The first clinical trial of IVIG to treat ITP was reported in 1981 and the increased platelet counts were soon confirmed by other investigators,4 resulting in IVIG becoming a standard treatment for ITP.
The exact mechanisms of action of IVIG are still unknown. Of many hypotheses, one involves blockage of Fc receptors by the IgG molecules in IVIG, as well as blockage (competitive inhibition of MPS sequestration of antibody-coated platelets) by patient red cells sensitized with blood group antibodies in the IVIG preparations. Antibodies shown to be present in IVIG include anti-A, -B, -D, and -K.5 This finding is consistent with the mild hemolysis associated with receiving IVIG, although in some patients severe transient hemolytic anemia has occurred.
Adverse effects of IVIG are common but generally mild, including headache, backache, nausea, and fever. However, renal failure, pulmonary insufficiency, and thrombosis, including stroke and myocardial infarction, have been reported as complications.2 In 1999 the U.S. Food and Drug administrationoman; (FDA) issued an alert of renal dysfunction and/or acute renal failure occurring following IVIG therapy, with most associated with sucrose-containing products.6
TraQ addition: IVIG has also been associated with transfusion-related acute lung injury (TRALI).15
- Part 1: Determining antibody specificity
- Part 2: Immmune thrombocytopenic purpura (ITP)
- Part 3. Intravenous immune globulin (IVIG) <--You are here
- Part 4: Intravenous RhIG therapy in ITP
- Part 4a: Passive antibodies (tools and resources)
- Part 4b: Severe hemolysis (tools and resources)