Drug Allergies

Introduction

Adverse drug reactions or drug allergy, account for 6-10% of all drug effects. There are a number of specific characteristics that are generally helpful in distinguishing drug allergy symptoms from other common drug allergies. They tend to occur in only a small fraction of patients, are producible with minute amounts of the drug, that can mimic other allergic reactions, and they do not resemble other known pharmacologic effects.

Many drug-hypersensitivity reactions can be classified according to the Gell and Coombs schema. This a synopsis of the manifestations of each reaction type. Penicillin allergy symptoms have been associated with all of them. In the Type I or anaphylactic mechanism, allergen is recognized by IgE bound by receptors to mast cells or basophils. The crosslinking of IgE by allergen results in cellular release of mediators, such as histamine, leukotrienes, and prostaglandins. The cytotoxic or Type II mechanism involves antibody recognition of cell-bound antigen; this antibody fixes complement, which causes cell damage. In addition to those drug allergy interactions hyperensitivities that are classifiable according to the Gell and Coombs schema, there are other adverse reactions which appear to be immunologically mediated that do not fit into this schema. Examples include pulmonary infiltrates from nitrofurantoin and interstitial nephritis from methicillin. Further, there are also adverse drug reactions that closely mimic the manifestations of immunologically mediated reactions, but no immunologic mechanism can be demonstrated. An example would be the anaphylactoid reactions to opiates that have been described in certain cases.