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allergic contact dermatitis

Dermatology / ImmunologyIntegumentary (Skin)Immune

Summary

Allergic contact dermatitis (ACD) is a Type IV (delayed-type, T-cell mediated) hypersensitivity reaction of the skin to a hapten after prior sensitization. It presents 48–72 hours after re-exposure as a pruritic, erythematous, eczematous, vesicular rash in the distribution of contact (e.g., poison ivy, nickel). Diagnosis is by history and patch testing; treatment is allergen avoidance plus topical corticosteroids.

Detail

**Mechanism (Type IV hypersensitivity, delayed-type):** - Sensitization phase (first exposure, no rash): Small haptens (<500 Da) penetrate the skin and bind self-proteins, forming hapten-protein complexes. Langerhans cells/dendritic cells process and present them on MHC II to naive CD4+ T cells in regional lymph nodes, generating allergen-specific memory T cells (Th1 predominantly; CD8+ cells also contribute). This takes about 10–14 days. - Elicitation phase (re-exposure): Memory T cells are activated and release IFN-γ, TNF and other cytokines, recruiting macrophages and causing keratinocyte injury and spongiotic dermatitis. The rash appears 48–72 hours after re-exposure (can range from 24 hours to 7 days). It is NOT antibody-mediated, and mast cells/IgE are not involved.

**Common causes:** - Toxicodendron (poison ivy, oak, sumac): urushiol. This is the classic cause. It produces linear streaks of vesicles/bullae. Fluid from blisters does not spread the rash. Urushiol remaining on skin, clothing or pets can spread it. - Nickel: jewelry, watch backs, belt buckles, jean snaps. This is the most common contact allergen overall. Look for periumbilical or earlobe dermatitis. - Others: neomycin and bacitracin (topical antibiotics), fragrances and balsam of Peru, preservatives (formaldehyde, parabens, methylisothiazolinone), rubber/latex accelerators (thiurams, carbamates), hair dye (p-phenylenediamine), topical anesthetics (benzocaine), chromates (cement, leather), gold, and cosmetics. - Latex can cause either a Type IV reaction (ACD, from rubber additives) or a Type I reaction (IgE-mediated urticaria/anaphylaxis).

**Clinical features:** - Acute: pruritic erythematous papules, vesicles and bullae with a sharply demarcated or geometric/linear pattern matching the exposure. - Chronic: lichenification, scaling, fissuring. - Distribution clues: eyelids (nail polish, cosmetics), hands (gloves, rubber), feet (shoe rubber/adhesives), earlobes/wrists/umbilicus (nickel). - The rash can spread by scratching only in the sense of additional allergen transfer; it is not contagious.

**Diagnosis:** - Clinical history and exam. Biopsy shows spongiosis (intercellular edema) with a perivascular lymphocytic infiltrate and sometimes eosinophils. - Gold standard is patch testing: allergens are applied under occlusion for 48 hours and read at 48–96 hours. A positive result shows erythema, edema and vesicles at the patch site. - Patch testing is a delayed-type hypersensitivity test, like the PPD/tuberculin skin test. Do not confuse it with prick/intradermal testing (Type I).

**Treatment:** - Identify and avoid the allergen. - Wash the skin with soap and water soon after exposure to urushiol. - Topical corticosteroids for localized disease. - Systemic corticosteroids (taper over 2–3 weeks) for extensive disease or involvement of the face/genitals. A short course may cause rebound. - Cool compresses and oral antihistamines for symptomatic relief; they act mainly through sedation.

**Key comparison with irritant contact dermatitis (ICD):** - ICD is more common, non-immune, and direct chemical or physical damage to keratinocytes (soaps, solvents, acids/alkalis, frequent hand washing). It needs no prior sensitization and occurs in anyone with enough exposure. - ICD tends to cause burning/stinging more than itching, appears within minutes to hours, and is dose dependent. - ACD requires prior sensitization, causes itching, involves only sensitized individuals, and can occur with trivial exposures.

**High-yield associations (Step 1 pearls):** - Type IV hypersensitivity mnemonic ACID: Allergic contact dermatitis, TB skin test (PPD), Cell-mediated, Graft-versus-host disease/transplant rejection, Delayed. It is also grouped with MS, Type 1 diabetes, and Hashimoto thyroiditis. - Transferred by T cells, not serum. It can be passively transferred with T cells but not with antibodies. - Treatment is with corticosteroids or calcineurin inhibitors (tacrolimus, pimecrolimus) for steroid-sparing use on the face/skin folds. - Step 2 pearl: for a rash with a linear or geometric pattern after outdoor exposure or new jewelry/cosmetics, think ACD; patch testing is indicated for persistent or recurrent dermatitis of unclear cause.

Sources

  • First Aid for the USMLE Step 1 (Immunology: Hypersensitivity Reactions; Dermatology: Contact Dermatitis)
  • Robbins & Cotran Pathologic Basis of Disease (Hypersensitivity, Type IV)
  • Fitzpatrick's Dermatology in General Medicine (Contact Dermatitis)
  • Pathoma (Fundamentals of Pathology) – Immunology/Dermatopathology
  • UpToDate: Clinical features and diagnosis of allergic contact dermatitis
  • Murphy's Janeway's Immunobiology (Delayed-type hypersensitivity)

Reviewed by Medusa editorial — medical student review. Information here is for study reference only and is not medical advice. Spotted an error? Let us know.