Table 4.

Mechanisms of APL-induced pregnancy morbidity

The possible mechanisms of action can be summarized as follows: 1. Inhibition of trophoblastic invasiveness, function and differentiation → early pregnancy loss rather than intervillous thrombosis 2. Decreased prostacyclin production by endothelial cells; platelets are therefore released to act in step 3 3. Increased thromboxane production by platelets; the outcome is increased platelet aggregation 4. Decreased protein C activation 5. Disruption of placental protein, annexin V 6. Activation of the complement pathways at the maternal fetal interface → local inflammatory response 7. Thrombosis of the uteroplacental vasculature → infarction of placenta → placental insufficiency (later in pregnancy) 8. Higher risk of thrombosis with lupus anticoagulant than with ACL antibodies