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.
