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This chapter discusses three auto-immune hematological conditions that may complicate pregnancy: immune/idiopathic thrombocytopenic purpura (ITP), autoimmune hemolytic anemia (AIHA), and autoimmune neutropenia (AIN). They are characterized by the development of an autoantibody specific for a surface antigen on the platelet, erythrocyte, or neutrophil. ITP usually occurs in isolation but may occur with other immune cytopenias or be secondary to a systemic autoimmune condition, e.g. SLE. The pathogenesis of AIN is similar to that of other maternal immune cytopenias. Patients with symptomatic neutropenia are likely to present outside of pregnancy and have an established diagnosis. The differential diagnosis includes: drugs, viral infections, immune mediated disorders, large granular lymphocyte (LGL) disease, benign ethnic neutropenia, and CIN. For patients presenting during pregnancy, the diagnosis of AIHA requires careful exclusion of other causes of anemia, biochemical evidence of hemolysis and serological evidence that the hemolysis is immune mediated.
Pre-eclampsia remains a leading cause of maternal and fetal morbidity and mortality. It is a pregnancy-specific multisystem disorder, occurring most commonly in primigravidae and characterized by the development of hypertension and proteinuria in the second half of pregnancy. The incidence in a second pregnancy is less than 1% in women who have had a normotensive first pregnancy, but is increased in women who have had pre-eclampsia in their first pregnancy, particularly in women whose first pregnancy was complicated by severe pre-eclampsia (Campbell et al., 1985). This issue is more completely discussed in the chapter by Dekker and Robillard in this book. The pathogenesis of pre-eclampsia is not fully understood but it is believed that genetic predisposition and immune maladaptation lead to placental ischemia and perturbation of the maternal vascular endothelium. Coagulation activation is an important feature and hypercoagulable states, including both inherited and acquired thrombophilias, have been associated not only with pregnancy thromboembolism but also with other adverse pregnancy events.
The primary initiator of coagulation is tissue factor. Tissue factor (TF) is expressed by epithelial, stromal and perivascular cells throughout the body but not normally by cells in contact with the circulation. Following vascular damage, membrane-bound TF complexes with factor VII (FVII). Cleavage of FVII results in the formation of activated FVIIa. Thereafter TF–FVIIa complex can directly activate factor X (FX). TF–FVIIa complex may also activate FX indirectly via activation of factor IX (FIX).
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