Last updated: 9 July 2009.
Introduction
Seborrheic dermatitis (SD) is a form of eczema and a common, inflammatory skin disorder that affects infants and adults. 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.
Incidence
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.
Causes
Whilst the cause of Seborrheic dermatitis is not entirely clear, many factors are thought to contribute to the disorder. These include:
- Malassezia yeast – increased numbers of a common yeast that lives on human skin has been implicated
- Oily skin – the sebaceous glands in the skin begin to produce too much oil (sebum)
- Genetic Factors – a family history of eczema
- Immune dysfunction/ deficiency – increased incidence of SD in immunocompromised patients (HIV/AIDS) suggests that they are unable to keep Malassezia numbers in check
- Neurological abnormalities – high frequency of patients with SD also have neurological disorders
The following risk and environmental factors may also increase the likelihood of developing SD:
- Cold, dry weather
- Stress
- Fatigue
- Skin injuries
- Obesity
- Nutritional deficiencies
- Various drugs and medications
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, 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.
Treatments
Infantile Seborrheic dermatitis is benign and will generally clear itself within a few weeks or months. It is not necessary to treat it, 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. 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.
Hygiene issues play a key role in controlling SD with frequent cleansing with soap or mild shampoos to remove oils from affected areas. Effective therapies for SD include:
- Anti-inflammatory (immunomodulatory) agents – anti-inflammatory properties and regulate different parts of the immune system
- Keratolytic agents – soften and remove/reduce scales and lesions
- Antifungal agents – control fungal growths
- Topical corticosteroids – anti-inflammatory properties and modify the body’s immune response to certain stimuli.
Introduction
Seborrheic dermatitis (SD) is a form of eczema and a common, inflammatory skin disorder. It 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 nasolabial folds, 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.
Epidemiology and prevalence
The prevalence rate of seborrheic dermatitis is 3-5%, with a worldwide distribution,n 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). It is found in up to 85% of patients with advanced HIV but in less than 5% of the general uninfected population. It may flare and subside overtime; generally worsening after severe illness. Persons with central nervous system disorders such as Parkinson’s disease and epilepsy also appear to be prone to the development of SD.
Clinical features
Infants:
The disease occurs primarily within the first few months of life as an inflammatory disease affecting the scalp. Other regions such as the face, neck and chest may also be affected. The scalp regions are covered with mild, oily scaling to widespread, thick, sticky crusts. Inflammation is very sparse and hair loss is uncommon. The disease can progress, with redness of the scales increasing and the scales extending pass the hairline. These clinical aspects can sometimes be mistaken for Psoriasis or Atopic dermatitis.
The disease is not dangerous nor caused by poor hygiene and will usually resolve itself over a few weeks or months. It is not contagious and therefore cannot be caught from another baby. Irritation generally leads to scratching, which may worsen the symptoms or lead to infections via broken skin.
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.
Etiology and pathogenesis
The etiology of Seborrheic dermatitis is not entirely clear. Several theories that contribute to SD currently exist.
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 furfur
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.
Genes
Having a family history of eczema might predispose one to developing SD. The actual genes involved, if any, are not known.
Immune dysfunction/deficiency
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. The increased incidence of SD in HIV and AIDS patients also supports the hypothesis that Seborrheic dermatitis has a strong immunological basis.
Neurological abnormalities
SD has been found to occur in high frequencies among patients with neurological disorders such as epilepsy and Parkinson’s disease. This points out a possibility that the nervous system may be involved, though there is no hard evidence as yet to support this theory.
Physical factors
It has been reported that SD usually worsens or is induced by the winter seasons where the climate is cold and dry. Other factors that may induce SD include emotional stress, fatigue, skin abrasions and obesity. Many drugs such as cimetidine, ethionamide, gold, arsenic, interferon-a, lithium and methyldopa have been known to induce SD like symptoms by an unknown mechanism. Nutritional deficiencies of zinc, riboflavin, niacin and pyridoxine have also been reported to cause SD like symptoms by unknown mechanisms.
Prevention
SD cannot be prevented but the severity of the disease can be decreased by controlling the risk factors and by maintaining skin care.
Treatment
Infants
In general, Seborrheic dermatitis clears itself spontaneously but some parents prefer to treat it as it is unsightly, even though it does not harm the infant in any way.
- Scalp – Treatment is directed toward loosening and removing scales and crusts. This can be done by washing and massaging the scalp with mild baby shampoos or soap. If regular washing and brushing does not seem to help, a dermatologist may prescribe a mild corticosteroid or antifungal medication.
- Non Scalp – When SD extends beyond the scalp, dermatologists will usually prescribe a topical medication such as antifungal creams or mild corticosteroids.
Adults
Adults should be informed of the chronic nature of the disease and how it cannot be cured; only controlled by treatment. 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 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.
Prognosis
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.
