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History and Epidemiology: Key Features

The document discusses differential diagnosis of intertriginous dermatoses in adults. Common causes include irritant/frictional intertrigo, seborrheic dermatitis, inverse psoriasis, and dermatophytosis. Less common causes include candidiasis. Uncommon causes include granular parakeratosis and other conditions.

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Aswin Krishna
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0% found this document useful (0 votes)
95 views8 pages

History and Epidemiology: Key Features

The document discusses differential diagnosis of intertriginous dermatoses in adults. Common causes include irritant/frictional intertrigo, seborrheic dermatitis, inverse psoriasis, and dermatophytosis. Less common causes include candidiasis. Uncommon causes include granular parakeratosis and other conditions.

Uploaded by

Aswin Krishna
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PDF, TXT or read online on Scribd
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CHAPTER

Fig. 13.3 Differential diagnosis of


DIFFERENTIAL DIAGNOSIS OF INTERTRIGINOUS DERMATOSES IN ADULTS
intertriginous dermatoses in
adults. Individual patients often
13

Other Eczematous Eruptions


Common Less common Uncommon have multiple disorders
superimposed upon one another.
Irritant/frictional intertrigo* Candidiasis Granular parakeratosis Bullous impetigo and streptococcal
• Ill-defined erythema/maceration • Intense erythema with intertrigo are considerably more
• Predisposing factors: obesity, desquamation and satellite
common in children than adults.
heat & humidity, hyperhidrosis, papules/pustules
diabetes mellitus, poor hygiene • Often involves scrotum as well
*Also referred to more
• Secondary infections common as skin folds nonspecifically as intertriginous
• Predisposing factors: occlusion, dermatitis or intertrigo. **The term
Seborrheic dermatitis**
hyperhidrosis, diabetes mellitus, ‘sebopsoriasis’ may be used when
• Well-demarcated, pink to red,
antibiotic or corticosteroid use, Systemic contact dermatitis, features of both seborrheic
immunosuppression symmetrical drug-related dermatitis and psoriasis are
moist patches/plaques
• Centered along inguinal creases intertriginous and flexural present. Insets: Courtesy, Luis Requena, MD;
• Involvement of scalp, face, ears exanthema, toxic erythema of Eugene Mirrer, MD; Louis A Fragola, Jr, MD;
chemotherapy David Mehregan, MD; Julie V Schaffer, MD.
Inverse psoriasis** Hailey−Hailey disease,
• Well-demarcated, pink to red Darier disease (depicted),
plaques pemphigus vegetans
• Shiny with little scale in folds
• Centered along inguinal creases
• Psoriasiform plaques elsewhere
(e.g. genitals, intergluteal cleft, Erythrasma
scalp, elbows/knees, hands/feet) • Pink−red to brown patches with
• Nail psoriasis (pitting, oil spots) fine scale
• Coral-red fluorescence with
Wood’s lamp illumination
Zinc deficiency, necrolytic
migratory erythema, other
“nutritional dermatitis”

Cutaneous Crohn disease

Dermatophytosis (tinea cruris)


• Less often centered along
inguinal creases
• Expanding annular lesions with
scaly erythematous border that
may contain pustules or vesicles Langerhans cell histiocytosis
• Extension to inner thigh,
buttock; usually spares scrotum
• Coexisting tinea pedis/unguium
very common

Extramammary Paget disease

Allergic contact dermatitis


• Consider if fails to respond to
usual therapy

common cause of xerosis is aging. Rarely, but especially when wide-


Key features spread and refractory to therapy, asteatotic eczema may be related to
■ Dry, rough, scaly and inflamed skin with superficial cracking that an underlying systemic lymphoma21.
resembles a “dried riverbed”
■ Sites of predilection are the shins, lower flanks, and posterior History and Epidemiology
axillary line Asteatosis as the cause of “nummular eczema” was first mentioned by
■ Associated with aging, xerosis, low relative humidity, and frequent Gross22 in the late 1940s. Dry skin probably occurs in everyone over
bathing the age of 60 years, but its severity is strongly linked to the exogenous
factors mentioned above.

Pathogenesis
Introduction Xerosis of aging skin is not caused by deficient sebum production, but
Dry skin (xerosis, exsiccosis, asteatosis) may result from both exoge- by a complex dysfunction of the stratum corneum (see Ch. 124)23.
nous and endogenous causes: a dry climate or low indoor humidity; There is a decrease of intercellular lipids with a deficiency of all key
excessive exposure to water, soaps and surfactants; marasmus and stratum corneum lipids24 and an altered ratio of fatty acids esterified
malnutrition; renal insufficiency and hemodialysis; and heritable con- to ceramide 125; this, plus a persistence of corneodesmosomes26 and 231
ditions such as ichthyosis vulgaris and atopic dermatitis. The most premature expression of involucrin and formation of the cornified
SECTION

3 PATHOGENETIC FACTORS IN STASIS DERMATITIS CUTANEOUS SIGNS OF CHRONIC VENOUS HYPERTENSION


PAPULOSQUAMOUS AND ECZEMATOUS DERMATOSES

Factor Consequence • Edema, often tender


• Varicosities, including venulectasias of the instep
Chronic venous insufficiency and the microvasculature
• Petechiae superimposed on a yellow–brown discoloration due to
Deposition of proteins, • Deposits inhibit oxygen diffusion and hemosiderin deposits (stasis purpura)
particularly fibrin, metabolic exchange in combination with • Stasis dermatitis
around vessels as interstitial edema • Lipodermatosclerosis, acute and chronic
hyaline cuffs • Stasis ulcerations, in particular above the medial malleolus
Slow blood flow • Upregulation of ICAM-1 and VCAM-1 on
• Acroangiodermatitis (pseudo-Kaposi sarcoma)
endothelia59
• Livedoid vasculopathy (“atrophie blanche”): porcelain-white scars
• Activation of neutrophils and surrounded by punctate telangiectasias and painful ulcerations*
macrophages60 *Need to exclude causes of hypercoagulability.
• Expression of L-selectin on neutrophils61
• Neutrophils attracted into and trapped Table 13.3 Cutaneous signs of chronic venous hypertension.
within affected areas, notably the medial
supramalleolar region62
Release of inflammatory • Pericapillary inflammation
Fig. 13.7
mediators, free radicals, Autosensitization
and proteases by dermatitis in a patient
neutrophils with venous ulceration.
Free iron ions released • Increase in free radical production and lipid Note the involvement of
from hemosiderin peroxidation the extensor surfaces of
deposits • Activation of matrix metalloproteinases63 the upper extremities in
this patient with an
Platelet accumulation • May trigger focal thrombosis allergic contact
within the dermatitis to neomycin,
microvasculature as well as stasis
Fibrosis and tissue • Lipodermatosclerosis – dermal sclerosis
dermatitis and venous
ulceration. Courtesy, Jean L
remodeling due to and septal sclerosis that present as
Bolognia, MD.
imbalances within the sclerosing panniculitis
capillary network • Lymphatic dysfunction
• “Atrophie blanche” – stellate sclerotic areas
depleted of capillaries with the formation of
peripheral giant capillaries
• May lead to the formation of venous ulcers
Elevated plasma levels • Hyperhomocysteinemia is associated with
of homocysteine64 an increased risk of thromboses
Complicating factors
Allergic contact • Sensitizers are often in topical agents used
dermatitis to combat pruritus, xerosis, and presumed
infection65,66
- A-ntibiotics, e.g. bacitracin, neomycin
- Lanolin derivatives
- Emulsifiers
- Antiseptics, e.g. iodine*
- Preservatives, e.g. parabens
- Balsam of Peru and other fragrances intraepithelial edema predominates, with fluid accumulation as micro-
- Chemicals of plant origin
or macrovesicles, accompanied by lymphocytes in a perivascular array
- Corticosteroids
in the superficial dermis and exocytosis of lymphocytes into the epi-
- Wound dressing components
dermis. There is usually focal parakeratosis. In the subacute phase,
• Patients with chronic venous insufficiency
often exhibit multiple contact allergies
spongiosis is still evident, but may be more subtle and intraepidermal
vesicles are less prominent. The epidermis thickens variably and para-
Irritant contact • The exudate from draining ulcers leads to keratosis is present (see Fig. 13.6B). Lymphocytes persist in the dermis
dermatitis maceration, increased inflammation, and and epidermis. In both acute and subacute stages, edema may be
bacterial colonization of surrounding skin present in the papillary dermis.
• Infectious eczematous dermatitis may occur In the chronic phase, thickening of the epidermis is more pronounced
*More commonly, irritant contact dermatitis. and it occurs in a regular, psoriasiform pattern or, more often, has a
more irregular profile. Inflammation and spongiosis are mild and may
Table 13.2 Pathogenetic factors in stasis dermatitis.
be absent. Changes in the granular layer are variable, from thickening,
simulating lichen simplex chronicus, to thinning, where the pattern
more closely approaches psoriasis; the latter is seen more often in num-
mular eczema. Ascribing a specific cause of the dermatitis based upon
Contact sensitization often leads to secondary dissemination. Patches this constellation of histologic findings is impossible, although indi-
of eczema arise in a strikingly symmetric distribution pattern, particu- vidually necrotic keratinocytes suggest the diagnosis of an irritant
larly on the anterior aspect of the contralateral leg, the anterior thighs dermatitis.
and the extensor surface of the upper extremities (Fig. 13.7); lesions In stasis dermatitis, biopsy specimens display the histologic features
may generalize to involve the trunk and face. just outlined, as well as signs of venous hypertension: dilated capillaries
surrounded by cuffs of fibrin, hemosiderin deposits, and hyperplastic
Pathology (and at times thrombotic) venules (Fig. 13.8). In later stages, there is
236 The histologic features of eczema, including stasis dermatitis, vary fibrosis of the dermal connective tissue and sclerosis of the adipose
according to the stage of the lesion. In acute eczematous eruptions, tissue (see Ch. 100).
SECTION

3 DIFFERENTIAL DIAGNOSIS OF DERMATITIS OF THE FOOT


PAPULOSQUAMOUS AND ECZEMATOUS DERMATOSES

Allergic contact dermatitis (footwear dermatitis)


• Dermatitis of the dorsal aspects of the feet and toes (allergen contained
in the “top” of the shoes)
• Dermatitis of the weightbearing areas of the soles (allergens contained
in the sole of the shoes)
• Most common allergens: dichromate, rubber accelerators, colophony,
dyes, formaldehyde resins; also consider topical antibiotics, e.g.
bacitracin
• Association with atopy and hyperhidrosis
• Distinguish from sock and stocking dermatitis where lesions extend
more proximally (popliteal area, thighs) – most common allergen is azo
dyes
Tylosis
• Mechanically induced hyperkeratosis, dryness, and fissuring
$ • Predilection sites: heels and weightbearing areas of the soles
• In middle-aged to elderly individuals
• Associated with obesity and hyperhidrosis
Acquired plantar keratoderma (keratoderma climactericum)
• Same as tylosis but more intense
• Typically occurs in women over the age of 45 years, but may also be
seen in men
• Similar lesions may appear on palms
Juvenile plantar dermatosis
See section in this chapter
Tinea pedis (athlete’s foot)
• Dermatophyte infections of the plantar skin are usually accompanied by
involvement of the interdigital spaces as well as lateral aspects of the
foot
• Often symmetric, accompanied by onychomycosis
• Lesions on the lateral and dorsal aspects of the feet have well-
demarcated circinate borders
• Occasionally vesicular variant
Psoriasis (see Ch. 8)
• Well-circumscribed plaques or diffuse erythema with thick adherent
% scales, dryness, and fissuring
• Psoriatic plaques found elsewhere on the body
Fig. 13.9 Dyshidrotic eczema. A Clinically, firm vesicles are seen along the side • Nail involvement, e.g. pitting and oil-drop changes
of the thumb and thenar eminence. Some of them are deep-seated. B
Histopathologically, spongiosis within the epidermis is accompanied by Dyshidrotic eczema
macrovesicles; the thickened stratum corneum points to an acral location. A, See section in this chapter
Courtesy, Louis A Fragola, Jr, MD; B, Courtesy, Lorenzo Cerroni, MD.
Recurrent focal palmar and plantar peeling
• Probably represents a mild form of dyshidrosis
• Dry, circinate, thin scales of palms and soles
from the primary site. Lastly, this disease should not be confused with • Vesicles are absent
HTLV-associated infective dermatitis (see above). Pustulosis of the palms and soles (see Ch. 8)
• A neutrophilic dermatosis, possibly related to pustular psoriasis
Juvenile Plantar Dermatosis • Chronic course with crops of non-pruritic, short-lived, superficial
pustules, particularly of the instep
• Yellow–brown macules admixed with pustules
Synonyms: ■ Atopic winter feet ■ Forefoot dermatitis ■ Dermatitis
plantaris sicca ■ Moon-boot foot syndrome ■ Sweaty sock dermatitis Sézary syndrome (see Ch. 120)
• Palms and soles are tender and exhibit scaling, which can be quite
thick
• Associated with hypertrophic onychodystrophy and erythroderma
Key features Other
■ Dry, scaly, glazed and fissured plantar surface of the forefoot • Atopic dermatitis
■ Prepubertal children are affected • Irritant contact dermatitis (e.g. due to occlusive footwear)
■ Association with atopy and exogenous factors • Pityriasis rubra pilaris
• Acrokeratosis paraneoplastica
• Keratoderma blennorrhagicum
• Inherited palmoplantar keratodermas (see Ch. 58)
Introduction • Palmoplantar keratoderma associated with hypothyroidism
The feet are a fairly common site for various eczematous dermatoses
• Crusted scabies
(Table 13.4). Juvenile plantar dermatosis is a characteristic condition Table 13.4 Differential diagnosis of dermatitis of the foot.
238 that occurs primarily (but not exclusively) in children with an atopic
diathesis.
CHAPTER
History Treatment
Juvenile plantar dermatosis was first reported by Mackie and Husain54. Juvenile plantar dermatosis is a chronic but self-limiting condition.
13
Patients should be advised to avoid wearing impermeable socks and

Other Eczematous Eruptions


Epidemiology shoes, and the application of emollients, keratolytics, and/or paraffin-
Juvenile plantar dermatosis occurs in prepubertal children, from the type ointments is beneficial. When shoes are removed, socks, if damp,
age of 3 years and upwards, when shoes are worn for longer periods of should also be removed and replaced by dry socks.
time. It is only rarely seen in adults. There is seasonal variation, with
worsening during the winter, and boys are affected slightly more often
than girls. Diaper Dermatitis
Pathogenesis
An atopic disposition is clearly a risk factor, but exogenous factors play Key features
an equally important role, including plastic- and rubber-constructed ■ Frequently, an irritant dermatitis of the diaper area due to
sports shoes that youngsters often wear all day long. The humid envi- occlusion and prolonged exposure to urine and feces
ronment leads to hydration of the horny layer, making it much less
resistant to wear and tear. When the stratum corneum is rubbed off by ■ Secondary infection with Candida albicans often occurs
friction, this leads to a characteristic glazed and thinned appearance of ■ May be associated with seborrheic dermatitis and psoriasis
the skin. As involved areas become xerotic, cracks are formed. The
inherently dry skin of atopic individuals may be a predisposing factor.
Adults have a much thicker horny layer of their plantar skin and are
thus less at risk of developing the condition. Epidemiology
Diaper dermatitis develops in at least 50% of infants, and it is respon-
Clinical features sible for a considerable percentage of dermatologic consultations in
The balls of the feet and the toe pads exhibit strikingly symmetrical infants and toddlers. Seborrheic dermatitis is a predisposing factor.
changes: fairly well demarcated shiny, reddish, tender, dry lesions with
some scaling (Fig. 13.10), and often accompanied by painful cracks Pathogenesis
and fissures. The dorsa of the feet, the interdigital spaces and the Diaper dermatitis is the cumulative result of several factors, in particu-
instep are typically spared. Less often, similar lesions are found on lar dampness and exposure to urine and feces. In the past, ammonia
the hands. derived from the urea in urine was held as primarily responsible for
diaper dermatitis. More recently, the blame has been placed on the
Pathology (alkaline) pH of the urine and the role of fecal bacteria. Enzymes pro-
Histologically, the features of a chronic dermatitis are seen (see section duced by fecal bacteria, as well as residual pancreatic proteases and
“Stasis dermatitis”). lipase in the stool, act as irritants and these enzymes are also activated
in the alkaline milieu55,56. In addition, ureases are produced by fecal
Differential diagnosis bacteria, resulting in a further increase of the urinary pH. This explains
Juvenile plantar dermatosis needs to be distinguished from allergic why diaper dermatitis is more likely to appear in cow milk-fed than in
contact dermatitis to chemicals contained in leather (e.g. chromates, breast-fed infants: cow milk formulas are colonized by a greater number
dyes) or rubber. However, the latter is rare in children and, if present, of urease-producing bacteria57.
often involves the dorsa of the feet as well. Tinea pedis is equally Prolonged use of diapers, dampness, and the factors detailed above
uncommon in children, and the interdigital spaces are usually predomi- lead to the breakdown of the horny layer barrier function. An alkaline
nantly affected. Patch testing and KOH preparations may help in estab- pH also facilitates the development of secondary C. albicans
lishing the diagnosis. infection.
As diaper dermatitis tends to be most prominent on the inner parts
of the thighs, genitalia and buttocks, friction between the skin and the
diaper material likely acts as a physical factor that leads to further
irritation. In addition, chemical constituents of the diaper and/or
topical preparations and baby wipes may lead to contact
sensitization.

Clinical features
Diaper dermatitis is strictly confined to the diaper area, presenting with
mild to pronounced erythema, erosions, and scaling. In the common
form due to irritant contact dermatitis, genitocrural folds are typically
spared. Depending on whether there is a secondary infection or an
underlying dermatosis (e.g. seborrheic dermatitis, psoriasis), the clini-
cal picture can vary (Fig. 13.11).

Differential diagnosis
The differential diagnosis is outlined in Fig. 13.11.

Treatment
In the acute phase, mild corticosteroid preparations are helpful. Topical
imidazole creams are added for secondary infection with Candida spp.
The major goal of long-term management is avoidance of the causative
factors. Frequent changing of highly absorbent disposable diapers is
associated with a lower incidence and severity of diaper dermatitis, and
it leads to a more physiologic pH58. Emollients containing white paraf-
Fig. 13.10 Juvenile plantar dermatosis in a child. Erythema and scaling of the fin (Vaseline®) or soft zinc pastes provide both protective and soothing
plantar surface of the great toes and fifth toes as well as the ball of the foot effects.
bilaterally. Note the glazed appearance of the skin of the left foot. Courtesy, Kalman 239
Watsky, MD. For additional online figures visit www.expertconsult.com
Online only content
CHAPTER
eFig. 13.1 Adult
seborrheic dermatitis of
the face and scalp. Note
13

Other Eczematous Eruptions


the diffuse scaling of the
scalp in addition to
erythema of the
forehead.

eFig. 13.2 Seborrheic dermatitis-like eruption due to dermatomyositis. This


patient presented with severe pruritus of the scalp. In addition to the scalp
involvement, she had Gottron papules and a photodistributed poikiloderma.
Courtesy, Jeffrey P Callen, MD.

eFig. 13.3 Asteatotic


eczema (eczema
craquelé). A The distal
lower extremity has areas
of dull erythema that
contain a criss-cross
pattern of superficial
cracks and fissures said to
resemble a dried river
bed. B A close-up of the
pattern.

eFig. 13.4 Nummular dermatitis.


%

239.e1
Online only content
SECTION
eFig. 13.5 Differential diagnosis of the “red leg”.
3 DIFFERENTIAL DIAGNOSIS OF THE “RED LEG”
PAPULOSQUAMOUS AND ECZEMATOUS DERMATOSES

Approach to the “red leg”

• Signs of chronic venous hypertension


• Edema +/or lymphedema
• Possible history of deep vein thrombosis

Stasis dermatitis Cellulitis Acute lipodermatosclerosis (LDS)

• Erythema with scale-crust • Fever, chills • Signs of chronic LDS − dull


• Pruritus • ↑ WBC or left shift pink to red−brown
• Often bilateral unless *
• Entry site (e.g. trauma ) color with induration
only one leg at risk • Rapidly expanding • No fever, chills, ↑ WBC
• No fever, chills, tender erythema or left shift
↑ WBC or left shift • Lighter shade than cellulitis

* may not have leg at risk

eFig. 13.7 Infectious


eczematous dermatitis.
Crusting and scaling at
the periphery of otitis
externa due to
Staphylococcus

eFig. 13.6 Dyshidrotic eczema. Firm papules and pseudovesicles on the palms
and volar sides of fingers. Annular collarette-like scaling in the dyshidrosis
lamellosa sicca (keratolysis exfoliativa) variant.

239.e2
SECTION

3 DIFFERENTIAL DIAGNOSIS OF DIAPER DERMATITIS


PAPULOSQUAMOUS AND ECZEMATOUS DERMATOSES

Common Less common Rare

Irritant contact dermatitis Bacterial infections Acrodermatitis


• Glazed erythema ± scale “punched out” erosions Bullous impetigo enteropathica, other forms
• Favors convex surfaces, often spares folds • Flaccid bullae, vesiculopustules, of “nutritional dermatitis”
• Prolonged contact with urine/feces (esp. if diarrhea), superficial shiny red erosions with
friction a collarette of scale
• Over time pseudoverrucous papules can develop • Gram stain +

Streptococcal perianal dermatitis


& intertrigo
• Sharply demarcated, bright red
erythema
• Usually no satellite lesions
• Perianal area, skin folds
• Pain, itch, foul odor
• ± Pharyngitis in patient or family Langerhans
members cell histiocytosis

Candidiasis Psoriasis
• Intense erythema with • Well-demarcated erythematous
desquamation/superficial plaques
erosions & peripheral • Shiny in folds, scaly on convex
scale/collarettes surfaces
• Satellite pustules • Psoriasiform lesions elsewhere,
• Favors folds, genitalia ± family history
• Yeast/pseudohyphae on
KOH preparation
• ± Recent antibiotic use, Other infections (e.g.
thrush congenital syphilis,
Allergic contact dermatitis* dermatophytosis)
• Consider if fails to respond to usual therapy
• “Holster” distribution if reaction to rubber additives in diaper elastics
Seborrheic dermatitis • May affect folds if reaction to components of baby wipes or topical
• Well-demarcated, preparations
Granular
salmon-colored to red, parakeratosis
moist or scaly patches
and plaques
• Favors folds Atopic dermatitis (AD)
• Involvement of other • Excoriations, lichenification
flexural sites, scalp • Favors skin at diaper margins and convex surfaces
• Often relative sparing of the diaper area Early Kawasaki
• Marked pruritus disease
• Other pruritic eczematous lesions in usual sites of AD

Fig. 13.11 Differential diagnosis of diaper dermatitis. While the most common etiologies are irritant contact dermatitis, cutaneous candidiasis and seborrheic
dermatitis, patients often have a combination with one disorder superimposed on another. Discrete papules or nodules are seen in scabies, granuloma gluteale
infantum and perianal pseudoverrucous papules, whereas congenital syphilis often presents with erosions and even ulcerations. *Potential allergens include
sorbitan sesquioleate (an emulsifier in diaper balms), fragrances, disperse dyes, rubber additives (e.g. mercaptobenzothiazole), and preservatives in baby wipes (e.g.
iodopropynyl butylcarbamate). Insets: Courtesy, Robert Hartman MD; Julie V Schaffer, MD.

REFERENCES
1. Unna PG. Das seborrhoische Ekzem. Monatsschr Prakt 7. Faergemann J. Pityrosporum species as a cause of dandruff, and seborrheic dermatitis. J Invest Dermatol
Dermatol 1897;6:827–46. allergy and infection. Allergy 1999;54:413–19. 1975;64:401–5.
2. Shuster S. The aetiology of dandruff and the mode of 8. Gupta AK, Kohli Y, Summerbell RC, et al. Quantitative 13. Parry ME, Sharpe GR. Seborrhoeic dermatitis is not
action of therapeutic agents. Br J Dermatol culture of Malassezia species from different body sites caused by an altered immune response to Malassezia
1984;111:235–42. of individuals with or without dermatoses. Med Mycol yeast. Br J Dermatol 1998;139:254–63.
3. Faergemann J. Management of seborrheic dermatitis 2001;39:243–51. 14. Faergemann J, Bergbrant IM, Dohse M, et al.
and pityriasis versicolor. Am J Clin Dermatol 9. Nakabayashi A, Sei Y, Guillot J. Identification of Seborrhoeic dermatitis and Pityrosporum (Malassezia)
2000;1:75–80. Malassezia species isolated from patients with folliculitis: characterization of inflammatory cells and
4. Xu J, Saunders CW, Hu P, et al. Dandruff-associated seborrhoeic dermatitis, atopic dermatitis, pityriasis mediators in the skin by immunohistochemistry. Br J
Malassezia genomes reveal convergent and divergent versicolor and normal subjects. Med Mycol Dermatol 2001;144:549–56.
virulence traits shared with plant and human fungal 2000;38:337–41. 15. Sullivan AK, Raben D, Reekie J, et al. Feasibility and
pathogens. Proc Natl Acad Sci USA 2007;104:18730–5. 10. Pechere M, Kirscher J, Remondat C, et al. Malasezzia effectiveness of indicator condition-guided testing for
5. Maietta G, Fornaro P, Rongioletti F, et al. Patients with spp carriage in patients with seborrheic dermatitis. J HIV: results from HIDES I (HIV indicator diseases across
mood depression have a higher prevalence of Dermatol 1999;26:558–61. Europe study). PLoS ONE 2013;8(1):e52845.
seborrhoeic dermatitis. Acta Derm Venereol 11. Ostlere LS, Taylor CR, Harris DW, et al. Skin surface lipids 16. Burton JL, Cartlidge M, Cartlidge NEF, Shuster S. Sebum
1990;70:432–4. in HIV-positive patients with and without seborrheic excretion in Parkinsonism. Br J Dermatol 1973;88:
6. Nenoff P, Reinl P, Haustein UF. Der Hefepilz Malassezia. dermatitis. Int J Dermatol 1996;35:276–9. 263–6.
240 Erreger, Pathogenese und Therapie. Hautarzt 12. McGinley KJ, Leyden JJ, Marples RR, Kligman AM. 17. Cowley NC, Farr RM, Shuster S. The permissive effect of
2001;52:73–86. Quantitative microbiology of the scalp in non-dandruff, sebum in seborrhoeic dermatitis: an explanation of the
CHAPTER

EYELID DERMATITIS – DIFFERENTIAL DIAGNOSIS AND MOST COMMONLY ASSOCIATED ALLERGENS 14

Allergic Contact Dermatitis


DIFFERENTIAL DIAGNOSIS
Endogenous

• Atopic dermatitis – lichenification


common
• Seborrheic dermatitis – scaling of
eyelid margins & accentuated in
creases
• Ocular rosacea – eyelid margin
• Dermatomyositis >> cutaneous lupus
– may have associated edema

Exogenous Allergens most commonly associated with ACD of the eyelids*

• Allergic contact dermatitis (ACD) – • Fragrances, including Myroxylon pereirae (balsam of Peru)
occasionally airborne • Preservatives – quaternium-15, DMDM hydantoin,
• Irritant contact dermatitis (ICD) methylchloroisothiazolinone, methyldibromoglutaronitrile
– topical medications (e.g. for acne), • Topical antibiotics – neomycin
anti-aging creams, cosmetics, • Metals – nickel, cobalt chloride, gold sodium thiosulfate
occupational exposures • Surfactants – cocamidopropyl betaine, amidoamine

*Adapted from North American Contact Dermatitis Group (2003–2004); Dermatitis. 2007;18:78–81.
Table 14.2 Eyelid dermatitis – differential diagnosis and most commonly associated allergens. There is often a
combination of endogenous plus exogenous causes. This patient had allergic contact dermatitis to neomycin.

COMPONENTS OF THE AMERICAN CONTACT DERMATITIS SOCIETY (ACDS) SCREENING SERIES (2013), THE T.R.U.E. TEST® SERIES, THE
AUSTRALIAN BASELINE SERIES, THE EUROPEAN BASELINE SERIES, AND THE NORTH AMERICAN CONTACT DERMATITIS GROUP (NACDG) 70

ACDS series T.R.U.E. Australian European


®
Allergen/hapten Conc/vehicle (2013) TEST baseline baseline NACDG 70
2-Bromo-2-nitropropane-1,3-diol (Bronopol®) 0.5% pet
Bacitracin 20% pet
Black rubber mix^ 0.6% pet
Budesonide 0.1% pet 0.01% pet
Carba mix 3% pet
Cobalt chloride 1% pet
Colophony (colophonium) 20% pet
Diazolidinyl urea 1% pet
Epoxy resin (bisphenol A) 1% pet
Ethylenediamine dihydrochloride 1% pet
Formaldehyde 1% aq 2% aq
Fragrance mix I 8% pet
Gold sodium thiosulfate 2% pet
Hydrocortisone-17-butyrate 1% pet
Imidazolidinyl urea 2% pet
Mercapto mix 1% pet 2% pet 2% pet
Mercaptobenzothiazole (MBT) 1% pet 2% pet
Methylchloroisothiazolinone/methylisothiazolinone 110 ppm aq 0.01% aq 200 ppm aq
Methyldibromoglutaronitrile 0.5% pet 2% pet*
Myroxylon pereirae resin (balsam of Peru) 25% pet
Neomycin 20% pet
Nickel sulfate 2.5% pet 5% pet 5% pet
^N-isopropyl-N′-phenyl PPD, N-cyclohexyl-N′-phenyl PPD, and N,N′-diphenyl PPD.

*Methyldibromoglutaronitrile combined with phenoxyethanol.


Table 14.3 Components of the American Contact Dermatitis Society (ACDS) Screening Series (2013), the T.R.U.E. TEST® Series, the Australian Baseline Series,
the European Baseline Series, and the North American Contact Dermatitis Group (NACDG) 70. The concentrations and vehicles are used in the ACDS Series
unless otherwise noted. Conc, concentration. aq, aqueous; pet, petrolatum; ppm, parts per million. 247
Continued

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