Practice Essentials
Serum sickness is a type III hypersensitivity reaction that results from the injection of heterologous or foreign protein or serum. Reactions to nonprotein drugs are clinically similar to serum sickness reactions.
Historically, the term serum sickness connotes a self-limited syndrome caused by deposition of immune complexes resulting from exposure to foreign proteins or haptens. Von Pirquet and Schick first described the syndrome in 1905, reporting fever, skin eruptions (mainly consisting of urticaria), joint pain, and lymphadenopathy in regions draining the site of injection after patients were given antitoxin in the form of horse serum. [1] Later, physicians reported a similar clinical picture after the injection of other equine-based antitoxins and antivenins. [2]
Certain medications (eg, penicillin, nonsteroidal anti-inflammatory drugs [NSAIDs]) have also been associated with serum sickness–like reactions. These reactions typically occur 1 to 3 weeks after exposure to the drug, but may occur as early as 1 to 24 hours afterward. Accelerated reactions are T-cell mediated, although an IgE mechanism cannot always be ruled out. [3]
Identifying serum sickness was a landmark observation in understanding immune complex diseases.
Withdrawal of the offending agent is the mainstay of treatment in serum sickness. Anti-inflammatory drugs and antihistamines provide symptomatic relief. Severe cases (multisystem involvement with significant symptoms [4] ) may warrant a brief course of corticosteroids. In some cases, plasmapheresis can attenuate serum sickness. [5]
