Seborrheic Dermatitis

Background

Seborrheic dermatitis is one of the most common skin manifestations of HIV infection. It occurs in 3-5% of the general HIV-uninfected population but in up to 85-95% of patients with advanced HIV infection. Among HIV-infected individuals, seborrheic dermatitis often begins when their CD4 counts drop to the 450-550 cells/µL range. The disease is more likely to occur among young adults (because they have oilier skin) and males, and is more common in areas with cold, dry winter air. It is rarely found in African blacks, unless the person is immunocompromised. It is more common during times of mental stress and severe illness.

Seborrheic dermatitis is a scaling, inflammatory skin disease that may flare and subside over time. It is characterized by itchy reddish or pink patches of skin, accompanied by greasy flakes or scales. It most commonly occurs in the scalp and on the face, especially at the nasolabial folds, eyebrows, and forehead, but also may develop on the ears, chest, upper back, axillae, and groin. Dandruff is considered to be a mild form of seborrheic dermatitis. Occasionally, seborrheic dermatitis may be severe, may involve large areas of the body, and may be resistant to treatment. Severe manifestations are more likely with advanced HIV infection.

The etiology of seborrheic dermatitis is not entirely clear. Malassezia yeast (formerly called Pityrosporum ovale), a fungus that inhabits the oily skin areas of 92% of humans, is the most likely culprit. This same yeast also is thought to cause tinea versicolor and Pityrosporum folliculitis. Overgrowth of the Malassezia yeast in the oily skin environment, failure of the immune system to regulate the fungus, and the skin's inflammatory reaction to the yeast overgrowth appear to be the chief factors that cause the dermatitis.

S: Subjective

The patient complains of a new rash, sometimes itchy, or of "dry skin" that will not go away despite the application of topical moisturizers.

O: Objective

Perform a thorough evaluation of the skin with special attention to the scalp, medial eyebrows, eyelashes and eyelids, beard and other facial hair areas, nasolabial folds, postauricular areas, the concha of the auricle, glabella, umbilicus, central chest, back, axillae, and groin. Seborrheic dermatitis appears as white to yellow greasy or waxy flakes over red or pink patches of skin; however, discrete fine scales may indicate a mild form of the disease. Around the eyes, seborrheic dermatitis can cause eyelid erythema and scaling. The distribution usually is symmetrical.

A: Assessment

The diagnosis of seborrheic dermatitis is based on the characteristic appearance. A partial differential diagnosis includes psoriasis, atopic dermatitis, contact dermatitis, erythrasma, tinea capitus (can be present on the scalp without hair loss), rosacea, and rarely, dermatomyositis.

P: Plan

Treatment

• Antiretroviral therapy, if otherwise indicated.
• Specific treatments are divided into three types: antimycotic (first choice), antiinflammatory (second choice), and keratolytic. Shampoos may be used on the entire body.
• Topical antifungal medications: The azoles and ciclopirox have been well studied and shown to have both antifungal and antiinflammatory activity. Various preparations are available; selection can be based on cost and availability. Antifungals may be used in combination with topical corticosteroid therapy (see below). Effective antifungals include but are not limited to the following:
  • Ketoconazole (Nizoral) 2% cream or shampoo; ketoconazole is one of the most widely studied of all topical treatments
  • Bifonazole ointment, miconazole cream (Monistat), terbinafine (Lamisil) 1% solution or cream, or clotrimazole (Lotrimin) 1% cream, lotion, or solution
  • Ciclopiroxolamine (Loprox) 1% shampoo, gel, or cream
  • Zinc pyrithione (keratolytic/antifungal) shampoo or cream
• Topical corticosteroids generally are effective and may be used in combination with topical antifungal therapy (see above). Low-potency agents (e.g., hydrocortisone 1%) rather than high-potency corticosteroids (e.g., betamethasone dipropionate, triamcinolone), are recommended, especially for the face, to reduce the risk of adverse effects associated with all corticosteroids (e.g., atrophy, telangiectasias, and perioral dermatitis). Clobetasol shampoo has antiinflammatory effects.
• Selenium sulfide/sulfur preparations (the most common is selenium sulfide shampoo).
• Whole coal tar, crude coal tar extract: shampoos, creams, and gels.
• Lithium succinate or lithium gluconate ointment, available in some countries as a combination of lithium succinate 8% and zinc sulfate 0.05% (may have antifungal or antiinflammatory effects). Not for use on the scalp.
• Honey, 90% diluted with warm water, may be used to treat seborrheic dermatitis and dandruff.
• Azelaic acid, 15% gel or 20% cream, has sebosuppressive, antimicrobial, antifungal, and antiinflammatory activity (also used for acne and rosacea).
• Noncorticosteroid topical immunomodulators (calcineurin inhibitors):
  • Tacrolimus
  • Pimecrolimus
• Oral therapy may be used for patients who are refractory to topical treatment (may interact with protease inhibitors and nonnucleoside reverse transcriptase inhibitors; check for possible drug-drug interactions with antiretroviral and other medications before prescribing). There are limited data regarding the efficacy of systemic medication.
  • Fluconazole 300 mg once weekly for 2 weeks
  • Itraconazole 200 mg once daily for 7 days
  • Ketoconazole 200 mg once daily for no more than 4 weeks
  • Terbinafine 250 mg once daily for 4 weeks

Potential adverse effects:

• With all topical products: skin burning, stinging, dryness; allergic or contact dermatitis. Tar shampoos may discolor light hair, leave an oily film on hair, and leave an odor. Coal tar may be carcinogenic; use shampoo no more than twice a week, leave on skin or hair for 5 minutes, and rinse well.
• Topical corticosteroids may cause skin atrophy, telangiectasias, folliculitis, striae, and excessive hair growth. Risk of adverse effects is low and can be mediated by using product infrequently, diluting the product, or limiting the amount of time the product is on the skin (shampoos are ideal).
• With oral therapy, monitor for hepatotoxicity.

Patient Education

• Although topical and oral medicines can relieve symptoms, recurrence is common. Effective antiretroviral therapy should be considered to control the effects of HIV on the immune system and thereby treat the underlying cause of seborrheic dermatitis.

References

• Bikowski J. Facial seborrheic dermatitis: A report on current status and therapeutic horizons. J Drugs Dermatol. 2009 Feb;8(2):125-33.
• Dunic I, Vesic S, Jevtovic DJ. Oral candidiasis and seborrheic dermatitis in HIV-infected patients on highly active antiretroviral therapy. HIV Med. 2004 Jan;5(1):50-4.
• Faergemann J, Bergbrant IM, Dohse M, et al. Seborrhoeic dermatitis and Pityrosporum (Malassezia) folliculitis: characterization of inflammatory cells and mediators in the skin by immunohistochemistry. Br J Dermatol. 2001 Mar;144(3):549-56.
• Gupta AK, Bluhm R. Seborrheic dermatitis. J Eur Acad Dermatol Venereol. 2004 Jan;18(1):13-26; quiz 19-20.
• Gupta AK, Ryder JE, Nicol K, et al. Superficial fungal infections: an update on pityriasis versicolor, seborrheic dermatitis, tinea capitis, and onychomycosis. Clin Dermatol. 2003 Sep-Oct;21(5):417-25.
• Levin NA. Beyond spaghetti and meatballs: skin diseases associated with the Malassezia yeasts. Dermatol Nurs. 2009 Jan-Feb;21(1):7-13, 51; quiz 14.
• Naldi L, Rebora A. Clinical practice: seborrheic dermatitis. N Engl J Med. 2009 Jan 22;360(4):387-96.
• Rigopoulos D, Paparizos V, Katsambas A. Cutaneous markers of HIV infection. Clin Dermatol. 2004 Nov-Dec; 22(6):487-98.
• Waldroup W, Scheinfeld N. Medicated shampoos for the treatment of seborrheic dermatitis. J Drugs Dermatol. 2008 Jul;7(7):699-703.