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Seborrheic Dermatitis

  • Author: Samuel T Selden, MD; Chief Editor: William D James, MD  more...
 
Updated: Feb 26, 2016
 

Practice Essentials

Seborrheic dermatitis is a papulosquamous disorder patterned on the sebum-rich areas of the scalp, face, and trunk (see the image below). In addition to sebum, this dermatitis is linked to Malassezia,[1] immunologic abnormalities, and activation of complement. Its severity ranges from mild dandruff to exfoliative erythroderma.

Seborrheic dermatitis may affect any hair-bearing Seborrheic dermatitis may affect any hair-bearing area, and the chest is frequently involved. Courtesy of Wilford Hall Medical Center Dermatology Teaching slides.

Signs and symptoms

History findings in seborrheic dermatitis may include the following:

  • Intermittent, active phases manifesting with burning, scaling, and itching, alternating with inactive periods; activity is increased in winter and early spring, with remissions commonly occurring in summer. This may be from sunlight effect on Malassezia.
  • In active phases, potential secondary infection in intertriginous areas and on the eyelids
  • Candidal overgrowth (common in infantile "napkin dermatitis")
  • Generalized seborrheic erythroderma (rare)

Physical findings may include the following:

  • Scalp appearance ranging from mild, patchy scaling to widespread, thick, adherent crusts; plaques are rare; lesions may spread from the scalp onto the forehead, the posterior part of the neck, and the postauricular skin
  • Seborrheic skin lesions manifesting as scaling over red, inflamed skin; hypopigmentation (in blacks); oozing and crusting; blepharitis (occurring independently)
  • Lesion distribution following the oily and hair-bearing areas of the head and the neck; extension to submental skin can occur
  • Either of 2 distinct truncal patterns: (1) annular or geographic petaloid scaling or (2) pityriasiform variety (rare)

Malassezia organisms are probably not the cause of seborrheic dermatitis but a cofactor linked to a T-cell depression, increased sebum levels, and an activation of the alternative complement pathway. Various medications may also flare or induce seborrheic dermatitis.[2, 3]

See Clinical Presentation for more detail.

Diagnosis

The diagnosis of seborrheic dermatitis is usually made on clinical grounds, based on a history of waxing and waning severity and by the distribution of involvement upon examination.

A skin biopsy may be needed in persons with exfoliative erythroderma, and a fungal culture can be used to rule out tinea capitis, though tinea capitis is rare in adults. Dermatopathologic findings of seborrheic dermatitis are nonspecific and typically include the following:

  • Hyperkeratosis
  • Acanthosis
  • Accentuated rete ridges
  • Focal spongiosis
  • Parakeratosis

See Workup for more detail.

Management

Early treatment of flares is encouraged. Behavior modification techniques in reducing excoriations are especially helpful with scalp involvement.

Pharmacologic agents that may be used include the following:

  • Topical corticosteroids (discouraged except for short-term use and at risk for tachyphylaxis when used as monotherapy)
  • For skin involvement, ketoconazole, naftifine, or ciclopirox creams and gels [4, 5, 6] ; alternatively, calcineurin inhibitors (ie, pimecrolimus, tacrolimus), [7, 8, 9] sulfur or sulfonamide combinations, or propylene glycol [10, 11, 12, 13, 14]
  • For acute flares, class IV or lower corticosteroid creams, lotions, or solutions
  • For severe or unresponsive lesions, systemic ketoconazole or fluconazole [15]

Treatment of dandruff may involve the following:

  • More frequent shampooing or longer lathering
  • Discontinuance of hair spray or hair pomades
  • Use of shampoos containing salicylic acid, tar, selenium, sulfur, or zinc [16, 17] ; selenium sulfide (2.5%), ketoconazole, and ciclopirox shampoos may help by reducing Malassezia yeast scalp reservoirs [18, 19, 20] ; an alternative to a shampoo with zinc is a conditioner rinse with zinc, 0.01% fluocinolone, and acetonide topical oil
  • Overnight application of tar, bath oil, or Baker’s P&S solution; Derma-Smoothe F/S oil is especially helpful for widespread plaques

See Treatment and Medication for more detail.

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Background

Seborrheic dermatitis is a papulosquamous disorder patterned on the sebum-rich areas of the scalp, face, and trunk. In addition to sebum, this dermatitis is linked to Malassezia,[1] immunologic abnormalities, and activation of complement. It is commonly aggravated by changes in humidity, changes in seasons, trauma (eg, scratching), or emotional stress. The severity varies from mild dandruff to exfoliative erythroderma. Seborrheic dermatitis may worsen in Parkinson disease and in AIDS.[21, 22]  Increased perspiration in Parkinson disease may be the link to seborrheic dermatitis.

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Pathophysiology

Seborrheic dermatitis is associated with normal levels of Malassezia but an abnormal immune response. Helper T cells, phytohemagglutinin and concanavalin stimulation, and antibody titers are depressed compared with those of control subjects. The contribution of Malassezia species to seborrheic dermatitis may come from its lipase activity—releasing inflammatory free fatty acids—and from its ability to activate the alternative complement pathway.[23]

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Frequency

International

The prevalence rate of seborrheic dermatitis is 3-5%, with a worldwide distribution. Dandruff, the mildest form of this dermatitis, is probably far more common and is present in an estimated 15-20% of the population.

Race

Seborrheic dermatitis occurs in persons of all races.

Sex

Seborrheic dermatitis is slightly worse in males than in females.

Age

The usual onset occurs with puberty. It peaks at age 40 years and is less severe, but present, among older people. In infants, it occurs as cradle cap or, uncommonly, as a flexural eruption or erythroderma.[24]

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Contributor Information and Disclosures
Author

Samuel T Selden, MD Assistant Professor Department of Dermatology Eastern Virginia Medical School; Consulting Staff, Chesapeake General Hospital; Private Practice

Samuel T Selden, MD is a member of the following medical societies: American Academy of Dermatology, International Society of Geriatric Dermatology

Disclosure: Nothing to disclose.

Specialty Editor Board

Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Texas Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

Jeffrey Meffert, MD Associate Clinical Professor of Dermatology, University of Texas School of Medicine at San Antonio

Jeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Robin Travers, MD Assistant Professor of Medicine (Dermatology), Dartmouth University School of Medicine; Staff Dermatologist, New England Baptist Hospital; Private Practice, SkinCare Physicians

Robin Travers, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Informatics Association, Massachusetts Medical Society, Women's Dermatologic Society, Medical Dermatology Society

Disclosure: Nothing to disclose.

References
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  3. Brodell EE, Smith E, Brodell RT. Exacerbation of seborrheic dermatitis by topical fluorouracil. Arch Dermatol. Feb 2011. 147(2):245-6. [Medline].

  4. Ford GP, Farr PM, Ive FA, Shuster S. The response of seborrhoeic dermatitis to ketoconazole. Br J Dermatol. 1984 Nov. 111(5):603-7. [Medline].

  5. Green CA, Farr PM, Shuster S. Treatment of seborrhoeic dermatitis with ketoconazole: II. Response of seborrhoeic dermatitis of the face, scalp and trunk to topical ketoconazole. Br J Dermatol. 1987 Feb. 116(2):217-21. [Medline].

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  17. Schwartz JR, Rocchetta H, Asawanonda P, Luo F, Thomas JH. Does tachyphylaxis occur in long-term management of scalp seborrheic dermatitis with pyrithione zinc-based treatments?. Int J Dermatol. 2009 Jan. 48(1):79-85. [Medline].

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  26. Prohic A, Kasumagic-Halilovic E. Identification of Malassezia species from immunocompetent and immunocompromised patients with seborrheic dermatitis. Eur Rev Med Pharmacol Science. Dec 2010. 14(12):1019-23. [Medline].

  27. Pontasch MJ, Kyanko ME, Brodell RT. Tinea versicolor of the face in black children in a temperate region. Cutis. 1989 Jan. 43(1):81-4. [Medline].

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  30. Elewski B. An investigator-blind, randomized, 4-week, parallel-group, multicenter pilot study to compare the safety and efficacy of a nonsteroidal cream (Promiseb Topical Cream) and desonide cream 0.05% in the twice-daily treatment of mild to moderate seborrheic dermatitis of the face. Clin Dermatol. 2009 Nov-Dec. 27(6 Suppl):S48-53. [Medline].

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Seborrheic dermatitis affecting the scalp line and the eyebrows with red skin and scaling. Courtesy of Wilford Hall Medical Center Dermatology slide files.
Seborrheic dermatitis may affect any hair-bearing area, and the chest is frequently involved. Courtesy of Wilford Hall Medical Center Dermatology Teaching slides.
African Americans and persons from other darker-skinned races are susceptible to annular seborrheic dermatitis, also called petaloid seborrheic dermatitis or seborrhea petaloides. Sarcoidosis, secondary syphilis, and even discoid lupus may be in the differential in such cases. Courtesy of Jeffrey J. Meffert, MD.
 
 
 
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