Diagnostic Summary

• Branny or greasy scaling over erythematous skin patterned on the sebum-rich areas of the scalp, face, and trunk. Facial areas include the forehead, eyebrows, eyelashes, nasolabial folds, and beard. Truncal involvement includes the presternal region, umbilicus, axillae, inframammary and inguinal folds, and perineum.

• The scalp appearance varies from mild, patchy dandruff to widespread, thick, adherent crusts; it may involve the anterior and posterior hairline and the periauricular skin. In infants it occurs as “cradle cap.”

• Usually nonpruritic, although active phases can manifest with burning and itching.

• Seasonal; worse in winter.

General Considerations

Seborrheic dermatitis is a common papulosquamous condition similar in appearance to psoriasis. Clinically it may be associated with excessive oiliness (seborrhea) and dandruff. The scale may be yellowish and either dry or greasy. The erythematous, follicular, scaly papules may coalesce to form large plaques or circinate patches. Flexural involvement is often complicated by candidal infection. The condition occurs either in infancy (usually between 2 and 12 weeks of age) or in the middle-aged or elderly and has a prognosis of lifelong recurrence.

Malassezia yeast organisms are probably not the cause but a cofactor linked to depressed helper T cells (seborrheic dermatitis is very common in AIDS); increased natural killer cells, which increase inflammatory cytokines; increased sebum levels; activation of the alternate complement pathway; and genetic susceptibility to a skin barrier dysfunction.¹ Malassezia species have lipase activity, which releases inflammatory arachidonic acid. Seborrheic dermatitis is aggravated by changes in humidity, scratching, emotional stress, diet, various medications, and androgen excess.

Therapeutic Considerations

Nutrition

Food Allergy

Seborrheic dermatitis usually begins as cradle cap and, although not primarily an allergic disease, has been associated with food allergy (67% of patients exhibit some form of allergy by 10 years of age).²

The underlying factor in infants may be a biotin deficiency.³ A syndrome clinically similar to seborrheic dermatitis has been produced by feeding rats a diet high in raw egg white (high in avidin, a glycoprotein that binds biotin, making it unavailable for absorption). Because a large portion of the human biotin supply is provided by intestinal bacteria, it has been postulated that the absence of normal intestinal flora may be responsible for biotin deficiency in infants.² A number of articles have demonstrated successful treatment of seborrheic dermatitis with biotin in both the nursing mother and the infant.^3,⁴

In adults, treatment with biotin alone is usually of no value.

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