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ALLERGIC CONTACT DERMATITIS TREATMENT

Allergic Contact Dermatitis (CD) is an immune system mediated inflammatory reaction of the skin to external agents, such as, allergens.

The first step in treatment of allergic Contact Dermatitis, as in any contact dermatitis case, is avoidance of the responsible agent. In certain environments, it may not be possible to totally remove the responsible allergen, so therapy is needed. In most cases, therapy is needed despite managing avoidance of the offending allergen.

Management of contact dermatitis

Topical Corticosteroids: Topical corticosteroids, when they were first introduced in the 50s, revolutionized the treatment of allergic contact dermatitis. Since then, these drugs have been the mainstay of allergic contact dermatitis treatment. Topical corticosteroids come in 7 grades of potency and consist of common steroids used by practitioners. These are broad spectrum medications where the two main mechanisms of action are inhibition of T-cell activation and leukocyte migration. When prescribing these drugs, certain factors are considered, such as, site and frequency of action, the vehicle i.e. cream, ointment, gel, lotion or solution and amount to be applied.

Effectiveness of corticosteroid treatment is now well established in allergic contact dermatitis cases. However, their effectiveness in irritant contact dermatitis treatment remains controversial with no agreement among clinicians on whether they should be used.

Oral and topical steroids are usually well tolerated when used for short periods. Long term and widespread use may result in side effects, such as, cutaneous skin atrophy, hirsutism, and systemic absorption.

Ultraviolet light: UV therapy is generally recommended for use in the more refractive cases of allergic contact dermatitis, unresponsive to corticosteroid treatment or on patients who cannot avoid all the triggering factors in their environment. UV light has innate immunosuppressive properties and several studies have shown the effectiveness of oral psoralen photochemotherapy (PUVA) and short wave UV light (UVB) in chronic allergic contact dermatitis of the hand.

In one study, however, UVB, treatment took almost 5 months to get a response and maintenance therapy was required. The study showed that PUVA is better than UVB in treating chronic hand dermatitis. Another study showed that PUVA elicited more photonic reactions, suggesting that it should be used only if UVB treatment fails.

Immunomodulators: The introduction of calcineurin inhibitors, a class of immunosuppressant drugs, in the last decade represented another milestone in the progress of allergic contact dermatitis treatment, providing a better alternative to corticosteroids. As compared to corticosteroids, these drugs have much milder adverse effects.

Calcineurin inhibitors also act by inhibiting T-cell activity, which they do by inhibiting the protein calcineurin. Cyclosporin was one of the first calicineurin inhibitors to be used successfully in skin treatment. The effectiveness of oral cyclosporin in treating refractory atopic dermatitis is well documented, but the topical preparation is not as effective, due to its limited skin penetrating ability.

Tacrolimus and pimecrolimus are the newer drugs in this category and are more effective topical medications than cyclosporin. Tacrolimus was initially used to treat atopic dermatitis but later it was approved for treating the clinical manifestations of contact dermatitis as well. A study proved tacrolimus to be effective in treating allergic contact dermatitis, while avoiding skin atrophy, usually associated with long-term use of corticosteroids. Pimecrolimus is three times less potent than either tacrolimus or cyclosporin, but has a higher skin affinity, suggesting it may be more skin-selective.

The most common side effects of these calcineurin inhibitors are burning and stinging at the site of application, lasting up to 3 days in most patients.

Biologic agents: Biologic agents may be the most promising drugs of the future. They moderate inflammation by targeting cytokine TNF-alpha which plays a role in many organs, including the skin. TNF-alpha has been implicated in both irritant contact dermatitis and allergic contact dermatitis development.

Two known drugs that target TNF-alpha, infliximab and ethanercept, have not been fully studied for contact dermatitis treatment, though their success in treating psoriasis is well established. It is hoped that further studies, in the future, will establish the efficacy of the aforementioned drugs in allergic contact dermatitis treatment

Some innovative drugs are also being tested for allergic contact dermatitis treatment. NADH or B-nicotinamide adenine dinucleotide has substantial antioxidant properties and in a study was shown to reduce erythema and edema on all nine subjects, without any adverse effects. Phosphodiesterase inhibitors have also been suggested as non-steroidal, anti-inflammatory treatments for allergic contact dermatitis.

Avoidance protocol: The new immunomodulatory drugs hold the promise of doing away with the avoidance protocols in contact dermatitis treatment. This, however, goes against the basic tenet of treating an exogenous skin disease, which is removal of the triggering agent. Also, in systemic contact dermatitis caused by food allergens, significant clinical improvement can be obtained by dietary modifications or restrictions, which control the intake of the offending agent. Therefore, despite new drugs, it may not be possible to do away with the allergen avoidance protocols.