[45-OR]: Thrombophilia and the origin of preeclampsia: Rumors of the past?

Objectives The contribution of thrombophilia to the etiology of preeclampsia is becoming less apparent. Previous case-control studies has shown possible associations between thrombophilia and preeclampsia, but later published prospective studies could not reproduce these associations. Whether the phenotypes of preeclampsia matter in these possible associations remains unclear. We wanted to test possible associations between thrombophilia and two important phenotypes of preeclampsia: with/without HELLP and with/without IUGR. Methods A retrospective cohort was formed of women who delivered between 1985 and 2010 in the Erasmus medical center, Rotterdam, The Netherlands, who were diagnosed with preeclampsia and were tested at least 6 weeks postpartum for thrombophilia. Tests included anti-cardiolipin antibodies (IgG and IgM), APTT lupus, APC-ratio, protein-C level (act and ag), Protein-S level (act and free), factor-V-Leiden mutation (heterozygous) and prothrombin gene mutation (heterozygous). Factor analysis with a 2-fixed axis model was used to test for associations and clustering of associations. Results 771 Women with preeclampsia were included in the cohort: 23% had no HELLP and IUGR, 27% only had IUGR, 17% only had HELLP and 33% had HELLP and IUGR. Factor-analysis showed clustering of protein-C and protein-S, as well as clustering of factor-Leiden, APC-ratio, APTT lupus and anti-cardiolipin IgM antibodies (added figure). However, the model could only explain 33% of the existing variance. Conclusions Since our model only explained one-third of the variance, we conclude that thrombophilia is poorly associated with HELLP and IUGR in preeclampsia. Combined with the absence of associations in previous prospective studies, this finding confirms that contribution of thrombophilia to the etiology of preeclampsia is limited. Therefore, testing for thrombophilia after preeclampsia should not be standard practice. Disclosures D. Berks: None. W. Visser: None. M.P. De Maat: None. E.A. Steegers: None. H.J. Duvekot: None.