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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5192_Библиотеки_им_академика_М_И_Перельмана.pdf
3.1 Papulosquamous Dermatoses
• Diffuse eruption (begins hours to weeks later): oval
patches/plaques on trunk and proximal extremities
■
Lesions appear similar to “herald patch,” but smaller
■
Vertical axes oriented along Langer’s lines (“Christmas
tree pattern”)
■
25% experience signicant pruritus
• Atypical PR: term utilized when rash has unusual features,
including:
■
Inverse PR pattern: prominent involvement of
intertriginous sites, or more prominent involvement of
limbs (.trunk)
■
Papular, vesicular, or targetoid morphology
PR is often more papular and extensive in African
American children
■
Oral involvement (e.g., ulceration)
• Drug-induced PR-like eruptions: ↑ inammation/pruritus,
lacks herald patch; older patient population
Histopathology
• Nonadherent thin mounds of parakeratosis (vs. thicker,
adherent mounds in guttate psoriasis), spongiosis,
perivascular lymphohistiocytic inltrate, and RBC
extravasation
Treatment
• Not required; symptomatic treatment w/ topical CS,
antipruritic lotions
• Oral erythromycin hastens clearance; NB-UVB for tough cases
Prognosis/clinical course
• Self-limited (6–8 weeks)
• Drug-induced PR-like eruptions resolve rapidly
(,2 weeks) after discontinuing drug
Intertriginous/axillary granular
parakeratosis
• Adult women . infants (diaper area)
• Pruritic, keratotic red-brown papules and plaques in
intertriginous areas (axillae . inguinal, inframammary)
• Possible defect in laggrin metabolism → retention of
keratohyalin granules in SC
■
Alternative theories: irritant dermatitis, reaction to
deodorants/antiperspirants
• Histology: characteristic thickened eosinophilic SC w/
prominent parakeratosis and retained keratohyalin
granules; vascular ectasia (Fig. 3.4)
• Can be chronic/recurrent
• Rx: topicals (CS, vitamin D analogs, keratolytics, and
antifungals), destructive (cryotherapy), and systemic
(isotretinoin, antifungals)
Erythroderma
Epidemiology
• M . F, average age 5 50 yo
Clinical features
• Erythema and scale involving more than 90% BSA
• Not a dened entity, but rather a clinical presentation of
various disorders (Box 3.1), characterized by:
■
Pruritus (.90% of cases, especially atopic dermatitis
[AD] or Sézary); lichenication (.30%);
dyspigmentation (.50%); PPK (30%); nail changes
(40%, typically “shiny nails”)
■
Other skin ndings: Staphylococcus aureus
colonization, eruptive seborrheic keratoses, ectropion,
and conjunctivitis
■
Systemic ndings: peripheral lymphadenopathy
(#1 extracutaneous nding), hepatomegaly
(20%), pedal/pretibial edema (50%), tachycardia
(40%), thermoregulatory disturbances
(hyperthermia . hypothermia), hypermetabolism,
and anemia
• Primary (erythema involves whole skin surface in days to
weeks) versus secondary (generalization of localized skin
disease)
Box 3.1 Causes of Erythroderma (SCALP-ID mnemonic)
S Sézary syndrome, Seborrheic dermatitis, Scabies
C CTCL, Contact dermatitis, Chronic actinic dermatitis
A Atopic dermatitis
L Leukemia/lymphoma, Lichen planus, LCH
P Psoriasis, PRP, Pemphigus/pemphigoid, Paraneoplastic
I Infection (HIV, SSSS), Idiopathic, Ichthyoses, Immunodeciencies
D Drug reactions, Dermatitis
A B
Fig. 3.4 (A) and (B) Axillary granular parakeratosis. Marked, compact parakeratosis with small bluish granules within the stratum corneum representing keratohyalin
granules. (Courtesy of Olayemi Sokumbi, MD.)
85
CHAPTER 3 • General Dermatology
• Causes:
■
Psoriasis (most common cause in healthy patients):
Usually preceded by typical plaques
25% are idiopathic; less scaly than typical psoriasis
lesions
Erythroderma is usually due to drug withdrawal
(steroid, MTX, or cyclosporine A)
Nails w/ characteristic psoriasis ndings
Histologically, changes of early psoriasis seen
■
Atopic dermatitis:
Typically have atopic history
Severe pruritus and lichenication
↑ Serum IgE and eosinophilia
■
Drug reactions:
Most common cause in HIV patients (40% vs. 23%
in non-HIV patients)
Lesions may become purpuric in the ankles and feet
Shorter duration than other erythrodermas (resolves
2–6 weeks after drug withdrawal, except in DRESS)
Most common drugs: allopurinol, sulfa (TMP-SMX,
dapsone), antiepileptics, isoniazid (INH), minocycline,
and highly active antiretroviral therapy (HAART)
■
Idiopathic erythroderma: elderly men w/ relapsing course
Lymphadenopathy (70%), PPK, and peripheral
edema seen frequently
■
Cutaneous T-cell lymphoma (CTCL) (Sézary and
erythrodermic mycosis fungoides [MF]):
Sézary: primary erythroderma; T-cell clone in blood
plus one of the following: (1) $ 1000 Sézary cells/
mL; (2) CD4:CD8 ratio of $ 10:1; or (3) ↑
percentage of CD41 cells w/ abnormal phenotype
(loss of CD7 or CD26)
Erythrodermic MF: secondary erythroderma; due to
progression from classic MF patches/plaques
■
Less common causes: PRP (salmon-orange color,
follicular keratotic papules on extensors, islands of
sparing), graft-versus-host disease (GVHD),
paraneoplastic erythroderma (usually lymphomas),
papuloerythroderma of Ofuji, chronic actinic
dermatitis, bullous dermatoses, and ichthyoses
(congenital ichtyiosiform erythroderma/non-bullous
congenitcal ichthyosiform erythroderma, epidermolytic
ichthyosis/bullous congenital ichthyosiform
erythroderma, Netherton syndrome)
Treatment
• Initial management: nutritional assessment, uid and
electrolyte correction; prevention of hypothermia;
treatment of secondary infections
• Tailor treatment to underlying condition: sedating
antihistamines, topical and/or systemic steroids (caution
when tapering; may need systemic steroids in drug reactions
and idiopathic presentation), wet dressings, and emollients
Conuent and reticulated
papillomatosis (CARP)
• Starts at puberty; F . M; Blacks . Whites
• Unknown etiology
• Red or brown, rough, keratotic, slightly raised
papules that rst appear in intermammary region →
Fig. 3.5 Conuent and reticulated papillomatosis. Multiple hyperpigmented papules that are conuent centrally and assume a reticulated pattern laterally. (From
James WD, Elston DM, McMahon PJ. Pityriasis rosea, pityriasis rubra pilaris, and
other papulosquamous and hyperkeratotic diseases. In: Andrews’ Diseases of
the Skin: Clinical Atlas . Philadelphia: Elsevier; 2018:139–151.)
spreads outward and forms reticulated pattern (Fig. 3.5)
laterally
• Histology: acanthosis nigricans-like (hyperkeratosis,
acanthosis, and papillomatosis)
• ToC: minocycline 100 mg BID 3 6 weeks (effective in 50%)
■
Other options: oral retinoids, oral antibiotics, or
topical antifungals
• Pseudoatrophoderma colli: variant that occurs on neck;
appears as vertically oriented hyperpigmented papillomatous
lesions w/ wrinkling; also responsive to minocycline
3.2 ECZEMATOUS DERMATOSES
Atopic dermatitis (AD)
Epidemiology
• Part of atopic triad: AD (often rst manifestation),
allergic rhinitis, and asthma
• More common in high-income and urban areas
(exposure to pollutants and lack of exposure to infectious
agents may → AD development)
• Affects 25% of children, 3% of adults; increasing in prevalence
• Subsets:
■
Early onset (most common): arises by 1 to 2 yo, 50%
have allergen-specic IgE antibodies, 60% resolve by 12 yo
■
Late onset: arises after puberty
■
Senile onset: arises after 60 yo
• Onset: 50%–60% by rst year of life (often 3–6 months),
90%–95% by 5 yo
Pathogenesis (Fig. 3.6)
• Complex interaction of epidermal barrier dysfunction,
immune dysregulation, and microbiome alteration
(e.g., AD skin signicantly more likely to be colonized by
S. aureus)
• Genetic factors are important
■
Twin studies (monozygotic . dizygotic concordance)
and family history (high probability that one or both
parents are atopic)
86
ATOPIC DERMATITIS: EPIDERMAL BARRIER DYSFUNCTION,
IMMUNE DYSREGULATION, AND ENVIRONMENTAL INFLUENCES
Environmental factors
↑↑ Penetration across skin barrier
Damage to epidermal barrier (e.g. scratching,
proteases)
Activation of immune responses
3.2 Eczematous Dermatoses
Impaired stratum corneum (SC) barrier function
↓
deficiencies →→ abnormal corneocyte
formation and impaired acid mantle (surface pH)
↑↑ Proteases (KLK5, KLK7) →→ corneocyte
dysadhesion
Abnormal lipids: impaired lamellar body and
lipid processing →→ ↑↑ SC permeability
Impairment of epidermal
barrier function
Immune dysregulation
Innate and adaptive responses to
environmental stimuli
Altered skin
microbiome
↑ S. aureus
↑
Adaptive
Innate
Allergens
Keratinocyte-derived
pro-Th2 and pro-innate
lymphoid cell (ILC) cytokines
TSLP, IL-1, IL-25, IL-33
Acute
Th2 responses:
IL-4, IL-5, IL-13, IL-31
IgE
Includes innate
lymphoid cells (ILC)
Irritants
Th1Th2
Th22 responses
Th17
Chronic
Th1, Th17,
Th22
Fig. 3.6 Atopic dermatitis results from defects in epidermal barrier function, immune dysregulation, and environmental inuences. KLK, Kallikrein; TEWL, transepidermal
water loss; TSLP, thymic stromal lymphopoietin. (Courtesy of Harvey Lui, MD. From McAleer MA, O’Regan GM, Irvine, AD. Atopic dermatitis. In: Bolognia JL, Schaffer
JV, Cerroni L. Dermatology. 4th ed. Philadelphia: Elsevier; 2018:208–227.)
■
Genes encoding epidermal proteins (e.g., FLG and SPINK)
Filaggrin (FLG) mutations (loss of function) cause
alterations in epidermal barrier (e.g., terminal
differentiation, ↓epidermal barrier proteins,
abnormal lipid organization); strongest genetic risk
factor a/w AD development; a/w severe disease,
early-onset AD that continues to adulthood, hand
dermatitis, food allergy
SPINK5 (encoding serine protease inhibitor LEKT1)
mutations → barrier alterations as well due to Dsg1
Th2 cytokines → ↓ laggrin, loricrin, involucrin; ↑ IL-31
(important in pruritus) and ↑ IL-17
Acute AD: Th2 predominance w/ eosinophilia,
↑ IgE production, and ↓ cutaneous antimicrobial
peptides (e.g., b-defensin 2/3)
Chronic AD: Th1 (and Th22) predominance w/
↑ IL-1, IFN-g
• Mediators of itch
■
Histamines less important than neuropeptides,
proteases, kinins, and certain cytokines
degradation
Barrier dysfunction causes transepidermal water loss
and xerosis, allowing penetration of allergens/irritants
■
↑ Transcription of genes encoding immunologic
proteins (TLR2, FCER1A, and DEFB1) and cytokines
(Th2 . Th1 [especially IL-4, IL-5, IL-10, and IL-13]);
Clinical features
• Clinical criteria
■
Essential: pruritus
■
Plus $3 of the following:
History of xerosis
87
CHAPTER 3 • General Dermatology
Personal history of allergic rhinitis or asthma
Onset , 2 yo
History of skin crease involvement (antecubital,
popliteal, ankle, neck, periorbital)
Visible exural dermatitis
• Acute form: erythema, edema, vesicles, oozing, and
crusting
• Subacute and chronic forms: lichenication, papules,
nodules, and excoriations
• Pediatric AD
■
Infantile (birth to 6 months of age)
Acute presentation and clinical features
Favors face, scalp, and extensor surfaces
May have overlap with seborrheic dermatitis
■
Childhood (2 yo to puberty)
Clinical manifestations more chronic in nature,
though acute ares may occur
Favors exures
Diffuse xerosis becomes more prominent
• Adolescent/adult AD (.12 yo)
■
Lichenied plaques . weeping eczematous lesions
■
Prominent involvement of exures, face, neck
(retroauricular), upper arms, back, acral sites
■
AD beginning during childhood is a/w more severe,
treatment-resistant disease as adults
■
May manifest as isolated prurigo nodularis, hand or
eyelid dermatitis
• Senile AD: marked xerosis rather than typical AD lesions
• Pruritus
■
Worse in evening
■
Triggers: wool clothing, sweat, and stress
• Associated features of AD: xerosis, ichthyosis vulgaris,
keratosis pilaris, palmoplantar hyperlinearity, DennieMorgan lines, periorbital darkening, circumoral pallor,
anterior neck folds, Hertoghe sign (diminished lateral
eyebrows), white dermatographism, follicular
prominence (favors darker skin types), “allergic shiners”
(gray infraorbital discoloration), and exaggerated linear
nasal crease (“allergic salute”)
■
Children have ↑ incidence of: pityriasis alba
(hypopigmentation seen on face/neck; more common
in darker skin types and more visible after sun
exposure), lichen spinulosis, nummular dermatitis,
dyshidrotic eczema, and juvenile plantar dermatosis
• Infectious complications: secondary to impaired barrier
function and immunologic factors
■
Bacterial: impetiginization w/ S. aureus . Streptococcus
pyogenes
■
Viral: eczema herpeticum, molluscum dermatitis, and
eczema vaccinatum (seen w/ smallpox vaccination)
• Ocular complications: atopic keratoconjunctivitis
(adults), vernal keratoconjunctivitis (children, warm
climates), posterior subcapsular cataracts, keratoconus
(elongation of the cornea), and retinal detachment
• Comorbidities: asthma, allergic rhinitis, food allergies,
alopecia areata, urticaria, depression, anxiety,
osteoporosis, bone fractures, skin infections
Regional variants
• Ear: erythema/scaling/ssuring under earlobe and
retroauricular region
• Eyelid: lichenication of periorbital skin
• Nipple dermatitis
• Frictional lichenoid eruption: occurs during spring and
summer in boys on the elbows/knees/dorsal hands
(clusters of small 1–2 mm lichenoid papules)
• Hand: may be intrinsic (atopic, psoriasis, dyshidrotic,
hyperkeratotic), extrinsic (irritant or water exposure, or
allergic), or infectious (tinea, S. aureus) in nature
■
Dyshidrotic eczema on lateral ngers and palms:
“tapioca-like,” rm and deep-seated pruritic vesicles
Pathogenesis is multifactorial (irritant, atopic, and
allergic contact)
Often chronic and recurrent/relapsing
• Diaper (napkin dermatitis; see Chapter 4)
• Id reactions (autosensitization)
■
Classic example: a vesicular eczematous id reaction of the
hands arising in a patient w/ tinea pedis; secondary id
reaction resolves when underlying dermatosis is treated
• Juvenile plantar dermatosis (see Chapter 4)
• Lip (cheilitis sicca): irritant contact dermatitis (ICD;
including “lip-licker’s eczema”) . allergic contact
dermatitis (ACD; fragrance mix most commonly) . AD
. eczema of unknown cause
■
Worse in winter; vermilion lip most affected
• Head and neck: occurs post-puberty, Malassezia may aggravate
Histopathology
• Acute: prominent spongiosis, intraepidermal vesicles/
bullae, and perivascular lymphohistiocytic inammation
w/ eosinophils
• Subacute: milder spongiosis w/ ↑ acanthosis; lacks
vesicles
• Chronic: marked irregular to psoriasiform acanthosis
(key feature), minimal to no spongiosis, 1/– dermal
brosis, and hyperkeratosis
Laboratory testing
• IgE not typically helpful
• In some patients, identication of allergens via
uorescence enzyme immunoassays, radioallergosorbent
(RAST) testing, skin prick testing, and atopy patch testing
may be warranted
• Consider testing for food hypersensitivity (eggs, milk,
peanuts, soy, and wheat) in children with severe/refractory
AD and reliable history of immediate reaction, or
worsening dermatitis after ingestion of specic food
■
Food allergy most commonly causes a type I
immediate hypersensitivity reaction
■
10%–15% of children with severe AD have coexistent
food allergies
• Consider testing for aeroallergens (dust mites, pollen,
animal dander, and fungi) in teens/adults w/ severe or
refractory AD on exposed skin surfaces
■
↑ Incidence of airborne allergy w/ ↑ age
Treatment
• Review 2022-2023 atopic dermatitis guidelines published
in the Journal of the American Academy of Dermatology
• Education regarding emollients, short lukewarm baths w/
minimal soap, bleach baths (especially if history of skin
infection), and wet dressings 1/– topical steroids
88
3.2 Eczematous Dermatoses
• Avoid irritants: overheating, wool, sweating, saliva, harsh
soaps, fabric softeners, bubble baths, and smoke
• Treatment ladder that ranges from topical treatments
(steroids, ruxolitinib, crisaborole, and calcineurin
inhibitors) to light therapy (NB-UVB . BB-UVB, UVA1, and
PUVA) to systemics (steroids, cyclosporine, azathioprine
[AZA], mycophenolate mofetil [MMF], MTX, tacrolimus,
dupilumab [anti-IL-4/-13 mab → reduces Th2 response],
tralokinumab [anti-IL-13 mab]) depending on severity
■
Topical CS are mainstay
■
May experience rebound ares after short courses of
systemic steroids
■
Sedative antihistamines as adjunctive treatment for
itch
■
Treat secondary infections (AD skin has ↓ antimicrobial
peptides and a compromised barrier → ↑ infection risk)
• Primary prevention via breastfeeding or formulas w/
hydrolyzed milk products for the rst 4 to 6 months of
life is protective in high-risk AD patients
■
Prenatal, followed by postnatal probiotic
supplementation, and postnatal prebiotic
supplementation, may ↓ risk of AD
Prebiotics 5 non-digestible plant bers/
oligosaccharides that help nourish “good gut
bacteria”
• If true IgE-mediated allergy → practice avoidance or
undergo allergen-specic immunotherapy through allergist
Prognosis/clinical course
• AD tends to clear in most children by puberty
■
Classic teaching: 75% resolve by adolescence
(however, new study suggests that only 50% remit by
early adulthood)
• If disease persists beyond childhood → tends to be
chronic
Asteatotic dermatitis (Eczema craquelé)
• Typically . 60 yo; worse in winter
• In elderly, ↓ natural moisturizing factor → ↓ water-
binding capacity → when humidity is low in winter, get
skin dehydration/xerosis → scaling, cracking, and
dermatitis
• Xerotic skin w/ ne cracking (resembles “cracked
porcelain” → hence eczema craquelé), erythema and scale
1/– oozing, and crusting
• Pruritic; favors lower legs
• Histology: xerosis (compact SC) 1 spongiotic dermatitis
• Rx: emollients to treat xerosis/prevent ares (applied
immediately after bathing); avoid aggravating factors;
topical CS and TCIs for ares
Nummular dermatitis
• Associated factors: external irritants, venous HTN,
infection, atopy, and xerosis
• Round or coin-shaped (“nummular”) pink plaques on
extremities; very pruritic; can have acute (eczematous) or
chronic (lichenied) appearance; tends to be more
recalcitrant
■
Secondary Staphylococcus infection common
• Histology: subacute-chronic spongiotic dermatitis
• Rx: mid- to high-potency topical steroids (ointments
preferable to creams), TCIs, and phototherapy; good skin
care w/ emollients
Progesterone dermatitis
• Cyclic ares of dermatitis during the luteal phase of
menstrual cycle (starts 1 week before menses → resolves
a few days after menses)
• Variable morphology (urticarial, vesicles, and oral erosions)
• Diagnostic test 5 intradermal injection of progesterone
→ skin reaction
• Rx 5 oral contraceptive pills (OCPs) or tamoxifen to
inhibit ovulation
• Estrogen dermatitis (chronic w/ exacerbations just prior
to menses; Rx 5 tamoxifen) is major DDx → intradermal
estrone test distinguishes
Contact dermatitis
Epidemiology
• ICD (80%) . ACD (20%)
• Occupations most affected:
■
Manufacturing/mining (United Kingdom)
■
Agricultural workers (United States)
• Most common causes of ACD:
■
Nickel (worldwide)
■
Poison ivy (United States)
• ICD is the most common form of occupational skin disease
■
Petrochemical, rubber, plastic, metal, and automotive
industries
■
Causes: soaps . wet work . petroleum products
. cutting oils . coolants
• Infants, elderly, and those w/ AD have ↑ risk, due to
↑ penetration of contactants
Pathogenesis
• ICD: direct damage of keratinocytes by irritant; not
immune-mediated, does NOT require previous
sensitization
■
Acute ICD: strong irritants (acids/bases) → direct
cytotoxic damage to keratinocytes
■
Chronic ICD (more common): repetitive use of mild
irritants (soap/water) → over time removes lipid and
water-retaining substances of keratinocytes → ↑
transepidermal water loss, ↑ epidermal turnover,
inammation
■
Frictional irritants: repeated rubbing, vibration, and
pressure
■
Cold temperature, low humidity → ↑ permeability to
irritants
■
Occlusion/maceration/↑ humidity may → ↑
permeability of water-soluble compounds
• ACD: immune-mediated, delayed-type (type IV)
hypersensitivity, initial sensitization to allergen is required
■
Sensitization can occur with just a few exposures, or
after years of exposure
■
Subsequent reexposure to allergen → T-cell mediated
release of cytokines/chemotactic factors → eczema
within 48 hours
89
CHAPTER 3 • General Dermatology
Only need exposure once every 3 weeks to keep
allergic reaction going
■
Cross-reactions and co-reactions can occur:
Cross-reaction: sensitization to one compound
results in sensitization to compounds w/ a similar
chemical structure (e.g., poison ivy and mango
peel; neomycin and gentamicin)
Co-reaction: sensitization to two chemicals
simultaneously because they are contacted/used
together, but otherwise allergy to one would not
result in allergy to the other (e.g., nickel and cobalt;
neomycin and bacitracin)
Clinical features
Irritant contact dermatitis
• Clinical presentation variable; burning may be more
common than itch
• Hands most common site of involvement; face is #2
• Ranges from acute ICD with vesiculation/necrosis that has
more clearly dened margins to chronic ICD w/ dryness,
scaling, lichenication, and ssuring
• Pustular/acneiform irritant ICD: metals, croton oil,
mineral oils, tars, greases, cutting and metal working
uids, and naphthalenes
• Airborne ICD: resembles photoallergic reaction, but
involves upper eyelids, philtrum, and submental region
• Phytophotodermatitis: furocoumarins 1 light (UVA;
320–400 nm) → erythema 1/– blistering (24–72 hours
postcontact) followed by hyperpigmentation (1–2 weeks
later)
■
Berloque dermatitis: pigmentation of neck/trunk/arms
from cologne application containing bergamot oil
(bergapten 5 5-methoxypsoralens; a furocoumarin)
• Can have concomitant ulceration, folliculitis, miliaria,
pigmentary alterations, alopecia, and urticaria
Allergic contact dermatitis
• Acute: erythema/edema/papules/oozing/vesiculation;
sharp demarcation between normal and involved skin
• Subacute: ↑ acanthosis, ↑ crusting/scaling, and
↓ vesiculation
• Chronic: marked lichenication/ssuring/scaling, no
vesicles, less well-dened than acute, and may spread
beyond site of exposure
• Distribution depends on exposure:
■
Linear streaks on extremities: rhus (poison ivy/poison
oak/poison sumac)
■
Fingertips in orists: owers (tulips #1)
■
Scalp is fairly resistant to allergens → often only the
surrounding skin is involved (neck, cheeks, and
postauricular)
Allergens: hair products (especially dyes), perms,
and rinse-off products (shampoo)
■
Perioral/baboon syndrome: avorings, foods,
cosmetics, shellac, meds, and sunscreens
■
Periocular/eyelid:
Nail products (tosylamide . acrylates,
formaldehyde, resin, glutaraldehyde, and
benzalkonium chloride)
Cosmetics (false eyelashes, adhesives, mascara,
rubber sponges for make-up, and eye-shadow)
Other allergens: gold (rings), other metals, volatile
gases, fragrances/balsam of Peru, aminoglycosides
(e.g., neomycin, gentamycin), sodium metabisulte
(excipient in topical antibiotics), anesthetics,
timolol, thimerosal, surfactants, and preservatives
■
Lips: gallates, dyes, avorings, sunscreens, and
propolis
■
Earlobe: nickel
■
Neck: fragrances and hair products
■
Wrist: chromates (leather)
■
Hands: gloves (latex, rubber [thiuram], and acrylates in
medical gloves)
■
Clothing dermatitis: spares the folds (axillary vault)
and is accentuated where clothing ts tightly
(waistline); most common allergens:
Fabric nishers (i.e., antiwrinkle and stain repellant):
formaldehyde and formaldehyde releasers
Dyes (disperse blue dyes 106 and 124)
Rubber (bleached underwear → bleaching causes
release of carbamates)
■
Cosmetics dermatitis: commonly on face/neck;
fragrances are #1 cause, preservatives are second most
common
■
Perianal: lidocaine and preservatives (e.g.,
methylchloroisothiozolinone/methyisothiozolinone
[MCI/MI])
■
Shoe dermatitis: spares toe webs, begins on base of
great toe and spreads over the dorsal surface (plantar
surfaces generally spared)
Causes: adhesives (colophony, p-tert-butylphenol
formaldehyde resin), rubber and rubber accelerators
(mercaptobenzothiazole), leather (chromates), and
dyes
■
Ulcers: bacitracin, neomycin, and lanolin
■
Oral stomatitis: dental llings (mercury/gold/amalgam
→ lichenoid reaction), epoxy resins, and avoring
(mint/cinnamon)
■
Airborne ACD: usually from plants (Compositae 5 #1
cause), but other chemicals also implicated
■
Systemic ACD: diffuse dermatitis due to systemic
allergen (e.g., systemic dermatitis from IV aminophylline
in patients w/ ethylenediamine sensitivity)
• Occupational ACD: rubber . nickel . epoxy and other
resins . aromatic amines
• Adhesives
■
Most tape reactions are ICD
■
ACD to tape: rubber, resins, and acrylates
Histopathology
• ICD: mild spongiosis, scattered necrotic keratinocytes,
and mild perivascular inammation
• ACD: spongiotic dermatitis (may be acute/subacute/
chronic, depending on stage), more prominent dermal
inammation
■
Versus ICD: ↑ spongiosis, ↑ dermal inammation w/
eosinophils, and lacks necrotic keratinocytes
Laboratory testing
• Patch testing will conrm diagnosis of ACD
■
Tailor the examined allergens to patient; NEVER apply
unknown product during patch testing (can cause
90
severe reaction/burn); determine relevance of any
positive reaction
■
Patches applied to upper back area free of dermatitis
on day 0; patches removed at 48 hours (day 2);
reactions recorded day 2 (rst reading) and days 3–7
(second reading, usually 96 hours)
Reactions that fade between rst and second
readings 5 irritant
Reactions that continue or develop between rst
and second readings 5 allergic
Delayed positive patch tests (arise after 7 days) can
be seen with: gold, neomycin, dodecyl gallate,
palladium, p-phenylenediamine, and CS
Gold can cause a persistent positive reaction at the
site of patch testing
■
TRUE test: currently 3 panels of 12 allergens each
(www.truetest.com)
Not as complete as comprehensive patch testing
• Repeat open application test (ROAT): use if patient cannot
do patch test, or to conrm patch test results
■
Apply product to single clear area of BID for 1 to 2
weeks → monitor for reaction
• Material safety data sheets (MSDS) and workplace visit
can help determine what workers are handling
Specic contactants
Irritant contact dermatitis
• Fiberglass dermatitis
■
Injury via skin penetration → pruritus/tinging → pink
papules
■
Rx: talcum powder
• Bodily uids (e.g., saliva, urine, feces) and water
■
Rx: provide barrier protection (e.g., zinc oxide paste,
improved hygiene)
• Alkalis
■
Strong alkalis are corrosive: dissolve keratin and
penetrate deeply → worse reactions than acids
■
Ca/Na/K hydroxides; ammonia; lye
■
Soap, detergent, bleaches, and depilatories
■
Treatment: apply weak acid (vinegar or lemon juice)
• Acids
■
Powerful acids are corrosive and weaker ones are
astringent (a compound that shrinks or constricts
tissues)
■
Sulfuric acid
Causes severe burns, produces brownish staining
Brass and iron workers, battery makers, jewelers,
weapon of vitriol attacks (“acid throwers”)
■
Nitric acid
Distinctive burns with yellow discoloration
Explosives, fertilizer
■
Hydrouoric acid
Penetrates very deeply due to low dissociation rate →
severe damage to bones, nerves; exquisitely painful;
symptoms may be delayed for up to 24 hours
Used for dissolving/etching glass in semiconductor
industry
Rx: neutralize w/ calcium gluconate gel, seek
emergency care
■
Hydrochloric acid
Supercial burn → produces blisters
3.2 Eczematous Dermatoses
■
Oxalic acid
Paresthesia of ngertips; cyanosis; gangrene
■
Phenol
Used in cosmetic peels
Produces white eschar and temporary anesthesia;
systemic absorption → glomerulonephritis and
arrhythmias
Neutralized by 65% ethyl or isopropyl alcohol
• Plants
■
May cause non-immunologic contact urticaria (CU),
irritant dermatitis (mechanical or chemical),
phytophotodermatitis, and ACD (discussed in Allergic
Contact Dermatitis section)
■
Non-immunologic CU:
Urticaceae family (nettle family): Urtica dioica
♦ Sharp hairs on plants contain toxins (histamine,
serotonin, and acetylcholine) → rapid edema,
pruritus, and burning
■
Mechanical ICD:
Opuntia spp. (prickly pear)
♦ Causes glochid dermatitis: mechanical ICD as a
result of larger spines or smaller glochids
(collections of short barbed hairs) that cause
penetrating injuries → inoculation of Clostridium
tetani, S. aureus, Sporothrix schenckii, and atypical
mycobacteria
♦ Remove larger pieces w/ tweezers; use glue and
gauze for smaller pieces
■
Chemical ICD (Boards favorite!):
Bromelin
♦ Ananas comosus (pineapples)
Calcium oxalate
♦ Family Amaryllidaceae/Liliaceae
Daffodil (Narcissus spp.), hyacinth, and tulip
bulbs
Most common cause of ICD in orists,
“daffodil itch”
♦ Family Araceae
Dumb cane (Dieffenbachia; house plant)
♦ A. comosus
Pineapple (also contains bromelin)
Capsaicin
♦ Family Solanaceae
Hot peppers
Neutralized with acetic acid (vinegar) or antacids
Phorbol esters
♦ Family Euphorbiaceae
Croton plant, spurges, and poinsettias
Also contains diterpenes (latex)
May cause temporary blindness
Protoanemonin/ranunculin
♦ Family Ranunculaceae
Buttercups and marigolds
Classic linear vesicles like
phytophotodermatitis, but NO
hyperpigmentation afterward
Thiocyanates
♦ Family Alliaceae
Garlic
♦ Family Brassicaceae
Black mustard, radish
91
CHAPTER 3 • General Dermatology
■
Phytophotodermatitis
Caused by furocoumarins in plants 1 UVA light
(320–400 nm) (Fig. 3.7)
Apiaceae/Umbelliferae
♦ Hogweed (Heracleum), cow parsley, and wild
chervil: “strimmer dermatitis” after weed
whacking
♦ Parsley, parsnips, celery, and carrots: “harvester’s
dermatitis” in gardeners
♦ Flowers easily identied as they are clustered on a
stalk and arise from a single point (mnemonic:
“Apiaceae/Umbelliferae phytophotodermatitis 5
Ape holding an Umbrella-looking plant to stay
protected from sun”)
Rutaceae
♦ Citrus (lemon, lime, grapefruit), rue
♦ Citrus bergamia (bergamot orange): causes
berloque dermatitis
♦ Pelea anisata (Hawaiian leis)
♦ Common cause in bartenders and spring
breakers
♦ “Mexican beer dermatitis:”
phytophotodermatitis variant that may be
widespread rather than linear, due to
aerosolization of lime-beer mixture
Moraceae
♦ Fig and g leaves
♦ Mulberry
Fabaceae (legumes):
♦ Bavachi/scurf pea (used as vitiligo treatment)
♦ Balsam of Peru (Myroxylon balsamum, Myroxylon
pereiae)
Allergic contact dermatitis
• Specic allergens involved in ACD (Table 3.1)
• ACD due to plants (Table 3.2)
■
Rhus dermatitis: Anacardiaceae family, Toxicodendron
species
Allergen: urushiol (an oleoresin)
♦ Sensitizing ingredient: pentadecylcatechol
Poison ivy/poison oak/poison sumac
♦ Contained in leaves, stems, and roots
Direct contact (plant/ngers) → linear/streaky
erythematous vesicles/bullae
Indirect contact (pet/burning plant) → diffuse
Black lacquer/spot dermatitis: sap from
Toxicodendron species turns black w/ oxidation
in stratum corneum
■
Asteraceae (Compositae; daisy/sunower family):
causes airborne ACD
Unlike photosensitive dermatitis, involves eyelids/
melolabial folds/submental/retroauricular sulci/
antecubital fossae
Classically affects middle-aged men
Worse in summer, resolves in winter
■
Essential oils: cinnamon oil (cassia), eucalyptus oil,
and citrus peel
■
Exotic hardwoods (cocobolo/rosewood): can cause
erythema multiforme (EM)-like reaction
■
Foods: variety of vegetables, fruits, and spices can cause
ACD
■
Photoallergic contact dermatitis
Allergen 1 light (usually UVA) → dermatitis via
immune mechanisms
Treatment
• Gold standard is education and avoidance of allergen/irritant
• Additional treatments similar to other dermatitides
• For ICD, many cases resolve spontaneously due to
“hardening” phenomenon
• After acute ACD exposure (i.e., poison ivy), whole area/
body should be rst washed with water, then soap can be
considered; systemic CS over 3 weeks are very effective
Fig. 3.7 Phytophotodermatitis; the patient had rinsed her hair with lime juice in
Mexico. (From James WD, Berger TG, Elston DM. Dermatoses resulting from
physical factors. In: Andrews’ Diseases of the Skin . 11th ed. Philadelphia:
Elsevier. 2011:18–44.)
92
Stasis dermatitis
• Incompetent valves of lower extremities → venous HTN
→ capillary distention and leak → extravasation of uid,
plasma proteins, and erythrocytes → edema, hemosiderin
deposition, brosis, ulceration, inammation, and
microangiopathy
• Contact sensitization (often from topical products [i.e.,
neomycin] or medicaments), irritant factors, and
superinfection may complicate the picture
• Pitting edema and hemosiderin deposits over distal
third of leg, scaling, inammation, and pruritus or
tenderness; skin changes often begin on medial ankle;
can become lichenied from rubbing
• A/w Lipodermatosclerosis (stasis panniculitis; “inverted
wine bottle” appearance w/ tight circular cuff over distal calf
from chronic inammation → adherent skin/subcutaneous
tissue/fascia; may need danazol or pentoxifylline treatment)
• Atrophie blanche and ulceration from venous changes can
occur (typically medial supramalleolar region)
3.2 Eczematous Dermatoses
Table 3.1 High-Yield Allergic Contact Dermatitis (ACD) Allergens
Metals and metal salts
Pure metals generally do not cause sensitivity; metals in salts more often cause reactions
Nickel
Chromates Sources: dyes (green felt fabric on pool table) , yellow-green pigment (tattoos/cosmetics), leather (shoe dermatitis),
Cobalt Sources: metal products, cosmetics, dyes ( blue-green dyes, paint, tattoos), glass/pottery, cement, vitamin B12 injec-
Mercury Common cause of oral lichenoid reaction (mercury amalgams)
Gold Common cause of oral lichenoid reactions and eyelid dermatitis
Aluminum Sources: sunscreen, cosmetics, dental restorations, food, vaccines, immunotherapy
Rubber and rubber additives
Sources: shoes, gloves, adhesives, elastic (if bleached), pacifiers, cosmetic applicators, latex (gloves, balloons, condoms), swim goggles, tires, fungicides
(thiurams), and neoprene (synthetic rubber)
Latex Derived from Hevea brasiliensis sap
Thiuram (tetramethylthiuram
disulfide)
Carba mix/carbamates Released from bleached elastic; perform use-test (patch test often false negative)
Mercaptobenzothiazole (MBT) #1 cause of allergic shoe dermatitis
Black rubber mix Found in heavy-duty rubber products (tires, rubber balls)
Dialkyl thioureas (neoprene) Wetsuit dermatitis and allergy to goggles
p-phenylenediamine (PPD) Sources: hair dye, black henna (temporary tattoos), black rubber (rubber vulcanization, antioxidant), photograph develop-
Adhesives
Substances used for gluing things together
Rosin (colophony and abietic
acid)
p-tert-butylphenol formaldehyde
resin (PTBP)
Epoxy resin (bisphenol A) Encountered in: PVC and plastic materials, electrical insulation, paint, artists, sculptors, glues
Cyanoacrylates Used for different purposes, depending on specic type
Methacrylate Very hard, rigid plastic; may also be used as adhesive in orthopedic and dental prostheses; isobornyl acrylate is found in
Preservatives
Added to anything with water in order to prevent spoilage; most commonly found in personal care products and cosmetics
Formaldehyde Frequent sensitizer, but decreased cosmetic use recently (formaldehyde releasers now more commonly used)
Most common positive patch test (relevance 50%)
Sources: jewelry (white gold, 14-carat gold), buckles, belts, cell phones, buttons, zippers, clothing hooks, musical instru-
ments, keys, doorknobs, European coins, and cement
Direct relationship between nickel allergy and number of pierced sites
Nickel in foods: cocoa, licorice, margarine, peanuts, brown lentils, walnuts, almonds, hazelnuts, and beans
Nickel testing: dimethylglyoxime in 10% ammonia test (turns pink in presence of nickel)
Safe metals for pts w/ nickel allergy: titanium, platinum, and sterling silver
cement, matches, and crude oils (engine/aircraft workers and photographers)
Cross-reacts w/ nickel and cobalt
tions (can lead to intractable hand dermatitis), and articial joints
Poral reaction: irritant reaction w/ purpuric pores
Cross-reacts w/ nickel and chromate
Cobalt testing: 1-Nitroso-2-naphthol-3, 6-disulfonic acid disodium salt can be used to detect trace cobalt in items
Sources: amalgams (dentistry), insecticides, industry (glues and starch pastes), felt hat workers, etching/artwork, and furs
Sources: jewelry (hand/facial/eyelid dermatitis) and amalgams/llings
Most frequent cause of persistently positive patch test reactions
Cross-reacts w/ nickel and cobalt
Aluminum hydroxide is the most allergenic aluminum salt
Far more likely to cause immunologic contact urticaria (type I hypersensitivity reaction) than type IV delayed-type hyper-
sensitivity reaction
Risk factors: healthcare profession, spina bida
Latex cross-reacts w/ “BACK Passion” (Bananas, Avocado, Chestnut, Kiwi, PASSION fruit)
Most common glove allergy and most common allergen in healthcare workers
Cross-reacts with disulram
May cause purpuric reaction
ment, photocopies, printer ink, other darkly colored cosmetics
Rubber workers p/w eczema of hands, wrists, forearms, eyelids, nose
Uses: de-epilation waxes, adhesives, painting, chewing gum, violin and other musical instruments
Used for gluing together leather products (watchbands, leather handbags, shoes)
Can cause depigmentation
Only produce ACD when in their liquid (non-cured, monomeric) state → fully polymerized product is non-sensitizing
Ethyl cyanoacrylate: KrazyGlue; used to glue-on articial nails ; is more toxic to skin than butyl- and octyl cyanoacrylates
→ not used for skin
Butyl cyanoacrylate (GluStitch): sutureless skin closures
Octyl cyanoacrylate (Dermabond): sutureless skin closures
glucose sensors and insulin pumps
Uses: articial nail plates, hard contact lenses, adhesive (“bone cement”) for articial joints, dental prostheses, dental sealant
Diffuses through rubber and polyvinyl gloves → paresthesias
Found everywhere—meds, textiles/clothing, paints, embalming process, and paper—but most notably wrinkle-free clothing
100% cotton or cotton/synthetic ber blends have most formaldehyde
Polyester has least formaldehyde of any textile
Continued
93
CHAPTER 3 • General Dermatology
Table 3.1 High-Yield Allergic Contact Dermatitis (ACD) Allergens—cont'd
Formaldehyde-releasing
preservatives (chemical
compounds that slowly release
formaldehyde)
Kathon CG
(methychloroisothiazolinone/
methylisothiazolinone (MCI/MI)
Parabens Preservative in topical medications, antiperspirants
Thimerosal (ethyl mercury) Mercury-containing preservative in vaccines, eye-drop solutions, cosmetics, and nasal sprays
Other preservatives 2-bromo-nitropropane-1,3-diol (Bronopol)
Vehicles, emollients, and emulsiers
Propylene glycol Vehicle base in many creams and lotions
Cocamidopropyl betaine Non-ionic surfactant found in shampoo, soaps
Ethylenediamine Found in topical steroid and antifungal creams ( Mycolog)
Lanolin Used in emollients
Propolis Made by bees from resinous exudates of plants
Alkyl glucosides Gentle eco-friendly surfactants used in cosmetic and household products
Fragrances
Fragrance allergy is #1 cause of all cosmetic-related ACD; almost all cosmetics contain fragrance; “fragrance free” ≠ no fragrance (still may have masking
fragrances!); fragrances are used for cologne, perfumes, food flavoring; patch test to balsam of Peru 1 fragrance mix detects 90% of fragrance allergies
Fragrance mix Patch test to mixtures of eight fragrances (cinnamic alcohol, cinnamic aldehyde, amyl cinnamic alcohol, eugenol, isoeugenol,
Balsam of Peru Derived from Myroxylon pereirea tree
Hair products
p-phenylenediamine (PPD) Potent sensitizer!
Perms Alkaline (home) perm: ammonium thioglycolate (rare sensitizer, more likely to cause ICD than ACD)
Hair bleach (contains
ammonium persulfate and
peroxides)
Nail products
Tosylamide (toluene-sulfonamide)
formaldehyde resin
Artificial nails Ethyl cyanoacrylate: KrazyGlue; used to glue-on articial nails
Medications
Transdermal patches Clonidine has highest rate of sensitization
Antihistamines
Formaldehyde-releasing preservatives are #2 cause overall of cosmetic-related ACD (fragrances are #1)
Quaternium-15 (Dowicil 200) : found in soaps, shampoos, moisturizers; #1 preservative sensitizer in the United States
Imidazolidinyl urea
Diazolidinyl urea
DMDM hydantoin
Found in wet wipes → common cause of perianal ACD
Also present in Eucerin and other personal care products
Cross-reacts with PPPASTA family (Para-aminosalicylic acid, PABA, PPD, Azo dyes, Sulfonamides, Thiazides, ester
Anesthetics
Positive thimerosal patch test almost never relevant! → ok to give vaccines even w/ positive patch test
Cross-reacts with piroxicam and mercury
Euxyl K 400 (methyldibromoglutaronitrile)
Benzylkonium chloride
Triclosan
Benzyl alcohol
Tea tree oil
Also in ECG and lubricant jelly, antifreeze, brake uid, food dyes/avorings
Derived from coconut oil
Cross-reacts w/ aminophylline and hydroxyzine → can develop systemic ACD if allergic and receive aminophylline!
Allergen is wax-wool alcohol (derived from sheep)
Allergy common among leg ulcer pts
Cross-reacts w/ Aquaphor and Eucerin
Most notable for ACD of lips (lip balms)
Found in many hypoallergenic, sensitive skin products, as well as sunscreen ingredient Tinosorb M
geraniol, hydroxycitronellal, oak moss absolute)
Rash typically limited to face, hands, arms, and tongue
Cross-reaction w/ propolis, colophony, turpentine
Detects 50% of fragrance-related ACD
Sources: hair dye, black henna (temporary tattoos) , black rubber (rubber vulcanization, antioxidant), photograph de-
velopment, photocopies, printer ink, and other darkly colored cosmetics
Hairdressers, photographers, rubber workers: eczema of hands, wrists, forearms, eyelids, nose
Clients who get hair dyed: scalp and hairline dermatitis
Beard dermatitis in those who dye their beards
Note: natural henna (Lawsonia inermis) is a traditional red-brown dye used in South Asian cultures; does not commonly
cause ACD
Acid (professional/salon) perm: glyceryl monothioglycolate (allergen); a common sensitizer, remains in hair shaft for .3
months, penetrates rubber and vinyl gloves
Neutral perm: cysteamine hydrochloride (uncommon sensitizer)
Ammonium persulfate → contact urticaria reaction and generalized histamine reaction
Nail lacquer/polish
Very common cause of eyelid, neck, and nger/periungual dermatitis
Methacrylate: rigid plastic material, forms articial (acrylic) nail plates
Doxepin . diphenhydramine
94