Factor V Leiden, prothrombin G20210A and antibodies against phospholipids in recurrent spontaneous abortion

Abstract

Recurrent idiopathic pregnancy loss is multifactorial, involving acquired (immunologic) and/or inherited factors, such as point mutations in factor (F) V G1691A/R506Q (FV-Leiden), and prothrombin (PRT; G20210A) genes [1]. Mounting evidences point to a link between autoimmunity and idiopathic pregnancy loss [2], as specific antiphospholipid (PL) autoantibodies including anticardiolipin antibodies (ACL [3]); and lupus anticoagulants (LA;[4]), described as major risk factor for thromboembolism [4], were detected in the sera of aborting women [5]. FV Leiden/R506Q and prothrombin (PRT) G20210A are G (r) A transition at nucleotide 1691 and 20210 in the FV and PRT genes, respectively, and are significant causes of inherited thrombophilia [6, 7]. The link between poor obstetrical outcome and high anti-PL levels [2] or FV-Leiden and PRT G20210A point mutations [8–10] was suggested by some [11], and disputed by others [12]. In view of the lack of data on North African population, in particular Tunisia, on the role of anti-PL antibodies and FV Leiden and PRT G20210A mutation on recurrent pregnancy loss, this study addresses their prevalence in 146 recurrent abortion women and 99 age-matched controls.