Histopathology in the placentae of women with antiphospholipid antibodies: A systematic review of the literature

Background: Antiphospholipid antibodies (aPLs) are a heterogenous group of autoantibodies associated with recurrent miscarriage, stillbirth, foetal growth restriction and premature birth. The cause of obstetric morbidity in women with aPLs is not completely understood. Workers have attempted to understand the role of aPLs in obstetric morbidity by investigating the histopathology of placentae from aPL-positive women. However, it is unclear from these diverse, and at times contradictory reports what histopathological lesions are common in the placentae of women with aPLs. This systematic review was undertaken to generate a complete picture of the placental features associated with aPLs in an attempt to understand the pathological processes that occur in pregnancies affected by aPLs. Methods: Pubmed, Scopus, Web of Science and Embase were searched on the 27th November 2014 using the keywords placenta OR trophoblast AND antiphospholipid antibody OR antiphospholipid antibody syndrome. Records that were relevant and eligible were qualitatively assessed and given a score out of 24. Results: Of the 1112 records that were retrieved from the systematic search, 34 records were eligible for review, and were qualitatively scored. Of the 44 histopathological features that were reported in 580 placentae from aPL-positive women, six features appeared to be more common in the placentae of aPL-positive women compared to control women, including: placental infarction, impaired spiral artery remodelling, decidual inflammation, increased syncytial knots, decreased vasculosyncytial membranes and the deposition of complement split product C4d. Conclusion: Based on the evidence in this systematic review, a human placental aPL fingerprint has been proposed. The diversity of the human placental aPL fingerprint suggests that multiple pathological processes may occur in pregnancies affected by aPL. (C) 2015 Elsevier B.V. All rights reserved.