Abstract

Morbilliform drug eruptions, also called exanthematous drug eruptions, are a form of delayed cutaneous hypersensitivity characterized by erythematous macules or papules that coalesce to form large plaques. The eruption usually occurs 5 days to 2 weeks after administration of the causative agent. The most common causes are antibiotics, anti-epileptics, allopurinol, non-steroidal anti-inflammatories (NSAIDS), anxiolytics, anti-hypertensives, and diuretics. They can also be associated with viral infections, illicit drug use, blood products, IV contrast media, and may have a genetic predisposition. With the cessation of the causative drug, morbilliform eruptions usually resolve within 1–2 weeks. The main histological features of morbilliform drug eruptions are a superficial and deep perivascular infiltrate and interstitial spongiotic and psoriasisiform dermatitis in conjunction with vacuolar interface changes. Although not completely understood, the immunological mechanisms for morbilliform drug eruptions involve a type IVb and IVc hypersensitivity reaction, as described by Gell and Coombs. Treatment for exanthematous drug reactions includes cessation of the causative agent and treatment of symptoms associated with the reaction, particularly pruritus.

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