Allergic contact dermatitis and photoallergy

Published on 19/03/2015 by admin

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Allergic contact dermatitis and photoallergy

Rosemary L. Nixon and Sarah E. Gamboni

Evidence Levels:  A Double-blind study  B Clinical trial ≥ 20 subjects  C Clinical trial < 20 subjects  D Series ≥ 5 subjects  E Anecdotal case reports

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Allergic contact dermatitis (ACD) is a delayed-type hypersensitivity reaction, usually occurring at the site of topical application of an allergen, to which the sufferer has already been sensitized. At first, the rash is localized to the site of contact with the causative allergen, but it may spread to other areas, either from transfer of the allergen or because of a so-called ‘id,’ or hypersensitivity eruption, also termed autosensitization dermatitis. Spread of the rash to other areas is very characteristic of ACD and clinically may help to differentiate it from irritant contact dermatitis.

Substances requiring activation by UV light in order to become allergenic are called photoallergens. The most important photoallergens are currently sunscreens, and perhaps some pesticides, but in the past fragrances (especially musk ambrette), halogenated salicylanilides, and topical non-steroidal agents (such as ketoprofen) were common photoallergens.

Some patients with an airborne contact dermatitis to sesquiterpene lactones, found in the Compositae group of plants, will develop photosensitivity, as evidenced by abnormal results on monochromator testing. This condition is generally termed chronic actinic dermatitis (CAD).

Localization may give clues to the causative allergen, for example involvement of the hands in cases of ACD caused by rubber accelerators in gloves; the ears and neck caused by nickel in costume jewellery; eyelid and neck dermatitis from preservatives or perfumes in moisturizing creams.

Determinants of whether sensitization will occur include the nature of the allergen involved, the duration and concentration of skin contact with the allergen, and individual susceptibility.

Management strategy

The primary responsibility is to identify and avoid further contact with the offending allergen, as well as any potentially cross-reacting agents. Such identification requires patch testing. From a public health perspective, it is important to reduce exposure to known allergens, particularly in the area of occupational dermatitis, which can be extremely disabling for the individual. The addition of ferrous sulfate to cement, initially in Denmark and now in the European Union, effectively reduces the available chromate through chemical reduction. In the European Union, legislation has been enacted to reduce the nickel content of jewellery that comes in contact with the skin.

In the workplace, other measures should be undertaken to reduce exposure to known allergens, such as substitution of known allergens, changing the design of an engineering process to limit skin contact with chemicals, installation of appropriate ventilation to reduce airborne exposure to substances, and the use of personal protective equipment.

It is most important to wear gloves that are appropriate for handling a particular chemical. In addition, it is often suggested that cotton gloves be worn underneath rubber or leather gloves to prevent sensitization to rubber accelerators and chromate, respectively. This is especially important in the context of work in hot environments, where sweating and leaching of allergens is likely.

The initial treatments involve the general principles of eczema therapy, including avoidance of skin irritants, such as water, soap, solvents, oils, heat, sweating, dust, and friction. Use of soap substitutes and moisturizing creams, together with topical corticosteroids, is recommended. More recently, tacrolimus and pimecrolimus have been used successfully. The use of barrier creams to prevent dermatitis has had limited success. Short courses of oral corticosteroids, such as prednisolone 25–50 mg daily for 1 week, are sometimes required in severe cases. Occasionally the dermatitis may become secondarily infected, so a course of antibiotics, such as cephalosporin, erythromycin, or flucloxacillin may be required. Topical antibiotics such as mupirocin or fusidic acid are often helpful, particularly for the treatment of persistently cracked or fissured skin that becomes infected.

Once the cause of ACD has been identified, long-term treatments other than avoidance of the allergen(s) are usually not required. Desensitization, commonly used in the treatment of allergies caused by immediate hypersensitivity reactions, has been of extremely limited value when employed in delayed hypersensitivity. However, severe episodes of dermatitis may precipitate a recurring eczematous condition, termed persisting post-occupational dermatitis. Recently, alitretinoin has been found to be effective in chronic hand eczema. However, not all of these patients studied had ACD.

In persistent cases, ultraviolet light therapy may be considered, such as with hand UVB or PUVA (psoralen plus UVA).

Systemic immunosuppression using azathioprine or cyclosporine may be considered. Other agents, such as methotrexate or acitretin (particularly if the hands are hyperkeratotic), are also used. Superficial X-ray and Grenz ray treatments have been successfully used in some cases.

In photoallergy, identification and avoidance of the photoallergen is of major importance. In the case of allergy to chemical sunscreening agents, this may involve substitution with physical sunscreening agents such as titanium dioxide.

In CAD, treatments have centered on reduction of UV exposure, including hospitalization and use of plastic films for windows to reduce UV transmission. Systemic therapies include azathioprine, prednisolone, hydroxychloroquine, cyclosporine, PUVA or UVB, and combinations of UV with prednisolone.


First-line therapies

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Allergic contact dermatitis
imagePrevent contact with allergen C
imageTopical corticosteroids B
imageEmollients and soap substitutes C
imageBarrier creams B
imageTacrolimus