Seborrheic Dermatitis

Seborrheic dermatitis is a common chronic, relapsing skin disorder that presents as erythematous plaques with greasy, yellow scales in susceptible areas (scalp, face, and trunk). Seborrheic dermatitis has a biphasic incidence, occurring in two peaks: first in infants, then in adolescence and early adulthood. Although the exact etiology is unknown, pathologic mechanisms have been observed involving the sebaceous glands and Malassezia on the skin. Topical medications are used for acute exacerbation or maintenance treatment. These options aim to inhibit skin colonization (antifungal agents), reduce inflammation (steroids, calcineurin inhibitors), and loosen scales and crusts (keratolytic agents). Severe and refractory seborrheic dermatitis may warrant the use of systemic antifungal medications.

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Epidemiology and Etiology

Seborrheic dermatitis is a common chronic skin disorder that is characterized by erythematous patches with greasy, yellowish scales that most often appear in areas with prominent sebaceous glands (scalp, face, upper trunk, and anogenital area).

Epidemiology

  • Prevalence: 3% of the general population
  • More common in men
  • Bimodal distribution: occurs in two peaks (first in infancy, then in adolescence and early adulthood)
  • Up to 70% of infants < 3 months of age are affected but improvement noted by 1 year
  • In adults, the disease peaks between the 3rd and 4th decades.

Etiology

Unclear, but may be affected by  the following:

  • Skin colonization of Malassezia and its interaction with lipids on skin surface
  • Individual susceptibility: 
    • Increased sebaceous gland activity (seborrhea)
    • Stress
  • Immunodeficiency:
    • HIV infection
      • Seborrheic dermatitis affects up to 85% of patients with AIDS.
      • Severe seborrheic dermatitis in patients with low CD4 counts
    • Lymphoma
    • Renal transplantation
  • Neuropsychiatric conditions:
    • Parkinson’s disease 
      • Increased sebum production
      • Improvement of seborrheic dermatitis with use of levodopa
    • Alzheimer’s dementia, depression
  • Alcoholism
  • Climate changes (worse in cold temperatures, some improve with sun exposure)
  • Medications: lithium, haloperidol, chlorpromazine, immunosuppressants, psoralen, dopamine antagonists

Pathophysiology

  • The exact pathophysiologic mechanism remains unknown.
  • Findings involve sebaceous glands and Malassezia colonization. Association is strongly suggested because antifungal agents decrease Malassezia organisms and effectively treat the disease.
  • Seborrheic dermatitis is found in areas with abundant sebaceous glands.
  • Malassezia (lipophilic yeast) on the skin interacts with sebum. Yeast produce lipases and phosphatases which cleave fatty acids from sebum → release inflammatory free fatty acids → aberrant keratinocyte production →  abnormal stratum corneum  → inflammatory response stimulated → skin eruption
  • Other factors include oxidative stress and cell-damaging oxygen radicals.

Clinical Presentation

General features

  • Pruritic, erythematous papules and plaques
  • Easily detachable greasy scales and yellow crusts
  • Remits and relapses

Seborrheic dermatitis in infants

  • Affected areas:
    • Head: 
      • Scalp (“cradle cap”)
      • Eyebrows, eyelids, nasolabial and retroauricular folds, and neck
    • Trunk: umbilicus and intertriginous areas (opposite of atopic dermatitis, which spares the intertriginous areas)
  • Leiner disease:
    • Rare disease associated with complement (C5) deficiency
    • Generalized severe seborrheic dermatitis
    • Also with diarrhea and/or vomiting, anemia, or failure to thrive

Seborrheic dermatitis in adults

  • Affected areas:
    • Scalp: dandruff/pityriasis sicca; fine, white, flaking scales on the scalp
    • Face:
      • Eyebrows, glabella, eyelids, sides of the nose, nasolabial folds (opposite of lupus, which spares the nasolabial folds)
      • Mustache and beard areas; improves with shaving
    • Trunk:
      • Intertriginous areas (axilla, inframammary folds, anogenital region) 
      • Upper chest and back

Seborrheic dermatitis in patients with HIV

  • In patients with CD4 counts < 400 cells/microL, lesions may be widespread and difficult to control.
  • Seborrheic dermatitis can be the initial clinical cutaneous marker for HIV/AIDS (sudden severe onset, atypical distribution of lesions or treatment resistance)
  • May improve with antiretroviral therapy

Diagnosis

  • Diagnosis is based on clinical findings.
  • Biopsy can be used if the diagnosis is uncertain. Findings on biopsy:
    • Superficial perivascular inflammatory infiltrate (neutrophils, lymphocytes)
    • Psoriasiform hyperplasia
    • Parakeratosis (retention of nuclei in the stratum corneum)
    • Focal spongiosis
    • Yeast species in the stratum corneum
  • In HIV: more parakeratosis, increased inflammatory infiltrate, and less spongiosis

Management

General approach

  • Avoid cold temperatures
  • Discontinue medications that can trigger flares
  • Treat associated comorbidities

Medical therapy

  • Topical agents containing:
    • Selenium sulfide: has antifungal properties
    • Tar: decreases inflammation and has antifungal properties
    • Sulfur: keratolytic and has antifungal properties
    • Salicylic acid: keratolytic; softens thick scales
    • Zinc pyrithione: has fungistatic and antibacterial properties
  • Antifungals:
    • Topical: ketoconazole, naftifine, ciclopirox
    • Systemic ketoconazole, fluconazole, or itraconazole if refractory or with extensive disease 
  • Topical steroids:
    • Only used for acute flares
    • Long-term use not recommended due to dermal atrophy and increased risk of recurrence and dependence
  • Calcineurin inhibitors (tacrolimus, pimecrolimus) used as steroid alternatives, especially for delicate areas (e.g., face).
    • Suppress cytokine production
    • Do not have adverse effects of steroids

Differential Diagnosis

Differential diagnoses of seborrheic dermatitis include the following conditions:

  • Atopic dermatitis: chronic, relapsing, inflammatory skin disease that often precedes asthma and other allergic disorders. The main features of this skin condition are intense pruritus and eczematous skin lesions.
  • Psoriasis: a chronic, recurrent, relapsing skin disorder characterized by inflammation and hyperproliferation of skin cells of the epidermis. Psoriasis presents with salmon-colored plaques with overlying silvery scales, which is why this disease is also called plaque psoriasis.
  • Impetigo: an infectious condition characterized by bacterial infection of the skin. Impetigo can present with bullous or nonbullous lesions. The crusts in nonbullous impetigo are honey-colored and located on the face and upper or lower extremities. Bullous impetigo, as the name implies, involves the formation of bullous skin eruptions.
  • Tinea versicolor: Malassezia furfur is the causative pathogen for this superficial infection of the skin, which presents with hypopigmentation or hyperpigmentation of the infected area.
  • Tinea capitis: infection of the skin caused by the dermatophyte fungi. There are 3 types of dermatophytes: trichophyton, epidermophyton, and microsporum. 
  • Pityriasis rosea: a common skin eruption that is characterized by a single skin patch that usually evolves into a widespread exanthem after 1 week. The condition typically lasts 6 weeks and is self-limited, with an excellent prognosis. 
  • Candidiasis: an opportunistic fungal infection that can affect the gastrointestinal tract or skin, or be systemic in immunocompromised patients. Clinical presentation varies and is dependent on the severity of immunosuppression and the anatomical site affected. 
  • Pemphigus vulgaris: a chronic, autoimmune, intraepithelial disease characterized by blister formation involving the skin and mucous membranes. Caused by autoantibodies, which are directed against target antigens present on the cell surface of keratinocytes.
  • Secondary syphilis: untreated primary syphilis becomes secondary syphilis. Patients present with a generalized non-pruritic maculopapular rash, generally on the palms and soles, along with pustular lesions. Various skin lesions include condylomata lata and white plaques.
  • Scabies: highly contagious skin infection caused by Sarcoptes scabiei mites that are transmitted via direct physical contact. Scabies causes erythematous, pruritic papules, scattered vesicles, and thin, curvilinear burrow tracks.
SiteDifferential diagnosis
ScalpPsoriasis, dandruff, atopic dermatitis, tinea capitis
FacePsoriasis, impetigo, contact dermatitis
Ear canalPsoriasis, contact dermatitis
EyelidsAtopic dermatitis, demodex folliculorum infestation
Chest and trunkPityriasis rosea, tinea versicolor
Intertriginous areasPsoriasis, candidiasis
All sites, rule outSecondary syphilis, pemphigus, scabies

References

  1. Berk, T.; Scheinfeld, N. (2010). Seborrheic dermatitis. P T., 35(6), 348–352. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2888552/
  2. Borda, L.; Wikramanayake, T. (2015). Seborrheic dermatitis and dandruff: a comprehensive review. J Clin Investig Dermatol, 3(2), 10.13188/2373–1044.1000019. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4852869/
  3. Clark, G.; Pope, S.; Jaboori, K. (2015). Diagnosis and treatment of seborrheic dermatitis. Am Fam Physician, 91(3), 185–190. https://www.aafp.org/afp/2015/0201/p185.html
  4. Johnson, B.; Nunley, J. (2000). Treatment of seborrheic dermatitis. Am Fam Physician, 61(9), 2703–2710.
  5. Sasseville, D.; Fowler, J. & Corona, R. (Eds.). (2020). Seborrheic dermatitis in adolescents and adults. UpToDate. Retrieved 25 Aug 2020, from https://www.uptodate.com/contents/seborrheic-dermatitis-in-adolescents-and-adults
  6. Scheinfeld, N. (n.d.). Seborrheic dermatitis. Medscape. Retrieved 26 Aug 2020, from https://www.medscape.com/viewarticle/499706
  7. Tucker, D.; Masood, S. (2020). Seborrheic dermatitis. https://www.ncbi.nlm.nih.gov/books/NBK551707/

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