Are You Confident of the Diagnosis?
What you should be alert for in the history
Patients with widespread, atypical, severe, erythrodermic, alopecic, scarring, treatment-resistant disease and those with systemic symptoms should be further evaluated for other conditions mimicking seborrheic dermatitis.
Characteristic findings on physical examination
Seborrheic dermatitis commonly presents with pink to erythematous, superficial patches and plaques with a yellow or skin-colored fine, branny, or greasy scale (Figure 1, Figure 2, Figure 3). There are several variations of seborrheic dermatitis such as petaloid (aka annular, which commonly occurs in darker skin types), follicular (may appear as micropustules on the face, trunk and other seborrheic dermatitis-prone areas), pityriasiform (mimics pityriasis rosea, but without a herald patch, oval superficial scaly patches and plaques on the trunk), and an eczematous form (poorly defined scaly patches).
Areas of the body with high concentrations of sebaceous follicles and active sebaceous glands are common sites of involvement including the face (forehead, glabella, eyebrows, eyelids, nasolabial folds, cheeks, mustache and beard distribution), scalp, ears (concha bowl, external canal, postauricular crease), upper trunk, and flexures (inguinal, inframammary, and axillary). Less often it may be found interscapular, umbilical, in the perineum, and the anogenital crease.
Expected results of diagnostic studies
Histopathology: In acute lesions there is folliculocentric scale crust composed of orthokeratosis and focal parakeratosis with scattered neutrophils, focal spongiosis, and a sparse superficial perivascular infiltrate of lymphocytes and histiocytes. Subacute lesions show numerous yeast species in the stratum corneum with mild psoriasiform hyperplasia 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.
In adult patients with severe, atypical, widespread or treatment-resistant forms of seborrheic dermatitis, consider checking a serum ELISA for HIV (human immunodeficiency virus) antibodies as these types are commonly seen in patients with HIV/AIDS (acquired immunodeficiency syndrome) when CD4+ counts are between 200 to 500 cells/mm3.
Leiner’s disease is a severe, widespread, erythrodermic form of infantile seborrheic dermatitis in which patients have symptoms of fever, anemia, diarrhea, vomiting, weight loss, and sometimes death if not treated properly. There is both a familial and nonfamilial form of Leiner’s. Complement deficiencies of C3 and C5 have been associated with the familial form resulting in defective opsonization of bacteria.
These patients may therefore need to be treated with fresh frozen plasma and whole blood to supplement these complement deficiencies in addition to intense IV hydration, temperature regulation, and antibiotics if they have a secondary bacterial infection.
There is a case report of an Israeli-Jewish-Moroccan family who presented with an autosomal dominant, seborrhea-like dermatosis. A mutation in (ZNF750) encoding a zinc finger protein (C2H2) was described in this family. No genetic tests are recommended despite this known association.
No imaging studies are needed or recommended in the work-up of seborrheic dermatitis.
Diffuse scalp dermatitis or inflammatory alopecia in children warrants fungal culture and KOH (Potassium Hydroxide) preparations to rule out Tinea capitis infections. A widespread, fine scaling variant of Tinea capitis can mimic seborrhea capitis as well.
Psoriasis vulgaris may also affect the scalp, hairline extending onto the forehead and ears mimicking seborrheic dermatitis. These patients may or may not also have a family history, characteristic nail involvement, and other classic sites involved such as knees, elbows and gluteal cleft.
Atopic dermatitis may also affect the face, eyelids, ears, scalp mimicking seborrheic dermatitis. These patients may also have characteristic eczematous dermatitis involving the flexures in addition to an atopic triad (eczema, seasonal allergies, asthma).
Impetigo contagiosum commonly presents on the face in addition to the trunk and extremities and usually has characteristic scales with yellow, honey crust and is highly pruritic and contagious.
Contact dermatitis of the eyelids, ear canals or concha bowls, axillae can mimic seborrheic dermatitis, and these patients should be carefully reviewed for common sensitizers including nail polish, eye drops, ear drops, and antiperspirants/deodorants.
Sarcoid and discoid lupus erythematosus of the face can mimic the petaloid variant of seborrheic dermatitis commonly seen in African Americans and other individuals with darker pigmented skins in which leaf-like or annular, dyspigmented, scaling patches and plaques are present on the cheeks. Sarcoidosis patients may have lacrimal gland enlargement, cutaneous lesions with an apple-jelly appearance on diascopy, and commonly have associated hilar adenopathy on chest X-ray.
Discoid lupus patients may complain of photosensitivity with scarring, dyspigmented patches and plaques on the scalp and conchae bowls as well. These patients usually have a negative ANA (anti-nuclear antibody), unless they have the rare, widespread, disseminated variant. The malar rash of systemic lupus erythematosus spares the nasolabial folds while seborrheic dermatitis classically involves them.
Patients with acne rosacea and demodex folliculorum infections may also have erythema and scaling of the eyelids and cheeks, and usually have follicular associated acneiform pustules in addition.
Widespread truncal types warrant scabies preps and an RPR to rule out secondary syphilis. Pityriasis rosea (Christmas tree pattern oval scaling on the trunk commonly associated with recent upper respiratory viral infection) and truncal psoriasis vulgaris (well-defined, erythematous plaques with thick white scale) may also mimic seborrheic dermatitis when widespread on the trunk.
Tinea versicolor on the central chest and back can appear similar to seborrheic dermatitis, but a KOH is positive for hyphae and spores in the former. Other conditions with widespread truncal involvement considered in the differential include drug eruptions (pityriasis rosea-like, other), pemphigus foliaceus and pemphigus erythematosus, and subacute cutaneous lupus erythematosus, which is commonly photodistributed.
All erythodermic types should be biopsied. Psoriasis, contact dermatitis, pityriasis rubra pilaris, drug eruptions, mycosis fungoides (Sezary syndrome), lichen planus, chronic actinic dermatitis, HIV/AIDS, Hodgkin’s disease, paraneoplastic syndrome, and leukemia cutis patients may all present with erythrodermic scaling that can mimic widespread, erythrodermic seborrheic dermatitis. Patients should be worked up appropriately based on systemic symptoms and other physical findings.
Who is at Risk for Developing this Disease?
Seborrheic dermatitis is primarily seen in two age groups, an infantile self-limited form seen during the first 3 months of life and a chronic, recurrent adult form. A male predominance is seen in all ages. There is no racial predilection, or horizontal transmission. It affects 3% to 5% of young adults, and 1% to 5% of the general population.
Seborrheic dermatitis is one of the most common dermatoses seen in HIV and AIDS patients. Patients with neurologic disorders have been shown to have a higher incidence of seborrheic dermatitis including Parkinson’s, Alzheimer’s, syringomyelia, epilepsy, cerebrovascular infarcts, post-encephalitis, mental retardation, poliomyelitis, quadriplegia, trigeminal nerve injury, other facial nerve palsies, and patients with depression and emotional stress, especially combat troops.
Severe forms are also seen in premature infants with immunosuppression, in patients with congestive heart failure, alcoholism, and endocrinologic diseases that lead to obesity.
It has been theorized that this increased incidence in these patients with neurologic disease leads to neuroendocrine dysregulation, resulting in increased sebum secretion and flares of seborrheic dermatitis. Others have postulated that patients with these neurologic disorders have facial immobility resulting in pooled sebum in which malessezia thrives.
What is the Cause of the Disease?
The etiology of seborrheic dermatitis remains to be elucidated. Many studies have linked Malassezia yeasts, sebum secretion and composition, immunologic abnormalities, and patient susceptibility to the development of seborrheic dermatitis. Disturbance in the host flora of Malessezia species and the resident flora Propionibacterium acnes have also been shown to flare seborrheic dermatitis.
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. A resultant inflammatory response ensues with stimulation of the alternative complement pathway with elevated levels of interleukin (IL)-10, and a drop in IL-2 and interferon-gamma. Both normal and elevated levels of antibodies to Malessezia furfur can be seen in patients with seborrheic dermatitis. Treatment and clearance of seborrheic dermatitis with antifungals and recurrence following cessation of therapy also supports the theory that Malessezia species are pathogenic.
Seasonal fluctuations are common, with flares during low humidity and cold temperatures in the winter and early spring, with some relief in the summer. Facial PUVA (psoralen plus ultraviolet radiation) treatments and facial trauma (scratching) can also trigger seborrheic dermatitis.
Many neurologic disorders have been associated with seborrheic dermatitis, with most of them resulting in varying facial immobility and sebum accumulation. These patients do not have increased rates of sebum, but rather excessive accumulation of sebum on the skin. Patients with seborrheic dermatitis may have increased activity of calmodulin resulting in epidermal hyperproliferation, which is also seen in psoriasis.
Seborrheic dermatitis has not been proven to be associated with any vitamin deficiency. Patients with zinc deficiency (acrodermatitis enteropathica) may have an eruption that appears similar to seborrheic dermatitis and improves with zinc supplementation, while seborrheic dermatitis patients do not improve. Infants with deficiency in biotin, holocarboxylase, biotinidase, and free fatty acids may also have seborrheic-like dermatitis. However, biotin supplementation has not been shown to improve seborrheic dermatitis.
Common medications known to trigger seborrheic dermatitis-like eruptions include the following: griseofulvin, cimetidine, lithium, methyldopa, arsenic, gold, auranofin, aurothioglucose, buspirone, chlorpromazine, ethionamide, haloperidol, interferon alfa, phenothiazines, stanozolol, thiothixene, psoralen, methoxsalen, and trioxsalen.
Systemic Implications and Complications
Patients with widespread, atypical, severe, erythrodermic, alopecic, scarring, treatment-resistant forms and those with systemic symptoms should be further evaluated for other conditions mimicking seborrheic dermatitis. See differential diagnosis above.
Appropriate workup based on history, review of symptoms, and physical examination may include skin biopsy, KOH preparation for hyphae, spores, demodex; fungal culture, bacterial culture, scabies preparation, Wood’s Lamp examination, RPR, ANA, patch testing (ie, TRUE test or North American Standard), and a careful medication history. Further workup depending on the patient setting may include calcium levels, ACE levels and chest X-ray to evaluate for/rule out sarcoidosis; zinc levels for acrodermatitis enteropathica, appropriate cancer screening for erythrodermic variants and CBC.
Shampoos with anti-dandruff activity, emollients, topical corticosteroids, topical antifungals, topical calcineurin Inhibitors, and other topicals.
Shampoos: Recommend lather on face, scalp and body; allow to soak then rinse; use daily until controlled and then two to three times weekly for maintenance. Examples include zinc pyrithione, selenium sulfide 1% to 2.5%, imidazoles (ie, ketoconazole 1% to 2%), salicylic acid 3%, coal tar, mild baby shampoos for infants and eyelid involvement; Baker’s P&S solution. Avoid aggressive manipulation of scale. Hair sprays and hair pomades should be stopped.
Emollients: Application of over-the-counter emollients, creams and lotions can help decrease the amount of scaling.
Topical corticosteroids: low-otency topical steroids (class IV or lower) such as hydrocortisone 1% cream or lotion applied once to twice daily for a few days; mid- or high-potency creams, lotions, or foams depending on the severity and the site can be considered as well. Excessive and long-term topical corticosteroid application should be discouraged as well to prevent steroid acne, steroid rosacea, perioral dermatitis, and rebound phenomenon.
Topical antifungals: Topical antifungals such as ketoconazole, miconazole, fluconazole, itraconazole, econazole, bifaconazole, climbazole, ciclopirox, ciclopiroxolamine. Allylamines may also be effective including butenafine and naftifine cream. All have all been used with varying success. Recommend once to twice daily application x 1 to 2 weeks until clear.
Topical calcineurin inhibitors: (1% pimecrolimus cream and 0.4% to 0.1% tacrolimus ointments) have anti-inflammatory and antifungal (tacrolimus) properties without the long-term side effects of topical corticosteroid use. Recommend once to twice daily application x 1 to 2 weeks until clear.
Other topicals: Sulfur or sulfonamide combinations; Benzoyl peroxide gels, creams, lotions or wash 5% to 10% can be used as well. Patients should avoid alcohol-containing solutions. Aluminum acetate solution can be used. 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. Topical lithium succinate and lithium gluconate (prescription ointments (Efalith) and creams, 8%, AAA 1 to 2 x daily x 2 to 4 weeks) have antifungal properties that can be used for treatment as well, especially in patients with HIV/AIDS. Vitamin D3 analogues (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; coal tar creams; coconut oil compound (ointment combination of coal tar, salicylic acid and sulphur).
Systemic therapy: Oral antifungals should be reserved for severe and refractory cases due to potential drug interactions and side effects, and include oral imidazoles (ie, oral fluconazole, 150 to 200 mg daily x 5 to 7 days; or 150 to 200 mg per week x 4 weeks; or a single 400 mg dose) and allylamines (i.e., oral terbinafine 250 mg daily x 4 weeks). 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). Off label use of oral isotretinoin in low doses (2.5 to 5 mg daily; or 0.1 to 0.3 mg/kg/day) over 3 to 5 months can be used in refractory disease, while observing requirements in child-bearing females.
Physical modalities: Phototherapy with narrowband ultraviolet B or psoralen plus ultraviolet A (PUVA) can also be used in severe and refractory disease, but may be ineffective if patients have thick hair. PUVA may also flare the condition as well.
Surgical Therapy: Not indicated or recommended.
Optimal Therapeutic Approach for this Disease
Treatment should be based on patient preference of topical (shampoo, lotion, cream, ointment, gel, foam, solution), cost of medication and side effect profile. Topical therapies are preferred over systemic treatments because of potential side effects of oral therapies and should be considered and screened for appropriately. Ideally, patients should be treated with a topical anti-inflammatory and anti-Malessezia (anti-dandruff, topical antifungal) combination therapy for maximum control.
Patients with severe and widespread or treatment resistant forms may warrant systemic therapy. Seborrheic dermatitis responds fairly rapidly with treatment, improving within days to one to two weeks with therapy with daily treatment. Maintenance can be used with shampoos or topicals listed above 1-3 times weekly to prevent recurrences.
Seborrheic dermatitis is a self-limited condition with a good prognosis in infants compared with the chronic, relapsing form commonly seen in adults. There is no evidence to suggest infants with seborrheic dermatitis will have disease as adults. The infantile form is self-limited, occurs during the first few weeks to 3 months of life, corresponding to the time when the neonate produces sebum.
The adult form, on the other hand, tends to be chronic and can persist from the fourth through the seventh decades of life, peaking at age 40 years old. The adult form typically begins during puberty corresponding with androgen activity resulting in an increase in size and activity of sebaceous glands. Prepubertal patients have not been shown to have excessive colonization of Malessezia. Generalized flares and erythroderma can sometimes occur in patients.
Monitoring, follow-up and maintenance of patients with seborrheic dermatitis can be done on an as-needed basis after initial therapy is instituted, if the condition worsens or if the patient fails to improve with the prescribed treatment. Discuss with the patient that this is a benign, inflammatory condition that is fairly easily controlled with therapy, but commonly recurs in adulthood, requiring repeat treatments.
The goal of therapy is to control the condition rather than completely cure it. Topical therapies are the preferred treatments due to less risk of side effects from systemic therapies, although some widespread and severe forms may mandate systemic treatments.
Unusual Clinical Scenarios to Consider in Patient Management
Patients with widespread, atypical, severe, erythrodermic, alopecic, scarring, treatment-resistant forms and those with systemic symptoms should be further evaluated for other conditions mimicking seborrheic dermatitis.
What is the Evidence?
Koc, E. “An open, randomized, prospective, comparative study of topical pimecrolimus 1% cream and topical ketoconazole 2% cream in the treatment of seborrheic dermatitis”. J Dermatol Treat. vol. 20. 2009. pp. 4-9. (This study looks at the efficacy and tolerability of pimecrolimus versus ketoconazole and concludes that they are equally effective, but side effects were more common in patients using pimecrolimus.)
DeAngelis, YM, Gemmer, CM. “Three etiologic facets of dandruff and seborrheic dermatitis: Malassezia fungi, sebaceous lipids, and individual sensitivity”. J Invest Dermatol. vol. 10. 2005. pp. 295-7. (This study shows that dandruff is mediated by Malassezia metabolites, specifically irritating free fatty acids released from sebaceous triglycerides. Reduction of Malessezia by pyrithione zinc is the easiest factor to control and therefore reduces free fatty acid production resulting in decreased scalp itching and flaking.)
Birnbaum, RY, Zvulunov, A, Hallel-Halevy, D, Cagnano, E, Finer, G, Ofir, R. “Seborrhea-like dermatitis with psoriasiform elements caused by a mutation in ZNF750, encoding a putative C2H2 zinc finger protein”. Nat Genet. vol. 38. 2006. pp. 749-51. (This article explores a genetic link for inheritance of a seborrhea-like dermatitis in an Israeli Jewish Morrocan family and finds a mutation in ZNF750, which is normally expressed in keratinocytes that encode a C2H2 zinc finger protein.)
Jacobs, JC, Miller, ME. “Fatal familial Leiner’s disease: a deficiency of the opsonic activity of serum complement”. Pediatrics. vol. 49. 1972. pp. 225-32. (This article looks at a family with C5 dysfunction and resultant Leiner’s disease with systemic symptoms and generalized seborrheic dermatitis. They noted that life saving therapy for these patients can be achieved with fresh frozen plasma that contains opsonically active C5.)
Abdel-Hamid, IA, Agha, SA. “Pityriasis amiantacea: a clinical and etiopathologic study of 85 patients”. Int J Dermatol. vol. 42. 2003. pp. 260-4. (This was a prospective study looking at pityriasis amiantacea and its causes and that concluded that this is a reaction pattern of the scalp to many inflammatory scalp dermatoses, most frequently psoriasis and seborrheic dermatitis with other common causes being tinea capitis and staphylococcal infections.)
Nnoruka, EN, Chukwuka, JC, Anisuiba, B. “Correlation of mucocutaneous manifestations of HIV/AIDS infection with CD4 counts and disease progression”. Int J Dermatol Suppl. vol. 2. 2007. pp. 14-8. (This article looked at key clinical indicators, mucocutaneous findings, of underlying immune status and disease progression based on CD4 counts [cells/cm3] and lymphocyte counts in HIV/AIDS patients, noting seborrheic dermatitis is an early finding in these patients when CD4 counts are greater than 200, wheareas Kaposi’s sarcoma is seen at less than 200 and cryptococcal skin disease seen at less than 50.)
Arora, V, Arora, S. “Management of infantile seborrheic dermatitis”. Am Fam Physician. vol. 75. 2007. pp. 807(This article is an excellent review of infantile seborrheic dermatitis and other things in the differential diagnosis to consider and a thorough treatment plan for infantile seborrheic dermatitis.)
Shin, H, Kwon, OS, Won, CH, Kim, BJ, Lee, YW, Choe, YB, Ahn, KJ, Eun, HC. “Clinical efficacies of topical agents for the treatment of seborrheic dermatitis of the scalp: a comparative study”. J Dermatol. vol. 36. 2009. pp. 131-7. (This article compared the efficacy of topical tacrolimus, betamethasone and zinc pyrithione in treating seborrheic dermatitis of the scalp and found that patients treated with zinc pyrithione had the longest sustained improvement over tacrolimus, which was more effective than patients treated with betamethasone. The latter two treatments used also caused a clinically evident scalp aggravation. They concluded the combination therapy of zinc pyrithione when used with either tacrolimus or betamethasone is effective.)
Bikowski, J. “Facial seborrheic dermatitis: a report on current status and therapeutic horizons”. J Drugs Dermatol. vol. 8. 2009. pp. 125-33. (This is an excellent review on the topic of facial seborrheic dermatitis and its current and future treatments.)
Birnbaum, RY, Zvulunov, A, Hallel-Halevy, D, Cagnano, E, Finer, G, Ofir, R. “Seborrhea-like dermatitis with psoriasiform elements caused by amutation in ZNF750, encoding a putative C2H2 zinc finger protein”. Nat Gen. vol. 38. 2006. pp. 749-51.
Cowley, NC, Farr, PM, Shuster, S. “The permissive effect of sebum in seborrheic dermatitis. An explanation of the rash in neurologic disorders”. Br J Dermatol. vol. 122. 1990. pp. 71-6.
de Souza Leão Kamamoto, C, Sanudo, A, Hassun, KM, Bagatin, E. “Low-dose oral isotretinoin for moderate to severe seborrhea and seborrheic dermatitis: a randomized comparative trial”. Int J Dermatol.. vol. 56. 2017 Jan. pp. 80-85. (This article shows that the use of low dose isotretinoin (10 mg every other day) is a potential treatment for seborrheic dermatitis.)
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