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.


  • Burton, J. L., Pye, R. J. (1983) ‘Seborrhea is not a feature of seborrheic dermatitis’. British Medical Journal. Vol 286, pp.1169-1170
  • Schwarz, R. A., Janusz, C. A., Janniger, C. K. (2006) ‘Seborrheic Dermatitis: An Overview’. American Family Physician. Vol 74, pp.125-130
  • Valia, R. G. (2006) ‘Etiopathogenisis of seborrheic dermatitis’. Indian Journal of Dermatology, Vereonology and Leprology. Vol 72, pp.253-255
  • Johnson, B. A., Nunley, J. R. (2000) ‘Treatment of Seborrheic Dermatitis’ American Family Physician. Vol. 61, pp.2703-2710
  • 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.
  • 2004, Therapeutic Guidelines: Dermatology, North Melbourne, Therapeutic guidelines Limited.
  • Seldon, S. (2007) ‘Seborrheic Dermatitis’ [Online] Available online from eMedicine. [Accessed on 8/12/2008]
  • Seborrheic Dermatitis (2007) [Online] Available online from Medline Plus. [Accessed on 8/12/2008]
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.


  • Barnetson, R S C & Rogers, M (2002). ‘Childhood atopic eczema’. British Medical Journal, Vol 324, pp. 1376-1379.
  • Bowcock, A M & Cookson, W O C M (2004). ‘The genetics of psoriasis, psoriatic arthritis and atopic dermatitis’. Human Molecular Genetics, Vol 13, pp. R43-R55.
  • Brown, S & Reynolds, S J (2006). ‘Atopic and non-atopic eczema’. British Medical Journal, Vol 332, pp. 584-588.
  • Buys, L M (2007). ‘Treatment Options for Atopic Dermatitis’. American Family Physician, Vol 75(4), pp. 523-528.
  • (2008) Atopic Dermatitis. [Online]. Available online [Accessed 03/12/2008].
  • 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.
  • (2008) Atopic Dermatitis. [Online]. Available online [Accessed 03/12/2008].
  • 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.


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