摘要: Multiple effectors are involved in reducing platelet survival. These include the spleen, liver, vascular endothelial system, elements of adaptive and innate immune systems, coagulation system. organs circulating factors typically act concert with one another – to varying degrees depending upon etiology pathological removal. Improved understanding molecular mechanisms has led increased recognition complement as an etiologic agent thrombocytopenia, leading new therapeutic possibilities. The activated cell promotes activation enhanced consumption, particularly setting heparin-induced thrombocytopenia where a significant prothrombotic state is promulgated despite thrombocytopenia. In other disorders, cofactors important regulation (atypical hemolytic uremic syndrome) or cleavage ultra large multimers von Willebrand factor (thrombotic thrombocytopenic purpura) reduced absent heightened consumption defects. Depending their specificity, elaboration autoantibodies (immune thrombocytopenia) alloantibodies (human leukocyte antigen alloimmunization, neonatal alloimmune posttransfusion results abnormal clearance. Due presence target antigens on donor platelets, transfusion unselected platelets these circumstances associated poor increments. A basic pathobiology processes may therefore improve diagnostic treatment decisions open doors research.