the disease. In addition to treatment, wearing soft clothing, exposure to cool temperatures and clothes washed with mild detergents and without a fabric softener reduce flare-ups of AD.

For mild to moderate atopic dermatitis, emollients (substances that soften and soothe the skin – e.g. petroleum based gels) and topical steroids are the mainstay of treatment. In addition, avoiding allergens and irritants and educating family members and patients about AD may improve treatment outcomes.

Topical corticosteroids

Topical corticosteroids have been the mainstay of treatment for atopic dermatitis flare-ups. A number of agents are available in varying doses and concentrations. Low-potency agents should be used on the face, groin and axillae, and in infants, to minimize side-effects, such as acne. Topical corticosteroids should be used for the shortest time possible to control flare-ups in order to minimize adverse effects. Once flare-ups are controlled, preventative strategies should be employed to control AD. Systemic side-effects, such as reduced linear growth in children and altered bone density in adults, can occur, but are rare.

Secondary bacterial infections due to overuse of topical steroids should be clinically reviewed.

Calcineurin inhibitors

For moderate to severe AD, topical or systemic calcineurin inhibitors, such as pimecrolimus, may be effective. These agents inhibit calcineurin in the skin, and blocks early T cell activation and release of cytokines. These drugs have side-effects including, skin irritation and burning sensations. The long-term safety of calcineurin inhibitors is unclear amid reports of cancer development in some patients.


Phototherapy with exposure to ultraviolet B light may help in some cases of atopic dermatitis, but the risk of skin cancer with such exposure should be considered.

Systemic treatments

For severe forms of AD, systemic treatments may be warranted. Short-term systemic corticosteroid therapy may be effective in controlling AD in adults. Rebound flare-ups and reduced effectiveness is of concern and may limit use. Immune modulators such as cyclosporine and interferon-gamma-1b may be effective in treating severe AD. On the other hand, the efficacy of other immune modulators, such as azathioprine and intravenous immunoglobulins, are unclear. Side effects of these agents include kidney and liver damage, increased risk of developing certain forms of cancer, and immune suppression.

Treatment of infections

Antibiotic treatments (such as cephalexin) and anti-viral treatments (e.g. acyclovir) may be used to treat secondary bacterial (particularly, S aureus) and viral (herpes simplex virus) infections respectively. Concerns about antibiotic resistance should be weighed up. Use of antiseptic baths and washes should be avoided.


Atopic dermatitis is a chronic disease and cannot be prevented or cured. Steps can be taken to manage symptoms and reduce flare-ups. Wearing soft clothing (such as cotton or other smooth fabrics), exposure to cool temperatures and clothes washed with mild detergents and without a fabric softener can reduce flare-ups of AD. Use of emollients and/or moisturizers twice a day to prevent dry skin is crucial in reducing the exacerbations of AD. Bathing in warm water using a mild, unscented soap or soap-free cleansers is helpful. Lubricating ointments may be used at night-time, because of their superior hydrating potential. Patients may develop allergies to foodstuffs and, where necessary, epinephrine / adrenaline (EpiPen) injections should be readily available. Avoiding known environmental triggers is beneficial.


Atopic dermatitis is a chronic condition that cannot be cured, but the symptoms can be controlled with treatment and appropriate preventative methods, such as moisturisation. Educating patients about the need to control and manage symptoms, and avoid allergens and irritants is vital in reducing the risk of flare-ups and complications. In children, AD usually resolves by adulthood. In adults, however, the disease is often recurring. Patients may develop complications, including bacterial and viral infections, asthma and allergic rhinitis and these should be managed appropriately. Regular follow-ups may be required to assess the progress of the disease and modify treatment regimes accordingly.


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  • Maintz, L & Novak, N (2007). ‘Getting more and more complex: the pathophysiology of atopic eczema’.European Journal of Dermatology, Vol 17(4), pp. 264-283.
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  • Solanki, L S, Srivastava, N & Singh, S (2008). ‘Superantigens: a brief review with special emphasis on dermatologic diseases’. Dermatology Online Journal, Vol 14(2).
  • Taieb, A (2007). ‘When and how to perform allergy tests in children and adults with atopic dermatitis’.European Journal of Dermatology, Vol 17(4), pp. 263-266.
  • Weatherhead, S, Robson, S C & Reynolds, N J (2007). ‘Eczema in pregnancy’. British Medical Journal, Vol 335, pp. 152-154.
  • Wuthrich, B, Cozzio, A, Roll, A, Senti, G, Kundig, T & Schmid-Grendelmeier, P (2007). ‘Atopic Eczema: Genetics or Environment?’. Annals of Agricultural and Environmental Medicine, Vol 14, pp. 195-201.
Acne Vulgaris

Acne vulgaris, commonly referred to as acne, is a skin condition characterised by whiteheads, blackheads and inflamed red pimples. It is a very common skin condition in adolescents and affects a significant minority of adults. Acne can severely impact an individual’s psychological well-being, as acne can lead to scarring. Although not a systemic disease (i.e. acne is usually confined to the skin and does not affect other tissues or organs), a rare and systemic form of acne, acne fulminans, can affect bones and other tissues. Other variants of acne that are often severe exist, but these are rare in comparison with acne vulgaris. Unless indicated otherwise, the discussion in this article pertains to acute vulgaris.


Acne affects 95 – 100% of adolescent boys and 83 – 85% of adolescent girls. Acne usually resolves before the age of 25 years. About 12% of women and 5% of men have acne at the age of 25 years. At 40 years of age, 1% of men and 5% of women have acne. Acne manifests in adulthood either for the first time or may recur in individuals who have had acne in adolescence.

It has been estimated that about 14% of affected individuals consult their general practitioners, while about 0.5% of individuals consult a dermatologist for their acne. Acne can occur in neonates and infants, predominantly in males, in the first year of life and can last up to four years. In females who develop acne earlier in life, there is an increased risk of developing more severe acne. Pre-menstrual flare-up of acne can occur in women.

A cross section of skin with acne

A cross section of skin with acne


The surface of the skin contains pores, each of which opens into a canal called a follicle. Each follicle contains a hair and an oil gland (sebaceous gland). The oil (sebum) from these glands lubricates the skin and helps remove dead skin cells. If too much sebum is produced, the pores may become blocked with the accumulation of dirt, debris and bacteria. The blockage is called a plug or a comedone. If these plugs rupture, the oil and bacteria can reach the surrounding vicinity, leading to inflammation. If the inflammation spreads deep down the skin, the pimples may enlarge to form cysts, which can be painful.

Acne can be caused (or exacerbated) by:

  • Family history of acne (i.e. genetic factors): A strong genetic component is believed to be associated with acne. Family history of acne predisposes an individual to developing acne. About 81% of the variance in acne can be attributed to genetic factors, whilst 19% of variance in acne can be attributed to environmental factors;
  • Excess androgen production, as can occur in some obese individuals, individuals with adrenal hyperplasia and other endocrine disorders: Structural modifications of the androgen receptors, thought to be genetic in origin, may play a role in altered response to peripheral androgens. Allelic variants in the cytochrome P450 gene, which may lead to defects in keratinocyte differentiation, have been observed in patients with acne;
  • Excessive combing or brushing of hair;
  • Sweating or a humid environment;
  • Comedogenic cosmetics, such as those containing the agent isopropyl myristate;
  • Stress;
  • Hormonal changes, as can occur during pregnancy or with the use of oral contraceptives;
  • Certain medications, including steroids and phenytoin.

Contrary to common perceptions, there is as much scientific evidence pointing to dietary factors as arguments against the significance of nutritional intake on the exacerbation of acne (e.g., fatty foods and chocolate). Consumption of healthy foods will, however, promote general well-being.


Acne Vulgaris

Acne Vulgaris

Acne is a chronic disease of the pilosebaceous follicle. The pathophysiology of acne can be divided into three steps:

  1. Stimulation of the sebaceous glands, resulting in seborrhoea. This step usually begins at puberty.
  2. Defects in the proliferation, adhesion and differentiation of keratinocytes lead to micro-comedone formation. Micro-comedones are the first elementary lesions of acne.
  3. Formation of inflammatory lesions constitutes the third step. Unlike the first two steps which are universal in the pathogenesis of acne, the third step does not occur in all individuals. Propionibacterium acnes (P acnes), a gram positive anaerobe, plays a crucial role in the formation of inflammatory lesions.

Androgens, in particular, a metabolite of testosterone, stimulate the production of sebum. A number of enzyme systems are present in the sebaceous glands and they convert cholesterol or weak androgens to stronger androgens that are capable of activating these glands. In patients with acne, the activity of these enzymes is increased. The rate of proliferation of sebocytes, the cells that form the sebaceous glands, and the potency of the enzyme systems varies between different cutaneous regions. This is believed to explain the predominance of facial acne. In addition, specific receptors (such as the PPAR receptor system that act via retinoid receptors) and neuromediators (such as substance P) can alter sebum production by modifying the proliferation of sebocytes and secreting specific substances respectively.

Obstruction of the follicular canal occurs due to defects in proliferation, adhesion and differentiation of keratinocytes. The keratinocytes fail to separate from each other, hence obstructing the canal and resulting in the formation of a micro-comedone, which is invisible to the naked eye. As the sebum production continues, dilation of the follicles occurs forming the comedone, which is visible. Anomalies in androgen metabolism are thought to play a role in causing the defects in keratinocyte proliferation, adhesion and differentiation. Interleukin-1α, a cytokine released by the keratinocytes in response to local irritation, is believed to play a role in micro-comedone formation. The phenomenon of seborrhoea, which decreases the concentration of linoleic acid in sebum by dilution, has been shown to affect keratinocyte differentiation and may contribute to the formation of micro-comedone.

P acnes plays a crucial role in the inflammatory phase of acne. P acnes proliferates in the micro-comedone and contains lipases that split triglycerides into free fatty acids and glycerol. The free fatty acids and bacterial fragments from P acnes migrate across the wall of the comedone and initiate an inflammatory response. Polynuclear neutrophils are recruited into the perifollicular tissue, where they secrete enzymes, including matrix metalloproteinases. These enzymes rupture the follicular wall and the inflammation invades the deeper layers. Other inflammatory mediators, such as T lymphocytes, prostaglandins, leukotrienes, complement, macrophages and cytokines, also play a role in the inflammatory response.


Acne usually occurs on the face and shoulders, but may also occur on the arms, legs and back. The symptoms of acne, in increasing order of severity, include:

  • Blackheads (open comedone);
  • Whiteheads (closed comedone);
  • Inflammatory papules and pustules;
  • Cysts; and/or
  • Scarring of the skin.

Diagnosis of acne is based on the appearance of the skin. Clinical tests are not performed, unless clinically warranted.

Clinical features

Acne is considered a polymorphic disease (that is, it presents in multiple forms) and two patterns of disease can usually be noted. In non-inflammatory acne, often seen in the peri-pubertal age group (8-16), increased sebum production in the face, chest, back and shoulders results in the formation of blackheads or open comedones. In some instances, appearance of whiteheads or closed comedones can occur, heralding the progression to inflammatory disease.

The inflammatory disease associated with acne is characterised by the presence of blackheads, whiteheads, papules and pustules. Cystic nodules and scarring can also be present. Redness and seborrhoea (greasy skin due to excess secretion of sebum) can also occur. The presence of acne may persist over years. Nodules may become more painful and an increased risk of scarring is present. Following the inflammatory phase, red or hyperpigmented changes can occur, which can last several months or even few years. On the upper chest and shoulders, hypertrophic or keloid scarring (a type of fibrous scar) may develop. Atrophic or “ice-pick” scars may usually develop on the face. In addition, small depressions and slight discolouration can develop and last for up to 12 months.

Clinical features of acne conglobata

In acne conglobata, a rare, severe variant of acne vulgaris, nodules are interconnected by channels, which contain haemorrhage and purulent exudate. When this evolves rapidly with fever, arthritis and neutrophil leukocytosis, the condition is termed acne fulminans.


Diagnosis of acne vulgaris is made clinically, based on the appearance of skin. Laboratory testing is rarely resorted to. Other conditions such as pustular drug eruptions and bacterial and fungal folliculitis can resemble acne, but can be distinguished by the absence of comedones. Acne rosacea can also resemble acne vulgaris, but the former is notable for its lack of comedones and nodules.

Although rarely performed, histological cultures may be helpful in ruling out gram-negative folliculitis (inflammation of the hair follicle) that is unresponsive to treatment. Histologically, a comedone is observed as a dilated follicle with a “plug” of loosely arranged keratin. As the disease progresses, dilation of the follicular opening occurs, resulting in an open comedone (blackhead). As the follicular wall thins, it may rupture. Bacteria and inflammatory mediators may be present. If the inflammation extends into the dermis, fibrosis and scarring can occur.


Self treatment

The following self-care steps may aid in decreasing the severity of acne:

  • Washing the skin with a mild, non-drying soap once or twice a day;
  • Avoiding excessive washing of the skin;
  • Avoiding comedogenic cosmetics, such as those containing the agent isopropyl myristate; and
  • Avoiding rubbing, squeezing, scrubbing or picking the pimples.

Acrylate glue based products, sold at pharmacies, may be used at home to extract comedones. It should be noted that this is not the same as picking at the spots, which can lead to scarring.

Professional treatments

Physicians (or beauty therapists) may choose to extract comedones manually. Pursuing this treatment once or twice a month may, in combination with other treatment options, may lead to a quicker resolution of acne.
Prescription medicines include:

  • Topical retinoid creams;
  • Topical and oral antibiotic therapy;
  • Benzoyl peroxide;
  • Hormonal therapies.

For severe cases of acne, chemical skin peeling, removal of scars and cysts or photodynamic therapy (see below) may be warranted.

Early stage acne treatment: Keratolytic agents

Keratolytic agents are the most effective topical treatment for early-stage acne. These agents target the occlusion of the follicles. Keratolytic agents include:

  • Retinoids: Tretinoin is considered as the gold standard against which new products are compared. It is the most potent of all the keratolytic agents. It acts by normalizing follicular epithelial cell turnover and preventing comedone formation. Side-effects include skin irritation, photosensitivity and an initial flare-up of acne. Adapalene, a synthetic napthoic acid derivative has comedolytic and anti-inflammatory properties and causes less irritation.
  • Azelaic acid: is a naturally occurring dicarboxylic acid that normalizes hyperkeratinisation and has anti-inflammatory effects. It has anti-bacterial properties and can stop the growth of P acnes. Itching and burning sensations are occasional adverse effects.
  • Alpha- and Beta-hydroxy acids: Both agents are comedolytics with limited efficacy.

Inflammatory phase acne treatment

For treatment of the inflammatory phase of acne that invariably involves P acnes, the following anti-inflammatory and antibiotic treatments are commonly prescribed:

  • Benzoyl peroxide: a bactericidal drug that is available as an over-the-counter preparation. It reduces the number of comedones and acts by sterilizing the follicle via its antibacterial effects on P acnes. Dry skin and allergy are possible side-effects.
  • Topical antibiotics: Clindamycin and erythromycin reduce numbers of P acnes. They also have anti-inflammatory actions by inhibiting neutrophil chemotaxis. A mixture of one of these agents with benzoyl peroxide may be more effective than either on its own and may aid in reducing antibiotic resistant strains of P acnes.
  • Oral antibiotics: These agents are used in patients with moderate to severe forms of acne who are at risk of scarring. Tetracyclines, erythromycin and trimethoprim are the agents of choice. Adverse effects, such as hepatic and renal impairment, may occur, especially with long-term use, and biochemical monitoring may be helpful.

Anti-androgenic therapy, including combination oral contraceptives, may prove useful in the treatment of acne. It should be noted, however, that in some instances, the use of oral contraceptives may worsen acne.

Administering isotretinoin orally is helpful in treating nodulo-cystic acne. It suppresses the production of sebum to pre-pubertal levels and an associated decrease in P acnes is observed. Common adverse effects include skin dryness, dry cracked lips, retinoid dermatitis and dry mucous membranes. These side-effects usually resolve after ceasing therapy. In rare cases, acute fulminans can occur with isotretinoin therapy. Psychological impairment, such as depression and suicidal tendencies, can occur. Concomitant use with certain drugs should be avoided. Isotretinoin is contraindicated during pregnancy because of its teratogenic effects.

Photodynamic therapy for acne

Light and laser therapy may be used in combination with other therapies for acne in patients who do not respond to a single treatment option alone, or who experience significant adverse effects with other modes of treatment. The use of blue and other longer wave visible light stimulates production of natural porphyrins in P acnes and destroy target cells. Lasers and radiofrequency devices that are capable of general upper dermal cooling and causing selective injury to sebaceous glands can be helpful in the treatment of acne.


Acne cannot be prevented. The following self-care steps may, however, aid in decreasing the severity of acne:

  • Washing the skin with a mild, non-drying soap once or twice a day, especially after exercise;
  • Avoiding excessive washing of the skin;
  • Avoiding comedogenic cosmetics; and
  • Avoiding rubbing, squeezing, scrubbing or picking the pimples.

No proven association exists between diet and acne, although consuming a healthy diet will promote general well-being.

Acne resolution

Acne usually resolves after adolescence. It may, however, recur or appear for the first time in adulthood in some individuals. Untreated acne can lead to the formation of painful cysts, and physical and emotional scarring. Consulting a general practitioner or dermatologist may be warranted, if the acne is severe or if it has not responded to over-the-counter treatments.

Although acne responds well to treatment, it may recur from time to time. The earlier the onset of acne, particularly in females, the more likely it is to recur in adulthood. It is important to note that like all medicines, treatment of acne may cause side effects – especially with tretinoin. Moreover, many of the commonly prescribed agents for acne are teratogenic and should be avoided during pregnancy.


  • (2008) Acne vulgaris. [Online]. Available online [Accessed 01/12/2008].
  • Goodman, G (2006). ‘Acne: natural history, facts and myths’. Australian Family Physician, Vol 35(8), pp. 613-616.
  • Goodman, G (2006). ‘Managing acne vulgaris effectively’. Australian Family Physician, Vol 35(9), pp. 705-708.
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  • Pawin, H, Beylot, T, Chivot, M, Faure, M, Poli, F, Revuz, J & Dreno, B (2004). ‘Physiopathology of acne vulgaris: recent data, new understanding of the treatments’. European Journal of Dermatology, Vol 14, pp. 4-12.
  • Purdy, S & de Berker, D (2006). ‘Acne’. British Medical Journal, Vol 333, pp. 949-953.
  • Taglietti, M, Hawkins, C N & Rao, J (2008). ‘Novel Topical Drug Delivery Systems and Their Potential Use in Acne Vulgaris’. Skin Therapy Letter, Vol 13(5), pp. 6-8.
  • Webster, G F (2002). ‘Acne vulgaris’. British Medical Journal, Vol 325, pp. 475-479.
  • Zaenglein, A L & Thiboutot, D M (2006). ‘Expert Committee Recommendations for Acne Management’. Pediatrics, Vol 118, pp. 1188-1199.
Sun 'Allergies'

Photosensitivity in children

Photosensitivity is the abnormal reaction of skin to light and sunlight, often referred to as a ‘sun allergy’. Its incidence in childhood is rare, but it is during childhood that some of the more severe ‘sun allergies’ (photosensitivity disorders) can first occur, causing children and parents great distress.

Generally a ‘sun allergy’ is neither an allergy, nor caused specifically by the sun. These disorders can be caused by a range of factors; some environmental, some chemical and others unknown. For most photosensitivity disorders, a particular wavelength of light is responsible, such as visible light or invisible ultraviolet (UV) radiation. A child may be sensitive to a specific type of radiation (the longer wavelength, UVA, is most common) or to a broad range. Symptoms of photosensitivity vary considerably, but commonly include sunlight-induced rashes (photodermatoses), skin reddening and blisters or lesions.


Causes of photosensitivity

Hydro vacciniforme is a rare photodermatoses which presents in children.Diseases which can cause photosensitivity in children include:

A variety of skin disorders, called photodermatoses, including – solar urticaria, hydroa vacciniforme, actinic prurigo and polymorphic light eruption (PLE)
Genetic skin disorders, such as the rare disease xeroderma pigmentosum
Metabolic conditions – the most common of these are the porphyrias, where photosensitising chemicals (porphyrins) build up in the skin (see more on EPP, one of the more common porphyrias to present in children)
Underlying skin disease, such as eczema (atopic dermatitis) or psoriasis, can sometimes be exacerbated by sun exposure

Other potential causes of photosensitivity:

Some medicines contain substances which can photosensitise the skin of susceptible people; be sure to mention to your doctor or dermatologist any medications your child might be taking
Contact with specific plants, dyes, fragrances or other chemicals can also induce photosensitivity

Diagnosis and treatment

Assessment of a suspected photosensitivity by a dermatologist includes a description of patient/family history and a physical examination. The clinician may then require laboratory tests (such as blood, urine and faecal tests) and skin biopsies or phototests (measured tests of the skin’s response to light) to determine the cause. The specific precautions necessary and treatments available will depend on the individual condition diagnosed or the stimulus of the photosensitivity. Many people with a photosensitivity do need to avoid excessive sun exposure, though the degree varies.

Parents who believe the sun is definitely the issue should seek a referral to a physician or dermatologist who specializes in photosensitivity disorders (such as a photodermatologist), as many children go undiagnosed or misdiagnosed due to the rarity of these conditions and the difficulty of identifying UV or light as the cause.


Garzon, MC & DeLeo, VA 1997, ‘Photosensitivity in the pediatric patient’, Current Opinion in Pediatrics, 9(4):377-387.

Sun safety

kids_on_bikesIt is well known that the ultraviolet (UV) radiation in sunlight can have damaging effects on human health. The vulnerable developing skin of children and babies can sunburn and scar easily. Excessive time spent in the sun can also have long-term, sometimes dangerous, effects including: eye damage (i.e. cataracts), skin cancer and premature skin aging (wrinkles; sagging; age spots and other lesions; broken blood vessels; thin, fragile, dry or leathery skin).

Importantly, the amount of sun exposure and sunburn a child incurs contributes significantly to their risk of developing skin cancer, including melanoma, later in life. Therefore, sun safety is vital for protecting the skin and reducing a child’s risk of skin cancer. There are a number of ways you can help to protect your child from the damaging rays of the sun and prevent these health problems. Furthermore, children whose parents set an example with sun safety tend to learn and carry them out more often.


Protective clothing

Light-weight, tight-weave clothing should be worn when spending time in the sun. It is best to cover as much as the body as possible, so long pants and shirts with sleeves and collars are recommended. Certain colours and types of fabric provide a better barrier between the skin and sun than others, for more information on sun safe clothes see the article on Sun protective clothing.


SunSmart Victoria recommends children and adults wear broad-rimmed hats to shade the scalp, face, ears and neck from sun damage. The hat’s brim should be at least 7 ½ cm wide, those of the bucket or legionnaire styles generally give good protection. Caps are not considered adequate protection as they don’t cover the ears and the back of the neck; common sites of sun overexposure and skin cancer development.


Most government health agencies advocate the use of wrap-around, polarised sunglasses to protect eyes from sun damage. Image: Aka Hige on FlickrMost government health agencies also advocate the use of wrap-around, polarised sunglasses to protect eyes from sun damage. When choosing sunglasses for children there are a few things you can look for to ensure they will shield adequately:

  • Check the label for the phrase “good UV protection”
  • Numbered categories 2, 3 or 4 – this indicates the glasses guard against a high level of UV
  • Text indicating that the glasses have met the Australian standard (AS/NZS 1067:2003)
  • An ‘Eye Protection Factor’ (EPF) rating of 9 or 10


When sun exposure is unavoidable, sunscreens can help to protect children’s skin, however it is important to remember that no sunscreen is 100% effective and should be used alongside other protective measures.

High SPF (minimum of 30+), broad-spectrum sunscreens block or absorb the most UV radiation and may be beneficial for preventing sun damage in all its forms. Proper, thorough application is essential to ensure the effectiveness of sunscreen – this means applying it regularly and liberally (roughly one teaspoon for each limb and your face). Use a generous amount of sunscreen 20 minutes prior to going out in the sun and reapply every two hours thereafter (more often if swimming or if skin is sweaty).

For more in-depth information on sunscreen use on children and babies, see the article on Sunscreen and pediatric skin on our Science of Skin website.

Avoiding the sun

Beach umbrella. Image: will ockenden on FlickrThe level of UV radiation generally spikes in the middle of the day when the sun is at its highest. Where possible, the World Health Organization (WHO) recommends limiting sun exposure during the hottest part of the day, from approximately 10am till 4pm. This may mean staying indoors, seeking shady spots outside or scheduling sports and other outdoor activities for the morning or late afternoon.

The forecast levels of UV radiation, known as the UV index, are often included as part of many weather reports. The Bureau of Meteorology provides information on the daily UV intensity throughout Australia,


SunSmart Victoria 2010, ‘For parents: protecting your family’, retrieved 5 April 2011, <>.

SunSmart Victoria 2010, ‘Sun protection’, retrieved 5 April 2011, <>.

Cuts, Bruises and Bites

Insect bites and stings

Mosquitoes, bees, wasps, fleas, spiders and ticks are the most common perpetrators of insect bites and stings in children. The symptoms and extent of the reaction your child experiences following a bite or sting will depend largely on how allergic they are, but most pain and irritation is only temporary. Often there is only slight, transient inflammation (redness and irritation) of the skin in the spot where the insect has bitten or stung. The bite/sting may be sore, tender or itchy and usually resolves within a few days. More intense reactions involve redness and swelling over a larger area which can take a week or so to settle. Very occasionally a child can have a severe allergic reaction to an…
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Bruises are one of the most common and visible injuries, often caused by intense or repeated contact of the skin with another object. Bruises frequently result from falls, accidents or sports injuries, but they may also be indicative of an underlying medical condition. For this reason, parents of children who bruise easily or experience regular, severe or unexplained bruising should seek medical treatment. What is a bruise? A bruise is a form of internal bleeding, known medically as a contusion. It is caused when muscle fibres, capillaries and venules (small veins) under the skin are damaged but the skin itself remains intact, causing blood to seep into the surrounding tissue. The skin around a bruise appears discoloured and is usually…
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In the event of a severe burn, consult emergency services immediately for professional treatment and advice. Burns are injuries to the skin caused by heat from flames, liquids, radiation, chemicals or electrical devices. The severity of a burn is determined by its depth, the age of the patient, the particular sites on the body burnt (hands, feet, face, genitals and joints are the most complicated) and the total surface area of the burns. While minor burns usually cause nothing more than temporary shock and mild discomfort, severe or widespread burns can be physically destructive, permanently debilitating and even fatal. Types of burns Burns can be classified by the depth of tissue they injure. The names for various types of burns…
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Healing cuts

Every child will, at some point, scrape a knee, cut a finger or break their skin open in some way. While more serious lacerations require medical attention, here are some basic tips for assisting in the healing of minor cuts and avoiding infection or irritation. First aid for minor cuts and abrasions Before treating a child’s injuries it is important to first wash your own hands, covering any breaks in the skin with bandages or gloves. Generally speaking, shallow cuts and abrasions stop bleeding on their own. However, if bleeding persists, it may be necessary to physically stem the flow of blood by gently holding a sterile dressing to the wound and applying pressure. Gently, but thoroughly, cleanse the cut…
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Skin During Pregnancy

Skin during pregnancy
The changes that occur in the skin during pregnancy are related to different aspects of the skin’s structure. We can group these into four types:

  1. changes in pigmentation (the colour of the skin);
  2. changes in the function of the skin’s glands;
  3. vascular changes (affecting the blood vessels beneath the skin); and
  4. changes in the connective tissue which holds skin together.

Many of these changes result from the altered levels of hormones which occur during pregnancy or from the physical stretch and strain on the skin. Fortunately, most are only temporary and subside or lessen shortly after delivery.

Skin changes during pregnancy

Pigmentation (colour changes)

Changes in skin pigmentation during pregnancy may involve an increase in pigment (skin darkening), or a loss of pigment (skin lightening).

Hyperpigmentation, or darkening of the skin, is extremely common; particularly during the first trimester of pregnancy. Up to 90% of pregnant women experience an increase in skin pigmentation on various parts of their bodies. It usually occurs on areas of skin which were darker to begin with, such as moles, freckles, nipples and genitals. Most experts attribute these changes to increased hormone levels (estrogen, progesterone and α-MSH) in the blood. It is thought that skin cells, called melanocytes, are stimulated by the hormones to produce more of the brown pigment (melanin) in the skin.

Melasma is common during pregnancy. Image: Jmh649 from Wikimedia commonsIt is well known that folic acid can reduce the risk of neural tube defects in babies, but studies have also shown a link between folic acid deficiency and hyperpigmentation. Ensuring you get enough folic acid, by taking supplements and eating plenty of folate-rich foods (leafy green vegetables, citrus fruits and legumes), can therefore help to minimise unwanted skin darkening.

Melasma, a type of facial skin darkening, and linea nigra, the formation of a dark line down the centre of the abdomen, are two common pigmentary changes to occur during pregnancy.


Most women will find that they sweat (perspire) more during pregnancy; in some cases this can be quite profuse. Once again, this is due to the increase in hormones affecting the operation of the sweat glands in the skin.

The influx of hormones during pregnancy can also stimulate the oil-producing (sebaceous) glands in your skin to secrete more oil (sebum). This can lead to worsening acne, particularly in women that had a preexisting problem or suffered from acne during adolescence.


A pregnant woman’s body also produces much more blood (some studies suggest up to 50% more) than normal to adequately supply the growing fetus. As a result, the small blood vessels beneath the skin surface dilate and become more permeable, those penetrating the skin can also become more numerous and visible. These changes in blood and vessels can cause unwanted spider and various veins, however the increased circulation is also responsible for the phenomenon of radiant skin known as the ‘pregnancy glow’.

Connective tissue

Pregnancy places a huge strain on the body, and the skin is no exception. Often the tissue beneath the skin tears if the skin is overstretched. This can create stretch marks on the abdomen as the skin is pulled over the expanding uterus, or on the breasts as they enlarge. Another change to the structure of the skin which is relatively common is skin tags, small, soft growths (usually in folds of skin) made up of collagen fibres and blood vessels.

Changes to the skin on the breasts

In addition to darker skin on the nipples, the areolas, the circular area surrounding the nipple, often expands during the first trimester. The small bumps on the areolas are actually specialised oil glands, called Montgomery’s tubercles, these may protrude more during pregnancy and lactation.

As well as stretch marks on your breasts, you may notice the veins beneath the skin become more obvious. Early in the pregnancy, your body begins to make colostrum, a thick, yellow liquid which the baby is first fed on. Small quantities of colostrum may leak from yours breasts towards the end of the pregnancy.

Skin care during pregnancy

Use a gentle cleanser that is oil and soap-free to wash your face twice each day. Rinse away any traces of cleanser with warm water and pat your face dry with a clean towel.
Avoid harsh chemicals, vigorous scrubbing or cleansing too often, as these can remove the natural oils from your skin, making it produce excess to compensate.
After cleansing, apply a mild, oil-free moisturising lotion to keep your skin soft, supple and hydrated.
Stay properly hydrated by drinking plenty of water; this helps your skin maintain its water content and appear smooth and bright.


BabyCenter 2010, ‘Breast changes during pregnancy’, retrieved 24 March 2011, <>.

Boutros, S, Régnier, S, Nassar, D, Parant, O, Khosrotehrani, K & Aractingi, S 2009, ‘Dermatological Manifestations Associated With Pregnancy’, Expert Review of Dermatology, 4(4):329-340.

Gentili, A & Vohra, M 2009, ‘Folic Acid Deficiency’, eMedicine, retrieved 30 March 2011, <>.

Pomeranz, MK 2010, ‘Physiologic changes of the skin, hair, nails, and mucous membranes during pregnancy, UpToDate, retrieved 24 March 2011, <>.

Nutrition for healthy skin


When it comes to nutrition, our skin often reflects what’s going on inside our body. Feeding children a balanced diet, high in essential vitamins and minerals, can have beneficial effects on the health of their skin. The following is a list of skin-friendly foods and the nutrients that they contain.



Berries (blueberries, cranberries, blackberries, strawberries, raspberries), plums, apples, green tea, artichokes, spinach, beans/legumes (black red and pinto), prunes, raisins, pecans.

These foods are all rich sources of antioxidants. Reactive oxygen species, or ROS, are molecules produced by the body in response to things like sun exposure and pollutants. When present in large amounts they can cause damage to both the structure and genetic information of skin cells. Antioxidants minimise the damage caused by ROS, protecting the cells to some extent. Antioxidants are also able to reduce skin inflammation. Inflammation can destroy the elastin and collagen fibres which give skin its plumpness and flexibility.

Shellfish (oysters, crab, lobster), nuts (cashew, brazil, peanuts, walnuts, pecan), seeds (sunflower, sesame, pumpkin), organ meats (liver, kidney, brain), legumes (beans and peas).

Copper is a mineral which aids in the development of elastin, the fibres which give skin both its elasticity and firmness.

Oily fish (salmon, mackerel, tuna, sardines, herring, trout), walnuts, flax seeds, canola or safflower oil.

Essential fatty acids (Omega 3) are necessary for maintaining the membranes (casings) of skin cells. As a result, EFAs play a role in skin flexibility and repair. The membranes of skin cells behave like a barrier, protecting the contents of the cell and allowing for the passage of material in or out. A robust membrane allows the skin cells to better retain moisture, appearing firmer and smoother. EFAs can also help reduce dry or irritated skin and combat inflammation.

Organ meat (liver, kidney, heart), lean meats (beef, lamb, pork fish, chicken), eggs, green leafy vegetables.

Iron assists with the production of elastin and collagen fibres in the skin, it is essential for proper skin growth and maintenance.

Brazil nuts, fish (tuna, halibut, sardines, salmon), shellfish (oysters, shrimp, mussels), liver, kidney, whole grain breads and cereals, wheat germ, brown rice, sunflower seeds.

As with vitamins C and E, selenium has antioxidant properties that help protect the skin from sun damage. Selenium works to increase the density of skin, making skin appear fleshier. It also affects skin condition, reducing dryness and roughness.

Carrots, liver, chili peppers, apricots, sweet potatoes, spinach, cantaloupe, low-fat dairy products, broccoli.

Vitamin A (carotenoids) is vital to the development, maintenance and repair of skin cells. Vitamin A increases the renewal of skin cells and deficiency can cause dry, flaky skin.

Broccoli, tomatoes, papaya, mangoes, red/yellow peppers, parsley, potatoes, kiwi fuit, grapefruit, guava, oranges.

Vitamin C is an effective antioxidant. Antioxidants neutralise and stabilise reactive oxygen species (ROS) – molecules which can damage skin cells. Antioxidants protect the cells by mopping up any excess ROS.

Sunflower seeds, safflower and sunflower oil, almonds, olives, spinach and other leafy greens, whole grains (wheat, oats, bran), tomatoes.

Vitamin E also acts as an antioxidant, reducing the harmful effects of ROS. When working together, vitamins C and E are particularly good at reducing the risk of damage from sun exposure which can lead to skin aging and cancer. Vitamin E also helps to heal and maintain skin tissue.

Water, herbal tea (not including sweetened or diuretic infusions), fruit or vegetable juice (in moderation).

Drinking plenty of water helps to keep skin hydrated, making it appear softer and suppler. Water is also important to skin health because without it skin cells cannot properly transport nutrients in and get rid of harmful waste products. Adequate fluid intake also aids in the process of sweating, keeping the skin clear.

Oysters, wheat germ, peanuts, pumpkin seeds, lean meat (beef, lamb, pork).

Zinc is a mineral which moderates the production of oil (sebum) by the skin, helping to clear acne.

*It is important to note that excess supplementation with some of these vitamins and minerals (vitamin A, copper, zinc and selenium) can be dangerous. Always speak to your child’s doctor before commencing dietary supplements.

**Nuts, dairy products and shellfish are some of the most common foods to induce allergic reactions. Introduce these foods to your child’s diet gradually and seek immediate medical attention if a reaction occurs.


Fraser, J 2006, ‘The top five foods for healthy skin’, retrieved 15 August 2011, <>.

Bouchez, C 2006, Foods for Healthy Skin: You Are What You Eat, WebMD, retrieved 15 August 2011,<>.

Newborn Skin

Newborn Skin

Caring for skin from birth to 18 months

No longer protected inside its mother, a newborn child must adjust to a host of changes in their new environment. The world outside the womb can be harsh and, as the external barrier, the skin is the body’s first defense against these conditions. An infant’s skin must adapt to tackle a variety of chemicals, weather conditions, physical stresses, skin disease and attack from microorganisms, such as bacteria or viruses.

Until recently, little has been known about the structure of babies’ skin due to ethical issues of using certain experimental methods on infants. With the advent of newer, noninvasive techniques, however, we are beginning to learn more about the unique qualities of young skin and how best to care for it.

Skin structure

An infant’s skin can be up to 5 times thinner than that of an adult, so it is far more delicate and sensitive – even compared to that of older children. At birth, babies have quite dry skin which quickly becomes hydrated within the first few weeks. This continues to such a point that older infants (8-24 months) actually have skin which is generally better hydrated than adults. Similarly, the skin of a baby is quite rough when they are first born, but quickly softens and smoothes out by around one month of age; this is linked to the increase in the water content of the skin.

While the amount of water is generally higher in baby skin, it does fluctuate more than in adult skin. One of the reasons for this is that skin cells contain a mixture of molecules called the NMF, or Natural Moisturising Factor. These molecules attract and absorb water, keeping the cells hydrated. Baby skin has less of these molecules, making it less able to retain moisture.

Babies have fewer lipids (fats) in their skin than adults. Lipids are important for creating a solid barrier of the skin, which could be one reason that infant skin does not function as such an effective defense against physical and chemical damage. Their skin is more vulnerable because this barrier role of the skin is still developing. Premature babies, in particular, have skin which is less well developed and are therefore more susceptible to a number of environmental factors, such as abrasion and water loss. Before 30 weeks gestation, the top layer of skin (called the epidermis) is weak, thin and relatively immature; its formation is mostly completed by 34 weeks.

Babies have smaller skin cells than adults and these are closely crowded together. This is because their skin cells multiply at a high rate, being more quickly renewed and sloughed off at the surface.

Caring for baby skin

The following guidelines for infant skin care are provided by the Royal Children’s Hospital in Melbourne.

Bathing a baby

Bathing a baby

It is recommended that a baby be bathed approximately 2-3 times per week in warm water; excessive bathing may remove the skin’s natural oils (sebum) and cause their skin to dry out. It is also advised that the use of harsh soaps be avoided as they may contain irritants or allergens.

When a cleanser is necessary, many brands offer gentler options. The skin should be dried carefully, particularly in the creases of the neck, groin and armpits. An emollient (a substance which moisturises and softens skin), in the form of a cream or lotion, should then be applied within three minutes. This can be applied up to three times daily and is particularly important for babies with dry, flaky or sensitive skin.

For babies with eczema or other dry skin conditions it best to avoid the use of soaps altogether, using moisturisers as a substitute when bathing, as well as applying them frequently at other times. Colder temperatures can also lead to excessively dry skin, at these times it may be necessary to wash less frequently and apply moisturiser more often.

Nappies (diapers)

Nappies should be changed regularly, and the skin in these areas cleansed with warm water and a small amount of mild soap or moisturiser. Given the sensitive nature of babies’ skin, along with its tenancy to absorb substances more easily, it is advised that the number of products you expose your baby to is minimised, sticking only to the essentials described above.

Baby suncare

Where possible, babies should be kept out of the sun. Where sun exposure or time outdoors is unavoidable, infants can be protected using sun protective clothing, hats, sunscreen, sunshades and ambient shade.

Temperature control

The skin and bodies of infants are not able to regulate temperature as well as adults. As a result, they are more vulnerable to over-heating or becoming too cold in extreme conditions. This is particularly important for babies and young children who are not capable of removing their bedding or adding an extra layer of clothing themselves.


The Royal Children’s Hospital Melbourne n.d., ‘Clinical Guidelines (Hospital): Skin care of the term baby and infant’, retrieved 26 July 2010.

Stamatas, GN et al. 2011, ‘Infant skin physiology and development during the first years of life: a review of recent findings based on in vivo studies’, International Journal of Cosmetic Science, 33(1):17-24.

St. Vincent’s Hospital Melbourne 2002, ‘Skin care in babies and young children’, retrieved 11 May 2011,

Mothers & Children

From the early stages of pregnancy and new motherhood to growing children and the independence of adolescence, skin faces a host of challenges – from healing wounds and keeping out foreign invaders to shielding against the ravages of light, heat and dehydration. As the largest organ of the body, the skin plays many important roles: it protects our bodies, senses physical stimuli, regulates temperature and helps to maintain a healthy balance of fluids and nutrients.

‘Atopic Mothers & Children’ offers unique insight into the functioning and health of skin throughout childhood and motherhood from the most common skin conditions to some of the rarest disorders.

UV and Light

The most important source of light and subsequent energy on earth is the sun. The sun emits energy that can be absorbed by organisms and molecules where it facilitates countless reactions, including photosynthesis, ozone production, vitamin D, and weather phenomena.

Ultraviolet radiation (UVR)

Sunburn and skin cancer are known to be correlated to the dose of UV radiation our skin encounters. UV radiation is emitted by the sun, and is a region in the electromagnetic spectrum between 400-200nm, that can be broken down into three categories: UVA which is between 400-320nm, UVB which is between 320-280nm, and UVC between 280-200nm. As the various types of UV radiation are at different wavelengths, they react differently with the atmosphere. Almost all of the UVC radiation, some of UVB and UVA is absorbed before it reaches the Earth’s surface. The dose of UVA, UVB and UVC changes as UV passes through the atmosphere mainly due to differences in rates of reflection, refraction, scattering and absorption. The change can be emulated on a UV index (Figure 1). A local UV index can be found in a variety of places reporting on meteorological data and forecasts. UVI depicts how much UV radiation is likely to be reaching the Earth’s surface and therefore which precautions should be taken to minimise human risk.

Figure 1. UV index

Figure 1. UV index

A UV index value of zero corresponds to no UVR reaching the Earth’s surface, which occurs at night time, and an index of 10 refers to roughly midday sun, when there is no cloud cover. UVR indices record well into the teens when the ozone layer reads low values. The index numbers are measured in watts/meters2, and the measurements reflect different wavelengths to be more harmful than others.

Note that the above precautions are provided for adults with moderately fair to dark skin tone, and that skin damage caused by sun exposure is accumulative over one’s lifetime.


Figure 2. Production of ozone in the atmosphere.

Figure 2. Production of ozone in the atmosphere.

As light enters the Earth’s atmosphere, it comes into contact with molecules in the stratosphere. The stratosphere is situated about 10km above sea level and continues up until 50km above sea level. It contains the ozone layer, which absorbs UV radiation. The ozone layer is composed of ozone, a molecule containing 3 oxygen atoms. Oxygen molecules are good absorbers of UVC radiation, using this energy the oxygen bonds break, forming two separate oxygen atoms. These atoms can rejoin, recreating the oxygen molecule, or binding to an oxygen molecule ultimately to form an ozone molecule. Ozone molecules are good absorbers of UVB, and to a lesser degree, UVA. Ozone molecules absorb the energy provided by UVB and UVA to undergo dissociation, releasing oxygen atoms that can combine to form oxygen molecules. These two reactions are in equilibrium, where neither really dominates. Ozone is an important molecule in reducing the amount of harmful UV radiation that passes through our atmosphere, but at low altitudes, such as on the surface of the Earth, it becomes a somewhat toxic and unstable molecule.

The amount of UV light that reaches the Earth’s surface varies and is dependent on a number of factors:

  • Latitude: Near the equator, where the sun is directly overhead, the distance from the sun to the ground is the shortest, and the UV has to pass through the least amount of radiation. Therefore, on the equator, the UV intensity is the highest. Likewise, on the poles, the sun appears low in the sky, meaning the light has to pass though more radiation-absorbing atmosphere to reach the surface.
  • Elevation: At higher altitudes there is less atmosphere to absorb UV radiation, therefore individuals are exposed to a greater amount of UVR.
  • Proximity to an industrial area: photochemical smog produced in industrial processes contains artificially produced ozone. The ozone produced can absorb more UV radiation, but also poses significant health risks if it is low lying.
  • Weather conditions: cloud cover can reduce the UV levels on the surface, but often incompletely.
  • Reflection: some surfaces are able to reflect UV radiation, meaning there is a greater chance of getting sun burnt, even in shady places. Snow, sand, grass and water are good reflecting surfaces.
  • Time of day/year: during the middle of the day, the sun is at its highest position in the sky, resulting in the least distance for radiation to travel, and more exposure to UV light. The summer months also provide the most intense UV radiation, as the sun’s angle (zenith angle) is reduced.
  • Ozone layer: the depth of the ozone layer plays a vital role in reducing exposure to UV light. The ozone layer has been found to be thinning in the past few decades. This is presumably due to the release of ozone degrading chemicals by industry.

Ozone depletion

In the past few decades, it has been observed that the ozone layer is thinning over certain regions of the globe, particularly over Antarctica. This has been attributed to chemicals that have been released by industry since the 1930’s, particularly gaseous chlorine and bromine containing substances, such as chlorofluorocarbons (CFC’s) and bromofluorocarbons (BFC’s).

Ozone can be broken down by natural and manmade sources. Atomic chlorine and bromine are two significant contributors, and can be released into the atmosphere by large volcanic eruptions and are also present in chemicals, especially those that where used by industry decades ago, such as CFC’s and BFC’s. CFC’s have been produced as a substitute for toxic and flammable chemicals used in industry, such as ammonia. They’re non-toxic, non-flammable, and their very stable nature made them perfect for propellants in aerosol cans and refrigerants. Their use have grown exponentially (in 1988 it was estimated that over one billion kilograms were being produced annually worldwide) until the discovery that CFS had the capacity of thinning the ozone layer. At this stage world leaders acted by signing the Montreal Protocol, which stipulated that consuming and producing chemicals capable of breaking down ozone be phased out by 2000.

CFC and other similar chemicals are so stable that they’re not destroyed in the troposphere, as they slowly rise towards the stratosphere. These stratospheric molecules are found to be able to break ozone down into an oxygen atom and molecule. This usually occurs at a slow rate, reducing the overall thickness of the ozone layer by about 4% per decade, but in the atmosphere above Antarctica, especially in spring, thinning occurs at an alarming rate. During its winter, Antarctica becomes cold enough (-80°C) for stratospheric clouds (termed Stratospheric Clouds Mother of Pearl, PSCs) to form in the ozone layer. On the surface of these clouds, chlorine and bromine are transformed into an active state and when the sun gains intensity in the spring, clouds disappear freeing chlorine and bromine to rapidly destroy ozone. As temperatures further continue to warm, wind vortexes holding the particles above Antarctica break up, mostly allowing ozone rich air to flow into ‘the hole’. The chlorine and other molecules capable of breaking ozone down can destroy up to a thousand molecules of ozone before it is converted into an inactive form, such as hydrochloric acid.

There are many complex reactions that destroy ozone, the simplest being: a free chlorine atom reacts with an ozone molecule, forming a chlorine and oxygen complex, ClO and an oxygen molecule, O2. The ClO then reacts with a free oxygen atom forming an oxygen molecule and a free chlorine atom. In this manner a circular process is initiated.

Although the Montreal Protocol, first signed in late 1988, will help assist to reduce the effects of destructive radicals in the atmosphere, the effects will not be instantaneous. As it takes years for the CFC’s and other molecules to reach the stratosphere, the reduction in emissions will have minimal effect in the stratosphere (the largest dimension of the hole over Antarctica was measured in 2006, being over three times the size of Australia). It is anticipated that it will take a decade before confirmation of recovery of the ozone can be given.

With the thinning of the ozone layer, less UVB radiation is absorbed resulting in more harmful radiation passing to the Earth’s surface. This would result in increased incidence of skin cancer, cataracts, and other UV related diseases.

Definitions and focus

Figure 3. A typical wavelength.

Figure 3. A typical wavelength.

Figure 4. Electromagnetic spectrum.

Figure 4. Electromagnetic spectrum.

The energy in the light emitted by the sun and all other sources, travels as mass-less, charge-less particles, photons. Photons can travel as both particles and waves, where each beam of light has its own wavelength (measured peak to peak: Figure 3), frequency (number of wave cycles passing a point per second, Hertz) and energy.

The wavelengths of visible light range from 400nm to 700nm. Once the wavelength drops outside of these values a different form of electromagnetic radiation transpires; these different forms can be found on an electromagnetic spectrum (Figure 4). As evident on Figure 4, the two main sources of electromagnetic radiation emitted by the sun (visible light and ultraviolet radiation – UVR) only occupy a small section of the spectrum.


The heat supplied by the sun has provided us with a suitable environment to survive. Once radiating energy is passed through the atmosphere, the photons collide with matter, transferring energy. This causes heat, wind, rain, clouds and other weather phenomena. Wind is a result of the varying temperatures of the air above land and water. The hot air rises, causing a flow of cooler air to occupy its previous place, and eventually cool air, high in the atmosphere, drops down to sea level, completing the cycle. When ocean water is heated, water particles evaporate into the air, where they culminate to form clouds. These clouds pushed over land by winds experience lower temperatures, causing condensation into droplets and precipitation. Differences in atmospheric moisture, pressure and temperature result in dramatic weather conditions as hurricanes, cyclones and tornadoes.

When the sun’s rays are shone on an organism, it can have harmful consequences. Different types of electromagnetic radiation have various effects on tissue and DNA. The ultraviolet region of the electromagnetic spectrum can cause serious damage to organic tissues, including human tissue. Humans are protected against ultraviolet radiation by various natural defense mechanisms. Ultraviolet radiation (UVR) can also cause damage to our eyes, both short and long term.

For instance the conjunctiva of the eye may show inflammatory reactions when exposed to intense UVR. Long-term eye (ophtalmis) exposure to sun may have deleterious effects on the retina, causing immediate, and sometimes permanent, visual loss. Long-term UV exposure contributes to cataract formation.


Figure 5. The process of photosynthesis.

Figure 5. The process of photosynthesis.

Photosynthesis is a process carried out by photo-autotrophs.Put simply, photosynthesis is water and carbon dioxide, in the presence of light, forming oxygen and glucose.

The oxygen produced is released out into the atmosphere through stomata while the carbohydrate, glucose, can be modified to produce various other carbohydrates, such as cellulose for plant walls, or starch, a glucose storage molecule.

The carbon dioxide is acquired through stomata, small gaps in plant leaves that are surrounded by two guard cells. These guard cells are able to open and close depending on the environmental conditions. For instance, if conditions are extremely dry, guard cells would swell to close the gaps, in order to minimize water loss. These gaps allow carbon dioxide and water vapor to enter the plant, and oxygen and water vapor to leave. In turn, water is acquired through the plant roots. Moisture obtained from the soil may travel through the roots up the plant to the leaves via the xylem (vascular tissue). The xylem is a tissue in vascular plants that carries water and minerals from the roots, to all other sections of a plant.

Figure 6. Diagram of a chloroplast.

Figure 6. Diagram of a chloroplast.

The energy within the sunlight is captured by chlorophyll, a pigment found in chloroplasts. Chlorophyll is of biological relevance due to its chemical structure, and subsequent absorption spectra. Also present in chloroplasts and involved in photosynthesis are grana, which are stacks of thylakoid discs, and the stroma, which is a dense fluid surrounding the grana (see Figure 6).

Photosynthesis is separated into two phases: the light dependent and independent stages. The light dependent stage involves the absorption of a photon and its conversion to an electron, a series of reactions follows, which conclude in an oxygen molecule being released into the atmosphere. The light independent reaction involves the absorption of carbon dioxide by an enzyme, RuBisCO, and results in the production of carbohydrates.

Light dependent reaction

Figure 7. Diagram of a photosystem.

Figure 7. Diagram of a photosystem.

The light dependent reaction can occur by two mechanisms: cyclic photophosphorylation and non-cyclic photophosphorylation. Non-cyclic photophosphorylation is the more common of the two in plants, produces ATP and NADPH and involves the use of two photosystems, photosystem I and II. Cyclic photophosphorylation occurs in plants when there is insufficient NADP+ to produce NADPH, involves photosystem I and only produces ATP.

A photosystem is an arrangement of pigments, such as chlorophyll, packed into a thylakoid membrane. The energy containing packets in light (photons) are absorbed by accessory pigments, passed to the primary pigment, and then collected where they initiate the production of energy in the form of ATP and NADPH. The primary pigment associated with photosystem I is P700, while P680 is associated with photosystem II. These numbers 700 and 680, refer to the wavelengths of light that the respective pigments can absorb.

Figure 8. Non-Cyclic photophosphorylation reaction.

Figure 8. Non-Cyclic photophosphorylation reaction.

Non-cyclic photophosphorylation (Figure 8) begins with photosystem 2. The photons present in light are absorbed by P680, where they excite an electron. This electron is then passed to a primary electron acceptor molecule through a process termed photoinduced charge separation. The positive charge left on the P680 molecule is alleviated by the extraction of electrons from water molecules, causing the release of atomic oxygen. The electron held by the primary electron acceptor is passed to pheophyton then down the electron transport chain. This creates a chemiosmotic gradient which leads to ATP being formed by ATP synthase in the light independent reaction. Once passed through the electron transport chain, the electron enters photosystem 1 where it is re-excited and begins its path down another electron chain. The electron is again passed through a series of reactions, eventually being added to NADP+ reductase to form NADPH.

Figure 9. Cyclic photophosphorylation reaction.

Figure 9. Cyclic photophosphorylation reaction.

Cyclic photophosphorylation only involves photosystem 1. P700 absorbs photons until an electron is raised to its excited state. The electron then passed undergoes photoinduced charge separation, before being passed down an electron transport chain, producing a chemiosmotic potential across the membrane. This ion gradient stimulates the production of ATP from ATP synthase. Once the electron reaches the end of the electron chain, it is passed back to the photosystem by electron acceptor molecules (see Figure 9). Cyclic photophosphorylation also occurs in certain photosynthetic bacteria.

Light independent reaction

Figure 10. Light independent reaction.

Figure 10. Light independent reaction.

Light independent reactions are also referred to as carbon fixation. Ribulose biophosphate (RuBP), with assistance from the enzyme RuBisCo, is combined with a carbon dioxide molecule. The end product is two, three-carbon, 3-phosphoglycerate (PGA), molecules. The ATP and NADPH produced in the light dependent reaction are used to reduce PGA to 3-phosphoglyceraldehyde (PGAL). Additionally, 5 of every 6 molecules of PGAL produced are reused in the production of RuBP, while the remaining molecule is used in the formation of carbohydrates, such as starch, cellulose and glucose (Figure 10).


  •, (2007). Photosynthesis [Online]. Available from: [Accessed on 29/04/2008].
  • de Gruijl, F R, Longstreth, J, Norval, M, Cullen, A P, Slaper, H, Kripke, M L, Takizawa, Y, (2003). Health effects from stratospheric ozone depletion and interactions with climate change, Photochemistry and Photobiology. Vol 2, pp 16-28.
  •, (2007). Photosynthesis [Online]. Available from: [Accessed on 29/04/2008].
  • Slaper, H, Velders, G J, Daniel, J S, de Gruijl, F R, van der Leun, J C, (1996) Estimates of ozone depletion and skin cancer incidence to examine the Vienna Convention achievements, Nature. Vol 384(6606). pp 256-258.
  •, (2006). Ozone [Online]. Available from: [Accessed on 29/04/2008].
Rare Skin Conditions

Congenital Erythropoietic Porphyria (CEP)

Snapshot Other common terms: CEP, Gunther’s disease, Uroporphyrinogen III synthase deficiency, UROS deficiency, Congenital porphyria, Congenital hematoporphyria, Erythropoietic uroporphyria ICD-10 classification: E80.0 Prevalence: Extremely rare; less than 200 cases reported. Usually manifests during infancy or early childhood. Causes: Genetic mutation in the UROS gene leading to reduced enzyme function. Symptoms: Symptoms may include: blistering, scarring, necrosis or excessive hair growth on light-exposed skin; disfiguration of the ears and nose; loss of fingers; anaemia; red-stained teeth; pink/red coloured urine and enlarged spleen. Treatments/cures: Treatment with blood transfusions, splenectomy, oral sorbents, beta-carotene…
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Actinic Prurigo (AP)

Snapshot Other common terms: AP, Hutchinson prurigo ICD-10 classification: Not defined, L55-59 Prevalence: Unknown. More common in Latin and Indigenous Americans Causes: Not well understood. Suggested that an immune-mediated response to UV light is responsible. Symptoms: Extremely itchy skin rash, red and inflamed bumps (papules), thickened patches (plaques) and/or lumps (nodules) following exposure of skin to sunlight. Treatments/cures: In some cases, actinic prurigo may resolve itself. Topical steroids, emollients, phototherapy, thalidomine and oral immunosuppressants. Differential diagnosis: Polymorphous light eruption, prurigo nodularis, lupus Actinic Prurigo (AP) is a rare chronic, idiopathic…
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Erythropoietic Protoporphyria (EPP)

For more on Atopic’s clinical program for EPP, click here. Snapshot Other common terms: EPP, protoporphyria, erythropoietic porphyria ICD-10 classification: E80.0 Prevalence: Rare; between 1:58,000-200,000. Estimates of between 5000-10,000 globally Causes: Inherited disease; defective enzyme causes inability to properly produce haem (heme). Symptoms: Phototoxicity: swelling, burning, itching and redness of the skin, occurring during or after exposure to sunlight, including light passing through windows. Liver toxicity in 5% of cases. Microcytic anaemia can occur. Treatments/cures: None proven fully effective to date. Phototoxicity can be avoided by complete avoidance of sunlight…
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Hydroa Vacciniforme (HV)

Snapshot Other common terms: HV, Bazin’s Hydroa Vacciniforme ICD-10 classification: L56.8 Prevalence: Rare. Prevalence data is scarce, reported as 0.34:100,000 in Scotland. Mainly presents in children aged 3-15. Causes: Exact cause unknown; there is correlation between diease symptoms and exposure of skin to UV (particularly UVA) radiation. Symptoms: Eruption of fluid-filled blisters on the skin following exposure to UV radiation. Treatments/cures: No known cure, HV commonly resolves in late adolescence. Phototherapy, fish oil and various drugs may reduce symptoms. Differential diagnosis: Porphyrias (erythropoietic protoporphyria, congenital erythropoietic protoporphyria), Polymorphous Light Eruption,…
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Porphyria Cutanea Tarda (PCT)

Snapshot Other common terms: PCT ICD-10 classification: E80.1 Prevalence: Uncommon; 1:25,000 Causes: Inherited disease; defective enzyme causes inability to properly produce haem (heme). Symptoms: Skin photosensitivity causing extremely fragile skin and changes in pigmentation (melanin). Discoloured urine. Treatments/cures: Cannot be cured. Avoidance of sunlight and certain artificial lights. Differential diagnosis: Erythropoietic protoporphyria, polymorphous light eruption Porphyria cutanea tarda (PCT) is the most frequently seen disease of a group of disorders (the Porphyrias) that can be acquired or inherited. It is caused by low levels of an enzyme (uroporphyrinogen decarboxylase or…
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Solar urticaria (SU)

Snapshot Other common terms: SU ICD-10 classification: L56.3 Prevalence: Very rare; 3.1:100,000 individuals globally. Solar urticaria is more likely to affect women Causes: Exposure of skin to light. Exact allergen is unknown. Symptoms: Systemic: anaphylaxis, breathing difficulty, nausea and headaches. Immediate localised reactions on skin: characteristic ‘wheal’ formation, erupting flares on exposed skin sites and to swelling of soft tissues. Treatments/cures: No known cure. Anti-histamines and topical steroids may be useful in some cases. Immunosuppressants and plasmaphoresis in extreme cases. Differential diagnosis: Polymorphous light eruption, drug induced photosensitivity, other allergies/physical…
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Urticaria Pigmentosa (UP)

Snapshot Other common terms: UP ICD-10 classification: Q82.2 Prevalence: Rare, exact prevalence is unknown but it is more common in Caucasians Causes: Excess of inflammatory mast cells due to an unknown cause; mast cells trigger histamine in the affected area. Environmental factors may trigger symptoms. Symptoms: Swelling, itchiness and a rash on the skin. May present as brown patches, hives, welts, rashes, blisters or facial flushing. Diarrhea, low blood pressure and an increased heart rate may present in certain cases. Treatments/cures: Avoidance of causes. Anti-histamines, mast cell stabilizers and topical…
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Xeroderma Pigmentosum (XP)

Snapshot Other common terms: XP ICD-10 classification: Q82.1 Prevalence: 1:250,000 globally except in Japan where incidence is 1:40,000 Causes: Inherited. Autosomal recessive disease. Symptoms: XP causes a defect in DNA repair, making affected individuals hypersensitive to UV light and causing an extreme susceptibility to skin cancers. Ocular and neurological issues are likely. Treatments/cures: No known cure. Treatment is limited to sun avoidance, and immediately treat skin cancers. Xeroderma Pigmentosum (XP) is a rare, hereditary disease where patients experience skin hypersensitivity to ultraviolet (UV) light. It is characterized by dry skin,…
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Common Skin Problems

Acne Vulgaris

Snapshot Other common terms: Acne vulgaris, pimples, zits, whiteheads, blackheads ICD-10 classification: L70.0 Prevalence: Very common; 95-100% of adolescent boys, 83-85% of adolescent girls Causes: Oil, dirt and bacteria build up in the skin. Family history, sweating, stress, certain cosmetics, hormonal changes and certain medications are among the causes of acne. Recent studies have shown that foods (including fatty foods, chocolate and other dairy) do not play a role in causing acne. Symptoms: Blackheads, whiteheads and inflammatory papules and pustules on the skin, most commonly on the face and shoulders,…
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Atopic Dermatitis

Snapshot Other common terms: AD, atopic eczema, eczema ICD-10 classification:L20.0, L30.0 Prevalance: Varies between populations from 2-20% of total population Symptoms: Blackheads, whiteheads and inflammatory papules and pustules on the skin, most commonly on the face and shoulders, but can occur anywhere. Severe acne can causes scarring of the skin. Treatments/cures: A range of over the counter and prescription medications. Antibiotics and hormonal therapies in moderate-severe cases. Chemical skin peeling, scar and cyst removal or photodynamic therapy in very severe cases. Differential diagnosis: Allergic reactions, seborrheic dermatitis Atopic Dermatitis Atopic…
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Polymorphic Light Eruption (PLE)

Snapshot Other common terms: Polymorphic Light Eruption, PLE, PMLE, sun sickness, sun allergy ICD-10 classification: 56.4 Prevalence: Between 5-20% reported in fair skinned populations, but can occur in any skin type Causes: Exact cause unknown; believed to be delayed hypersensitivity to sunlight. Symptoms: Non-scarring, itchy or burning, red papules, vesicles or plaques appear on sun-exposed skin 30 minutes to several hours following exposure to sunlight. Treatments/cures: Sun avoidance to prevent disease onset, including broad spectrum sunscreens. Topical steroids and phototherapy can be used. Differential diagnosis: Solar urticaria, erythropoietic protoporphyria (EPP),…
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Snapshot Other common terms: None ICD-10 classification: L40 Prevalence: Common; 2-3% of the global population, estimated 125 million affected globally Causes: Thought to be a genetic disease. Symptomatic onset can be due to a range of environmental factor such as infections, stress, skin trauma and certain medications. Symptoms: Reoccurring outbreaks of distinct red areas of skin, covered by silvery-white flaky skin. Five different sub-types have their own specific symptoms. Treatments/cures: Treatments vary according to psoriasis type and location. Topical emollients and steroids are often used, with immunosuppressants and phototherapy used…
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Snapshot Other common terms: Acne rosacea ICD-10 classification: L71 Prevalence: Common, more common in Caucasian population. Approx 14 million Americans are affected by rosacea Causes: Sunlight and UV, certain food and drinks (including alcohol), stress, environmental factors Symptoms: Frequent or prolonged flushing/blushing; spider veins (usually on the nose); papules and pustules (acne like appearance); facial burning and stinging; swelling of facial areas; enlargement of sebaceous glands giving the nose a bulbous appearance; dry and flaky facial skin. Treatments/cures: No known cure. Avoidance of stimulants is key. Topical steroids and oral…
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Seborrheic dermatitis (SD)

Snapshot Other common terms: SD, seborrhoeic dermatitis eczema, cradle cap ICD-10 classification: L21 Prevalence: Very common; affects approximately 3-5% of the global population Causes: Exact cause is unknown. Environmental factors contribute to the onset of symptoms. Symptoms: Reddish or pink patches of skin, accompanied by greasy, yellowish flakes or scales. May become inflamed, itchy or infected with scratching Treatments/cures: Anti-inflammatory agents, topical steroids, keratolytic agents and antifungals. Differential diagnosis: Atopic dermatitis Seborrheic Dermatitis Seborrheic dermatitis (SD) is a form of eczema and a common, inflammatory skin disorder that affects infants…
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Melanin in Biology

Melanin is a complex polymer synthesized by living organisms. A polymer is a large chemical compound often made up of hundreds of smaller chemical parts, monomers. A variety of melanins can be found through biology, most commonly being composed of derivatives of acetylene, a black monomer.

Human Melanin

Melanins are found in a wide variety of organs in humans. They have been found in a few regions of the brain, where they are termed neuromelanins. Their exact function is unknown, but it has been suggested that they could be a byproduct of the synthesis of a neurotransmitter. Neuromelanin is probably the only source of these specific neurotransmitters with a variety of neurodegenerative compounds coupled with a reduction in neuromelanin. In the inner ear melanin protects against hearing damage, this is presumed to be because it has been found that it is the best sound absorber known. In the eye it protects the iris against UV damage, similar to the way it protects the skin. It is has also been discovered in the birth canal and adrenal gland. All of these melanins have different structures, they might be slight alterations of each other, or distant relatives.

Melanin in the skin

Human skin and hair contain both the reddish pigment pheomelanin and brownish eumelanin, where eumelanin is the most abundant in the human body. Pheomelanin is more present in females, leaving females with a more reddish skin.

Where reference is made to melanin in the text, eumelanin is implied. The precise function of melanin is the subject of much debate; its exact role is still unclear. In the dermis (skin), the pigment is a primary determinant of both skin and hair colour. Melanin is produced by melanocytes, special skin cells located in the basal layer of the epidermis (Figure 1). The process of activating pigmentation in the skin is termed melanogenesis, and is initiated after cellular damage following exposure to UV radiation or the sun. Visibly, increased melanin in the skin results in a darker skin complexion, and better protection.

Figure 1. Melanosomes leaving the melanocyte as a result of sunburn in the upper epidermis.

Figure 1. Melanosomes leaving the melanocyte as a result of sunburn in the upper epidermis.

Both melanins are synthesized in the basal layer, which is located at the bottom of the epidermis (top layer of the skin), above the dermis (see Figure 1). Special cells, melanocytes, produce melanin containing packets, called melanosomes. These melanosomes are spread throughout the epidermis by tentacle-like projections called dendrites. The dendrites, which are connected to the melanocytes, transfer the melanosomes to separate keratinocytes (skin cells). Once the melanosomes reach the end of the projections they are squeezed out, into the keratinocytes. The melanin containing packets spread out above the nucleus, where they stay, protecting the DNA inside the organelle from harmful UV radiation. The skin cells eventually rise to the top of the epidermis where they die and are desquamated (shed away).

All humans appear to almost have the same number of melanocytes and keratinocytes (at a ratio of 1:36). The size and number of melanosomes, however, can vary dramatically between individuals. People with fair skin tend to produce small melanocytes, containing little melanin, which is portrayed as a fine brown dust covering the nucleus of keratinocytes. Dark skin individuals produce larger melanin containing packets that are seen as dark patches covering the nucleus. Both of these forms of melanosomes protect the DNA in two ways, by scattering incoming ultraviolet radiation and by absorbing it. Because of this protective ability that melanin posses, it is called a photoprotectant, that is a substance that can protect an organism from damage caused by the absorption of photons from a radiating source, particularly the sun. This degradation is called photodegradation.

The more incoming UV radiation that is randomly scattered, the less the chance of DNA’s exposure to it. The amount and direction of the scattering is dependent on both the wavelength of the incident ray, and the size of the particle that it is striking.

Research has shown that the smaller a particle size, the greater the evenness of scattering. It has been revealed that even though some radiation passes through the melanin, if the layer is thick enough, it will eventually be dispersed or absorbed elsewhere.

Figure 2. Scattering caused by different sized particles when subject to the same wavelength of light.

Figure 2. Scattering caused by different sized particles when subject to the same wavelength of light.

The sizes of human melanosomes range from around 228nm to 684nm. It is therefore desired, on a scattering basis, to have melanosomes closer to 230nm rather than 690nm.

On the other hand, light absorption is favored by a larger surface area, which requires larger melanosomes. Once the energy is absorbed by the melanin, it raises electrons to excited states and, in turn, passes the energy to the cell it is situated in. The cell is then assumed to use this energy to regulate its conditions and drive chemical reactions, a role similar to that of chlorophyll in photosynthesis.

As a photoprotectant, melanin can be artificially produced and incorporated into products and substances that seek to offer protection against UV radiation. In other domains, similar types of melanin have also been used in conjunction with plastics, plastic films, and optical lenses.


In the same way that melanin provides skin and hair colour, it also provides the colour of birds’ plumage, amphibians’ and reptiles’ skin or scales, and other animals’ fur. Pigmentation in animals provides bright colours that attract mates in the animal kingdom and is used for camouflage, as illustrated by the cuttlefish, which releases an ink composed of melanin particles, to distract and confuse its predators. It is thought to also be involved in the defense of fungi and bacteria against ionizing UV radiation, chemical strain and biochemical strain.

Additionally, in pathogenic microbes, melanin is used to protect the microbe from immune responses by its host. Also, in some organisms, melanin is involved in a self-defense mechanism, it encapsulates invading pathogens and is accompanied with the production of radical byproducts, it aids in the killing of pathogens.

Recently, due to the presence of melanin, fungi have shown to survive under harsh radioactive conditions. It is thought that melanin is converting ionizing radiation into a useable energy source, which promotes growth. This was first noticed after the melt down at the Chernobyl nuclear power plant in Ukraine. A sample taken of a black fungus found inside a reactor was found to contain melanin, triggering the speculation that the polymer melanin was harnessing the energy from the radioactive rays into a usable energy.

Melanin structure

The chemical structure of the different forms of melanin have proven difficult to analyze, due to the properties of the molecule. They are found to be insoluble, amorphous, and cannot be studied as a solution or in crystal form. To overcome the frustrating properties, a partial degradation process has been used to study the separate components of each melanin structure. Two of the main melanins in the human body are eumelanin and pheomelanin (Figure 3).

The pathway to synthesize melanins is also not fully understood. It is known that tyrosine is the starting reactant, and tyrosinase the enzyme that catalyses the reaction (Figures 4 and 5).


  • Chedekel, Zeise, Fitzpatrick (1994) ‘Melanin: Its role in human photoprotection’, Publish city: United Kingdom. John Murray.
  • Dadachova, E, Bryan, R A, Huang, X, Moadel, T, Schweitzer, A D, Aisen, P, Nosanchuk, D J, Casadevall, A. (2007). ‘Ionizing Radiation Changes the Electronic Properties of Melanin and Enhances the Growth of Melanized Fungi’ PLoS ONE Vol 2(5).
    Miyamoto, K, Baba, K, (1987) ‘Stereological Method for Unfolding Size-Shape Distribution of Spheroidal Organelles from Electron Micrographs’, Journal of Electron Microscopy, Vol 36(3) pp 90-97.
  • Nosanchuk, J D, Casadevall, A. (2006). Impact of Melanin on Microbial Virulence and Clinical Resistance to Antimicrobial Compounds, Antimicrobial Agents and Chemotherapy . Vol 50, pp 3519-3528.
  • (1997), Skin Pigmentation [Online]. No longer available online. Accessed on 29/04/2008.
Skin Layers

The skin (dermis, cutis, derma, integument, and cuticle) is the largest organ of the human body (approximately 20 square feet), weighing approximately 16% of bodyweight. Skin thickness varies and is on average 1mm thick; the thinnest on eyelids at 0.5mm and the thickest at 1.5mm on the palms and soles. Skin consists of multiple layers (stratified), epidermis, dermis and hypodermis (deepest layer).



Skin cross section showing the epidermis (not to scale)

The upper most outer layer of the skin, the epidermis, consists of squamous cells (flat and scale-like in shape) and underneath basal cells (round shaped). The process of keratinisation (formation of horny layer) occurs over the course of 4 to 6 weeks when keratinocytes (85% of the epidermal cells) migrate upwards through the skin to be desquamated (shedding of old skin) at the skin surface. Renewal of the upper layer is continuously initiated by the keratinocytes.

The mitotic layer (single line) is the area where the division of keratinocytes takes place, held together by desmosomes (macula adherens) resisting shearing of the epidermal layer. Mitosis (cell division) occurs in the ratio of 1:2, with each keratinocyte producing two identical new cells. One cell remains in place to enable it to divide again, as the other migrates to the differentiation layer, the upper and thickest layer of the epidermis (5-15 cells thick). After initial growth, a newly formed layer, the Malphigian layer, gives rise to the production of keratin, an insoluble sulphur-based fibrous protein. In the Malphigian layer, Langerhans cells play a role in the recognition of antigens and interaction with epidermal T-cells (lymphocytes), as an immunologic response.

In the deepest layer of the epidermis, called the stratum basale, Merkel cells are found, these cells are part of the cell-neuron complex: a close association with an afferent nerve ending, the sensory part of the epidermis.


A cross section of skin highlighting keratinocytes, the epidermis and dermis (not to scale)

A cross section of skin highlighting keratinocytes, the epidermis and dermis (not to scale)

As the keratinocytes migrate upwards, they lose their content of the cell nucleus (anucleate) and become flat in structure. When reaching the outermost layer of the epidermis, the keratinocytes become corneocytes, with relatively little biological activity. This is the end-stage of the keratinocytes. The keratinocyte at this stage is filled with keratin and ceramides; these are lipids and fatty acids, enabling the dermis to retain moisture. The most external epidermal layer in contact with the external environment is the stratum corneum. The external corneocyte is distinguished in 2 layers, a compact and a sloughing layer. When the junction, corneodesmosomes, between these layers breaks down, desquamation (skin shedding) occurs.

Melanocytes and melanogenesis

A cross section of skin highlighting melanocytes, the epidermis and dermis (not to scale)

A cross section of skin highlighting melanocytes, the epidermis and dermis (not to scale)

The deeper layer of the epidermis contains the pigment producing (melanogenesis) cells, melanocytes. These produce the dark brown pigment in the epidermis, eumelanin. The melanocyte forms part of the epidermal unit in a ratio of 1:36 keratinocytes. Melanin production is initiated through the up regulation of the receptors on the melanocyte, called the melanocortin 1 receptor (MC1R). The melanocyte produces intracellular eumelanin through a tyrosinase mediated biochemical pathway. Once eumelanin is formed within the cell organelle melanosome, the eumelanin granules are transferred after dendrite formation by the melanocyte.

Melanin has a photoprotective function (shields against UV and light damage) to the skin. The second form of melanin is pheomelanin, reddish-yellow pigmentation. Pheomelanin is the major type of pigmentation in red hair and also predominates in the epidermis of skin types I and II (fair skinned individuals). Eumelanin, on the other hand, is present in large amounts in individuals with dark skin and hair (skin types III-VI). It is generally accepted that eumelanin provides greater photoprotection than pheomelanin.


A cross section showing the dermis (not to scale)

A cross section showing the dermis (not to scale)

The dermis is the deeper skin layer consisting of two layers: the papillary and elastic, both containing collagen. Blood vessels (capillaries) and nerves are found in this layer.

The principle structural component of the dermis is the protein collagen, produced by fibroblasts dispersed throughout the dermis. A quantity of collagen molecules are bundled together throughout the dermis, making up for three-quarters of the dry weight of skin. Collagen is mainly responsible for dermal strength, representing connective tissue, the glue or cement holding together smooth muscles tissues found throughout the body. Collagen is, along with elastin, a pivotal component of bones, cartilage, tendons, the skin, lung tissue and blood vessels. Most of all, collagen is the main structure to provide firmness to body tissues, while elastin provides flexibility to these tissues.

As part of the dermal sensory system, nerves transmit and evoke pain, itch, and temperature from the dermis. Specialized nerve cells, Meissner’s and Vater-Pacini corpuscles, transmit the sensations of touch and pressure. Also present in the dermis are eccrine, apocrine, sebaceous glands and hair follicles.


The hypodermis contains specialized cells and structures, and adnexae, such as hair follicles, each follicle being attached to the arector pili muscle. Oil, scent and sweat, sebaceous, apocrine and eccrine glands are all associated with the follicle. The hypodermis is characterized with a high density of lipocytes, adipose or fat cells. The adipose layer serves as the largest reservoir of fatty acids. There is gender difference in distribution and size of adipose cells (in females predominantly in the buttocks and thigh area; in males in the abdominal region). This hypodermis also contains sweat and eccrine glands.

Hair is regarded as “dead epidermal cells” that have evolved through continuous modified epidermal keratinization. Upon close examination, hair is characterized by the expression of specific keratin proteins that are intensely cross-linked by disulfide bonds. Hair stems from hair follicles, which are epidermal invaginations that project into the dermis or hypodermis. There are two types of hair: vellus – fine short, soft, fine, and pale hair; and terminal – thick hard, large, coarse, long and dark hair. The number of hairs on all primates is similar, but mostly seen is vellus on humans and terminal on other primates. Hair can be “mobilized” by arector pili muscles, a smooth muscle enabling hair to stand on end most likely for better insulation (the phenomenon of goose bumps/pimples). The hair follicle undergoes a cycle of active and resting phases during which a new hair is started and then falls out, respectively. Melanocytes are seen to be scattered throughout the hair shaft. The melanocytes render colour to the hair. With age, tyrosinase production decreases and the hair turns gray.

Eccrine sweat glands are simple coiled tubular glands located in the deep dermis or underlying hypodermis and are present throughout the body. They develop as invaginations of the epithelium of the epidermal ridge and grow into the dermis, and the deep aspect eventually develops into the glandular portion of the sweat gland. Eccrine sweat glands have two regions: a secretory region and a duct region. The secretory portion is comprised of simple coils of cuboidal epithelium containing two kinds of cells. Dark cells produce sialo-mucins, while clear cells produce water and electrolytes. Myoepithelial cells support and constrict the gland in response to cholinergic stimulation. Secretion is controlled by heat stress in most of the body but is under emotional control in palms and soles. The duct portion of the sweat gland is stratified cuboidal epithelium (2 layers), whose cells resorb ions (Na+, K+, Cl-) from the glandular secretion. The final product is hypotonic (99% water) containing salts, lactate and urea. Adults are able to produce between 0.5-1.0 litre/day. Apocrine sweat glands are simple tubular glands that empty into hair follicles in axillary and anogenital regions. The secretion is a mixture of proteins, carbohydrates, and ferric ions, odourless when secreted, but which is acted on by commensal bacteria. They begin to function at puberty; but their function remains unknown.

Function of the skin

Human skin has numerous functions, it is the major interface between the environment and the human organs and so it serves many specialised functions that facilitate survival. It regulates body temperature to protect against hyperthermia and hypothermia. Water loss is controlled to protect against dehydration and is involved in controlling a balance of body fluids, mineral and waste product loss.

Skin also protects from the invasion of noxious substances, UV light, heat and micro-organisms. Langerhans cells have been found to be involved in a number of reactions to protect against micro-organism invasion and pain. They have antigen-presenting capacity, force keratinocytes to secrete immune regulating cytokines and T-cells, and are involved in delaying hypersensitivity.

The skin is also the most extensive sensory organ of the body for detection of tactile, thermal and painful stimuli for the start of vitamin D production – which is pivotal for bone growth – and serves other important immunological functions. Wound healing of the skin is regulated by an intact immunological defense mechanism.


  • Marks, R (2004). ‘The Stratum Corneum Barrier: The Final Frontier’, The Journal of Nurtition, Vol 134(8). pp2017-2021.
  • Jablonski, N & Chaplin, G. (2000), ‘The Evolution of human Skin Coloration’ Journal of Human Evolution. Vol 39. pp 57-106.
  • Chedekel, M R, Zeise, L & Fitzpatrick, T B (1994). Melanin: Its Role in Human Photoprotection. Overland Park: Valdenmar Publishing Company.
  • Anderson, R R & Parrish, J A. (1981), ‘ The optics of human skin’, Journal of Investigative Dermatology. Vol 77(1). pp 13-19.