Seborrheic Dermatitis

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.

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 hairbearing 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

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)

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]

Overnight application of tar, bath oil, or Bakers P&S solution; Derma-Smoothe F/S oil is especially
helpful for widespread plaques
See Treatment and Medication for more detail.

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 toMalassezia,[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 diseaseand in AIDS.[21, 22]

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 activityreleasing inflammatory free fatty acidsand from its ability to activate
the alternative complement pathway.[23]

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.

Mortality/Morbidity

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]

History
Intermittent, active phases of seborrheic dermatitis manifest with burning, scaling, and itching, alternating
with inactive periods. Activity is increased in winter and early spring, with remissions commonly occurring in
summer.
Active phases of seborrheic dermatitis may be complicated by secondary infection in the intertriginous
areas and on the eyelids.
Candidal overgrowth is common in infantile napkin dermatitis. Such children may have a diaper dermatitis
variant of seborrheic dermatitis or psoriasis.
Generalized seborrheic erythroderma is rare. It occurs more often in association with AIDS, [21, 22] congestive
heart failure, Parkinson disease, and immunosuppression in premature infants.

Physical
The scalp appearance of seborrheic dermatitis varies from mild, patchy scaling to widespread, thick,
adherent crusts. Plaques are rare. From the scalp, seborrheic dermatitis can spread onto the forehead, the
posterior part of the neck, and the postauricular skin, as in psoriasis. Note the images below.

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 hairbearing area, and the chest is frequently involved. Courtesy of Wilford Hall Medical Center Dermatology Teaching
slides.

Seborrheic dermatitis skin lesions manifest as branny or greasy scaling over red, inflamed skin.
Hypopigmentation is seen in blacks. Infectious eczematoid dermatitis, with oozing and crusting, suggests
secondary infection. A seborrheic blepharitis may occur independently.
Distribution follows the oily and hair-bearing areas of the head and the neck, such as the scalp, the
forehead, the eyebrows, the lash line, the nasolabial folds, the beard, and the postauricular skin. An
extension to submental skin can occur. Presternal or interscapular involvement is more common than
nonscaling intertrigo of the umbilicus, axillae, inframammary and inguinal folds, perineum, or anogenital
crease, which also may be present.
Two distinct truncal patterns of seborrheic dermatitis can occasionally occur. An annular or geographic
petaloid scaling is the most common. A rare pityriasiform variety can be seen on the trunk and the neck,
with peripheral scaling around ovoid patches, mimicking pityriasis rosea. Note the image below.

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.

Causes
Malassezia organisms are probably not the cause but are a cofactor linked to a T-cell depression,
increased sebum levels, and an activation of the alternative complement pathway. Persons prone to this
dermatitis also may have a skin-barrier dysfunction.[25, 26]

Because seborrheic dermatitis is uncommon in preadolescent children, and tinea capitis is uncommon after
adolescence, dandruff in a child is more likely to represent a fungal infection. A fungal culture should be
completed for confirmation.
Various medications may flare or induce seborrheic dermatitis. These medications include auranofin,
aurothioglucose, buspirone, chlorpromazine, cimetidine, ethionamide, fluorouracil, gold, griseofulvin,
haloperidol, interferon alfa, lithium, methoxsalen, methyldopa, phenothiazines, psoralens, stanozolol,
thiothixene, and trioxsalen.[2, 3]

Diagnostic Considerations
Xerotic eczema
Chronic granulomatous disease
Exfoliative erythroderma
Facial chapping
Infectious eczematoid dermatitis
Letterer-Siwe disease
Scaling drug eruptions
Sebopsoriasis
Staphylococcal blepharitis
Tinea amiantacea
Tinea versicolor[27]
Vitamin B and/or zinc deficiency

Differential Diagnoses

Acute Cutaneous Lupus Erythematosus (ACLE)

Allergic Contact Dermatitis

Asteatotic Eczema

Cutaneous Candidiasis

Dermatologic Manifestations of Gastrointestinal Disease

Dermatologic Manifestations of Glucagonoma Syndrome

Drug Eruptions

Drug-Induced Photosensitivity

Erythrasma

Extramammary Paget Disease

Impetigo

Intertrigo

Irritant Contact Dermatitis

Langerhans cell histiocytosis

Lichen Simplex Chronicus

Nummular Dermatitis

Omenns syndrome

Pediatric Atopic Dermatitis

Pemphigus Erythematosus

Pemphigus Foliaceus

Perioral Dermatitis

Pityriasis Rosea

Rosacea

Tinea Capitis

Tinea Corporis

Tinea Cruris

Tinea Versicolor

Laboratory Studies
A clinical diagnosis of seborrheic dermatitis is usually made based on a history of waxing and waning
severity and by the distribution of involvement upon examination.

Procedures
A skin biopsy may be needed in persons with exfoliative erythroderma, and a fungal culture can be used to
rule out tinea capitis, although tinea capitis in the adult is rare.

Histologic Findings

Dermatopathologic findings of seborrheic dermatitis are nonspecific. Hyperkeratosis, acanthosis,

accentuated rete ridges, focal spongiosis, and parakeratosis are characteristic. Psoriasis is distinguished
by regular acanthosis, thinned rete ridges, exocytosis, parakeratosis, and an absence of spongiosis.
Neutrophils may be seen in both diseases.

Medical Care
Early treatment of flares is encouraged. Behavior modification techniques in reducing excoriations are
especially helpful with scalp involvement.
Topical corticosteroids may hasten recurrences, may foster dependence because of a rebound effect, and
are discouraged except for short-term use. Skin involvement responds to ketoconazole, naftifine, or
ciclopirox creams and gels.[4, 5, 6] Alternatives include calcineurin inhibitors (ie, pimecrolimus, tacrolimus), [7, 8,
9]
sulfur or sulfonamide combinations, or propylene glycol. [10, 11, 12, 13, 14] Class IV or lower corticosteroid creams,
lotions, or solutions can be used for acute flares. Systemic ketoconazole or fluconazole may help if
seborrheic dermatitis is severe or unresponsive.[15] Combination therapy has been recommended.[28]
Dandruff responds to more frequent shampooing or a longer period of lathering. Use of hair spray or hair
pomades should be stopped. Shampoos containing salicylic acid, tar, selenium, sulfur, or zinc are effective
and may be used in an alternating schedule. [16, 17] Overnight occlusion of tar, bath oil, or Baker's P&S solution
may help to soften thick scalp plaques. Derma-Smoothe F/S oil is especially helpful when widespread scalp
plaques are present. Selenium sulfide (2.5%), ketoconazole, and ciclopirox shampoos may help by
reducing Malasseziayeast scalp reservoirs.[18, 19, 20] Shampoos may be used on truncal lesions or in beards
but may cause inflammation in the intertriginous or facial areas.
Siadat et al reported that 1% metronidazole gel is effective for seborrheic dermatitis of the face. [29] Some
suggest using a nonsteroidal cream. [30] Bikowski recommends azelaic acid.[31] Seborrheic blepharitis may
respond to gentle cleaning of eyelashes with baby shampoo and cotton applicators. The use of
ketoconazole cream in this anatomical region is controversial.

Medication Summary
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Antifungals
Class Summary
The mechanism of action may involve alteration of RNA and DNA metabolism or an intracellular
accumulation of peroxide that is toxic to fungal cells.
View full drug information

Ketoconazole topical

Ketoconazole topical is available as ketoconazole cream 2% (Nizoral), ketoconazole foam (Extina),

ketoconazole shampoo 2% (Nizoral 2%; prescription only in United States), and ketoconazole shampoo 1%
(Nizoral A-D Shampoo; over-the-counter in United States). It is an imidazole broad-spectrum antifungal
agent. It inhibits the synthesis of ergosterol, causing cellular components to leak, resulting in fungal cell
death.

Corticosteroids

Class Summary
Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. They
also modify the body's immune response to diverse stimuli.
View full drug information

Betamethasone topical (Valisone)

Betamethasone is a medium-strength topical corticosteroid for body areas. It decreases inflammation by

suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability.
Betamethasone affects the production of lymphokines and has inhibitory effects on Langerhans cells.
View full drug information

Desonide

Desonide is used for inflammatory dermatoses responsive to steroids. It decreases inflammation by

suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability.

Keratolytics
Class Summary
Keratolytics cause cornified epithelium to swell, soften, macerate, and then desquamate.
View full drug information

Coal tar shampoo (DHS Tar, MG217, Theraplex T, Psoriasin); Scytera foam

Coal tar shampoo inhibits deregulated epidermal proliferation and dermal infiltration; it is antipruritic and
antibacterial.

Immunosuppressants
Class Summary
Immunosuppressants exert anti-inflammatory affects by inhibiting T-lymphocyte activation. They are safer
than topical steroids for prolonged use or in skin folds.
View full drug information

Tacrolimus ointment (Protopic)

Tacrolimus ointment is a nonsteroidal anti-inflammatory agent. It should not cause steroid-type skin
atrophy. It is currently indicated only for atopic dermatitis in immunocompetent patients aged 2 years and
older.

View full drug information

Pimecrolimus (Elidel cream 1%)

Pimecrolimus is a nonsteroidal anti-inflammatory agent. It should not cause steroid-type skin atrophy. It is
currently indicated only for atopic dermatitis in immunocompetent patients aged 2 years and older. Use
cream sparingly to avoid maceration in skin folds.

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