Allergic and immune-related disorders Atopic dermatitis (Eczema) Relapsing inflammatory skin disorder Pruritis (*Intense itching

) Lichenification Commonly associated w/ asthma + allergic rhinitis Triggers: Climate, food, contact w/ allergens, physical/chemical irritants, emotional factors Contact (including hand) dermatitis Type IV hypersensitivity rxn from contact w/ allergen pt was previously exposed and sensitized to Pruritis, rash Frequent allergens: poison ivy, poison oak, nickel, soaps, detergents, cosmetics, rubber products containing latex (gloves, elastic bands in clothing) Pathogenesis: Allergens passed through epidermis  taken up by langerhans cells  carried to LNs  exposed to T lymphocytes Common in infancy Infants: Erythematous, weeping, pruritic patches on face, scalp, diaper area Children: Dry, scaly, pruritic, excoriated patches in flexural areas + neck Adults: Lichenification and dry, fissured skin, often limited to hands Distributions where makeup, clothing, perfume, nickel jewelry, and pants contact skin Begins in area of contact w/ antigen Acute: 24-48 hrs after contact. Erythematous – tiny blisters  scale + crusts. Intense pruritis Subacute: episodic exposure or weak allergen. Chronic: extended exposure. Erythema, lichenification w/ fissuring, often w/ superimposed acute dermatitis More common in Adults Sebhorrheic dermatitis Inflammatory papulosquamous dz associated w/ sebaceous follicle regions Related to abnormal immune response to Malassezia (Pityrosporum) – common skin yeast **Pts w/ HIV/AIDS can develop severe seborrheic dermatitis or overlapping syndrome *Suspect HIV in young person w/ severe seborrheic dermatitis Psoriasis T-cell mediated inflammatory dermatosis  dermal inflammation and epidermal hyperplasia Well-defined pink to erythematous patches covered with silvery scales, revealing small bleeding points on scraping (Auspitz sign) 5% have also have seronegative arthritis Psoriatic nails: pitting, “oil spots,” and onycholysis (lifting of nail plate) Provoked by:  Local irritation, trauma (Koebner’s phenomenon)  Step infxn  cutaneous immune complex deposition  triggers guttate  B-blockers, lithium, ACEIs Psoriatic arthritis:  Begins on hands (“sausage digits”)  Pts w/ spinal involvement = HLA-B27 + Pustular psoriasis (less common)  Life-threatening when generalized  Fever, electrolyte abnormalities, loss of serum proteins Urticaria (Hives) Type I hypersensitivity response: Mast cells release vasoactive substances (histamine, protaglandins) Acute: response to trigger (food, drug, virus, insect bite, physical stimulus) Chronic: Idiopathic Superficial, intense edema in localized area Elevated papules or plaque reddish or white, variable size. Widespread, last a few hours. Severe rxs  extracutaneous manifestations: Tongue swelling, angiodema (deeper, more diffuse swelling), asthma, GI sx, joint swelling, fever Eruptions: 7-14 days after exposure  If pts reascts w/in 1-2 days of starting new drug (i.e. never taken before) – that drug not likely causative agent  Widespread, relatively symmetrical, + pruritic Clinical impression Histo: eosinophils D/c offention agent Symptoms: Antihistamines Clinical Biopsy: perivascular edema Systemic antihistamines *Topical meds = NO benefit Areas w/ oily skin – scalp, eyebrows, nasolabial folds, midchest Infants: severe, red diapher rash w/ yellow scale, erosions, + blisters. Thick crust (cradle cap) seen on scalp. Children/Adults: Red, scaly patches around ears, eyebrows, nasolabial fold, midchest, scalp Starts in puberty or young adulthood Extensor surfaces: elbows, knees, lumbosacral regions  Initially very small (guttate)  May slowly enlarge and become confluent Clinical Biopsy: thickened epidermis, elongated rete ridges, absent granular layer, preserved nuclei, and sterile neutrophilic infiltrate (munro’s microabscess) in stratum corneum Topical steroids + keratolytic agents, tar, or anthralin + UV therapy (PUVA) Severe: Methotrexate Arthritis:  NSAIDs  Methotrexate  *Avoid systemic steroids (tapering  flares) Clinical r/o contact dermatitis and psoriasis Scalp:  Selenium Sulfide  Zinc pyrithione shampoos Other areas:  Topical antifungals  Topical corticosteroids Clinical Possible  eosinophils and  IgE r/o seborrheic dermatitis, contact dermatitis, pityriasis rosea, drug eruption, and CTCL Clinical Patch test Differential:  Atopic dermatitis  seborrheic dermatitis  Impetigo  HSV  Herpes zoster  Fungal infection Topical or systemic corticosteroids Prophylaxis:  Moisturizers  Nondrying soaps (Dove)  Avoid triggers Topical steroids

Prophylaxis:  Avoid allergen

Drug Eruption

Maintain high suspicion in hospitalized pts who develop rash Can cause all four types of hypersensitivity rxns

+ Nikolsky’s sign. Cephalosporins  Seizure meds (phenytoin. carbamazepin)  Allopurinol  Corticosteroids  NSAIDs Erythema Nodosum Panniculitis (inflammation of fat cells under skin) Triggers:  Infection (Strep. TB)  Drug rxns (Sulfas. Triggers: Recurrent HSV infxn of lip. NSAIDs). Behcet’s) **Pts may have false-+ VDRL (as in SLE) Pemphigus vulgaris *Involves mucous membranes Life-threatening autoimmune condition w/ intraepidermal blister  widespread painful erosions of skin and mucous membranes Abs against desmoglein molecules responsible for keratinocyte adherence  loss of cellular attachment Middle-aged 40-60 Initial: mucous membrane involvement (mouth ulcers) w/ progression to skin Severe mucosal erosions w/ widespread erythematous. electrolyte disturbances. UC. myalgias. stable blister on erythematous skin  Often preceded by uriticarial lesion  . anticonvulsants. erythematous nodules on pts lower legs  Slowly spread turning brown or grey May present w/ fever and joint pain TEN: full-thickness eosinophilic epidermal necrosis Possibley preceded by EM (Flu-like prodrome. Crohn’s. w/ hx of new drug  Penicillin. face. Coccidoides. HA. or painful mouth lesions) BIOPSY: SJS: degeneration of basal layer of epidermis Pts have same complications as burn victims (Thermoregulatory difficulties. extremities) each tim pt is exposed to triggering agent  When lesions resolve  brown pigmentation Extreme complications: erythroderma and TEN Erythema multiforme Cutaneous rxn pattern w/ classic targetoid lesions w/ many triggers. OCPs)  Chonic inflammatory diseases (Sarcoid. Yersinia. barbs. epidermal detachment Mucous membranes of eyes. penicillin. mycoplasmal infections Target appearance (erythematous macules  centrally cleared  blister) Palms + soles affected Possible systemic sx (Fever. various antibiotics. arthralgias) Minor form: Uncomplication.Nikolsky’s sign  Form crusts + erosions Mucous membranes less commonly involved than in pemphigus Clinical Biopsy: subepidermal blister. Often recurrent. cutaneous macules or atypical targetoid lesions  Epidermal lesions become confluent. Qunilones. acquired autoimmune blistering dz w/ Abs against hemidesmosomal Ag  separation at epidermal BM MC: 60-80 yo Pathogenesis: Abs agains bullous pemphigoid Ag (lies superficially in BM zone (BMZ)) Ag-Ab complexes  activate complement + eosinophil degranulation  inflammation rxn  separation at BMZ Blisters are stable d/t nearly normal epidermis roof Firm. drugs (sulfas. 2 infxns) Tx:  Skin coverage  Maintenance of fluid + electrolyte balance High risk of mortality Clinical Hx of recurrent labial herpes Should be sought in all cases w/ multiple recurrences Symptomatic tx Minor: antipruritics Major: Treat as burns Pts w/ HSV: suppressive acyclovir may  frequency of rashes *Corticosteroids no benefit Diff:  Graft-vs-host rxn (after BM transplant)  Radiation therapy  Burns Clinical Histo: nonspecific panniculitis Workup:  ASO titer  PPD test (in high risk)  CXR (r/o sarcoid)  Small bowel series (r/o IBD in pts w/ GI sx) Clinical + Nikolsky’s sign (produce blister by rubbing skin adjacent to natural blister) Skin bx w/ IF: Acantholysis (intraepidermal split w/ freefloating keratinocytes in blister) IF + ELISA = confirmatory for antidesmoglein Abs Remove triggering factor and treat underlying dz NSAIDs can be used but may  EM Long term tx required Intital:  Systemic corticosterois at high doses  Steroid-sparing agents introduced early to steroid SEs (mycophenolate mofetil and azathioprine) Bullous (and cicatricial) pemphigoid Chronic. w/ eosinophil-rich infiltrate  IF Linear IgG + C3 Ig + Complement at dermalepidermal junction Systemic corticosteroids Topical steroids can help prevent blister formation when applied to early lesions . skin tenderness. localized to skin Severe: Can  TEN or SJS (Pts very ill. Sulfonamides. and genitals often become eroded and hemorrhagic Painful. Short-lived (gone 1-2 weeks after cessation) Exception: Fixed drug eruption  Reddish macules/papules that develop in same area (genitalia. maculopapular drug rash. involved at least 2 mucosal surfaces) StevensJohnson Syndrome (SJS)/Toxic Epidermal Necrolysis (TEN) Life-threatening exfoliative mucocutaneous dz often caused by drug0induced immunologic rxn SJS: epidermal separation <10% BSA TEN: >30% BSA Assoc. mouth.

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