HE INCREASED utilization of automated blood counts T by obstetricians has led to the realization that pregnancy may often be complicated by the development of thrombocytopenia. Thrombocytopenia in pregnant individuals may result from the effects of several diverse processes, which may be either physiologic or pathologic. In addition to disorders that may cause thrombocytopenia in nonpregnant women, pregnant patients are at risk for the development of thrombocytopenia caused by syndromes such as preeclampsia, which are unique to pregnancy. Thus, determining the significance of thrombocytopenia in a pregnant patient depends on the accurate identification of its underlying cause. In this report we review the major causes of thrombocytopenia that occur during pregnancy, and discuss their pathogenesis and management. These include the syndromes of immune thrombocytopenic purpura (ITP), preeclampsia and the HELLP syndrome (hemolysis, elevated liver function tests, low platelets), thrombotic thrombocytopenic purpura (TTP), and the hemolytic uremic syndrome (HUS). Other causes of thrombocytopenia in pregnancy, such as systemic lupus erythematosus (SLE), type I1 von Willebrand disease (vWD), and disseminated intravascular coagulation will be discussed only briefly. It is likely that ihe pathophysiology of these diverse syndromes involves complex interactions between platelets and the vessel wall, antiplatelet antibodies and IgG-containing immune complexes. The integrity of the maternal and fetal reticuloendothelial systems, as well as the efficiency of platelet production by megakaryocytes within fetal and maternal bone marrow (BM), also play important roles in determining the severity of thrombocytopenia that may develop in a particular individual. These considerations highlight the need to further clarify the complex processes that influence the maternal and fetal platelet counts during pregnancy.