SERUM SICKNESS & VASCULITIC (TYPE III) REACTIONS
Immunologic reactions to drugs resulting in serum sickness are more common than immediate anaphylactic responses, but type II and type III hypersensitivities often overlap. The clinical features of serum sickness include urticarial and erythematous skin eruptions, arthralgia or arthritis, lymphadenopathy, glomerulone-phritis, peripheral edema, and fever. The reactions generally last 6–12 days and usually subside once the offending drug is elimi-nated. Antibodies of the IgM or IgG class are usually involved. The mechanism of tissue injury is immune complex formation and deposition on basement membranes (eg, lung, kidney), fol-lowed by complement activation and infiltration of leukocytes, causing tissue destruction. Glucocorticoids are useful in attenuat-ing severe serum sickness reactions to drugs. In severe cases plas-mapheresis can be used to remove the offending drug and immune complexes from circulation.
Immune vasculitis can also be induced by drugs. The sulfon-amides, penicillin, thiouracil, anticonvulsants, and iodides have all been implicated in the initiation of hypersensitivity angiitis. Erythema multiforme is a relatively mild vasculitic skin disorder that may be secondary to drug hypersensitivity. Stevens-Johnson syndrome is probably a more severe form of this hypersensitivity reaction and consists of erythema multiforme, arthritis, nephritis, central nervous system abnormalities, and myocarditis. It has fre-quently been associated with sulfonamide therapy. Administration of nonhuman monoclonal or polyclonal antibodies such as rattle-snake antivenin may cause serum sickness.