WITH the discovery of agammaglobulinemia in 1952,1 a pressing need emerged for antibody-replacement therapy to prevent serious bacterial infections. Intramuscularly administered immune serum globulin resulted in a remarkable decrease in the incidence of such infections in patients with this type of immunodeficiency; however, the injections were painful, and the IgG was absorbed slowly and was subject to local proteolysis. Intravenous administration of immune serum globulin resulted in shocklike episodes, chills, and hyperpyrexia, especially in sick and acutely infected children. Beginning in the early 1960s, many attempts were made to modify immune serum globulin so that it could be given safely . . .
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Oates et al. (1991) studied this question.
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