3 Chapter 26 :: Seborrheic Dermatitis
:: Dae Hun Suh
AT-A-GLANCE
■ Seborrheic dermatitis is a common inflammatory
skin disease affecting various age groups.
■ Erythematous, greasy, scaling patches and plaques
appear on scalp, face, ears, chest, and intertriginous
Part 3
areas.
■ Severe forms, like generalized erythroderma, rarely
occur.
::
■ Etiology is unclear but may be related to abnormal
immune mechanism, Malassezia, sebaceous glands,
Dermatitis
and individual susceptibility.
■ Treatment is based on symptomatic control.
Seborrheic dermatitis (SD) is clinically character-
ized by erythematous, scaly patches on sebaceous
gland–rich sites, including scalp, face, upper trunk,
and intertriginous areas.1 The affected areas present
as various appearances from mild pinkish and some-
times greasy scaling to solid adherent crusts. Patients
with this condition complain of discomfort, with
symptoms of itching and burning, and also have some
serious cosmetic problems, leading to psychosocial
distress that has a negative impact on their quality of
life.2 SD arises in all races and ethnic groups and has
a worldwide distribution, but a higher incidence and
more-severe forms are observed in AIDS patients and
individuals with certain neurologic conditions, such
as Parkinson disease.3
CLINICAL FEATURES
GENERAL FEATURES
SD usually appears as a chronic and relapsing pat-
tern in adolescents and young adults when the activ-
ity of sebaceous glands increases from hormonal
effects, with the incidence increasing in patients
with older than 50 years of age.4 SD can also affect
babies as young as age 2 weeks with peak incidence at
3 months of age, which is called infantile seborrheic der-
matitis (ISD; Fig. 26-1). The overall prevalence of SD
in general population is between 2.35% and 11.30%,
depending on the study.5 A male predominance is
observed in all ages without any racial or regional
predilection. SD is often influenced by a seasonal
impact. It becomes more common and severe in the
cold and dry climates, whereas it may be mitigated
by sun exposure. However, several cases induced by
Kang_CH026_p0428-0437.indd 428
treatment of psoralen plus ultraviolet A (PUVA) ther-
apy have been reported.6
The symptoms of SD are mainly chronic, persistent,
and recurrent. The red, flaking, and greasy lesions
of scalp and face are easily observed, particularly on
nasolabial folds (Fig. 26-2); eyebrows, upper eyelid,
forehead, postauricular areas (Fig. 26-3); external audi-
tory canal and auricle (Fig. 26-4), with generally sym-
metrical distribution. SD can appear in other sites,
such as occiput and neck. When the sternal area on
the chest (Fig. 26-5), upper back (Fig. 26-6), and umbi-
licus are involved, petaloid or arcuate lesions with
fine pink scale can be seen. In contrast, intertriginous
areas, including inguinal and axillary regions, show
less scale, making SD easily confusable with intertrigo.
However, variations of these clinical appearances are
common. Scalp involvement is more common in the
male patient, in the patient with long disease duration,
and in the patient with a history of acne.1 The sever-
ity of SD varies from mild erythema and pruritus to
severe, oily, thick scale with a burning or tingling sen-
sation. Some patients with SD also may present with
Pityrosporum folliculitis and blepharitis. Pityrosporum
folliculitis typically manifests as a diffuse papulopus-
tular eruption with peripheral erythema on the trunk
and arises more in immunocompromised patients. Seb-
orrheic blepharitis usually appears as a type of anterior
blepharitis, inducing flaking and scaling on the eyelids
and creating uncomfortable, irritating problems.
Characteristically, ISD has a relatively different
feature in contrast with SD in older ages. The non-
pruritic skin eruption generally affects the frontal
or vertex areas (or both areas) of the scalp and the
central areas of the face with dry, thick, adherent,
and flaking scale, and may be accompanied by ery-
thematous rash on intertriginous folds of the trunk
and extremities (Fig. 26-7). The extensive involve-
ment of the scalp, commonly called “cradle cap,” is
one of the typical appearances observed in ISD. ISD
normally resolves spontaneously within the first 6 to
12 months of life. Extensive and serious conditions
should be differentiated from immunosuppressed
status.
LEINER DISEASE
The term Leiner disease was first introduced by Carl
Leiner in 1908, to describe infants with desquamative
erythroderma, sparse hair, frequent loose stools, and
failure to thrive.7 Later, Miller reported other patients
with similar clinical features who had generalized SD.
Miller also found a lack of opsonization by the serum
of the patients.8 Since Miller’s findings it has become
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 3

Chapter 26 :: Seborrheic Dermatitis

A

Figure 26-1 Cradle cap or infantile seborrheic

dermatitis. (Photo contributed by University of North
Carolina Department of Dermatology. From Tintinalli JE,
et al. Rashes in infants and children. In Tintinalli JE, et al.
Tintinalli’s Emergency Medicine: A Comprehensive Study
Guide. 8th ed. New York, NY: McGraw-Hill Education;
2016:934-952, Fig. 141-30.)

clear that Leiner disease is an umbrella phenotype

rather than a single-disease entity, and a variety of
immunologic defects have been identified.9 Congeni-
tal or acquired deficiencies of C3, C5, and phagocytic
activity results in defective opsonization of yeast and
bacteria. Association of Leiner disease and Netherton
syndrome was also suggested.9 Secondary bacterial
infection can bring death to a Leiner disease patient, so
appropriate treatment, such as IV hydration, tempera-
ture regulation, and antibiotics, is essential. Infusion of
fresh-frozen plasma or whole blood can be beneficial
in supplementing the deficient factors in a hereditary
form of Leiner’s disease.8 The prognosis of Leiner dis-
ease depends on the nature of the underlying immuno-
logic abnormality of the patients.

PITYRIASIS AMIANTACEA
B
Asbestos-like scalp, called pityriasis amiantacea, was Figure 26-2 Seborrheic dermatitis with involvement
first described by Alibert in 1832. Pityriasis amianta- of (A) nasolabial folds, cheeks, eyebrows, and nose in
cea is also called tinea asbestina, tinea amiantacea, white person and (B) nasolabial folds in a person of Asian
keratosis follicularis amiantacea, and porrigo ami- descent.
antacea. Pityriasis amiantacea is an inflammatory
429

Kang_CH026_p0428-0437.indd 429 06/12/18 3:22 pm

 3

Figure 26-3 Seborrheic dermatitis of the postauricular area.

Part 3

condition of the scalp that is characterized by large

::

plates of thick, silvering scale firmly adherent to

Dermatitis

both the scalp and hair tufts (Fig. 26-8). This can be
a localized or diffuse condition, and is attributed to
diffuse hyperkeratosis and parakeratosis with follic-
ular keratosis surrounding each hair with a sheath
of corneocytes and debris. It is more common in
females and it may occur at any age, often without
evident causes. Alopecia, which is generally revers-
ible but is sometimes cicatricial, is a common feature
of pityriasis amiantacea.10 Concomitant secondary
bacterial infection, mostly Staphylococcus aureus, may
result in scarring alopecia, so early and appropriate
treatment is necessary. The most frequent skin dis- Figure 26-5 Seborrheic dermatitis of the chest.
eases associated with pityriasis amiantacea are pso-
riasis (35%) and eczematous conditions like SD and
atopic dermatitis (34%). Of pediatric patients with lichen simplex chronicus, superficial fungal, or pyo-
pityriasis amiantacea, lesions in 2% to 15% develop genic infection, or as an adverse effect of molecu-
into typical psoriasis.11 Pityriasis amiantacea may larly targeted therapy such as vemurafenib.12,13 In
also manifest as a complication of lichen planus, these cases, therapy should be directed toward the
underlying etiology.

Figure 26-4 Seborrheic dermatitis of the ear: external

430 canal, concha bowl, and auricle. Figure 26-6 Seborrheic dermatitis of the upper back.

Kang_CH026_p0428-0437.indd 430 06/12/18 3:22 pm


Figure 26-7 Seborrheic dermatitis in an infant. Wide-
spread pattern of seborrheic dermatitis with psoriasiform
lesions on the trunk and groin.
Figure 26-8 Pityriasis amiantacea. Masses of sticky silvery
scales adhere to the scalp and cause matting of hairs they
surround.
Kang_CH026_p0428-0437.indd 431
ASSOCIATIONS OF HIV
3
AND AIDS
SD arises in more extensive and refractory patterns in up
to 83% of HIV-seropositive and AIDS patients (Fig. 26-9).4
The initial clinical symptom may appear as a butterfly-
like rash seen in systemic lupus erythematosus. SD is
associated with reduction of T-cell function, and gets
worse as the CD4+ lymphocyte count decreases, making
SD an indicator for evaluating the progression of AIDS.14
ETIOLOGY AND
Chapter 26 :: Seborrheic Dermatitis
PATHOGENESIS
Many studies to uncover the pathogenesis of SD in
adult and adolescent patients have been conducted,
but the etiology has not been clearly identified yet.
B
Figure 26-9 Wide spread unusual distribution pattern
of seborrheic dermatitis in a patient with AIDS. A, Moist
patches on the centrofacial region, beard, and scalp.
B, Moist lesions on the chest. In patients with AIDS, sebor- 431
rheic dermatitis responds poorly to conventional therapy.
06/12/18 3:22 pm
 3 Multifactorial causes, including several endogenous
and exogenous predisposing factors, are associated
with SD. The role of sebaceous glands in pathogenesis
of SD is notable considering time and lesional distri-
bution of SD. The immunologic status of patients or
the susceptibility to SD can be an important factor
because SD is much more seen in those with certain
underlying diseases such as AIDS and Parkinson dis-
ease. Malassezia may also be one of the causes of SD as
antifungal medications are effective. The relationship
of the SD lesions with seasonal fluctuations or sun
exposure implies that multiple exogenous factors can
contribute to the development of SD.
Part 3
IMMUNE RESPONSE AND
::
INFLAMMATION
Dermatitis
The immune component may be important in the
pathogenesis of SD because SD is much more common
in immunosuppressed patients. The DBA/2 2C TCR
transgenic mouse, which has a defect in expression
of CD4+ and CD8+ cells owing to the lack of T-cell
progenitor thymocytes, exhibited SD-like eruptions.15
Several studies have focused on the cellular immu-
nity and humoral immunity in SD, but there are some
controversies. One study showed a normal CD4+-to-
CD8+ ratio, whereas another study demonstrated a
decreased CD4+-to-CD8+ ratio in 68% of patients.16 A
decrease in the number of B cells in 28% of patients
and a rise of the number of natural killer cells in
48% of patients were reported. In addition, 60% of
patients showed an increase in CD8+ cells and 70%
of patients showed a diminished CD4+-to-CD8+ ratio.
Also, it was stated that SD patients had an increased
production of immunoglobulin (Ig) A and IgG anti-
bodies in serum.16 However, there was no change
in the total amount of antibodies against Malassezia
in SD, suggesting that changes to the antibodies are
not likely linked with Malassezia.17 The alteration of
inflammatory cytokines in patients with SD has been
demonstrated by immunohistochemical studies. The
production of interleukin (IL)-1α, IL-1β, IL-4, IL-12,
tumor necrosis factor-α, and interferon (IFN)-γ was
increased in the lesions compared with the normal
skin.18 Significantly increased IL-1RA–to–IL-1α and
IL-1RA–to–IL-8 ratios, as well as overproduction of
histamine, were also shown to occur in SD when com-
pared with healthy controls.19 An investigation of gene
expression by DNA microarrays in 15 patients with
dandruff showed the reciprocal expression of induced
inflammatory genes and repressed lipid metabolism
genes compared with nondandruff individuals.20 The
expression of induced inflammatory genes was dis-
tinctly observed in uninvolved skin of the patients
as well, indicating the presence of predisposing fac-
tors related to inflammation in patients with SD. Fur-
thermore, inflammation induced by oxidative stress
432 through reactive oxygen species may have a potential
role in the pathogenesis of SD.21
Kang_CH026_p0428-0437.indd 432
MICROBIAL EFFECTS
Malassezia, normal flora that inhabits human skin, is
suggested to be important in SD. This opinion is based
on the evidences that the common lesions of SD are
related to the distribution of sebaceous glands where
Malassezia preferentially colonizes, and that antifungal
medications have therapeutic effects on SD. A decline
in the number of Malassezia by use of antifungal agents
corresponds with the relief of the symptoms.4 More-
over, pityriasis versicolor and Pityrosporum folliculitis,
induced by Malassezia, are commonly accompanied by
SD. However, there is a lack of difference in Malassezia
counts between patients with SD and healthy indi-
viduals. In addition, a mycelial form of Malassezia, a
pathogenic form observed in pityriasis versicolor, has
not been detected in SD.17 These facts propose a com-
plex causative role of Malassezia for SD. The prevalence
and types of the most predominant Malassezia species
found on SD lesions differ among studies, countries,
or parts of body, but Malassezia globosa and Malassezia
restricta are considered to be the most important of
the 14 Malassezia species identified.4,22 The complete
genome sequences of M. globosa and M. restricta have
been determined and these genomes encode lipase and
phospholipase, making the species lipophilic or lipid-
dependent.23 The primary role of these enzymes is to
metabolize lipid into fatty acids to produce fungal cell
walls responsible for virulence, including invasion and
dissemination.24 Not all M. globosa or M. restricta strains
were found in SD, implying that there may exist spe-
cific strains capable of causing the disease.25 Also, an
increased amount of Malassezia furfur was observed in
patients with SD versus healthy controls.26 The high
concentration of M. furfur can disturb protective skin
barriers and induce inflammation. Malassezin, gener-
ated by M. furfur or M. restricta, can serve as agonists
to aryl hydrocarbon receptor, which is involved in the
differentiation of T-helper 17 cells and the mediation of
contact sensitivity.27
LIPID AND HOST
SUSCEPTIBILITY FACTORS
Several analyses of skin surface lipids in patients
with SD or dandruff have shown alterations in those
irrespective of HIV status.28 These findings were not
consistent with one another, but they introduced the
causative relationship between SD and the composi-
tion of skin surface lipids. Specifically, irritating free
fatty acids, such as oleic acid produced by lipase of
M. globosa, could mediate dandruff-like flaking in the
dandruff-susceptible individuals with SD but not in
nonsusceptible individuals.29 Individual susceptibility
is considered to be associated with a disrupted epi-
dermal barrier that allows penetration of the irritating
metabolites. The process for Malassezia to reach the
aryl hydrocarbon receptor in the granular and spinous
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 layers also may depend on such defective skin char-
acter. This host susceptibility factor could explain the
lack of a positive correlation between the number of
Malassezia and the severity of dandruff.
EPIDERMAL
HYPERPROLIFERATION
Increased epidermal turnover in SD, which is also
shown in psoriasis, implicates SD in a disorder of
hyperproliferation, and Malassezia can be considered
as one of the incidental outcomes derived from the
phenomenon. SD resembles psoriasis in many aspects,
both clinically and histologically, and it is sometimes
difficult to differentiate the two diseases even after a
skin biopsy. There are case reports that keratolytics
and antiinflammatory medications were successful in
the treatment of the patients with SD whose treatment
with amphotericin B had failed.30 This alteration of epi-
dermis may be related with the increased activity of
calmodulin and explains the basis of use of cytostatic
medications such as azelaic acid.31
NEUROTRANSMITTER
ABNORMALITIES
SD expressed in Parkinson disease has been thought
to result from the elevated levels of sebum allowing
the proliferation of Malassezia. Bilateral seborrhea
observed in unilateral parkinsonism suggests the
changes of sebum levels are presumably triggered
by endocrine effects rather than neurotrophic effects.
It may be associated with an increased circulating
α-melanocyte–stimulating hormone in Parkinson dis-
ease.32 Because the severity of SD in Parkinson disease
does not correlate with the sebum excretion rate, the
sebum accumulation by facial immobility may play
a key role. Administration of levodopa can clinically
improve the skin symptoms by reducing the sebum
production or secretion by restoring the production
of melanocyte-stimulating hormone-inhibiting factor.
The prevalence of SD is also increased in patients with
other neurologic disorders, including mood disorder,
Alzheimer disease, syringomyelia, epilepsy, cerebro-
vascular infarcts, postencephalitis, mental retardation,
poliomyelitis, quadriplegia, trigeminal nerve injury,
and alcoholism. Indoor lifestyle with less sunlight
exposure and hygiene status of the patients may func-
tion in this association.4
OTHER FACTORS
Low humidity and cold temperatures worsen SD, espe-
cially in the winter and early spring. Facial trauma (eg,
scratching) and PUVA therapy also are aggravating
Kang_CH026_p0428-0437.indd 433
factors.6 Multiple drugs can lead to SD-like eruptions,
including griseofulvin, cimetidine, lithium, meth-
3
yldopa, arsenic, gold, auranofin, aurothioglucose,
buspirone, chlorpromazine, ethionamide, haloperidol,
IFN-α, phenothiazines, stanozolol, thiothixene, pso-
ralen, methoxsalen, and trioxsalen. The SD-like der-
matitis also appears in patients with zinc deficiency
(acrodermatitis enteropathica and acrodermatitis
enteropathica–like conditions) or biotin deficiency, but
the skin eruptions do not respond to zinc or biotin sup-
plementation.33 It is noted that the familial form of SD
was reported in an Israeli Jewish family of Moroccan
descent, which was caused by autosomal dominant
genetic mutation (ZNF750) encoding a zinc finger pro-
Chapter 26 :: Seborrheic Dermatitis
tein (C2H2).34
DIAGNOSIS
The diagnosis of SD remains a clinical one, based on
SD’s characteristic morphology and patterns. Dermos-
copy enables the detailed identification of morphologic
structures, which is especially helpful in diagnosing
SD of the scalp. The typical magnified vascular pat-
terns observed by dermoscopy are twisted loop, red
dots and globules, and glomerular vessels in scalp pso-
riasis, but arborizing vessels and atypical red vessels in
SD.35 A skin biopsy is not routinely required, but may
be useful when the diagnosis is unclear. The various
histopathologic features can be observed depending
on the different stages of the disease: acute, subacute,
and chronic. Acute and subacute SD may exhibit slight
to moderate spongiotic dermatitis with mild pso-
riasiform hyperplasia, folliculocentric crust contain-
ing scattered neutrophils at the tips of the follicular
opening, orthokeratosis with focal parakeratosis, and
superficial perivascular lymphohistiocytic infiltration.
Chronic SD shows a more intense pattern of the fore-
going features with minimal spongiosis and markedly
dilated superficial vessels. However, the histopatho-
logic picture in chronic cases is sometimes similar
to those of psoriasis, and careful attention should be
paid to the histopathology reading. HIV-associated
SD is histologically distinctive from the ordinary SD,
showing very severe patterns such as extensive para-
keratosis, leukoexocytosis, necrosis of keratinocytes,
and superficial perivascular infiltrate of plasma cells
(Table 26-1).36 Lesion scraping for a potassium hydrox-
ide preparation can be beneficial to confirm the diagno-
sis of accompanied Pityrosporum folliculitis. It should
be kept in mind that SD can simultaneously occur
with other dermatoses. When SD occurs in infants,
the classic diagnostic criteria suggested by Beare and
Rook can be used in diagnosing ISD. It is composed
of early onset (before 6 months of age); erythematous
and scaling rash distributed in the scalp, diaper, or
flexural areas; and the relative absence of pruritus.37
Involvement of the diaper area alone is considered as a
characteristic sign favoring a psoriasiform type of ISD.
Above all, the clinician should remember that there is
not a characteristic pathognomonic feature or labora- 433
tory test to establish the accurate diagnosis of SD.
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 3 TABLE 26-1
Histopathologic Differences between Classic
Seborrheic Dermatitis and AIDS-Associated
Seborrheic Dermatitis
CLASSIC SEBORRHEIC AIDS-ASSOCIATED
DERMATITIS SEBORRHEIC DERMATITIS
Epidermis
Limited parakeratosis Widespread parakeratosis
Rare necrotic keratinocytes Many necrotic keratinocytes
No interface obliteration Focal interface obliteration with
Prominent spongiosis clusters of lymphocytes
Sparse spongiosis
Dermis
Part 3
Thin-walled vessels Many thick-walled vessels
Rare plasma cells Increased plasma cells
No leukocytoclasis Focal leukocytoclasis
::
From Soeprono FF, Schinella RA, Cockerell CJ, Comite SL. Seborrheic-like
Dermatitis
dermatitis of acquired immunodeficiency syndrome. A clinicopathologic
study. J Am Acad Dermatol. 1986;14(2):242-248, with permission.
DIFFERENTIAL DIAGNOSIS
Several diseases should be considered in the dif-
ferential diagnosis of SD (Tables 26-2 and 26-3),
especially as ISD is easily confused with atopic der-
matitis, psoriasis, histiocytosis, and scabies; some-
times it is impossible to distinguish among these
diseases in infants younger than 3 months of age.
Checking family history and pruritus and taking cer-
tain laboratory tests including serum IgE levels and
multiple allergen stimulation tests may give a clue to
whether it is atopic dermatitis or ISD. When the skin
eruption arises solely on the scalp, an involvement
of frontal hair lines is a distinctive feature for scalp
psoriasis.38 Langerhans cell histiocytosis, previously
called Letterer-Siwe disease has more generally pur-
puric lesions and tends to desquamate on the scalp
and ulcerate on the folds and the mucosal areas.
Severe itching that includes the palms and soles sug-
gests scabies. Intertrigo, contact dermatitis, neonatal
erythroderma, and multiple carboxylase deficiency
should also be excluded in infants.39
CLINICAL COURSE AND
PROGNOSIS
Generally SD in adolescents or adults has a chronic and
recurrent relapsing course. Consequently, the primary
goal of treatment should be control of symptoms like
pruritus, erythema, and scales, rather than cure of dis-
ease. Also, patients should be informed that they need
to prepare for a future re-outbreak and avoid aggra-
vating factors of SD. However, ISD has a benign, self-
limited course; ISD spontaneously disappears by 6 to
12 months of age. Severe exacerbation with exfoliating
434 dermatitis may occur, albeit rarely, but its prognosis is
usually favorable. ISD does not progress to adulthood.
Kang_CH026_p0428-0437.indd 434
TABLE 26-2
Site-Specific Differential Diagnosis of Seborrheic
Dermatitis
Scalpa Psoriasis, atopic dermatitis, impetigo, tinea
capitisa (mimics dandruff in children)
Face Psoriasis, rosacea, contact dermatitis, impetigo,
discoid lupus, sarcoid (petaloid type in African
Americans), drug-induced photosensitivity
Ear canal Psoriasis, contact dermatitis
Eyelids Atopic dermatitis, psoriasis, Demodex folliculorum
infestation
Chest, back Pityriasis rosea, tinea versicolor, subacute
cutaneous lupus, psoriasis vulgaris
Groin, buttock Intertrigo (fungal, Candida, erythrasma),
glucagonoma, extramammary Paget disease,
zinc deficiency
Intertriginous Inverse psoriasis, candidiasis, erythrasma, contact
dermatitis, tinea intertrigo, Langerhans cell
histiocytosis (Letterer-Siwe disease in infants)
Generalizedb Scabies, secondary syphilis, pemphigus foliaceus,
pemphigus erythematosus, Leiner disease
(infants), drug eruption
Erythrodermicc Psoriasis, contact dermatitis, pityriasis rubra
pilaris, drug eruption, mycosis fungoides
(Sézary syndrome), lichen planus, chronic
actinic dermatitis, HIV, Hodgkin disease,
paraneoplastic syndrome, leukemia cutis
a
Diffuse scalp dermatitis or inflammatory alopecia in children warrants
fungal culture, potassium hydroxide preparation.
b
Widespread truncal types warrant scabies prep and rapid plasma reagin
to rule out syphilis.
c
Erythrodermic type should be biopsied.
MANAGEMENT
Basically, using emollients (eg, mineral oil, vegetable
oil, or petroleum jelly) can help improve symptoms
such as scales. Soft rubbing with a brush or comb aids
removing thick, adherent scales, but aggressive scrap-
ing should be avoided because it can induce further
inflammation. The main recommendations for the first-
line treatment of SD are topical medications, including
corticosteroids, calcineurin inhibitors, antifungal drugs,
and keratolytics. In the case of topical corticosteroids,
mild-potency formulations are recommended to be
used first because of their cutaneous adverse effects
and frequent rebound phenomena. Treatment with
corticosteroids is highly effective for reducing ery-
thema, scaling, and pruritus rapidly, resulting in total
clearance more often than placebo.40 Topical calcineu-
rin inhibitors (tacrolimus and pimecrolimus) manifest
good effects on SD by blocking calcineurin, thus pre-
venting both inflammatory cytokines and a signaling
pathway in T-lymphocyte cells. No difference between
topical calcineurin inhibitors and topical corticoste-
roids in total clearance was identified in short-term
trials.40 There is no risk of telangiectasia and skin atro-
phy, so topical calcineurin inhibitors are recommended
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 TABLE 26-3
3
Comparison of Infantile Seborrheic Dermatitis with Differential Diagnoses
INFANTILE SEBORRHEIC
DERMATITIS “NAPKIN” PSORIASIS ATOPIC DERMATITIS LETTERER-SIWE DISEASE

Occurs in the first few weeks to Onset at 3 months Onset within first 2 months of life, Occurs in newborns; other types
3 months most within the first year of Langerhans cell histiocytosis
(LCH) may occur between 1 and
3 years of age
Self-limited, regresses Self-limited Severity decreases with age Fatal if untreated; other variants of
spontaneously LCH have differing prognoses
Vertex scalp most commonly Diaper commonly affected; Face primarily involved Trunk and scalp involved
affected scalp and face may be affected

Chapter 26 :: Seborrheic Dermatitis

Adherent, yellow-brown,
greasy scale
Face, neck, trunk, and extremities
may be affected with inter-
triginous sites affected (axillae,
groin); isolated diaper lesions
more suggestive of seborrheic
dermatitis
Macerated, shiny erythema on
diaper region
Similarly extensive involvement,
but less scaling on intertriginous
sites; diaper region primarily
affected
Intensely pruritic, erythematous
papules with excoriation,
vesicles and serous exudate;
skin appears dry
Forearms and shins (extensors)
often affected, axillae are
spared; diaper area usually
spared
Slightly raised, rose-yellow
papules on trunk that may crust
and ulcerate
Extensive involvement with moist
erythematous plaques and pete-
chial lesions on intertriginous
areas; scalp involvement similar
to seborrheic dermatitis

for application to the susceptible regions instead of
topical corticosteroids. There are no studies comparing
the efficacy of tacrolimus with pimecrolimus in SD.
Maintenance therapy with topical calcineurin inhibi-
tors may be useful in preventing the relapse or exacer-
bation, but their long-term safety has not been verified.
Based on the presumed etiologic roles of Malassezia,
ketoconazole has been the most heavily investigated
topical agent for SD. Several randomized studies have
demonstrated that 1% to 2% ketoconazole significantly
lowers and improves the severity of SD versus pla-
cebo, achieving an equal remission rate with cortico-
steroids, with nearly 44% fewer adverse events.41 The
use of 1% ciclopirox also improved skin symptoms. In
single studies for evaluating the short-term efficacy of
clotrimazole and miconazole, those had almost equiv-
alent impacts on SD compared with corticosteroids.41
Other topical antifungal agents, such as bifonazole,
terbinafine, fluconazole, and zinc pyrithione, are also
likely to be useful.4 Dandruff or pityriasis simplex
capillitii may be treated by shampoos containing zinc
pyrithione, selenium sulfide, ketoconazole, salicylic
acid, ciclopirox, and coal tar. Lithium seems to have an
antiinflammatory role inhibiting the release of arachi-
donic acid and restricting availability of free fatty acids
essential for the growth of Malassezia.42 Topical lithium
has shown good results in total clearance both in HIV-
negative patients and in AIDS-associated SD. Topical
sulfur, propylene glycol, metronidazole, and benzoyl
peroxide wash have also been used. Seborrheic blepha-
ritis should be managed by long-term eyelid hygiene
with warm compresses, followed by proper topical
antibiotics and topical corticosteroid to reduce the bac-
terial load and marked inflammation, respectively.43
Aluminum acetate solution can be used to decrease
the symptoms of seborrheic otitis externa. In cases
refractory to topical treatment, systemic therapies can
be prescribed for uncontrolled multiple widespread
lesions and severe cases. Low doses of systemic glu-
cocorticoids may be used for a short period. Patients
should know that SD can be controlled but not eradi-
cated. SD patients treated by glucocorticoids should
be informed of the side effects and rebound flares that
occur after discontinuation of glucocorticoids. Oral
antifungals may be tried for severe and refractory
cases. Itraconazole, fluconazole, and pramiconazole
have been used with various regimens.44 For exam-
ple, itraconazole 200 mg/day for the first 7 days of
the month for several months is a regimen used to
get clinical improvement. The daily administration of
isotretinoin 0.1 to 0.5 mg/kg also may be effective in
severe cases.
The basic principle of treatment is the same for
infants. When ISD involves the diaper areas, the use
of superabsorbent disposable diapers with frequent
changes prevents the aggravation of the symptoms.45
Soap and alcohol-containing compounds are not rec-
ommended in cleaning the diaper lesions. Topical
medications having antifungal and antiinflammatory
activities are effective choices that have a high clinical
cure rate. A mild-potency steroid, such as 1% hydro-
cortisone, is preferred but used with caution because
of its adverse effects. In more refractory cases, a mid-
potency topical steroid, such as 0.1% betamethasone
valerate, may be required but usable only for a short
time. Keratolytic agents, including salicylic acid and
selenium sulfide are dangerous to neonates because
of the possibility of its percutaneous absorption.
Lotion containing 0.025% licochalcone, an extract 435
from Glycyrrhiza inflata, was shown to have a similar

Kang_CH026_p0428-0437.indd 435 06/12/18 3:22 pm

 3 effect compared to 1% hydrocortisone.46 If second-
ary infection with fungi or bacteria is accompanied,
appropriate systemic drugs should be prescribed.
Dietary controls and vitamin supplementation are
not beneficial in ISD.
Many researchers have proposed various alterna-
tive methods to treat SD as well, in preparation for the
antifungal resistance and the adverse effects of exist-
ing therapies. Homogeneous mixture of biodegradable
elements, such as urea, propylene glycol, and lactic
acid, was shown to be highly effective in treatment of
SD of the scalp.47 Tea tree oil, derived from nature, was
found to be of benefit in improving severity, pruritus,
and greasiness in a randomized single-blind study.
Part 3
The antifungal property of tee tree oil, mostly to M.
furfur, was established in an in vitro study.48 Narrow-
band ultraviolet B phototherapy was confirmed as an
additional choice and to be both safe and effective in
::
an open-label prospective study. Its role in SD may be
Dermatitis
associated with its immunomodulatory and antiin-
flammatory function.49
ACKNOWLEDGMENTS
The author acknowledges the contributions of Chris D.
Collins, MD, FAAD, and Chad Hivnor, MD, the former
authors of this chapter, and thanks Jungyoon Moon,
MD, for his devoted assistance.
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