INFLAMMATORY AND IMMUNE-MEDIATED SKIN DISORDERS

Allergic Contact Dermatitis

Classification: Type IV delayed hypersensitivity to an allergen contacting the skin (Norris, 2020; Pincus & McCalmont, 2019).

Key diagnostic discriminator: Pruritic eczematous eruption that follows the distribution of contact and appears 24–48 hours after re-exposure. Patch testing identifies delayed allergens (Gohara et al., 2012; Pincus & McCalmont, 2019).

Clinical priority: Facial/eyelid/genital involvement, widespread blistering, severe swelling, occupational exposure, or inability to avoid the allergen warrants specialist input (Gohara et al., 2012; Pincus & McCalmont, 2019).

Etiology and risk factors

  • Common allergens include urushiol/poison ivy, nickel, fragrances, preservatives, rubber accelerators, hair dyes, adhesives, and topical antibiotics (Gohara et al., 2012; Norris, 2020; Pincus & McCalmont, 2019).
  • Risk depends on sensitization, repeated exposure, impaired skin barrier, occupation/hobbies, and use of topical/cosmetic products. Any exposed person may become sensitized (Gohara et al., 2012; Norris, 2020; Pincus & McCalmont, 2019).

Pathophysiology

  • Sensitization phase: allergen penetrates epidermis, binds proteins, is processed by Langerhans/dendritic cells, and generates allergen-specific memory T cells (Norris, 2020; Pincus & McCalmont, 2019).
  • Elicitation phase: re-exposure activates memory T cells and cytokines, causing epidermal spongiosis and inflammation after a delay. Chronic exposure produces hyperplasia, scale, fissuring, and lichenification (Norris, 2020; Pincus & McCalmont, 2019).

Clinical manifestations

  • Acute disease: intense pruritus, erythema, edema, papules, vesicles/bullae, weeping, and crusting. Borders/distribution often map to exposure; spread beyond the exact site may occur (Gohara et al., 2012; Pincus & McCalmont, 2019).
  • Chronic disease: scale, fissures, lichenification, hyperpigmentation, and thickening. Linear streaks suggest plant exposure; earlobe/waist/wrist patterns may suggest metal (Gohara et al., 2012; Pincus & McCalmont, 2019).

Findings that argue against or redirect

  • Burning and immediate onset after a strong irritant, including first exposure, favor irritant contact dermatitis (Gohara et al., 2012; Pincus & McCalmont, 2019).
  • Migratory wheals lasting less than 24 hours favor urticaria. Dermatomal grouped vesicles with pain favor herpes zoster (Gohara et al., 2012; Pincus & McCalmont, 2019).
  • A negative limited patch panel does not exclude an untested allergen or an exposure missed by timing/distribution (Gohara et al., 2012; Pincus & McCalmont, 2019).

Diagnostic evaluation

  • Use a detailed exposure timeline covering work, home, hobbies, plants, gloves, metals, cosmetics, personal-care products, topical medications, and recent product changes. Examine distribution and protected areas (Gohara et al., 2012; Pincus & McCalmont, 2019).
  • Patch testing is the diagnostic standard for delayed contact allergy when disease is recurrent, chronic, occupational, or unclear. Biopsy can confirm spongiotic dermatitis but usually cannot identify the allergen (Gohara et al., 2012; Pincus & McCalmont, 2019).

Expected diagnostic and laboratory findings

  • Positive patch test reproduces an eczematous delayed reaction to a tested allergen and is clinically meaningful only when exposure relevance is established (Gohara et al., 2012; Pincus & McCalmont, 2019).
  • Histology shows spongiosis with variable vesiculation and inflammation; chronic lesions show acanthosis/hyperkeratosis. Findings overlap with other eczematous disorders (Gohara et al., 2012; Pincus & McCalmont, 2019).

Differential diagnosis

  • Irritant contact dermatitis: direct toxic injury, often burning/pain and exposure to wet work/chemicals; no sensitization required (Gohara et al., 2012; Pincus & McCalmont, 2019).
  • Atopic dermatitis: chronic relapsing flexural pattern with atopic history and barrier dysfunction (Gohara et al., 2012; Pincus & McCalmont, 2019).
  • Tinea: annular active edge and fungal elements on KOH/culture (Gohara et al., 2012; Pincus & McCalmont, 2019).
  • Cellulitis: pain, warmth, tenderness, systemic symptoms, and no vesicular exposure pattern (Gohara et al., 2012; Pincus & McCalmont, 2019).

Treatment and management

  • Identify and eliminate the allergen. Restore the skin barrier with gentle cleansing, emollients, and protective practices that reduce repeat exposure (Norris, 2020; Pincus & McCalmont, 2019).
  • Use site- and severity-appropriate topical corticosteroids. More extensive acute disease may require clinician-directed systemic corticosteroid therapy. Treat secondary infection only when it is present (Norris, 2020; Pincus & McCalmont, 2019).

Additional complications and red flags

  • Rapidly progressive pain, fever, purulence, or disproportionate tenderness suggests infection rather than uncomplicated dermatitis (Gohara et al., 2012; Pincus & McCalmont, 2019).

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References

Gohara, M. A., Schaffer, J. V., Abbasi, N. R., Kingsley, M. M., Sheehan, J. M., & Arndt, K. A. (2012). Inflammatory dermatoses (rashes). In M. C. Henderson, L. M. Tierney, Jr., & G. W. Smetana (Eds.), The patient history: An evidence-based approach to differential diagnosis (2nd ed.). McGraw-Hill.

Norris, T. L. (2020). Porth’s essentials of pathophysiology (5th ed.). Wolters Kluwer.

Pincus, L. B., & McCalmont, T. H. (2019). Diseases of the skin. In G. D. Hammer & S. J. McPhee (Eds.), Pathophysiology of disease: An introduction to clinical medicine (8th ed.). McGraw-Hill Education.