Pre-eclampsia as a manifestation of antiphospholipid syndrome: assessing the current status.

Abstract

The presence of antiphospholipid antibodies is considered a risk factor for pre-eclampsia. Two meta-analyses and a number of case-control and cohort studies have found associations between pre-eclampsia and lupus anticoagulant, anticardiolipin, and/or anti-β2 glycoprotein I. However, existing literature is inconsistent, with varying severity of pre-eclampsia phenotype examined, differing aPL titer cutoffs used to define positive status, and an overwhelming lack of repeat confirmatory aPL testing. This calls into question the link between aPLs and pre-eclampsia, or at least makes it less well defined. There is evidence for a mechanistic pathway between aPLs and adverse pregnancy outcomes (APOs) including pre-eclampsia via the complement pathway. Complement appears to be overactive in pregnancies affected by APOs. A mouse model has show that the fetal wastage caused by treatment with human aPLs can be salvaged by either creating genetic knockouts along the complement, TNF-alpha, and tissue factor pathways or be treating mice with monoclonal antibodies blocking key complement factors. Thus, this is worth further investigation to clarify the likely association of aPLs and pre-eclampsia in humans, as well is to further evaluate the interaction with complement in human pregnancies.