ABC of allergies: Allergy and the skin. II---Contact and atopic eczema

Publisher Website
Google Scholar
Abstract
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. View larger version: In this window In a new window Allergic contact eczema due to nickel in studs and buttons on jeans 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. Mechanisms When skin sensitisers penetrate the epidermis, they are taken up by Langerhans' cells—bone marrow-derived members of the macrophage family that function as “professional antigen presenting cells.” The Langerhans' cells leave the epidermis and migrate to the regional lymph nodes, where they enter the paracortical areas, the home of naive T lymphocytes. Probably while en route to the lymph node, the Langerhans' cells process the sensitiser so it is physically associated with the HLA-DR molecules on the cell surface. In the node, the Langerhans' cells “present” the sensitiser to T lymphocytes of the immune system. If T cells with the appropriate specific receptor recognise the complex of sensitiser and HLA-DR, they proliferate to establish “immunological memory.” The memory T cells that mediate allergic contact eczema are of the Th1 subtype, characterised by the production of interleukin 2 and interferon gamma. The induction of sensitisation and establishment of immunological memory takes 8-14 days. Should re-exposure to the sensitiser occur, Langerhans' cells carry it down into the dermis, where they present it to memory T cells travelling through the tissues. These are activated to release cytokines (including interferon gamma) that attract other cells and activate vascular responses, resulting in the characteristic inflammation of contact eczema. Clinical presentation After re-exposure to a sensitiser, at sites of skin contact with the offending agent, an itchy erythematous rash starts to develop within 6-12 hours The reaction progresses and reaches a peak between 48 and 72 hours after contact Sensitivity may range from weak to strong Strongly sensitised people may need very little contact to evoke an acute, weeping eczematous reaction Nickel in keys, money, or clothing studs can be eluted by minimal perspiration through several layers of clothes View larger version: In this window In a new window Irritant contact eczema (dermatitis) of the hand Differential diagnosis Allergic contact eczema must be distinguished from irritant contact eczema. Clinically the two may be indistinguishable, but irritant eczema usually occurs on the hands. It is the result of repeated “insult” to the skin with caustic, irritant, or detergent substances. Photoallergic eczema occurs on light exposed areas—face, nape of neck, and backs of hands. It is usually a response to photosensitisation by ingested drugs such as thiazide diuretics or quinine. View larger version: In this window In a new window Patch testing for diagnosing causal sensitiser in allergic contact eczema Management The causal agent should be identified by epicutaneous patch tests. Contact allergy can be induced by a huge range of substances encountered daily. Sometimes the history of flare ups after contact with something is sufficient to permit reasonably confident identification. Often a short list of possible culprits can be arrived at. Definitive proof of causal significance, however, requires patch testing. This is normally performed in dermatology clinics with the requisite expertise and range of test materials. The patient should then be advised to avoid the causal agent. Treatment will vary: • Acute weeping eczema should be “dried” by soaking with potassium permanganate (1/10 000) daily for four to five days; • Anti-inflammatory steroids of category 3 or 4 (category 1 is the weakest, 4 the strongest—see British National Formulary) during the acute phase; • Systemic steroids may be required for severe cases; • For irritant hand eczema, avoiding contact with soaps, detergents, and solvents, together with generous use of greasy emollients, is vital. Pathogenesis Eczema is triggered or exacerbated by interactions between a genetic predisposition and environmental...

This publication has 0 references indexed in Scilit: