Allergic Contact Dermatitis Medication
- Author: Daniel J Hogan, MD; Chief Editor: William D James, MD more...
The goal of pharmacotherapy is to reduce morbidity and to prevent complications. Topical glucocorticosteroids are the mainstay of therapy. Topical calcineurin inhibitors (immunomodulators) may be preferred for persistent facial particularly periocular dermatitis. When choosing a topical glucocorticosteroid, match the potency to the location of the dermatitis and the vehicle to the morphology (ointment for dry scaling lesions; lotion or cream for weeping areas of dermatitis).
For severe acute allergic contact dermatitis (eg, poison ivy dermatitis, erythroderma), systemic glucocorticosteroids or other immunosuppressive medications (eg, azathioprine) may be occasionally needed for widespread and severe chronic dermatitis, particularly to airborne allergens such as feverfew (Parthenium hysterophores).
In some cases, allergic contact dermatitis may prove persistent despite avoidance of the allergen. In some of these cases (eg, nickel), ingestion of minute amounts of the allergen is believed to drive the process, and chelation therapy with disulfiram can be beneficial. In other instances, the cause of persistence remains enigmatic; many allergens penetrate through rubber gloves. Psoralen–ultraviolet A (PUVA) therapy can be helpful in these cases.
Oral antihistamines may help diminish pruritus caused by allergic contact dermatitis.
These agents modify immune processes that promote inflammation.
Pimecrolimus is indicated for eczema and atopic dermatitis. It was the first nonsteroid cream approved in the United States for mild-to-moderate atopic dermatitis. Pimecrolimus is derived from ascomycin, a natural substance produced by fungus Streptomyces hygroscopicus var ascomyceticus.
This agent selectively inhibits production and release of inflammatory cytokines from activated T cells by binding to cytosolic immunophilin receptor macrophilin-12. The resulting complex inhibits phosphatase calcineurin, thus blocking T-cell activation and cytokine release. Cutaneous atrophy was not observed in clinical trials, a potential advantage over topical corticosteroids.
Tacrolimus reduces itching and inflammation by suppressing release of cytokines from T cells. It also inhibits transcription for genes that encode interleukin 3 (IL-3), IL-4, IL-5, granulocyte-macrophage colony-stimulating factor (GM-CSF), and tumor necrosis factor–alpha (TNF-alpha), all of which are involved in the early stages of T-cell activation.
Additionally, tacrolimus may inhibit release of preformed mediators from skin mast cells and basophils and may down-regulate expression of high-affinity IgE receptor (FCeRI) on Langerhans cells.
Tacrolimus is approved for moderate-to-severe atopic dermatitis and can be used in patients as young as 2 years. It is more expensive than topical corticosteroids. This agent is available as ointment in concentrations of 0.03 and 0.1%.
Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli.
A class I superpotent topical steroid, clobetasol suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction. Use 0.05% cream or ointment.
Hydrocortisone is an adrenocorticosteroid derivative suitable for application to skin or external mucous membranes. It has mineralocorticoid and glucocorticoid effects resulting in anti-inflammatory activity. Use 0.2% cream or ointment.
Prednisone is an immunosuppressant for treatment of autoimmune disorders; it may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear neutrophil (PMN) activity. Prednisone stabilizes lysosomal membranes and suppresses lymphocytes and antibody production.
Triamcinolone is indicated for inflammatory dermatosis responsive to steroids; it decreases inflammation by suppressing migration of PMNs and reversing capillary permeability. Intramuscular injection may be used for widespread skin disorder or intralesional injections may be used for localized skin disorder.
Antihistamines act by competitive inhibition of histamine at the H1 receptor. They may control itching by blocking effects of endogenously released histamine. These agents have no role in treating allergic contact dermatitis beyond possibly decreasing pruritus via sedating effects.
Hydroxyzine antagonizes H1 receptors in the periphery. It may suppress histamine activity in the subcortical region of the central nervous system.
The tricyclic antidepressant doxepin is used in contact dermatitis for its sedative and antihistaminic properties. Oral doxepin may be considered if oral antihistamines are not helpful. Topical doxepin should be avoided because of the risk of iatrogenic allergic contact dermatitis.
Doxepin inhibits histamine and acetylcholine activity and has proven useful in the treatment of allergic dermatologic disorders. The oral form is marketed as an antidepressant but is used also for its antihistaminic/antipruritic effects. The dosage is 10-25 mg at night in adults; if necessary, this can be gradually increased to a maximum dose of 75 mg/d for dermatoses. The topical form is approved for pruritus in adults with atopic dermatitis or lichen simplex chronicus.
Although marketed as a treatment for alcoholism, disulfiram chelates nickel, which then is excreted in the urine. Lowering systemic levels of nickel has been reported to benefit individuals with pompholyx (dyshidrosis) and demonstrated hypersensitivity to the metal. Consider this therapy only for severe disabling dyshidrosis refractory to all other treatment in a patient proven allergic to nickel who does not drink alcohol and who consents to regular blood tests to identify liver toxicity from the medication.
Disulfiram is a thiuram derivative that interferes with aldehyde dehydrogenase. In patients highly allergic to nickel with severe vesicular hand dermatitis, the chelating effect of disulfiram is helpful in reducing the body's nickel burden in the individual allergic to nickel. Do not administer if patient has ingested alcohol within last 12 hours.
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