It is not precisely known how antiphospholipid antibodies cause damage, but it is likely that their actions are multifactorial. Platelets may be damaged directly by antiphospholipid antibody or indirectly by binding 32-glycoprotein I, which causes platelets to be susceptible to aggregation (Giannakopoulos, 2013). One theory proposes that phospholipid-containing endothelial cell or syncytiotrophoblast membranes may be damaged directly by the antiphospholipid antibody or indirectly by antibody binding to either 3z-glycoprotein lor annexin V (Rand, 1997, 1998). his prevents the cell membranes from protecting the syncytiotrophoblast and endothelium. This exposes the basement membrane, to which damaged platelets can adhere and form a thrombus.
Pierro and associates (1999) reported that antiphospholipid antibodies decreased decidual production of the vasodilating prostaglandin E2. Diminished protein C or S activity and greater prothrombin activation may also be contributory (Zangari, 1997). Evidence also supports that thrombosis with APS stems from activation of the tissue factor pathway (Amengual, 2003). Finally, uncontrolled placental complement activation by anti phospholipid antibodies may playra role in fetal loss and growth restriction (Holers, 2002).
Complications from APS cannot be completely explained by thrombosis alone. Animal models suggest that efects are due to inflammation rather than thrombosis (Cohen, 2011). Some investigators hypothesize that APS-associated clotting is triggered as a "second hit" from innate inflammatory immune responses. These investigators recommend treatment with antiinlammatory agents (Meroni, 2011).
Overall, antiphospholipid antibodies are generally associated with higher rates of fetal wastage (Chap. 18, p. 353). In most early reports that describe these outcomes, however, women were included because they had had repeated adverse outcomes.
Both antibody prevalence and miscarriage are common-recall that the incidence of antiphospholipid antibodies in the general obstetrical population is about 5 percent and early pregnancy loss approximates 20 percent. Accordingly, current data are too limited to conclude the exact risks for adverse efects of these antibodies on pregnancy outcomes. Fetal deaths, however, are more characteristic with APS than are first-trimester miscar riages (Oshiro, 1996; Roque, 2004). Moreover, women with higher titers have worse obstetrical outcomes compared with those with low titers (Hadar, 2017; Nodler, 2009).