MODULE III
ALLERGIC CONTACT DERMATITIS
EPIDEMIOLOGY
Contact allergy caused by ingredients found in personal care
products (cosmetics, toiletries) is a well-known problem, with
approximately 6% of the general population estimated to have
a cosmetic-related contact allergy.
Age
-an important cause of childhood dermatitis
-most common allergens identified differ between the age
groups.
Gender and Race
-gender differences in the development of ACD are largely
unknown
-role of race, if any, in the development of ACD to some potent
allergens such as para-phenylenediamine (PPD), remains
controversial
ETIOLOGY AND PATHOGENESIS
-represents a Type IV Hypersensitivity Reaction
-results from expo- sure and subsequent sensitization of a
genetically susceptible host, to an environmental allergen,
which on reexposure triggers a complex inflammatory reac-
tion
-erythema, edema, and papulo-vesiculation, usually in the dis-
tribution of contact with the instigating allergen, and with
pruritus as a major symptom
-To mount such reaction, the individual must have sufficient
contact with a sensitizing chemical, and then have repeated
contact with that substance later. This is an important
distinction to irritant contact dermatitis (ICD) in which no
sensitization reaction takes place, and the intensity of the
irritant inflammatory reaction is proportional to the dose—
concentration and amount of the irritant
Sensitization Phase
-most environmental allergens are small, lipophilic molecules
with a low molecular weight (<500 Daltons)
-unprocessed allergen is more correctly referred to as a
hapten. Once the hapten penetrates the skin, it binds with
epidermal carrier proteins to form a hapten–protein complex,
which produces a complete antigen.
-lasts 10-15 days and is often asymptomatic
-Sub- sequent exposure to the antigen, or rechallenge, leads to
an elicitation phase
Elicitation Phase
-both the APCs and the keratino- cytes can present antigen
and lead to subsequent recruitment of hapten-specific T cells
-T cells release cytokines, including IFN-g and TNF-a, which,
in turn, recruit other inflammatory cells while stimulating
macrophages and keratinocytes to release more cytokines.
-An inflammatory response occurs as monocytes migrate into
the affected area, mature into macrophages, and thereby
attract more T cells
-localized proinflammatory state results in the classical clinical
picture of spongiotic inflammation: redness, edema, papules
and vesicles, and warmth
CLINICAL APPROACH
Consideration of the Diagnosis
-character and distribution of the dermatitis should raise the
index of suspicion for ACD.
-any patient who presents with an eczematous dermatitis
should be regarded as possibly having ACD
-consider contact allergy in patients with other types of der-
matitis (e.g., atopic) that is persistent and recalcitrant despite
appropriate standard therapies, as well as in patients with
erythroderma, or scattered generalized dermatitis.
-patients with stasis dermatitis are at increased risk of
developing ACD from topical medications and lotions which are
often applied under occlusion over chronically inflamed and
broken skin
-the first step in the diagnosis of ACD is a careful medical and
environmental exposure history. His- tory taking should begin
with a discussion of the present illness focusing on the site of
onset of the problem and the topical agents used to treat the
problem (including over the counter and prescription
medications).
-past history of skin disease, atopy, and general health should
be routinely investigated.
-detailed history of the usage of personal care products (soap,
shampoo, conditioner, deodorant, lotions, creams,
medications, hair styling products, etc.), and investigation of
the patient’s avocations or hobbies
-occupation should be ascertained as well, and if it appears
contributory, or there are potential allergenic exposures, then a
thorough occupational history should be taken
CLINICAL MANIFESTATIONS
Cutaneous Findings
-classic presentation of ACD is a pruritic, eczema- tous
dermatitis initially localized to the primary site of allergen
exposure
-Geometric or linear patterns or involvement of focal skin
areas, may also be suggestive of an exogenous etiology
-A linear or streaky array on the extremities, for example, often
represents ACD from poison ivy, poison oak, or poison sumac.
-relevant historic data gathered from thoughtful ques- tioning
may prove as useful as the distribution of the lesions
-Acute lesions: marked by edema, erythema, and vesicle
formation. As the vesicles rupture, oozing ensues and papules
and plaques appear. Stronger allergens often result in vesicle
formation, whereas weaker allergens often lead to papular
lesion morphology, with surround- ing erythema and edema
-Subacute ACD will present with erythema, scaly juicy papules
and weeping
-Chronic ACD can present with scaling, fissuring, and
lichenification
-A key symptom for allergy is pruritus, which seems to occur
more typically with allergy, than a complaint of burning.
Topographic Approach
-usually the single most important clue to the diagnosis of ACD
-area of greatest eczematous dermatitis is the area of greatest
contact with the offending allergens
-location, in fact, can be one of the most valuable clues as to
which chemical might be the culprit of a patient’s ACD.
-an eczematous dermatitis in the peri/infraumbilical area
suggests contact allergy to metal snaps in jeans and belt
buckles, whereas eczema distributed around the hairline and
behind the ears suggests contact allergy to an ingredient in
hair products (hair dyes, shampoo, conditioners, styling
products)
-facial, eyelid, lip, and neck patterns of dermatitis should
always raise suspicion of a cosmetic-related contact allergy
-Occasionally, the topographic approach does not hold, and
the distribution can actually be misleading. This mainly refers
to cases of ectopic ACD or airborne ACD
- Ectopic ACD can follow two circumstances: Autotransfer, in
which the allergen is inconspicuously transferred to other body
sites by the fingers—the classical example being nail lacquer
dermatitis located on the eyelids or lateral aspects of the neck;
and heterotransfer, in which the offending allergen is
transferred to the patient by someone else (spouse, parent,
etc.)
-FACE: women are more commonly affected than men,
particularly by cosmetic- associated allergens such as
fragrances, PPD, preservatives, and lanolin alcohols. Allergens
can be applied to the face directly but can also be indirectly
transferred from airborne or hand-to-face exposure
-SCALP: allergens applied to the scalp most often produce
patterns of dermatitis on the forehead and lateral aspect of the
face, eyelids, ears, neck, and hands; whereas the scalp
remains uninvolved, suggesting that the scalp is particularly
“resistant” to contact dermatitis. Patients sensitive to certain
ingredients in hair products such as PPD or glyceryl
monothioglycolate may show a marked scalp reaction with
edema and crusting. PPD is one of the most potent sensitizers
known and is widely used as an ingredient in hair dyes
-EYELID: eyelids are one of the most sensitive skin areas, and
are highly susceptible to irritants and allergens perhaps due to
the thinness of the eyelid skin and perhaps because they can
accumulate the offending chemical in the skin folds. Volatile
agents may affect the eyelids first and exclusively, causing
airborne eyelid contact dermatitis. Sources of contact
dermatitis of the eyelids include cosmetics such as mascara,
eyeliners and eye shadows, adhesive in fake eyelashes, and
nickel and rubber in eyelash curlers. Furthermore, marked
edema of the eyelids is often a feature of hair-dye dermatitis.
-LIPS: approximately one-third of patients with cheilitis—
without other areas of dermatitis—are typically found to have
an allergen as a contributing factor. Allergic contact cheilitis
(ACC) has been reported to result from the use of a wide array
of products including cosmetics such as lip balms, lipsticks, lip
glosses, moisturizers, sunscreens, nail products, and oral
hygiene products (mouthwashes, toothpastes, dental floss)
-NECK: highly reactive site for ACD. Cosmetics applied to the
face, scalp, or hair often initially affect the neck. Nail-polish
ingredients (tosylamide formaldehyde resin and epoxy resin)
are common culprits in this region. In a fragrance-sensitized
individual, the practice of repeated application of fragrances to
the anterior neck may result in the appearance of a dermatitic
plaque on the neck, which has been coined the “atomizer
sign.” Metal allergy can mani- fest as chronic eczematous
dermatitis from exposure to necklaces and jewelry clasps that
contain nickel and/ or cobalt.
-TORSO: encounter fragrances, preservatives, surfactants,
and other chemicals from the use of personal care products;
yet it is also susceptible to allergens found in textiles.
-AXILLAE: Heat, humidity, and friction of the axillary fold may
contribute to the leaching of textile resins and dyes and
dermatitis accentuation in these areas.74 The axillary region is
also uniquely exposed to deodor- ants and antiperspirants.
These products contain most notably the contact allergens
fragrances and preservatives (formaldehyde releasers,
parabens, etc.). A commonly observed effect with the use of
these products is the sparing of the axillary vault, mainly
secondary to perspiration diluting the allergens
-HANDS AND FEET: Hand dermatitis has a particularly high
incidence secondary to the fact that the hands are the main
means of interaction with the environment, with increased
possibility for numer- ous allergen exposures. Accounts for as
much as 80% of the occupationally related skin diseases,
especially in certain “wet work” occupations such as health
care workers, food handlers, etc.
TREATMENT
-identification and removal of the inciting agent should always
be the goal in the diagnosis and treatment of ACD
IRRITANT CONTACT DERMATITIS
-cutaneous response to contact with an external chemical,
physical, or biologic agent; endogenous factors such as skin
barrier function and preexisting dermatitis also play a role
Epidemiology
-no previous exposure to the causative agent is necessary in
eliciting irritant reactions
-often occupation-related
-caused by personal care products and cosmetics is also
common; however, very few patients with these irritant
reactions seek medical help because they manage by avoiding
the offending agent
Etiology and Pathogenesis
-Four interrelated mechanisms have been associated with ICD:
(1) removal of surface lipids and water-holding substances, (2)
damage to cell membranes, (3) epidermal keratin denaturation,
and (4) direct cytotoxic effects.
-characterized by the release of proinflammatory mediators,
particularly cytokines, from nonimmune cutaneous cells
(keratinocytes) in response to chemical stimuli. This is a
process that does not require previous sensitization.
-Disruption of the skin barrier leads to release of cytokines
such as interleukin (IL) 1α, IL-1β, and tumor necrosis factor-α
(TNF-α)
-loss of function polymorphisms in the filaggrin gene, an
important protein for skin barrier function, have been
associated with an increased susceptibility to chronic ICD
-EXOGENOUS FACTOR: The irritant potential of compounded
formulations may be more difficult to predict. Factors to be
considered include: (1) chemical properties of the irritant: pH,
physical state, concentration, molecule size, amount,
polarization, ionization, vehicle, and solubility; (2)
characteristics of exposure: amount, concentration, duration
and type of contact, simultaneous exposure to other irritants,
and interval after previous exposure; (3) environ- mental
factors: body region and temperature; (4) mechanical factors
such as pressure, friction, or abra- sion; and (5) ultraviolet (UV)
radiation.
When one or more irritants are combined or used
simultaneously, a synergistic or antagonistic effect may occur
as a consequence of specific cellular interactions between the
compounds, or an alteration in the skin permeability by one or
more of the compounds, that would not occur when an irritant
is used alone.
-ENDOGENOUS FACTORS: genetic predisposition to irritant
susceptibility may be specific for each irritant, majority of
clinical ICD affects the hands and women account for a
majority of these patients, children <8 yo are more susceptible
to percutaneous absorption of chemicals and to irritant
reactions, erythema is decreased in older persons while
invisible skin irritation (barrier damage) might be increased in
the elderly, significant site differences in barrier function,
making the skin of the face, neck, scrotum and dorsal hands
more susceptible to ICD with palms and soles comaparatively
more resistant, history of atopy is a well-known risk factor for
irritant hand dermatitis because of lower threshold for skin
irritation, impaired skin barrier function and a slower healing
process
Common Irritants
-water, hard water, skin cleansers depending on the chemistry
of their constituents
-preservatives
-food such as citrus peels, garlic, flour, spices, pineapple juice
can act as irritants
-animal products from seafood and meat, from caterpillars,
carpet beetles, and moths, from insect secretions; cosmetics,
especially when applied to the eyelids; alkalis, present in soap,
bleaches, detergents, oven cleansers, and toilet bowl cleaners
-Animal products
-Cosmetics
-Degreasing agents
-Detergents Dusts/friction Foods
-Low humidity
-Metal working fluids
-Tear gases
-Topical medicaments
-Solvents
-Water/wet work
Treatment
-Identification and elimination of the irritants and protec- tion
from further exposure are important in the manage- ment of
ICD
-once dermatitis develops, topical treatment is helpful. The role
of topical corticosteroids in the management of ICD is
controversial, but they may be helpful because of their anti-
inflammatory effect.
-emollients or occlusive dressings may improve barrier repair
in dry, lichenified skin. Traditional pet- rolatum-based
emollients are accessible, inexpensive, and have been shown
to be as effective as emollient con- taining skin-related lipids
-ICD is a risk factor for the development of ACD because the
impaired skin barrier may facilitate the potential for the
induction and elicitation of ACD. Thus, the prevention of irritant
dermatitis reduces the risk of ACD
-prognosis for acute ICD is good if the causative irritant can be
identified and eliminated
ATOPIC DERMATITIS
Chronically relapsing skin disease that occurs most commonly
during early infancy and childhood. It is frequently associated
with abnormalities in skin barrier function, allergen sensiti-
zation, and recurrent skin infections
Major Features of Atopic Dermatitis:
Pruritus
Rash on face and/or extensors in infants and young children
Lichenification in flexural area in older children
Tendency toward chronic or chronically relapsing dermatitis
Personal or family history of atopic disease: asthma, allergic
rhinitis, atopic dermatitis
EPIDEMIOLOGY
-prevalence in children of 10–20% in the United States,
Northern and Western Europe, urban Africa, Japan, Australia,
and other industrialized countries.
-prevalence of AD in adults is approximately 1–3%
-prevalence of AD is much lower in agricultural regions of
countries such as China and in Eastern Europe, rural Africa,
and Central Asia
-AD is a disease with high prevalence, affecting patients in
both developed and developing countries.4 There is also a
female pre- ponderance for AD, with an overall female/male
ratio of 1.3:1.0.
-potential risk factors that may be associated with the rise in
atopic disease include small family size, increased income and
education both in whites and blacks, migration from rural to
urban environments, and increased use of antibiotics
-“hygiene hypothesis”: allergic diseases might be prevented by
“infection in early childhood transmitted by unhygienic contact
with older siblings.”
-Autoimmune diseases such as diabetes, abnormalities in T
regulatory cells have also been implicated.
ETIOLOGY AND PATHOGENESIS
Decreased Skin Barrier Function
-associated with a marked decrease in skin barrier function
due to the downregulation of cornified envelope genes
(filaggrin and loricrin), reduced ceramide levels, increased
levels of endogenous proteolytic enzymes, and enhanced
transepidermal water loss
-Addition of soap and detergents to the skin raises its pH,
thereby increasing activity of endogenous proteases, leading to
further breakdown of epidermal barrier function
-epidermal barrier may also be damaged by exposure to
exogenous proteases from house dust mites and
Staphylococcus aureus (S. aureus)
-decreased skin barrier function could act as a site for allergen
sensitization and predispose such children to the development
of food allergy and respiratory allergy
Immunopathology of Atopic Dermatitis
-Acute eczematous skin lesions are characterized by marked -In older children, and in those who have long-standing skin
intercellular edema (spongiosis) of the epidermis disease, the patient develops the chronic form of AD with
-Dendritic antigen-presenting cells in lesional and, to a lesser lichenification and localization of the rash to the flexural folds of
extent, in nonlesional skin of AD exhibit surface-bound the extremities
immunoglobulin E (IgE) molecules. -AD often subsides as the patient grows older, leaving an adult
-Chronic lichenified lesions are characterized by a hyperplastic with skin that is prone to itching and inflammation when
epidermis with elongation of the rete ridges, prominent exposed to exogenous irritants. Chronic hand eczema may be
hyperkeratosis, and minimal spongiosis. Increased numbers of the primary manifestation of many adults with AD
eosinophils are observed in chronic AD skin lesions.
TREATMENT
Cytokines and Chemokines
-orchestrated by the local expression of proinflammatory
-successful treatment of AD requires a systematic,
cytokines and che- mokines.12 Cytokines such as tumor
multipronged approach that incorporates education about the
necrosis factor-a (TNF-a) and interleukin 1 (IL-1) from resident
disease state, skin hydration, pharmacologic therapy, and the
cells [keratinocytes, mast cells, dendritic cells (DCs)] bind to
identification and elimination of flare factors such as irritants,
receptors on the vascular endothelium, activating cellular
allergens, infectious agents, and emotional stressors
signaling pathways, which leads to the induc- tion of vascular
-treatment plans should be individualized to address
endothelial cell adhesion molecules. These events initiate the
each patient’s skin disease reaction pattern, including the
process of tethering, activa- tion, and adhesion to vascular
acuity of the rash, and the trigger factors that are unique to the
endothelium followed by extravasation of inflammatory cells
particular patient
into the skin.
-Acute AD is associated with the production of T helper 2 type
Cutaneous Hydration
(Th2) cytokines, notably IL-4 and IL-13,13 which mediate
-Patients with AD have abnormal skin barrier function with
immunoglobulin isotype switching to IgE synthesis and
increased transepidermal water loss and decreased water con-
upregulate expres- sion of adhesion molecules on endothelial
tent and dry skin (xerosis) contributing to disease morbidity by
cells.
the development of microfissures and cracks in the skin, which
-In chronic AD, there is an increase in the production of IL-5,
serve as portals of entry for skin pathogens, irritants, and
which is involved in eosinophil development and survival.
allergens.
Increased production of granulocyte macrophage colony-
-Warm soaking baths for approximately 10 minutes followed by
stimulating factor in AD inhibits apoptosis of monocytes,
the application of an occlusive emollient or topical medication
thereby contributing to the persistence of AD
to retain moisture can give such patients excellent
symptomatic relief.
Key Cell Types in Atopic Dermatitis Skin
-Use of an effective emollient combined with hydration therapy
Antigen-presenting Cells
helps to restore and preserve the stratum corneum barrier, and
T cells
may decrease the need for topical glucocorti- coids.
Keratinocytes
General Skin Care measures:
Genetics
-Education
-AD is a complex disease that is familially transmit- ted with a
-Appropriate skin hydration and use of emollients/skin barrier
strong maternal influence.
repair measures
-Genome-wide linkage studies of families with AD have
-avoidance of irritants
implicated chromosomal regions that overlap with other
-Identification and avoidance of proven allergens
inflammatory skin diseases such as psoriasis.
-Anti-inflammatory therapy (topical steroids, topical calcineurin
inhibitors)
CLINICAL FINDINGS
-Antipruritic interventions (sedating antihistamines, behavioral
modification)
Cutaneous Lesions
-Identification and treatment of complicated bacterial, viral or
-Intense pruritus and cutaneous reactivity are car- dinal
fungal infections
features of AD.
-treatment of psychosocial aspects of disease
-Pruritus may be intermittent throughout the day but is usually
worse in the early evening and night. Its consequences are
scratching, prurigo papules, lichenification, and eczematous
skin lesions. NUMMULAR ECZEMA
-Acute skin lesions: characterized by intensely pruritic,
erythematous pap- ules associated with excoriation, vesicles
-Also known as discoid eczema
over erythematous skin, and serous exudate
-Papules and papulovesicles coalesce to form nummular
-Subacute dermatitis is characterized by erythematous, excori-
plaques with oozing, crust, and scale.
ated, scaling papules
-Most common sites of involvement are upper extremities,
-Chronic AD is characterized by (1) thickened plaques of skin,
including the dorsal hands in women, and the lower extremities
(2) accentuated skin markings (lichenification), and (3) fibrotic
in men.
papules (prurigo nodularis). In chronic AD, all three stages of
-Pathology may show acute, subacute, or chronic eczema.
skin reactions frequently coexist in the same individual. At all
-predominantly a disease of adulthood
stages of AD, patients usually have dry, lackluster skin
-Men are more frequently affected than women
-distribution and skin reaction pattern vary according to the
-The peak incidence in both males and females is around 50–
patient’s age and disease activity
65 years of age.
-During infancy, the AD is generally more acute and primarily
-There is a second peak in women around 15–25 years of age.
involves the face, scalp, and the extensor surfaces of the
extremities. Diaper area is usually spared.
Pathogenesis
-pathogenesis of nummular eczema is still unknown
-The vast majority of patients with nummular eczema do not
have a personal or family history of atopy, although nummular
plaques may be seen in atopic eczema.
Clinical Findings
-Well-demarcated coin-shaped plaques form from coalescing
papules and papulovesicles. Pinpoint oozing and crusting
eventuate, and are distinctive.
-Crust may cover the entire surface
-plaques range from 1-3 cm in size.
-surrounding skin is generally normal but may be xerotic
-pruritus varies from minimal to severe
-central resolution may occur, leading to annular forms.
-Chronic plaques are dry, scaly and lichenified.
-Classic distribution of of lesions is the extensor aspects of the
extremities
-In women, the upper extremities, including the dorsal aspects
of the hands, are more fre- quently affected than the lower
extremities.
-Exudative discoid and lichenoid dermatitis of Sulzberger-
Garbe may represent a variant of nummular dermatitis
Laboratory Tests
-Patch testing may be useful in chronic recalcitrant cases to
rule out a superimposed contact dermatitis
Complication
Nummular eczema maybe complicated by secondary bacterial
infection
Prognosis
Course is usually chronic. Recurrence at prior sites of
involvement is a feature of the disease
Treatment
-Topical steroids in the mid to high potency range are the
mainstay of treatment
-Calcineurin inhibitors, and tar preparations are also effective
-Emollients can be added adjunctively if there is accompanying
xerosis.
-Oral antihistamines are useful if pruritus is severe
-Oral antibiotics are indicated when secondary infection is
present.
-For widespread involvement, phototherapy with broad- or
narrow-band ultraviolet B may be beneficial.
LICHEN SIMPLEX CHRONICUS
-chronic, severely pruritic disorder characterized by one or
more lichenified plaques
-most common sites of involvement are scalp, nape of neck,
extensor aspect of extremities, ankles and anogenital area
-pathology consists of hyperkeratosis, hypergranulosis,
psoriasiform epidermal hyperplasia and thickened papillary
dermal collagen
Epidemiology
-affects adults, predominantly from ages 30 to 50.
-Females are affected more commonly than males.
-Prurigo nodularis may occur at any age, but most patients are
between 20 and 60 years.
-Men and women are equally affected.
-Patients with coexistent atopic dermatitis have been found to
have any earlier age of onset as compared to the nonatopic
group.
Etiology and Pathogenesis
-induced by rubbing and scratching secondary to itch.
-a variable association between lichen simplex chronicus and
atopic disorders has been reported, ranging from around 26%
to 75%
-Environmental factors have been implicated in induc- ing itch,
such as heat, sweat, and irritation associated with anogenital
lichen simplex chronicus
-The presence of emotional or psychological factors in patients
with lichen simplex chronicus has been alluded to in the
literature. Lichen simplex chronicus patients had higher
depression scores in one study. Whether these emotional
factors are secondary to the primary dermatologic disease or
whether they are primary and causative, altering perception of
itch, is unclear. It has been postulated that neurotransmitters
that affect mood, such as dopamine, serotonin, or opioid
peptides modulate perception of itch via descending spinal
pathways. Obsessive-compulsive disorder (OCD) has also
been associated with picking in these disorders
Clinical Findings
-severe itching is the hallmark of simplex chronicus.
-itching may be paroxysmal, continuous or sporadic
-rubbing and scratching may be conscious and to the point of
replacing the sensation of itch with pain
Itch severity is worth with sweating, heat irritation from clothing
and in times of psychological distress
-cutaneous lesions: repeated rubbing and scratching gives rise
to lichenified, scaly plaque with excoriations
Cutaneous Lesions
-repeated rubbing and scratching gives rise to a lichenified,
scaly plaque with excoriations.
-hyper- and hypopigmentation are seen with chronicity
-usually, only one plaque is present, however, more than one
site may be involved
-most common sites of involvement are the scalp, the nape of
the neck (especially in women), the ankles, the extensor
aspects of the extremities, and the anogenital region.26
-the labia majora in women and the scrotum in men are the
most common sites of genital involvement
-the upper inner thighs may also be affected.
-patients with atopic eczema: intervening skin is often
lichenified and xerotix
-nonatopic patients: cutaneous signs of underlying systemic
disease or lymphadenopathy, signifying lymphoma may be
present
Treatment
-aimed at interrupting the itch-scratch cycle
-systemic causes of itch should be identified and addressed
-first-line measures to control itch include potent
topical steroids as well as nonsteroidal antipruritic preparations
such as menthol, phenol, or pramoxine
-emollients are an important adjunct
-Intralesional steroids, such as triamcinolone acetonide, given
in varying concentrations according to the thickness of the
plaque or nodule are beneficial.
SEBORRHEIC DERMATITIS
-characteristically found in regions of the body with high
concentrations of sebaceous follicles and active sebaceous
glands including the face, scalp, ears, upper trunk, and
flexures (inguinal, inframammary, and axillary)
-most common dermatoses seen in human immu- nodeficiency
virus (HIV) and acquired immunodefi- ciency syndrome (AIDS)
patients

Epidemiology
-separated into two age groups, an infantile self-limited form
primarily during the first 3 months of life and an adult form that
is chronic
-male predominance is seen in all ages, without any racial
predilection, or horizontal transmission
Etiology and Pathogenesis
-exact pathogenesis of seborrheic dermatitis is yet to be fully
elucidated, but this dermatosis is commonly linked with the
yeast Malessezia, immunologic abnormalities, sebaceous
activity, and patient susceptibility.
-amount of sebum produced is not an essential factor, as not
all patients with seborrheic dermatitis will have increased levels
of sebum production
-abnormal immune response to it resulting in a depressed
helper T cell response and less production of
phytohemagglutinin and concanavalin
-seasonal fluctuations in humidity and temperature are noted to
flare this disease, particularly with low humidity and cold
temperatures in the winter and early spring, with some relief in
the summer. Facial PUVA (psoralen plus ultraviolet radiation)
treatments and facial trauma (scratching) are also reported to
trigger seborrheic dermatitis as well
-clearance of seborrheic dermatitis with antifungals and
recurrence following cessation of therapy also supports the
premise that Malassezia species is pathogenic
-drugs known to trigger seborrheic dermatitis like eruptions
including griseofulvin, cimetidine, lithium, methyldopa, arsenic,
gold, auranofin, aurothioglucose, buspirone, chlorpromazine,
ethionamide, haloperidol, interferon-α, phenothiazines,
stanozolol, thiothixene, psoralen, methoxsalen, and trioxsalen.
-neurologic disorders have been associated with seborrheic
dermatitis, with most of them resulting in some facial immobility
and sebum accumulation. These include Parkinson’s,
Alzheimer’s, syringomy- elia, epilepsy, cerebrovascular
infarcts, postencephalitis, mental retardation, poliomyelitis,
quadriplegia, trigeminal nerve injury and other facial nerve
palsies
-patients with seborrheic dermatitis may have epidermal
hyperproliferation or dyskeratinization related to increased
activity of calmodulin, which is also seen in psoriasis
Clinical Findings
-Seborrheic stage: which is often combined with a gray–white
or yellow–red skin discoloration, prominent follicular openings,
mild to severe pityriasiform scales
-infantile: scalp (cradle cap), trunk (flexures and napkin area),
Leiner’s disease (nonfamilial and familial C3/C5 dysfunction). It
occurs during the first few weeks to 3 months of life, is self-
limited, and corresponds to the time when the neonate
produces sebum, which then regresses until puberty.
-adult: scalp, face, eyelids (blepharitis), trunk (petaloid,
pityriasiform, flexural, eczematous, follicular, generalized,
erythrodermic), tends to be chronic and can persist from the
fourth through the seventh decades of life, with a peak at age
40. Lesions may also be seen on the face with prominent
symmetry particularly medial eyebrows, forehead, upper
eyelids, nasolabial folds and lateral nares
Treatment
-infants: benign, self-limited form responds readily to
shampoos, emollients, and mild topical steroids. Infants with
prolonged inflammation on the scalp or intertriginous areas can
be treated with low potency topical corticosteroids
(hydrocortisone 1% cream or lotion for a few days), followed by
topical imidazoles.
-adult: patients should be informed that the aim of treatment
will be to control rather than cure the dis- ease. Scalp
seborrheic dermatitis can be treated with shampoos containing
zinc pyrithione, selenium sulfide, imidazoles, ciclopirox (cream,
gel, and shampoo), salicylic acid (shampoos, creams), coal tar
(creams, shampoos), or mild detergents. Treatment of the
face, trunk, and ears includes short courses of low potency
topical glucocorticoids (Class IV or lower) to suppress the initial
inflammation.
-recommend patients to avoid alcohol-containing solutions that
flare the disease. Aluminum acetate solu- tion can be used to
maintain seborrheic otitis externa. Patients with seborrheic
blepharitis can be treated with warm to hot compresses and
washing with baby shampoo followed by gentle cotton tip
debridement of thick scale.
Prognosis
-Self-limited with a good prognosis in infants compared to
chronic and relapsing in adults
-No evidence to suggest infants with seborrheic dermatitis will
have disease as adults
Generalized flares and erythroderma can sometimes occur
PERIORAL DERMATITIS
-characterized by small, discrete papules and pustules in a
periorificial distribution, predominantly around the mouth
-classic presentation is an eruption with overlapping features of
an eczematous dermatitis and an acneiform eruption.
Epidemiology
-predominantly affects women
-pediatric perioral dermatitis may have a slight female
preponderance and is seen equally among those of different
races
-the granulomatous form of peri-oral dermatitis has been
reported mostly in children of prepubertal age
-Perioral dermatitis can occur as early as 6 months.
Etiology and Pathogenesis
-relationship of perioral dermatitis to the misuse of topical
corticosteroids
-patients often reveal a history of an acute steroid-responsive
eruption around the mouth, nose, and/or eyes that worsens
when the topical corticosteroid is discontinued. Dependency on
the use of the topical corticosteroid may develop as the patient
repeatedly treats the recurrent eruption.
-disease is predominant in young women
Clinical Findings
-primary lesions of perioral dermatitis are discrete and grouped
erythematous papules, vesicles, and pustules
-lesions are often symmetric but may be unilateral and appear
in the perioral, perinasal, and/or periocular regions
-background erythema and/or scale may be present
-a distinct 5 mm clear zone at the vermilion edge is well-
described
-granulomatous variant of perioral dermatitis presents with
small flesh-colored, erythematous or yellow-brown papules,
some with confluence and shares the distribution of perioral
dermatitis in adults
Treatment
-topical corticosteroids being used should be discontinued.
-If fluorinated corticosteroids are being applied, initial
substitution with a low-potency hydrocortisone cream may
minimize a flare of the dermatitis.
-Patients should be educated about the link between
application of topical corticosteroids and exacerbation of the
dermatitis.
-In most cases, effective therapy is oral tetracycline,
doxycycline, or minocycline, for a course of 8 to 10 weeks, with
a taper over the last 2 to 4 weeks
-In children under 8 years of age, nursing mothers, or
tetracycline-allergic patients, oral erythromycin is
recommended
INTERTRIGO AND DIAPER DERMATITIS
Diaper Dermatitis
-may be the result of prolonged or too frequent contact with
urine or fecal residues
-also called diaper rash, napkin dermatitis, and nappy rash
-most common skin eruption in infants and toddlers
-typically occurs on convex skin surfaces that are in direct
contact with the diaper, including the buttocks, lower abdomen,
genitalia, and upper thighs.
-there is sparing of the genitocrural flexures
Intertrigo
-inflammation caused by skin-to-skin friction, most often in
warm, moist areas of the body, such as the groin, between
folds of skin on the abdomen, under the breasts, under the
arms or between the toes. The affected skin may be sensitive
or painful, and severe cases can result in oozing sores,
cracked skin or bleeding.
-Intertrigo usually clears up if the affected areas are kept as
clean and dry as possible.
-wearing loose clothing and reducing skin-to-skin friction in
affected areas
-applying an ointment to the skin can help
-weight loss may be helpful as well.
ASTEATOTIC DERMATITIS
-also known as xerotic eczema or “winter itch”
-mildly inflammatory dermatitis that develops in areas of
extremely dry skin, especially during the winter months
-exsiccation eczematid usually occurs in elderly patients who
frequently shower without applying moisturizers to their skin. -
Clinical features: fine cracks and scale, with or without
erythema, characteristically develop in areas of dry skin
especially on the anterior surfaces of the lower extremities in
elderly patients
-bathing and the use of harsh soaps exacerbate asteatotic
eczema
Treatment
-responds well to topical moisturizers and the avoidance of
cutaneous irritants
STASIS DERMATITIS
-papulosquamous plaques with dyschromia located on the
shins and medial surfaces of the lower legs, with presence of
concomitant varicosities
-patches of erythema and scaling on background of
hyperpigmentation associated with signs of venous
insufficiency
-develops on the lower extremities secondary to venous
incompetence and chronic edema
-patients may give a history of deep venous thrombosis and
may have evidence of vein removal or varicose veins
-Early findings in stasis dermatitis consist of mild erythema and
scaling associated with pruritus
-The typical initial site of involvement is the medial aspect of
the ankle, often over a distended vein
-may become acutely inflamed, with crusting and exudate
(easily confused with cellulitis)
-symmetrical and bilateral involvement is more likely stasis
dermatitis, whereas unilateral involvement may represent
cellulitis
-Chronic stasis dermatitis is often associated with dermal
fibrosis that is recognized clinically as brawny edema of the
skin.
-As the disorder progresses, the dermatitis becomes
progressively pigmented due to chronic erythrocyte
extravasation leading to cutaneous hemosiderin deposition.
Stasis dermatitis may be complicated by secondary infection
and contact dermatitis.
-Severe stasis dermatitis may precede the development of
stasis ulcers
Treatment
-patients benefit greatly from leg elevation
-routine use of compression stockings with a gradient of at
least 30-40 mmHg
-use of emollients and/or mid-potency topical glucocorticoids
and avoidance of irritants are also helpful in treating stasis
dermatitis
-protection of the legs from injury, including scratching and
control of chronic edema are essential to prevent ulcers
DYSHIDROTIC ECZEMA
-presents with multiple, intensely pruritic, small papules and
vesicles on the thenar and hypothenar eminences and the
sides of the fingers
-Lesions tend to occur in crops that slowly form crusts and then
heal.
-common distribution: palms, soles, sides of fingers and toes
HOUSEWIVES’ DERMATITIS
-develops as a result of repeated insults to the skin
-chemicals involved are often multiple and weak and would not
in themselves be strong enough to cause irritant dermatitis
-most common marginal irritants: soap, detergents,
surfactants, organic solvents and oils which may also act as
perpetuating factors once the dermatitis has become
established
-(+) history of atopy
-common distribution: dorsum of finger or hand with sparing of
the palms
-clinical features: pruritic, ill-defined, rough, pinkish fissured
patches
Treatment
-reduce exposure to offending agent
-emollients should be sued liberally