Seborrheic DermatitisContributor Information and
DisclosuresAuthorSamuel T Selden, MDAssistant 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 EssentialsSeborrheic
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
toMalassezia,[1]immunologic abnormalities, and activation of
complement. Its severity ranges from mild dandruff to exfoliative
erythroderma.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
symptomsHistory 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)Malasseziaorganisms 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]SeeClinical Presentationfor more detail.DiagnosisThe 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 outtinea 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 ParakeratosisSeeWorkupfor
more detail.ManagementEarly 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
reducingMalasseziayeast 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
plaquesSeeTreatmentandMedicationfor more
detail.BackgroundSeborrheic 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 inParkinson diseaseand inAIDS.[21,
22]PathophysiologySeborrheic dermatitis is associated with normal
levels ofMalasseziabut an abnormal immune response. Helper T cells,
phytohemagglutinin and concanavalin stimulation, and antibody
titers are depressed compared with those of control subjects. The
contribution ofMalasseziaspecies to seborrheic dermatitis may come
from its lipase activityreleasing inflammatory free fatty acidsand
from its ability to activate the alternative complement
pathway.[23]FrequencyInternationalThe 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/MorbidityRaceSeborrheic dermatitis occurs in
persons of all races.SexSeborrheic dermatitis is slightly worse in
males than in females.AgeThe 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
aflexural eruptionorerythroderma.[24]HistoryIntermittent, 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.PhysicalThe 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 hair-bearing 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, mimickingpityriasis 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.CausesMalasseziaorganisms 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 ConsiderationsXerotic
eczemaChronic granulomatous diseaseExfoliative erythrodermaFacial
chappingInfectious eczematoid dermatitisLetterer-Siwe
diseaseScaling drug eruptionsSebopsoriasisStaphylococcal
blepharitisTinea amiantaceaTinea versicolor[27]Vitamin B and/or
zinc deficiencyDifferential 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 VersicolorLaboratory StudiesA 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.ProceduresA skin biopsy may be needed in persons with
exfoliative erythroderma, and a fungal culture can be used to rule
outtinea capitis, although tinea capitis in the adult is
rare.Histologic FindingsDermatopathologic 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
CareEarly 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 reducingMalasseziayeast 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 SummaryThe goals of pharmacotherapy are to
reduce morbidity and to prevent complications.AntifungalsClass
SummaryThe 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 informationKetoconazole
topicalKetoconazole 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.CorticosteroidsClass
SummaryCorticosteroids 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
informationBetamethasone 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 informationDesonideDesonide is used
for inflammatory dermatoses responsive to steroids. It decreases
inflammation by suppressing the migration of polymorphonuclear
leukocytes and reversing capillary permeability.KeratolyticsClass
SummaryKeratolytics cause cornified epithelium to swell, soften,
macerate, and then desquamate.View full drug informationCoal tar
shampoo (DHS Tar, MG217, Theraplex T, Psoriasin); Scytera foamCoal
tar shampoo inhibits deregulated epidermal proliferation and dermal
infiltration; it is antipruritic and
antibacterial.ImmunosuppressantsClass SummaryImmunosuppressants
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 informationTacrolimus 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
informationPimecrolimus (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.References1. Zisova LG. Malassezia species and seborrheic
dermatitis.Folia Med (Plovdiv). 2009 Jan-Mar.
51(1):23-33.[Medline].2. Litt JZ, Powlak WA.Drug Eruption Reference
Manual. 5th ed. Cleveland, Ohio: Wal-Zac Enterprises; 1966. 465.3.
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].6.
Skinner RB Jr, Noah PW, Taylor RM, et al. Double-blind treatment of
seborrheic dermatitis with 2% ketoconazole cream.J Am Acad
Dermatol. 1985 May. 12(5 Pt 1):852-6.[Medline].7. Tatlican S, Eren
C, Eskioglu F. Insight into pimecrolimus experience in seborrheic
dermatitis: close follow-up with exact mean cure and remission
times and side-effect profile.J Dermatolog Treat. 2009.
20(4):198-202.[Medline].8. Cook BA, Warshaw EM. Role of topical
calcineurin inhibitors in the treatment of seborrheic dermatitis: a
review of pathophysiology, safety, and efficacy.Am J Clin Dermatol.
2009. 10(2):103-18.[Medline].9. Ozden MG, Tekin NS, Ilter N,
Ankarali H. Topical pimecrolimus 1% cream for resistant seborrheic
dermatitis of the face: an open-label study.Am J Clin Dermatol.
2010. 11(1):51-4.[Medline].10. Cunha PR. Pimecrolimus cream 1% is
effective in seborrhoeic dermatitis refractory to treatment with
topical corticosteroids.Acta Derm Venereol. 2006.
86(1):69-70.[Medline].11. Firooz A, Solhpour A, Gorouhi F, et al.
Pimecrolimus cream, 1%, vs hydrocortisone acetate cream, 1%, in the
treatment of facial seborrheic dermatitis: a randomized,
investigator-blind, clinical trial.Arch Dermatol. 2006 Aug.
142(8):1066-7.[Medline].12. High WA, Pandya AG. Pilot trial of 1%
pimecrolimus cream in the treatment of seborrheic dermatitis in
African American adults with associated hypopigmentation.J Am Acad
Dermatol. 2006 Jun. 54(6):1083-8.[Medline].13. Schwartz RA, Janusz
CA, Janniger CK. Seborrheic dermatitis: an overview.Am Fam
Physician. 2006 Jul 1. 74(1):125-30.[Medline].14. Cook BA, Warshaw
EM. Role of topical calcineurin inhibitors in the treatment of
seborrheic dermatitis: a review of pathophysiology, safety, and
efficacy.Am J Clin Dermatol. 2009. 10(2):103-18.[Medline].15.
Zisova LG. Fluconazole and its place in the treatment of seborrheic
dermatitis--new therapeutic possibilities.Folia Med (Plovdiv).
2006. 48(1):39-45.[Medline].16. Kligman AM, Marples RR, Lantis LR,
McGinley KJ. Appraisal of efficacy of antidandruff formulations.J
Soc Cosmet Chem. 1974. 225:73-91.17. 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].18. Carr MM, Pryce DM, Ive FA. Treatment of
seborrhoeic dermatitis with ketoconazole: I. Response of
seborrhoeic dermatitis of the scalp to topical ketoconazole.Br J
Dermatol. 1987 Feb. 116(2):213-6.[Medline].19. Waldroup W,
Scheinfeld N. Medicated shampoos for the treatment of seborrheic
dermatitis.J Drugs Dermatol. 2008 Jul. 7(7):699-703.[Medline].20.
Seite S, Rougier A, Talarico S. Randomized study comparing the
efficacy and tolerance of a lipohydroxy acid shampoo to a
ciclopiroxolamine shampoo in the treatment of scalp seborrheic
dermatitis.J Cosmet Dermatol. 2009 Dec. 8(4):249-53.[Medline].21.
Groisser D, Bottone EJ, Lebwohl M. Association of Pityrosporum
orbiculare (Malassezia furfur) with seborrheic dermatitis in
patients with acquired immunodeficiency syndrome (AIDS).J Am Acad
Dermatol. 1989 May. 20(5 Pt 1):770-3.[Medline].22. Odom RB.
Seborrheic dermatitis in AIDS.J Int Postgrad Med. 1990. 2:18-20.23.
Belew PW, Rosenberg EW, Jennings BR. Activation of the alternative
pathway of complement by Malassezia ovalis (Pityrosporum
ovale).Mycopathologia. 1980 Mar 31. 70(3):187-91.[Medline].24.
Elish D, Silverberg NB. Infantile seborrheic dermatitis.Cutis. 2006
May. 77(5):297-300.[Medline].25. Tajima M, Sugita T, Nishikawa A,
Tsuboi R. Molecular analysis of Malassezia microflora in seborrheic
dermatitis patients: comparison with other diseases and healthy
subjects.J Invest Dermatol. 2008 Feb. 128(2):345-51.[Medline].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].28. Shin H, Kwon OS,
Won CH, et al. Clinical efficacies of topical agents for the
treatment of seborrheic dermatitis of the scalp: a comparative
study.J Dermatol. 2009 Mar. 36(3):131-7.[Medline].29. Siadat AH,
Iraji F, Shahmoradi Z, Enshaieh S, Taheri A. The efficacy of 1%
metronidazole gel in facial seborrheic dermatitis: a double blind
study.Indian J Dermatol Venereol Leprol. 2006 Jul-Aug.
72(4):266-9.[Medline].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].31.
Bikowski J. Facial seborrheic dermatitis: a report on current
status and therapeutic horizons.J Drugs Dermatol. 2009 Feb.
8(2):125-33.[Medline].
