Peripheral and visceral thromboses are also a feature. For example, Ahmed and associates (2009) reported a postpartum ing a mesenteric vessel infarction. Obstetrical complications relected by fetal-growth restriction, stillbirth, preeclampsia, and preterm birth. Treatment using aspirin, anticoagulation, and close monitoring has increased live birth rates to more than 70 percent in these women (Schreiber, 2016).
A small proportion of these patients develop the catastrophic drome. his is deined as a rapidly progressive thromboembolic or tissues (Schreiber, 2016). It has a high mortality rate from activation of a cytokine storm. In half of cases, a "triggering" event is identiied.
As mentioned, several antibodies in APS are directed against a speciic phospholipid or phospholipid-binding protein: 1.
32-Gycoprotein I-also known as apolipoprotein H-is a phospholipid-binding plasma protein that inhibits prothrombinase activity within platelets and inhibits platelet aggregation (Giannakopoulos, 2013). hus, its normal action is to limit procoagulant binding and thereby prevent coagulation cascade activation. Logically, antibodies directed against this glycoprotein would reverse its anticoagulant activity and promote thrombosis. This is important from an obstetrical viewpoint because 32-glycoprotein I is expressed in high concentrations on the syncytiotrophoblast surface. Complement activation may contribute to its pathogenesis (Avalos, 2009; Tsokos, 2011). Teleologically, this seems appropriate because the decidua intuitively should be a critical area to prevent coagulation that might lead to intervillous space thrombosis. Another possibility is that 32-glycoprotein I may be involved in implantation, and this glycoprotein may result in pregnancy loss via an inlammatory mechanism (Iwasawa, 2012; Meroni, 2011).
2.
Lupus anticoagulant (LAC) is a heterogeneous group of antibodies directed against phospholipid-binding proteins. This antibody group induces prolongation in vitro of the prothrombin, partial thromboplastin, and Russell viper venom times. hus, paradoxically, this so-called anticoagulant is actually powerfully thrombotic in vivo.
3.
Anticardiolipin antibodies (ACAs) are directed against one of the many phospholipid cardiolipins found in mitochondrial membranes and platelets.
Some anti phospholipid antibodies are also directed against the natural anticoagulant proteins C and S (Robertson, 2006). Another is directed against the anticoagulant protein annexin V, which is expressed in high concentrations by syncytiotrophoblast
TABLE 59-5. Some Clinical Features of Antiphospholipid Syndrome
Venous thrombosis-thromboembolism, thrombophlebitis, livedo reticularis
Arterial thrombosis-stroke, transient ischemic attack, Libman-Sacks cardiac vegetations, myocardial ischemia, distal extremity and visceral thrombosis and gangrene
Hematological-thrombocytopenia, autoimmune hemolytic anemia
Other-neurological manifestations, migraine headaches, epilepsy; renal artery,
Pregnancy-preeclampsia syndrome, recurrent miscarriage, preterm delivery, fetal-growth restriction, fetal death
Data from Giannakopoulos, 2013; Moutsopoulos, 2015.