With the decline in use of heterologous serum products since the beginning of this century, there has been a marked reduction in the incidence of serum sickness in humans. Current heterologous proteins still in use are antithymocyte globulin and anttsnake venom which carry with them a dose-dependent risk of serum sickness. Reactions resembling serum sickness have been associated with various nonprotein drugs, in particular cefaclor, (3-lactam antibiotics, streptokinase and p blockers. This serum sickness-like illness has been postulated to be due to drug-related hapten antibodies, but this has never been proven. Other plausible alternatives arc direcr toxicity to the vessel wall, development of autoantibodies to endothelial cells and cell-mediated cytotoxicity. Most cases of drug-induced serum sickness are not associated with hypocomplementemia, which is a feature of classic serum sickness.
The typical clinical presentation of serum sickness in humans is seen 8-14 days after antigen exposure unless sensitization has occurred. The commonest clinical presentation is the development of fever, Ivm-phadenopathy and morbilliform rash which normally starts in the extremities. Urticaria may occur, but is less common. Fifty per cent of cases have associated visceral involvement of which arthralgia and arthritis are the most common. Significant systemic vasculitis and glomerulonephritis are uncommon although transient abnormalities are often noted on urinalysis. Classically there is depletion of complement; investigations reveal low C3 and C4 levels.
Treatment involves withdrawal of the suspected antigen, symptomatic relief with antihistamines, analgesics and steroids if indicated. Effective treatments in animal studies include antioxidants, cyclosporine and plasmapheresis; these have not been subject to clinical trials in humans.
See also: Heterophil antibodies; Hypersensitivity reactions; Immune complexes.
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