Seborrheic dermatitis

OVERVIEW: What every practitioner needs to know

Are you sure your patient has seborrheic dermatitis? What should you expect to find?

Immunocompetent patients with seborrheic dermatitis present similarly to those without HIV infection; however, an atypical and more extensive presentation is common in those infected with HIV (Figure 1).

Figure 1.

Eroded and scaly plaques on face; note scaling on anterior hairline

  • Itching and rash: Patients commonly complain of itching of their scalp, ears, beard area, and axillae or groin if involved. Patients may complain of dandruff and/or rash around the nose, in the eyebrows, ear canals, beard and mustache, axillae, or groin. If erythrodermic, patients may complain of full-body itching along with rash.

  • Scaly scalp: This is the most common clinical finding and may be the only sign in mild disease; may be fine white or greasy, yellow scale.

  • Rash: Symmetrical erythematous macules, patches and thin papules or plaques with yellow, greasy scale


    Eyebrows and glabella

    Peri-alar and melolabial (nasolabial) fold

    External auditory canals and post-auricular skin

    Beard and mustache area

    Central chest and inframammary folds

    Axillae and groin/perineum

    Rarely, the patient will have erythroderma.

  • Except those on the scalp, lesions tend to be sharply demarcated.

How did the patient develop seborrheic dermatitis?

  • Seborrheic dermatitis is common.

    2-5% of the normal population

    More common in males

  • There are two incidence peaks:

    Infancy, a self-limited condition (i.e., cradle cap)

    4-6th decades in adults

  • In those with HIV:

    Prevalence ranges from 7 to 80%

    Occurs early in HIV infection

    Can be seen at all stages of disease, however, atypical and more extensive involvement can be associated with worsening immunodeficiency.

    May be presenting sign of HIV infection

  • Malassezia species

    Thought to be involved in pathogenesis of disease

    Reduction in density correlates with treatment success

Which individuals are of greater risk of developing seborrheic dermatitis?

Seborrheic dermatitis is more common in certain populations, some of which have been outlined in the previous section. Additional settings in which seborrheic dermatitis may be seen include:

  • Underlying neurological disease: Parkinson’s disease, stroke, facial nerve injury, seizure disorder

  • Obesity and diabetes

  • Celiac sprue

  • Intestinal malabsorption

Beware: there are other diseases that can mimic seborrheic dermatitis:

The differential diagnosis of seborrheic dermatitis includes:

  • Psoriasis

    Plaques tend to be thicker with more pronounced erythema or redness.

    Scale is “silvery.”

    It tends to be less itchy

    Nails, elbows, knees are involved.

    The scalp may be involved, similar to seborrheic dermatitis, but facial involvement is uncommon.

  • Atopic Dermatitis

    Scale on scalp tends to be fine, white.

    Dry skin presents overall.

    There is involvement of antecubital and popliteal fossae.

  • Intertriginous Candida

    It is beefy red.

    There are satellite pustules at periphery of main plaques.

    Lack of scalp involvement exists.

  • Rosacea

    Erythematous papules and pustules in central facial distribution occur.

    There is a lack of typical seborrheic dermatitis distribution.

  • Langerhan’s cell histiocytosis

    Yellow-brown perifollicular papules occur.

    Intertriginous fissures occur.

What laboratory studies should you order and what should you expect to find?

The diagnosis of seborrheic dermatitis is most commonly made by history and physical examination alone.

Results that confirm the diagnosis

When needed, a skin biopsy may help confirm the clinical suspicion of seborrheic dermatitis and rule out some diseases in the differential diagnosis (Langerhans cell histiocytosis).

  • Skin biopsy: often nonspecific and subtle

    Irregular acanthosis with variable amounts of spongiosis and lymphocytic exocytosis

    Neutrophil exocytosis

    Parakeratosis and scale-crust especially adjacent to follicular ostia

What consult service or services would be helpful for making the diagnosis and assisting with treatment?

If you decide the patient has seborrheic dermatitis, what therapies should you initiate?

Dermatology is often consulted, especially if the patient presents with erythroderma.

Key principles of therapy
  • Seborrheic dermatitis is thought to be related to overgrowth of or an inflammatory response to Malassezia species, a fungal member of the normal skin flora.

  • The mainstay of therapy remains topical antifungals with creams, gels, foams, liquids, and shampoos.

    The azole antifungals are commonly employed in this disease.

  • Griseofulvin is not effective against Malassezia and should not be used.

  • In mild disease, treating the scalp with shampoo often contributes to improvement or resolution of disease elsewhere.

  • Anti-inflammatory medications, such as topical corticosteroids or calcineurin inhibitors, may also be used, especially if the disease is resistant to initial antifungal treatment.

    The use of topical steroids should be limited and appropriate for the body site to limit the risk of side effects, including epidermal and dermal atrophy, skin dyspigmentation, telangiectasia, and striae.

    The site of involvement will not only help determine which anti-inflammatory to use, but also which formulation.

    For example, ointments do not work well in hairy areas, because they are difficult to apply.

  • If significant hyperkeratosis is present, topical keratolytics (salicylic acid) may be used to reduce the scale.

What other treatments may be helpful?

  • Substitute the use of soap with a light emollient cleanser if the face is significantly scaly.

What should you tell the patient about the prognosis?

Seborrheic dermatitis is a chronic disease that tends to wax and wane in severity. Patients may see worsening of their disease with stress, changes in environment, and travel. In general, seborrheic dermatitis is more difficult to treat in those with HIV infection and may be resistant. These patients often have more areas involved and are at increased risk of developing erythroderma, although this is a rare complication of seborrheic dermatitis.

If the patient presents with erythroderma

  • It is important to discuss the case with a dermatologist at the point of care.

  • These patients are at risk of increased insensible losses, volume depletion, and high-output cardiac failure if allowed to persist for long periods of time with extensive skin disease. Treatment setting depends on the severity of illness; if the patient is tachycardic and volume depleted, it may be best to admit the patient for IV fluid resuscitation. However, most patients can be treated effectively as outpatients with close clinical follow-up.

  • Initial therapy may include a medium-potency topical steroid (triamcinolone can be prescribed in a 1 pound jar) ointment applied to affected skin (avoiding facial skin) twice every day. The addition of the soak and smear method (soak in a warm water tub with no soap for 15-20 minutes; while still wet, apply the topical steroid, then dress in cotton pajamas and/or a vinyl sauna suit, preferably worn over damp cotton pajamas) will often speed improvement, as well as reduce pruritus dramatically. Patients must be cautious not to employ this modality for longer than 1-2 weeks to prevent side effects.

How do you develop seborrheic dermatitis and how frequent is this disease?

It is unclear why seborrheic dermatitis develops. As mentioned, seborrheic dermatitis is more common in men. Although the exact incidence and prevalence are unknown, seborrheic dermatitis typically begins in two age groups. The infantile form begins at about 1 week of age and may last for several months but is a self-limited disease. The adult type begins in the 4-6th decades of life and is a chronic, waxing and waning skin condition. There is no evidence of horizontal spread of seborrheic dermatitis.

What pathogens are responsible for this disease?

Although the exact mechanism by which this disease occurs is unknown, it is apparent that Malassezia species are involved. Malassezia is a commensal fungus on the skin; it can be easily isolated from the skin of those with seborrheic dermatitis and, although there is no specific threshold at which seborrheic dermatitis develops, successful treatment is associated with reductions in the number of Malassezia on the skin.

How do these pathogens cause seborrheic dermatitis?

A role for immune mechanisms against Malassezia in the development of seborrheic dermatitis has been suspected but has yet to be confirmed. M. fufur specific antibodies do not seem to be increased in those with seborrheic dermatitis versus controls. Although it may not be specific to Malassezia, is it apparent that patients with seborrheic dermatitis show upregulation of several cytokines including interleukin (IL)-6, 4, 10 and interferon (IFN)-γ, as well as increased recruitment of natural killer cells. There appears to be a decrease in IL-2.

What other additional laboratory tests may be ordered?

The diagnosis is most often made clinically. The following tests may be useful if questions still remain:

  • A PAS stain performed on a skin biopsy may reveal fungal organisms in the stratum corneum.

  • A KOH preparation of scale from the skin may show characteristic “spaghetti and meatballs” appearance of Malassezia spores and hyphae.

WHAT'S THE EVIDENCE for specific management and treatment recommendations?

James, WD, Berger, TG, Elston, DM.. Andrews' diseases of the skin. 2011. pp. 188-9. (This is an excellent review of the salient features of seborrheic dermatitis, including clinical presentation, histologic findings, and treatment.)

Fritsch, PO, Reider, N., Bolognia, JL, Jorizzo, JL, Rapini, RP. “Other eczematous eruptions”. Dermatology. 2008. pp. 197-200. (This is an outstanding review of seborrheic dermatitis, including its relationship to HIV infection.)

Maniar, J, Kamath, R., Tyring, SK, Lupi, O, Hengge, UR. “HIV and HIV-associated disorders”. Tropical Dermatology. 2006. pp. 112(This is a brief review of seborrheic dermatitis in the setting of HIV infection.)

Williams, J, Coulson, I., Lebwohl, MG, Heymann, WR, Berth-Jones, J, Coulson, I. “Seborrhiec eczema”. Treatment of Skin Disease Comprehensive Therapeutic Strategies. 2010. pp. 694-6. (This book evaluates the evidence for treatments for many different diseases of the skin.)

Kastarinen, H, Oksanen, T, Okokon, EO, Kiviniemi, VV. “Topical anti-inflammatory agents for seborrhoeic dermatitis of the face or scalp”. Cochrane Database Syst Rev.. 2014 May 19. pp. CD009446(This thorough review finds no evidence for superiority of any treatment compared to topical steroids, but most of the included studies were small and short.)


DRG code 596: If the patient requires admission for erythrodermic seborrheic dermatitis.

, 690.10, or 690.18.

Table I.
Disease Location Anitfungal Topical Steroid Alternative
Scalp Shampoos – lather, leave in 5 minutes, then rinse; 2-3 times/week·         Ciclopirox 1% (probably most effective; Evidence level A)·         Ketoconazole 2% (Evidence level A)·         Zinc pyrithione 1% (Evidence level B)·         Coal tar 0.5%, 1%·         Selenium sulfide 1%, 2.25% (least effective; Evidence level C) Clobetasol 0.05% shampoo (likely not appropriate for long-term use; Evidence level A) ·         Propylene glycol lotion 15% (applied to wet hair after shampooing, leave on for 5 minutes, then rinse; Evidence level A)For recalcitrant disease: ·         Oral itraconazole 200mg daily for 1 month, then 2 days each of the following 11 months·         Oral terbinafine 250mg daily for 4-6 weeks
Face, ears (including EAC), intertriginous, and trunk Ketoconazole 2% cream BID (Evidence level A)·         Ciclopiroxolamine 1% cream BID (Evidence level A)·         Clotrimazole 1% cream BID·         Miconazole 2% cream BID·         Econazole 1% cream BID Hydrocortisone 1%, 2.5% cream, ointment BID (Evidence level A)·         Desonide 0.05% cream, ointment BID·         Fluocinolone 0.01% oil BID (for use in EAC)·         Triamcinolone 0.1% cream, ointment BID (for persistent disease on the trunk only) ·         Lithium succinate or gluconate 8% ointment BID (Evidence level A)·         Topical pimecrolimus 1% cream BID (Evidence level B)·         Topical tacrolimus 0.1% ointment BID (Evidence level C)For recalcitrant disease:·         Oral itraconazole 200mg daily for 1 month, then 2 days each of the following 11 months (Evidence level B)·         Oral terbinafine 250mg daily for 4-6 weeks (Evidence level A)
Erythroderma Triamcinolone 0.1% ointment BID, using soak and smear and/or sauna suit