ABSTRACT
Following the pioneering work by Barandun at the ZLB Central Laboratory in Berne on the formulation of immunoglobulin suitable for intravenous infusion (IVIG)1, the first substantial clinical studies of IVIG were reported in the early 1980s. Patients with severe anti-body deficiency had previously relied on regular plasma infusions or intramuscular injections of pooled immunoglobulin (IMIG), with a strong clinical impression that this replacement therapy reduced the incidence of infection. Many immunologists had assumed that only small amounts of specific antibody were necessary to protect against infection, but it soon became clear that higher doses reduced the infection rate. The first indication of this came from the Medical Research Council (MRC) trial in the late 1960s where two doses of intramuscular immunoglobulin were compared, with a significant reduction in signs of infections with the higher dose (50mg/kg/week)2. It was not practicable to increase the amount of IMIG any further because of the discomfort and frequency of reactions after injection. Nevertheless, there was a growing consensus that higher doses given intravenously would be beneficial, and subsequent trials comparing IVIG with IMIG supported this view (reviewed in reference 3).
