COMMENTARY: Thrombophilia and pregnancy loss in first intended pregnancy

Abstract

To cite this article: Brenner B. Thrombophilia and pregnancy loss in first intended pregnancy. J Thromb Haemost 2005; 3: 2176-7. See also Lissalde-Lavigne G, Fabbro-Peray P, Cochery-Nouvellon E, Mercier E, Ripart-Neveu S, Balducchi J-P, Dauré s J-P, Perneger T, Qué ré I, Dauzat M, Maré s P, Gris JC. Factor V Leiden and prothrombin G20210A polymorphisms as risk factors for miscarriage during a first intended pregnancy; the matched case-control 'NOHA first' study. This issue, pp 2178-84. Recurrent pregnancy loss is a common health problem affecting 1-5% of women at the reproductive age and bears significant emotional, social and economical impact [1]. A number of case-control and cohort studies have suggested an association between inherited thrombophilia and recurrent pregnancy loss while others refuted this occurrence [2-6]. Several recently reported meta-analysis support an association between maternal factor V Leiden (FV Leiden) and factor II G20210A genotypes and pregnancy loss [7-9]. These findings have lead to the introduction of thrombo-philia workup in women at risk, particularly in those with recurrent or late pregnancy loss. Documentation of thrombo-philic risk factors in women with pregnancy complications may have significant therapeutic implications as a number of clinical studies have demonstrated the potential efficacy of prophylaxis with low molecular weight heparin (LMWH) in these settings [10,11]. While interpretation of the results of these studies arose some debate [12-22], it is clear that the field of thrombophilia and pregnancy complications continues to be in the focus of medical research and clinical practice. Studies on the association of thrombophilia and gestational complications in populations of pregnant women have revealed conflicting results [6,23] partly explained by variance in incidence of thrombophilic polymorphisms in different ethnic backgrounds and studies not powered for evaluation of the potential associations. Differences in type of pregnancy loss i.e. primary or secondary, isolated or recurrent, consecutive or non-consecutive and timing of its occurrence i.e. first, second or third trimester may also influence the magnitude of these associations [24-26].

Thrombophilia and anticoagulation in pregnancy: indications, risks and management

“…Although there is accumulating evidence that inherited thrombophilia can be associated with placental vascular complications such as fetal loss, intrauterine growth restriction, placental abruption and pre-eclampsia [31][32][33]38,85], there is a controversy concerning the precise risk of these complications and the causal relationship to thrombophilia [28,86]. Comprehensive debates have been published on that in the recent literature [87,88].…”

“…Women with thrombophilia show an increased risk for pregnancy loss at the end of the first and in the second trimester [31,32] and those with FVL or prothrombin gene variant show a higher risk of late pregnancy loss (424 weeks) [4,13]. Recurrent pregnancy loss has been linked to inherited thrombophilia, particularly with protein C and S deficiency, FVL and a prothrombin gene variant [29,37,38], but the evidence is limited. A significant association with increased risk for placental abruption was only observed with heterozygous FVL and the prothrombin gene variant [13,39].…”

Thrombophilia and Pregnancy Complications

“…primary or secondary, isolated or recurrent, consecutive or nonconsecutive and timing of its occurrence i.e. first, second or third trimester may also influence the magnitude of these associations (19)(20)(21).…”

Evaluation of factor VIII value in normal women and whom encountered recurrent pregnancy loss: is there any significant difference?

“…15,[17][18][19][20][21][22] It is hypothesized that thrombophilia may increase the risk of placental insufficiency because of placental micro and/ or macro-vascular thrombosis, as well as effects on trophoblast growth and differentiation. 1,23,24 Factor VIII (FVIII) is an essential blood-clotting protein, also known as anti-hemophilic factor (AHF). in humans the factor VIII is encoded and produced by the F8 gene shown in (Figure 1).…”