The effect of antiplatelet autoantibodies on megakaryocytopoiesis

Abstract

Immune thrombocytopenic purpura (ITP) is a disorder manifested by isolated thrombocytopenia. In vivo infusion studies in the 1950s and 1960s provided evidence that the thrombocytopenia was due to autoantibody-induced platelet destruction. However, there is mounting evidence that platelet production in this disorder may also be suppressed by antibodies. Early morphologic studies showed megakaryocytic damage in ITP, and these results have been confirmed by ultrastructural studies. Autologous platelet turnover studies in the 1980s showed that most ITP patients have either normal or reduced platelet turnover rather than increased turnover, as would be expected if platelet destruction were the only pathogenetic mechanism. More recently, in vitro culture studies of both adult and pediatric ITP have shown that some ITP plasmas suppress both megakaryocytopoiesis and thrombopoiesis. In view of these findings, both platelet destruction and suppression of platelet production seem likely to be involved in the pathogenesis of ITP.