Allergy and the skin. II—Contact and atopic eczemaBMJ 1998; 316 doi: https://doi.org/10.1136/bmj.316.7139.1226 (Published 18 April 1998) Cite this as: BMJ 1998;316:1226
- P S Friedmann
Allergic contact eczema
Eczema is characterised by erythema, pruritus, vesiculation, and, in more chronic forms, scaly desquamation. Contact eczema may be due to chemically induced irritation or allergic sensitisation. Allergic contact eczema is a cell mediated (delayed type) hypersensitivity reaction to environmental chemical “sensitisers.” Hence, it occurs at body sites that make physical contact with the eliciting sensitiser. The term dermatitis is often used for eczema caused by exogenous agents.
Distribution of allergic contact eczema
Nickel sensitivity involves ears, skin under buckles, and often the hands; accidental spread from hands can involve the face
Hair products (for example, dyes, perms, and setting agents) often affect the face, neck, and ears
Clothing dyes in socks and shoe leather often affect the feet
Ingredients in drugs used around leg ulcers often induce a dermatitis of the leg
Prevalence and aetiology
In the working population of Western countries, contact eczema (both irritant and allergic) accounts for 85-90% of all occupational skin disease. Hand eczema has been estimated to affect 2-6.5% of all populations in Western countries.
The development of allergic reactions to exogenous substances seems to be the result of the intrinsic “sensitising potency” of the compound and various host factors that determine susceptibility. Small molecular chemicals vary in their potential to induce allergic sensitivity: primula can sensitise most people, nickel sensitises 10-20% of women, while many other agents sensitise a smaller minority. The sensitising potency of a chemical is thought to be related to its chemical reactivity and ability to bind to proteins, which act as “carriers,” facilitating the presentation of the substance to the immune system. Host susceptibility is related to as yet uncharacterised genetic factors, which include variation in metabolic pathways that handle exogenous chemicals.
When skin sensitisers penetrate the epidermis, they are taken up by Langerhans' cells—bone marrow-derived …