As an interesting aside, Galanaud and coworkers (2010) hypothesized that a paternal thrombophilia could increase the risk of maternal thromboembolism. Specifically, these investigators found that a paternal thrombophilia-the PROCR 6936G allele-afects the endothelial protein C receptor. his receptor is expressed by villous trophoblast and thus is exposed to maternal blood. Although this research is preliminary, it could help explain the pathogenesis of recurrent idiopathic thromboses in pregnant women.
Some examples of acquired hypercoagulable states include anti phospholipid syndrome (APS), heparin-induced thrombocytopenia (p. 1015), and cancer.
his prothrombotic disorder can afect both the venous and arterial circulations. The deeper veins of the lower limbs and the cerebral arterial circulation are the most frequent sites of venous and arterial thrombosis, respectively (Connors, 2017; Giannakopoulos, 2013). Besides thrombosis, the other major clinical manifestations of the APS are obstetrical (Table 18-5, p. 353). Criteria include: (1) at least one otherwise unexplained fetal death at or beyond 10 weeks; (2) at least one preterm birth before 34 weeks' gestation because of eclampsia, severe preeclampsia, or placental insuiciency; or (3) at least three unexplained consecutive spontaneous abortions before 10 weeks.
Once one of the above clinical criteria-thrombosis or obstetrical-is met, anti phospholipid antibody testing should be performed to diagnose APS. hese patients should be tested for the presence of three factors: (1) lupus anticoagulant, (2) anticardiolipin immunoglobulin G and M (IgG and IgM) antibodies, and (3) anti-�2-glycoprotein I IgG and IgM antibodies. If any of these laboratory test results are positive, a conirmatory test is performed 12 weeks later (Connors, 2017).
Based on their study of 750 singleton pregnancies complicated by APS, Saccone and associates (2017) found that anticardiolipin antibody is the most common sole antiphospholipid antibody present; but anti-�rglycoprotein I is associated with the lowest live birth rate and highest incidences of preeclampsia, fetal-growth restriction, and stillbirth compared with anticardiolipin antibodies or lupus anticoagulant alone. hese investigators also observed that despite therapy with lowdose aspirin and prophylactic LMWH heparin, the chance of a liveborn neonate was only 30 percent for women with positive test results for all three antibodies.
The thrombosis risk rises signiicantly during pregnancy in women with APS. Indeed, up to 25 percent of thrombotic events in women with APS occur during pregnancy or in the puerperium. Looking at this a diferent way, women with APS have a 5-to 12-percent risk of thrombosis during pregnancy or the puerperium (American College of Obstetricians and Gynecologists, 2017 a). This syndrome is discussed in more detail in Chapter 59 (p. 1143).
Attention has been directed toward possible relationships between inherited thrombophilias and pregnancy complications other than thromboses. Summarized in Table 52-3 are the findings of 25 studies systematically reviewed by Robertson and associates (2005) and incorporated into the recommendations of the American College of Chest Physicians (Bates, 2012). Importantly, the considerable heterogeneity and wide conidence intervals illustrate the uncertainty of these associations.
Other investigations underscore the heterogeneity of results.