Treatment of Seborrheic Dermatitis
FREE PREVIEW Log in or buy this issue to read the full article. AAFP members and paid subscribers get free access to all articles. Subscribe now .
FREE PREVIEW Subscribe or buy this issue. AAFP members and paid subscribers get free access to all articles.
BETTY ANNE JOHNSON, M.D. PH.D. and JULIA R. NUNLEY, M.D. Medical College of Virginia Campus of Virginia Commonwealth University, Richmond, Virginia
Am Fam Physician. 2000 May 1;61(9):2703-2710.
Seborrheic dermatitis is a chronic inflammatory disorder affecting areas of the head and trunk where sebaceous glands are most prominent. Lipophilic yeasts of the Malassezia genus, as well as genetic, environmental and general health factors, contribute to this disorder. Scalp seborrhea varies from mild dandruff to dense, diffuse, adherent scale. Facial and trunk seborrhea is characterized by powdery or greasy scale in skin folds and along hair margins. Treatment options include application of selenium sulfide, pyrithione zinc or ketoconazole-containing shampoos, topical ketoconazole cream or terbinafine solution, topical sodium sulfacetamide and topical corticosteroids.
The etiology of seborrheic dermatitis remains unknown, although many factors, including hormonal, have been implicated. This chronic inflammatory skin disorder is generally confined to areas of the head and trunk where sebaceous glands are most prominent. When seborrheic dermatitis occurs in the neonatal period, it usually disappears by six to 12 months of age, suggesting that it may be a response to maternal hormone stimulation.1
Seborrheic dermatitis frequently affects persons in postpuberty. Additional evidence of hormonal influence is provided by research demonstrating that the human sebocyte responds
to androgen stimulation.2
Pityrosporum ovale. a lipophilic yeast of the Malassezia genus, has been implicated in the development of this condition.3 It has been suggested that seborrheic dermatitis is an inflammatory response to this organism, but this remains to be proved.4 P. ovale is present on all persons. Why some persons develop seborrheic dermatitis and others do not is unclear. The colonization rate of involved skin by this organism may be lower than that of uninvolved skin.3 Nonetheless, the fact that seborrheic dermatitis responds to antifungal medications is strongly suggestive of the role of yeast in this disorder.
Genetic and environmental factors, as well as other comorbid diseases, may predispose specific populations to the development of seborrheic dermatitis. Although seborrheic dermatitis affects only 3 percent of the general population, the incidence in persons with acquired immunodeficiency syndrome may be as high as 85 percent. The exact mechanism whereby human immunodeficiency virus infection promotes an atypical and explosive onset of seborrheic dermatitis (and other common inflammatory skin disorders) is unknown, but many factors have been explored, including CD4-positive T lymphocyte counts,5 P. ovale density6 and nutritional factors.7
Persons with central nervous system disorders (Parkinson's disease, cranial nerve palsies, major truncal paralyses) also appear to be prone to the development of seborrheic dermatitis, tend to develop more extensive disease and are frequently refractory to treatment. It has been postulated that seborrheic dermatitis in these patients is a result of increased pooling of sebum caused by immobility. This increased sebum pool permits growth of P. ovale. which induces seborrheic dermatitis.8