Chapter 22. Seborrheic Dermatitis

Seborrheic dermatitis is a common, chronic papulosquamous disorder affecting infants and adults alike. It is characteristically found in regions of the body with high concentrations of sebaceous follicles and active sebaceous glands including the face, scalp, ears, upper trunk, and flexures (inguinal, inframammary, and axillary).1 Less commonly involved sites include interscapular, umbilical, perineum, and the anogenital crease.2 The dermatitis presents with pink to erythematous, superficial patches and plaques with a yellow, branny and sometimes greasy scale. Excessive flaking on the face and scalp can lead to social embarrassment which can have a negative impact on one's quality of life, especially in women, younger patients, and those with a higher educational level.3 Mild forms are most commonly encountered, but severe psoriatic and erythrodermic forms can be seen as well.1 Seborrheic dermatitis is one of the most common dermatoses seen in human immunodeficiency virus (HIV) and acquired immunodeficiency syndrome (AIDS) patients along with certain neurological disorders such as Parkinson disease.4,5 These patients tend to have widespread, erythrodermic, and treatment resistant forms. Severe forms are also seen with immunosupression in premature infants and congestive heart failure patients.6,7 African-Americans and other darkly pigmented races are susceptible to the annular or petaloid variant of seborrheic dermatitis, which may be confused for discoid lupus, secondary syphilis, or sarcoidosis.8 A rare pityriasiform variety of seborrheic dermatitis with ovoid scaling patches can be seen on the trunk and the neck, mimicking pityriasis rosea and secondary syphilis. A higher incidence of seborrheic dermatitis is also seen in patients with alcoholism and endocrinologic diseases that lead to obesity.9

Seborrheic dermatitis is separated into two age groups, an infantile self-limited form primarily during the first 3 months of life and an adult form that is chronic. A male predominance is seen in all ages, without any racial predilection, or horizontal transmission. The prevalence of seborrheic dermatitis is 3%–5% of young adults, and 1%–5% of the general population, although its lifetime incidence is significantly higher.10

The exact pathogenesis of seborrheic dermatitis is yet to be fully elucidated, but this dermatosis is commonly linked with the yeast Malessezia, immunologic abnormalities, sebaceous activity, and patient susceptibility.14,15 The amount of sebum produced is not an essential factor, as not all patients with seborrheic dermatitis will have increased levels of sebum production. On the other hand, some patients with elevated sebum levels may not have seborrheic dermatitis either.16 Patients with seborrheic dermatitis show higher skin surface lipid levels of triglycerides and cholesterol, but lower levels of free fatty acids and squalenes. Both Malassezia species and the resident flora Propionobacterium acnes have lipase activity resulting in transformation of triglycerides into free fatty acids.17 All seven species of Malassezia are lipophilic except the zoophilic species, Malassezia pachydermatis. The free fatty acids and reactive oxygen radicals produced in turn have antibacterial activity that alters the normal skin flora. Some authors believe this disturbance in flora, lipase activity, and free oxygen radicals may be more closely linked to seborrheic dermatitis than an altered immune response.18

Many patients have normal levels of Malassezia species on the skin, but have an abnormal immune response to it resulting in a depressed helper T cell response and less production of phytohemagglutinin and concanavalin when compared to control subjects.19,20 Levels of antibodies are the same in both patients with and without seborrheic dermatitis. Malassezia species also play a role in the inflammatory response with stimulation of the alternative complement pathway.21 A disturbed lymphocytic cellular immune response to Malassezia, results in elevated levels of interleukin (IL)-10, with a drop in IL-2 and interferon-γ.22 Both normal and elevated levels of antibodies to Malassezia furfur can be seen in patients with seborrheic dermatitis. Malassezia can lead to inflammation on the skin from metabolic products produced and complement activation via the direct and alternative pathways.

Seasonal fluctuations in humidity and temperature are noted to flare this disease, particularly with low humidity and cold temperatures in the winter and early spring, with some relief in the summer.23 Facial PUVA (psoralen plus ultraviolet radiation) treatments and facial trauma (i.e., scratching) are also reported to trigger seborrheic dermatitis as well.24

The pathogenesis of seborrheic dermatitis has been disputed since it was originally described over a hundred years ago. The presence or imbalance of microbial flora likely plays a role in the disease. Although some patients may have cultures showing Candida albicans, Staphylococcus aureus, Propionobacterium acnes, and other aerobic bacteria, none have been linked to the pathogenesis of seborrheic dermatitis.25 Infants commonly have secondary contamination and infection with Candida species. The pathogenic role of Malassezia furfur (previously known as Pityrosporum ovale) is also controversial. The number of yeasts on the skin does not directly correlate with the severity of seborrheic dermatitis also. Patients with both dandruff and seborrheic dermatitis generally have abundant yeast counts when compared to controls supporting the role of yeast in the disease. A higher rate of seborrheic dermatitis is also seen in patients with Pityrosporum folliculitis and tinea versicolor.26 Clearance of seborrheic dermatitis with antifungals and recurrence following cessation of therapy also supports the premise that Malassezia species is pathogenic.27

Several drugs are known to trigger seborrheic dermatitis like eruptions including griseofulvin, cimetidine, lithium, methyldopa, arsenic, gold, auranofin, aurothioglucose, buspirone, chlorpromazine, ethionamide, haloperidol, interferon-α, phenothiazines, stanozolol, thiothixene, psoralen, methoxsalen, and trioxsalen.

Many neurologic disorders have been associated with seborrheic dermatitis, with most of them resulting in some facial immobility and sebum accumulation. These include Parkinson's, Alzheimer's, syringomyelia, epilepsy, cerebrovascular infarcts, postencephalitis, mental retardation, poliomyelitis, quadriplegia, trigeminal nerve injury and other facial nerve palsies.28 The fact that administration of l-dopa improves seborrheic dermatitis in some Parkinson patients, and some neuroleptic drugs that induce Parkinsonian symptoms can induce seborrheic dermatitis suggests that neurotransmitters may play a role in this dermatitis.29 Depression and emotional stress have also been reported to trigger seborrheic dermatitis.30 A high rate of this dermatitis is also seen among combat troops.31 In summary, these groups of patients do not have increased rates of sebum, but rather excessive accumulation of sebum on the skin.

Patients with seborrheic dermatitis may have epidermal hyperproliferation or dyskeratinization related to increased activity of calmodulin, which is also seen in psoriasis.32 This explains why patients with seborrheic dermatitis improve while being treated with a number of different cytostatic medications such as azeleic acid.12

Seborrheic dermatitis has not been proven to be associated with any vitamin deficiency. Patients with zinc deficiency (acrodermatitis enteropathica, and acrodermatitis enteropathica like conditions) may have an eruption that appears similar to seborrheic dermatitis and improves with zinc supplementation, while seborrheic dermatitis patients do not improve with zinc supplementation.33 Infants with deficiency in biotin, holocarboxylase, biotinidase, and free fatty acids may also have seborrheic-like dermatitis. But again, biotin supplementation has not been substantiated to improve seborrheic dermatitis.34

A family history of seborrheic dermatitis is often reported, but only recently has a mutation (ZNF750) encoding a zinc finger protein (C2H2) been described resulting in a seborrhea-like dermatitis. This Israeli Jewish Moroccan family presented with an autosomal dominant seborrhea-like dermatosis.35

The controversial term sebopsoriasis is often used in patients when there appears to be an overlap of psoriasis and seborrheic dermatitis. It tends to localize to the scalp, face, and presternal chest as seen with seborrheic dermatitis. However, the margins tend to be better defined, more erythematous and with thicker scales than those seen with seborrheic dermatitis. The biopsy can be indistinguishable from psoriasis, similar to the chronic form of seborrheic dermatitis.36

In all patients with seborrheic dermatitis, there is a so-called seborrheic stage, which is often combined with a gray–white or yellow–red skin discoloration, prominent follicular openings, and mild to severe pityriasiform scales. Several forms can be distinguished (Table 22-1).

Self-limited with a good prognosis in infants compared to chronic and relapsing in adults. There is no evidence to suggest infants with seborrheic dermatitis will have disease as adults. Generalized flares and erythroderma can sometimes occur.37

The infantile form occurs during the first few weeks to 3 months of life, is self-limited, and corresponds to the time when the neonate produces sebum, which then regresses until puberty.38 It is commonly concentrated on the vertex of the scalp (i.e., cradle cap) with adherent, yellow–brown, greasy scale, which can sometimes spread to the entire scalp with inflammatory, erythematous, and oozing crusts. Lesions can be seen on the face, neck and can be disseminated to the trunk and extremities with inflammatory glistening plaques in intertriginous sites such as the axillae and groin (Fig. 22-1). A differential diagnosis should be undertaken in any infant with a widespread form of seborrheic dermatitis (Box 22-1). Atopic dermatitis patients tend to have lesions on the forearms and shins, while sparing the axillae. Lesions isolated to the diaper region suggest seborrheic dermatitis. Radioallergosorbent assay test screening to egg whites, milk antibodies, soybean, and total immunoglobulin E levels, may be helpful in discerning infantile seborrheic dermatitis from atopic dermatitis. Some authors believe that infantile seborrheic dermatitis is actually a variant of atopic dermatitis rather than a separate entity. Extensive involvement plus lesions on the palms and soles with severe pruritis suggests scabies. Infantile psoriasis can also be extensive, with erythematous plaques and scale, with less scale in intertriginous sites. Extensive involvement with moist erythematous plaques and petechial lesions of intertriginous sites and the scalp suggests Langerhans cell histiocytosis (Letterer–Siwe) and should be biopsied for confirmation and treated appropriately.

The adult form on the other hand, tends to be chronic and can persist from the fourth through the seventh decades of life, with a peak at age 40. Lesions may also be seen on the face with prominent symmetry (Fig. 22-2), particularly medial eyebrows, forehead, upper eyelids, nasolabial folds (Fig. 22-3), and lateral nares. Other sites commonly involved include retroauricular regions, external auditory canal, auricle, and conchae bowl (Fig. 22-4), scalp (Fig. 22-5), occiput, and neck. The presternal region of the chest, upper back (Fig. 22-6), and umbilicus can be involved as well, and can be petaloid or arcuate with fine pink scale. Intertriginous sites such as axillary and inguinal regions show less scale and mimic intertrigo. See Box 22-2 for site-specific differential diagnosis of seborrheic dermatitis. Erythema and pruritis are common, as well as burning or tingling sensitivity reported as well, particularly on the scalp. Pityrosporum folliculitis can be seen as well with diffuse monomorphic tiny pustules and papules with peripheral erythema on the trunk. Diagnosis can be confirmed with a KOH (potassium hydroxide) preparation. Immunocompromised patients more commonly get this form of folliculitis. The adult form typically begins during puberty corresponding with androgen activity, which results in an increase in size and activity of sebaceous glands. Prepubertal patients tend to not get seborrheic dermatitis because of this lack of androgen stimulation of sebaceous glands, and have also not been shown to have excessive colonization of Malessezia species.

Leiner first described this controversial condition in 1908, dermatitis seborrhoides infantum, and is considered a severe, widespread, erythrodermic form of infantile seborrheic dermatitis.39 These patients have symptoms of fever, anemia, diarrhea, vomiting, weight loss, and sometimes death if not treated properly with intense IV hydration, temperature regulation, and antibiotics if they have secondary bacterial infection. There is both a familial and nonfamilial form of Leiner's. The hereditary form has been associated with deficiencies of complement C3, C5, and phagocyte malfunction therefore resulting in defective opsonization of bacteria. Patients with the hereditary form may necessitate treatment with fresh frozen plasma and whole blood to supplement these complement deficiencies.40

Pityriasis amiantacea was first described by Alibert in 1832, and is also known as asbestos scalp, tinea asbestina, keratosis follicularis amiantacea, and porrigo amiantacea.41 The use of the term tinea amiantacea is discouraged since tinea capitis is rarely associated with pityriasis amiantacea. This is a localized or diffuse condition, in which inflammation and massive silvery scaling of the scalp results in thick, matted, sticky hair (Fig. 22-7). This condition can occur at any age, especially adolescents and young females. It is most commonly seen with psoriasis (35%), and eczematous conditions like seborrheic dermatitis and atopic dermatitis (34%).42 Case reports of patients with lichen planus and Darier's have had associated pityriasis amiantacea.43 Middle-aged females with lichen simplex chronicus can have patches of pityriasis amiantacea as well. Alopecia may result and is nonscarring unless secondary scalp infection occurs with Streptococcus or Staphylococcus and should be treated appropriately. Staphylococcal isolates in the matted hairs can be found in up to 96% of patients.42 Young females commonly have concomitant postauricular scale and fissures.

Patients with HIV and AIDS have severe and extensive seborrheic dermatitis (Fig. 22-8) that tends to be refractory to standard therapy.44 Treatment with 400 mg of oral ketoconazole daily for 2 weeks may be necessary. The initial facial eruption may appear as a butterfly rash, similar to the acute facial eruption associated with systemic lupus erythematosus. The histopathology also differs from seborrheic dermatitis in HIV seronegative patients in that they have much more parakeratosis, necrosis, lymphocytes, and focal leukocytosis.45 Seborrheic dermatitis usually occurs when CD4+ counts are between 200–500 cells/mm3 and as one of the earliest skin manifestations of HIV patients.46

Depending on the stage of the lesion biopsied, the changes seen include acute, subacute, and chronic spongiotic dermatitis. In acute lesions there is folliculocentric scale crust composed of orthokeratosis and focal parakeratosis with scattered neutrophils, mild focal spongiosis, and a sparse superficial perivascular infiltrate of lymphocytes and histiocytes. Subacute lesions show mild psoriasiform hyperplasia and numerous yeast species in the stratum corneum in addition to the above findings. Chronic lesions show even more psoriasiform hyperplasia and crusting scales in a folliculocentric distribution, superficial dilation of capillaries and venules, and minimal spongiosis. The chronic form may be difficult to distinguish from psoriasis clinically and pathologically, but the folliculocentric distribution supports seborrheic dermatitis.

HIV and AIDS patients with seborrheic dermatitis show histopathologic findings consistent with severe, chronic seborrheic dermatitis (Table 22-2). Patients with pityriasis amiantacea show, spongiosis, mild exocytosis of lymphocytes and acanthosis. The asbestos-like scale seen is due to a thick layering of hyperkeratosis and parakeratosis surrounding the outer hair shafts. Patients with dandruff (pityriasis simplex capillitii, aka pityriasis capitis) show minimal parakeratotic foci of scale, without any spongiosis or inflammatory infiltrates.47

Infantile Seborrheic Dermatitis

This benign, self-limited form responds readily to shampoos, emollients, and mild topical steroids. Infants with prolonged inflammation on the scalp or intertriginous areas can be treated with low potency topical corticosteroids (hydrocortisone 1% cream or lotion for a few days), followed by topical imidazoles (2% ketoconazole cream, lotion, or 1% shampoo). Aggressive removal of scale with keratolytics or mechanical removal is discouraged to prevent further inflammation. However, mild baby shampoos, with or without 3% salicylic acid applications, can help remove thick, stubborn scale on the scalp. Secondary infections with candidiasis or Staphylococcus should be treated appropriately. Infants with seborrheic dermatitis do not respond to dietary alterations or restrictions (milk-free, etc.) and vitamin supplementation that may help patients with atopic dermatitis.38,48–51

Adult Seborrheic Dermatitis

Adults tend to have chronic and recurrent disease, and as such, the patients should be informed that the aim of treatment will be to control rather than cure the disease. Scalp seborrheic dermatitis can be treated with shampoos containing zinc pyrithione, selenium sulfide (1%–2.5%), imidazoles (1%–2% ketoconazole shampoo, creams, lotions, or foams), ciclopirox (cream, gel, and shampoo), salicylic acid (shampoos, creams), coal tar (creams, shampoos), or mild detergents. Dandruff (pityriasis simplex capillitii) involves the face and scalp as well with extensive scale, but shows minimal to no inflammation and erythema. Dandruff responds to more frequent shampooing or a longer period of lathering. Shampoos may be used on the scalp, beard and chest, but may flare the disease if used on the face or other intertriginous areas if left on for extended periods. Xanthotrichia or yellow hair has been reported in patients using selenium sulfide shampoo. Severe and thick scale on the scalp can respond to overnight application of topical corticosteroids (low-, mid-, or high-potency creams, lotions, or foams depending on the severity) with shower cap occlusion as needed, Baker's P&S solution, tar shampoo, or salicylic acid (ointment or shampoo, especially for patients with pityriasis amiantacea). Alternative effective treatments include coconut oil compound (ointment combination of coal tar, salicylic acid and sulfur). Patients should avoid aggressive manipulation. Hair sprays and hair pomades should be stopped. Treatment of any underlying secondary microbial infection should be treated as well. Patients with severe inflammatory disease that fail the above regimens may respond to a 1-week course of systemic glucocorticoids (prednisolone 0.5 mg/kg body weight/day), while cautioning the patient of side effects and informing them of potential rebound flares following discontinuation of the medication.52–57

Treatment of the face, trunk, and ears includes short courses of low potency topical glucocorticoids (Class IV or lower) to suppress the initial inflammation. Excessive and long-term topical corticosteroid application should be discouraged as well to prevent steroid acne, steroid rosacea, perioral dermatitis, and rebound phenomenon. Topical calcineurin inhibitors (pimecrolimus and tacrolimus) have anti-inflammatory and antifungal (tacrolimus) properties without the long-term side effects of topical corticosteroid use. Topical antifungals such as ketoconazole, miconazole, fluconazole, itraconazole, econazole, bifonazole, climbazole, ciclopirox, and ciclopiroxolamine have all been used with varying success. Sulfur or sulfonamide combinations, or propylene glycol topical have also been used. Benzoyl peroxide wash 5%–10% can be used as well. Recommend patients to avoid alcohol-containing solutions that flare the disease. Aluminum acetate solution can be used to maintain seborrheic otitis externa. Patients with seborrheic blepharitis can be treated with warm to hot compresses and washing with baby shampoo followed by gentle cotton tip debridement of thick scale. Avoid ocular glucocorticoids. Ophthalmic sodium sulfacetamide ointment can be used for resistant seborrheic blepharitis.58–68

There are many other alternative treatments. Oral antifungals should be reserved for severe and refractory cases due to potential drug interactions and side effects. Allylamines may also be effective including topical butenafine and naftifine cream for mild cases versus oral terbinafine for extensive involvement. Lithium succinate and lithium gluconate, both available in some countries, have antifungal properties that can be used for treatment as well. Vitamin D3 analogs (calcipotriol cream or lotion) have both anti-inflammatory and antifungal properties and can be used in selected patients as well. Other alternatives include topical metronidazole cream or gel, once to twice daily. Oral isotretinoin in low doses (2.5–5 mg daily; or 0.1–0.3 mg/kg/day) over 3–5 months can be used in refractory disease, of course while observing requirements in child-bearing females. Phototherapy with narrowband ultraviolet B or psoralen plus ultraviolet A can also be used in severe and refractory disease, but may be ineffective if patients have thick hair.17,69,74

We would like to thank Gerd Plewig and Thomas Jansen for their previous editions of this chapter on seborrheic dermatitis and the use of their format, tables, boxes, and photos while revising this chapter.