What is contact dermatitis?
Contact dermatitis is an eczematous skin reaction caused by direct and usually repeated exposure to harmful objects or chemicals. Dependent on the point of contact, it can occur anywhere on the body including mucous membranes. It is typically characterized by itching papules or vesicles but may vary from slight hyperkeratosis (thickening of the outermost horny layer) and small fissures to extensive redness, swelling and oozing. A histopathological examination of a biopsy shows an acute inflammation in the outermost layers of the dermis with involvement of the epidermis. Only superficial parts of the skin are thus involved, and healing is complete with no residual scars. The main pathogenetic mechanisms are damage to the skin barrier and/or immunological reactions.
There are four different forms of contact dermatitis:
Irritant contact dermatitis
Irritant contact dermatitis with synonyms toxic, traumiterative or housewifes eczema and non-allergic contact dermatitis is the most common variant with a point prevalence of 1-2 % in the healthy population. Localized almost exclusively to the hands it occurs most frequently in 'wet work' occupations such as hairdressers, health care personnel, cleaners, cooks and caterers. Contactants are detergents and surfactants, acid and alkaline solutions, organic solvents, sometimes even water. The deleterious effect of these agents is the removal of the fat emulsion on the skin surface, a damage to the function of the epidermal skin barrier, and a removal of the water- binding substances of the horny layer. A single exposure is usually harmless but by repetition can be destructive. The damage can be documented by an increased epidermal water loss.
The clinical consequences are desiccation, scaling and fissuring, progressing to eczematous dermatitis. Promoting factors for the development of this type of contact dermatitis are individual, such as the presence of an atopic constitution, thickness of the horny layer, a previously damaged skin barrier etc, physicochemical, such as type of contact with the agent, concentration and pH of the offending material, solubility of the substance etc, and environmental, such as room temperature and humidity.
Diagnostic tests have not been developed, and a biopsy for histopathology is not contributary. The diagnosis is clinical, often by exclusion. A frequent complication is contact allergy. The best therapy is prohylaxis, i.e. avoidance of harmful contacts including a change of living pattern, and frequent use of moisturizing creams. The healing period is often protracted.
Allergic contact dermatitis
Allergic contact dermatitis is the clinical expression of contact allergy. This type of hypersensitivity is always acquired and may develop anytime during life. The allergy-inducting agents or antigens are low-molecular weight so-called haptens, e.g. inorganic or organic salts, ionized metals etc. Soluble haptens penetrate the skin surface, are coupled to epidermal proteins to form complete antigens, and then transported by Langerhans cells through lymphatic vessels to regional lymph nodes. Here immunocompetent lymphocytes are stimulated to clonal proliferation so that cytotoxic and memory T lymphocytes are formed and circulated. In man, this induction process to sensitization (the subject now being allergic) takes a minmum of ten days. Contrary to other allergic diseases, e.g. asthma or hay-fever allergic contact dermatitis is cell-mediated (type 4 allergy) and not mediated by circulating antibodies.
Common contact allergens are metals (nickel, chromium, cobalt, gold), fragrances (perfume chemicals), colophony resin, rubber chemicals, topical drugs (neomycin, corticosteroids), preservatives, plastic chemicals (acrylates, epoxy resins), dyes, formaldehyde, plants etc. In a patient with an established contact allergy the interval between skin contact and the following eruption of dermatitis is longer than in cases of antibody-mediated allergies, viz. a matter of hours/days (delayed allergy). This efferent link involves aggregation of specific T lymphocytes at the site of cutaneous exposure to the antigen and release of biologically active cytokines resulting in clinical disease.
An acquired contact allergy cannot be obliterated by treatment but is persistent for many years. If it possible to avoid contact with the allergen, the dermatitis may, however, stay in remission. In principle, individuals are allergic to one chemical only -- the allergy is antigen specific -- but cross sensitivity may be present: the patient may react with eczema to a chemically similar substance even if it is met in quite another product. Example: the patient may become sensitized to p-phenylene diamine in a hair coloring preparation but later flare up with eczema from p-aminobenzoic acid in a sunscreen.
Contact allergy is demonstrated through patch testing by a dermatologist. Small amounts of standardized and other suspected allergens are applied with an adhesive on the skin of the back for 48 hours. A positive test shows up as a miniature eczema during the following few days. It is important to carefully consider the relevance of all positive patch tests since some of them may constitute immunological residues from eczematous episodes earlier in life.
The main treatment for allergic contact dermatitis is by topical corticosteroids, often supplemented by moisturizing creams, sometimes even ultraviolet radiation. In order to prevent a recurrence it is necessary for the patient to avoid further contact with the allergen.
Photocontact dermatitis is the result of an interaction between a harmful substance present in the skin and ultraviolet radiation. In other words, no dermatitis evolves from the chemical alone (e.g. if the subject stays indoors) but UV exposure is also required. Photocontact dermatitis is therefore always localized to light-exposed skin, viz. on face, ears, dorsal aspects of hands, and other areas not protected by clothing. The radiation responsible is within the longwave UV (320-400 nm, UVA).
The interaction between chemical in the skin and UVA can lead to a direct damaging effect on the skin tissue by the disposal of accumulated energy or by the formation of new photoproducts. The result is a phototoxic reaction, hitting everybody if the two requirements are fulfilled: sufficient amounts of photosensitizer in the skin and of UVA. (Even in Northern Europe there is enough UVA on sunny days the year for these reactions to occur.) Common photosensitizers are the psoralens, found in ubiquitous plants of the Umbelliferae family (wild parsnip, giant hogweed); the ensuing disease is often called phytophotodermatitis. The psoralens are actually used in dermatological therapy (PUVA).
The pathogenetic mechanism may also involve an immunological component in addition to the skin absorption of a photosensitizer and exposure to UVA. In a photoallergic reaction a sensitization similar to contact allergy is also required and therefore, only a few subjects in the population suffer. Common causal agents are Musk ambrette (in after shave-products), salicylic anilids (in soaps and detergents), p-aminobenzoic acid (in sunscreens), fragrances and balsams (for skin care). A photoallergic reaction can be diagnosed by photopatch testing similar to regular patch testing but with (and without) the exposure to artificial UVA. This is not possible in phototoxic reactions since everybody reacts under proper circumstances; instead, research interest has to be focused on the potency of chemicals to be activated by UVA.
Contact urticaria deviates from regular contact dermatitis in the type of clinical reaction, its time sequence, the causal agents, and the pathogenetic mechanism. True, the clinical reaction appears on the site of direct contact, usually the fingers, but consists of small, itching wheals, emerging within 10-20 minutes after contact and rapidly disappearing. Causal agents may be latex rubber in gloves, animal proteins or other food stuffs, the patients often being health care personnel, as well as chefs and workers in meat or fish industry.
Pertinent allergens are high-molecular, complete antigens, normally not absorbed through the skin. Therefore, preceding damage to the skin barrier. e.g. a discrete irritant dermatitis, would be a prerequisite. Pathogenetically, this is a type 1 allergy based on specific IgE antibodies, and the patients usually have an atopic constitution.
A regular 48 hour patch test will give a false negative reaction. Instead, a short term (20 min) prick test or scratch-chamber test with the suspected material, e.g. shrimps or rubber, will provoke a positive, immediate, wheal reaction. In latex cases, also specific IgE in blood may be demonstrated. It should be pointed out, however, that a non-immunological variant of contact urticaria also exists.