|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 (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;
- Skin injuries;
- Nutritional deficiencies of zinc, riboflavin, niacin and pyridoxine;
- Various drugs and medications such as cimetidine, ethionamide, gold, arsenic, interferon-a, lithium and methyldopa.
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]
- Pennstate Medical Centre - A - Z Health and disease information
- Mayo Foundation for Medical Education and Research
- University of Maryland Medical Centre
- Mercks Online Medical Library
- Dermatology Information System
- American Osteopathic College of Dermatology