Purpose of review: Pregnancy is a hypercoaguable state. The hypothesis has been developed that many cases of recurrent miscarriage and of later pregnancy complications are caused by a defective maternal haemostatic response leading to thrombosis of the uteroplacental vasculature and subsequent fetal loss. The evidence upon which this hypothesis is based is reviewed.
Recent findings: The majority of studies report an increased prevalence of genetic thrombophilic mutations in the female partner of couples with recurrent miscarriage. It is important to note, however, that this is not a uniform finding. A sub-group of women with recurrent miscarriage has been demonstrated to be in a prothrombotic state before pregnancy, and that women in such a state are at an increased risk of miscarriage in future untreated pregnancies. Furthermore, the long-term health implications of this hypercoaguability have been highlighted in a large retrospective study reporting an increased risk of ischaemic heart disease among women with a history of pregnancy loss.
Summary: Although recurrent miscarriage is a heterogeneous condition and no single abnormality will account for all cases of pregnancy loss, the relationship between abnormalities in the haemostatic pathways and pregnancy outcome is increasingly recognized. The challenges we face are how to discriminate between women with a thrombophilic defect who are destined to miscarry from those whose pregnancy will be successful, the pathology of pregnancy loss associated with thrombophilic defects, the role of the fetal genotype in determining pregnancy outcome, and the management of women with thrombophilic defects both during and beyond their reproductive years.