Seborrheic dermatitis

Seborrheic dermatitis is a chronic inflammatory disease of the skin of unknown cause or origin, characterized by moderate erythematic, dry, moist or greasy scaling and yellow-crusted patches on various areas of the body. This skin condition that essentially causes flaking of the skin usually affects sebum rich areas of the body such as the face, scalp and the chest. The condition is more common in men than in women. In patients with chronic seborrheic dermatitis, the lesions often worsen in the winter. The effect of increased sunlight on seborrheic dermatitis is unclear, but it seems that low air humidity may exacerbate the seborrheic dermatitis.

The name "seborrheic dermatitis" implies an oily inflammation of the skin. Yet the disease is much more complex than the name implies. Although research has indicated that the skin of patients with seborrheic dermatitis is not necessarily oilier than that of other individuals, there still appears to be some co-relation between seborrheic dermatitis and sebum levels.

The exact cause of seborrheic dermatitis is not known. The root cause may be different in infants and adults. Although seborrheic dermatitis in adults may be clinically similar to infantile seborrheic dermatitis (including cradle cap), the converse is not true. The two primary lesions of infantile seborrheic dermatitis are commonly called ‘cradle cap’ and ‘diaper rash’, though not all cases of ‘diaper rash’ are the results of infantile seborrheic dermatitis. Typically, infantile seborrheic dermatitis occurs within the first 6 months of life and disappears spontaneously by 8 months of age.

Seborrheic dermatitis in adults may be related to hormones, and the disorder is especially common in adolescents and young adults, with the incidence increasing again in patients past the age of 50 years.

Seborrheic dermatitis is often seen in conjunction with other skin diseases, including rosacea (a chronic dermatitis of the face, especially of the nose and cheeks, characterized by a red or rosy coloration with deep-seated papules and pustules), blepharitis or ocular irritation, and acne vulgaris (common acne).

Seborrheic dermatitis is also common in patients with other skin diseases associated with Malassezia species, such as pityriasis versicolor and Malassezia folliculitis. Malassezia is an organism that is normally present on the skin in small numbers. Sometimes the numbers of the Malassezia organism increase, resulting in skin problems, leading some authors to suggest a causative role of Malassezia yeasts in the presentation of seborrheic dermatitis. The species of Malassezia that have been commonly identified with seborrheic dermatitis are M. globosa and M. restricta. While the possibility of Malassezia being the fundamental cause of seborrheic dermatitis is open to question, it does seem to be a complicating factor at least. It is likely that the environment of seborrheic dermatitis, with oil and dead skin being a rich nutrient supply, promotes the growth of Malassezia species.

Seborrheic dermatitis can be associated with immune deficiency, and is much more common in HIV-positive and AIDS patients than in the general population. Seborrheic dermatitis in HIV-positive and AIDS patients is relatively severe and lesions of the extremities are common. As the immune deficiency in these patients deteriorates, the lesions of seborrheic dermatitis get progressively worse. The differences in the clinical presentation, histological and molecular presentation of seborrheic dermatitis in HIV-positive and AIDS patients have led to the suggestion by many researchers and authors that the ‘seborrheic-like’ dermatitis associated with AIDS should be regarded as a distinct clinical condition that is secondary to the immune deficiency.

In addition to its association with immunosuppression, seborrheic dermatitis is common in patients with Parkinson’s disease, probably because of the severe elevation in sebum levels in affected individuals. Authors speculate that the pooling effect of sebum on the face of patients with Parkinson’s disease, whose faces often demonstrate decreased mobility, augments the growth of Malassezia yeasts.

Seborrheic dermatitis is also common in patients with mood disorders. However, it is not definite whether there is a neurological cause for this association, or whether lifestyle and hygiene factors play a pro-active role.

Research studies have documented that seborrheic dermatitis is also associated with chronic alcoholic pancreatitis, hepatitis C virus, various cancers and is also common in patients with genetic disorders, such as Down’s syndrome, Hailey disease and cardio-facio cutaneous syndrome.

The use of varying terms such as "sebopsoriasis", "seborrheic eczema", "seborrheic dermatitis", "dandruff" and "pityriasis capitis" may sometimes make it difficult to interpret the documentation on this disorder. The relationship between seborrheic dermatitis of the scalp and ‘dandruff’ is unclear. Some authors regard a diagnosis of ‘seborrheic dermatitis of the scalp’ as a way of describing severe dandruff, whereas others believe that the term ‘dandruff’ is for any flaking of the scalp, regardless of etiology.

Studies on the causes and treatment of seborrheic dermatitis often focus on the appearance and course of the disease in special populations, specifically, infantile seborrheic dermatitis (ISD), seborrheic dermatitis in AIDS patients and seborrheic dermatitis in patients with Parkinson’s disease. Differences in the course of the condition and its histopathology suggest that the underlying disease process is not the same. In many cases, seborrheic dermatitis may be a sign of disease, rather than the disease itself.

Seborrheic dermatitis clinical features

Seborrheic dermatitis is characterized by the appearance of red, flaking, greasy areas of skin, most commonly on the scalp, nasolabial (relating to the nose and upper lip) folds, ears, eyebrows and chest. However, variations in this clinical picture are common. The extent of redness, degree of flaking and ‘greasy’ appearance of lesions varies from case to case, and it is not unusual to see involvement of other body areas, especially flexural regions.

The lesions of seborrheic dermatitis may resemble those of psoriasis. Their distribution, however, is generally different, with psoriasis manifesting generally on the elbows and knees while seborrheic dermatitis is most commonly present on the sebaceous areas of the skin: the scalp, face, chest and back.

Seborrheic dermatitis pathology

Lesions of seborrheic dermatitis typically show a ‘spongiform’ appearance that distinguishes them from psoriasis. Over time, the lesions become less spongiotic and develop follicular plugs with orthokeratotisis (the formation of an anuclear keratin layer), parakeratosis (retention of nuclei in the cells of the stratum corneum of the epidermis) and uneven ridges.

The histological findings in HIV-positive and AIDS patients are different. Biopsies of lesions from such patients indicate widespread parakeratosis, keratocytic necrosis (death), leukoexocytosis, and a superficial perivascular infiltrate of plasma cells. Hyperkeratosis or hypertrophy of the cornea (horny layer of the skin) also develops in long-standing lesions.

At a molecular level, biopsies taken from lesional skin of AIDS patients show presence of heat-shock proteins (HSP65 and HSP72), which is not evident in HIV-negative patients with seborrheic dermatitis or psoriasis.

Seborrheic dermatitis treatment

Earlier treatments for seborrheic dermatitis tended to focus on anti-inflammatory agents. The current practice is to treat seborrheic dermatitis with antimycotics (anti fungal agents) and other non-specific treatment agents. Some antifungal agents may also reduce the frequency of relapse of seborrheic dermatitis. The following treatment measures have provided relief from seborrheic dermatitis:

• The condition may be treated with over the counter keratolytic agents, which act by peeling and sloughing to unblock the comodones. Selenium sulphide / sulphur preparations like selenium sulphide shampoos have keratolytic action due to the interaction of sulphur with keratinocytes and the subsequent formation of hydrogen sulphide.
• Both whole coal tar and crude coal tar extract have been shown to be effective against seborrheic dermatitis.
• Lithium succinate ointment, available in some countries as a combination of 8% lithium succinate and 0.05% zinc sulphate, may be effective in the treatment of seborrheic dermatitis, both in immuno-competent individuals and in those with AIDS. While some authors believe that lithium succinate is effective in vitro against Malassezia species, others report that it has an anti-inflammatory effect rather than an antifungal one.
• Successful treatment of seborrheic dermatitis has also been reported using benzoyl peroxide, propylene glycol and bufexamac cream.
• The efficacy of corticosteroids, probably due to their anti inflammatory action, ensures that they remain a popular treatment choice for seborrheic dermatitis. Frequently, these agents are prescribed in conjunction with antibiotics. However, they must be used with caution, as even the lower potency steroids may sometimes be associated with atrophy, telangiectasias or perioral dermatitis.
• Zinc pyrithione has both a non-specific keratolytic and an antifungal activity.
• Azoles like Bifonazole and Miconazole may be effective in the treatment of seborrheic dermatitis of the scalp. Ketoconazole is the most commonly prescribed azole medication and is preferred over topical steroids, as it does not carry a risk of patients developing atrophy or telangiectasias with prolonged use. Ketoconazole is available as a 2% cream, a 2% shampoo, an oil-in-water emulsion, and a foaming gel. Fluconazole is another azole medication that is commonly used to treat dermatosis caused by Malassezia. Metronidazole may be a promising new treatment for seborrheic dermatitis.
• Ciclopirox olamine has a broad-spectrum antifungal action, including efficacy against Malassezia SPP, as well as an anti-inflammatory effect.
• Terbinafine is a fungicidal allylamine and works by both improving the lesions of seborrheic dermatitis and reducing the number of Malassezia organisms colonizing the affected areas.
• A new class of medications called topical tacrolimus ointment and pimecrolimus cream are being recommended for treating seborrheic dermatitis. They not only lack side effects associated with the use of corticosteroids, they also have anti fungal activity against M. furfur and Pityrosporum ovale.
• When the seborrheic dermatitis is widely diffuse, or when resistance to topical preparations is observed or in cases when chronic application of topical steroids should be avoided, an oral medication may be preferred by both physician and patient. Despite its efficacy, oral ketoconazole has the potential for adverse effects, particularly with prolonged use and is not advisable. Oral Itraconazole, 200 mg per day for 7 days, is the preferred oral treatment option of seborrheic dermatitis. Oral terbinafine may also be effective against seborrheic dermatitis.

Seborrheic dermatitis references

• Gupta AK, Nicol K, Batra R. Related Articles, Links Role of antifungal agents in the treatment of seborrheic dermatitis. Am J Clin Dermatol. 2004;5(6):417-22. Review. PMID: 15663338
• Gupta AK, Batra R, Bluhm R, Boekhout T, Dawson TL Jr. Skin diseases associated with Malassezia species. J Am Acad Dermatol. 2004 Nov;51(5):785-98. PMID: 15523360
• Gupta AK, Bluhm R.Ciclopirox shampoo for treating seborrheic dermatitis. Skin Therapy Lett. 2004 Jun-Jul;9(6):4-5. PMID: 15334279
• Gupta AK, Cooper EA, Ryder JE, Nicol KA, Chow M, Chaudhry MM. Optimal management of fungal infections of the skin, hair, and nails. Am J Clin Dermatol. 2004;5(4):225-37. PMID: 15301570
• Gupta AK, Kogan N. Seborrhoeic dermatitis: current treatment practices. Expert Opin Pharmacother. 2004 Aug;5(8):1755-65. PMID: 15264990
• Gupta AK, Madzia SE, Batra R. Etiology and management of Seborrheic dermatitis. Dermatology. 2004;208(2):89-93. PMID: 15056994
• Gupta AK, Ryder JE, Nicol K, Cooper EA. Superficial fungal infections: an update on pityriasis versicolor, seborrheic dermatitis, tinea capitis, and onychomycosis. Clin Dermatol. 2003 Sep-Oct;21(5):417-25. PMID: 14678722
• Gupta AK, Bluhm R. Seborrheic dermatitis. J Eur Acad Dermatol Venereol. 2004 Jan;18(1):13-26; quiz 19-20. PMID: 14678527
• Gupta AK, Bluhm R, Cooper EA, Summerbell RC, Batra R. Seborrheic dermatitis. Dermatol Clin. 2003 Jul;21(3):401-12.PMID: 12956195
• Crespo Erchiga V, Delgado Florencio V. Malassezia species in skin diseases. Curr Opin Infect Dis. 2002 Apr;15(2):133-42. PMID: 11964913
• Faergemann J. Management of seborrheic dermatitis and pityriasis versicolor. Am J Clin Dermatol. 2000 Mar-Apr;1(2):75-80. PMID: 11702314
• Hay RJ, Graham-Brown RA. Dandruff and seborrhoeic dermatitis: causes and management. Clin Exp Dermatol. 1997 Jan;22(1):3-6. PMID: 9330043
• Aly R, Berger T. Common superficial fungal infections in patients with AIDS. Clin Infect Dis. 1996 May;22 Suppl 2:S128-32. PMID: 8722840
• Bergbrant IM. Seborrhoeic dermatitis and Pityrosporum yeasts. Curr Top Med Mycol. 1995;6:95-112. PMID: 8724243
• Bergbrant IM, Faergemann J. The role of Pityrosporum ovale in seborrheic dermatitis. Semin Dermatol. 1990 Dec;9(4):262-8. PMID: 2149500