Allergic Contact Dermatitis

A type four, T cell mediated delayed hypersensitivity reaction of the skin occurring in response to direct cutaneous contact with a specific sensitising allergen, distinct from irritant contact dermatitis, which results from direct chemical or physical damage to the skin without an immunological mechanism, though the two frequently coexist and can be difficult to distinguish clinically.

Pathophysiology and common allergens

Sensitisation occurs on first exposure, with the allergen acting as a hapten that binds to skin proteins and is processed by Langerhans cells, priming allergen specific T cells. Subsequent re exposure triggers a delayed inflammatory response, typically developing over one to several days, mediated by these sensitised T cells recruiting and activating macrophages in the skin.

Common allergens include nickel (jewellery, clothing fasteners), fragrances and preservatives in cosmetics and skincare products, topical medications (particularly neomycin and corticosteroids themselves), rubber accelerators, hair dye components (paraphenylenediamine) and certain plants.

An eczematous, itchy rash develops at the site of contact with the allergen, typically with well demarcated borders that often correspond to the shape or distribution of the contact (a linear pattern from a plant brush, a circular pattern beneath a metal button or watch clasp), an important clue distinguishing it from other forms of dermatitis.

Acute reactions present with erythema, oedema and, in more severe cases, vesiculation and weeping, while chronic or repeated exposure produces lichenification, scaling and skin thickening.

Onset is typically delayed, developing over twenty four to seventy two hours after exposure in a previously sensitised individual, though can take longer with initial sensitisation.

The distribution of the rash frequently provides the most important diagnostic clue, correlating with sites of contact with jewellery, clothing, cosmetics or occupational exposures, and a careful history exploring the temporal and spatial relationship between exposure and rash onset is essential.

Chronic hand dermatitis, particularly in occupational settings with repeated exposure to relevant allergens (healthcare workers, hairdressers, cleaners), can be significantly disabling and career limiting if the causative allergen is not identified and avoided.

Diagnosis is supported by a careful history identifying the pattern and timing of exposure relative to rash onset, together with the characteristic distribution of the lesions corresponding to sites of contact.

Patch testing is the diagnostic test of choice, involving application of a standardised panel of common allergens (supplemented by specific products or substances the patient is exposed to) to the back under occlusion for forty eight hours, with reading of the reaction at forty eight and again at ninety six hours given the delayed nature of the hypersensitivity response, since some reactions only become apparent at the later reading.

Interpretation of patch testing requires clinical correlation, since a positive reaction indicates sensitisation to that allergen but does not by itself confirm that the allergen is responsible for the patient's current dermatitis, which must be assessed against the clinical history and exposure pattern.

Distinguishing allergic from irritant contact dermatitis can be clinically challenging, though irritant dermatitis typically develops more rapidly after exposure, is less clearly itchy and more often burning or stinging in character, and does not require prior sensitisation, occurring on first exposure to a sufficiently irritant substance.

Skin biopsy is rarely required but, where performed, shows spongiotic dermatitis, a non specific pattern shared with other eczematous conditions rather than one specific to allergic contact dermatitis.

Identification and strict avoidance of the causative allergen, guided by patch testing results and a thorough review of the patient's personal care products, occupational exposures and clothing or jewellery, is the cornerstone of management and, where achieved, is frequently curative.

Topical corticosteroids, of a potency appropriate to the site and severity of the dermatitis, are first line treatment for the acute inflammatory phase, with emollients used liberally alongside to support skin barrier repair.

Topical calcineurin inhibitors (tacrolimus, pimecrolimus) offer a steroid sparing alternative, particularly useful for sensitive sites such as the face and eyelids where prolonged corticosteroid use carries greater risk of skin atrophy.

Severe, widespread or refractory disease occasionally requires a short course of oral corticosteroids, with systemic immunosuppression (methotrexate, azathioprine) reserved for chronic, severe, occupationally disabling disease where allergen avoidance has proven insufficient or impractical.

Occupational contact dermatitis requires specific attention to workplace modification, appropriate protective equipment, and in some cases occupational health referral or, where avoidance within the current role is not feasible, consideration of redeployment given the potential for significant and recurrent disability.

Patient education regarding reading product ingredient labels, recognising alternative names for known allergens, and understanding that even products labelled as hypoallergenic may contain the relevant sensitising substance, supports long term successful avoidance and prevention of recurrence.