Activated Protein C Resistance and Factor V Leiden Mutation can be Associated with First‐ as well as Second‐Trimester Recurrent Pregnancy Loss1

Js, Younis; Brenner, Benjamin; Ohel, Gonen; Tal, J.; Lanir, Naomi; Ben‐Ami, Moshe

doi:10.1111/j.8755-8920.2000.430106.x

Cited by 119 publications

(99 citation statements)

References 15 publications

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“…Grandone et al (1997) reported a 31.2% prevalence of factor V Leiden in women with second trimester fetal losses compared to 4.2 % in matched controls. These findings were further supported by Younis et al (2000) who described a significantly higher incidence of factor V Leiden in women with first trimester and second trimester losses compared to a control group; 16%; 22% and 6% respectively. Reznikoff-Etievant et al (2001) also found a higher incidence of factor V Leiden; 10.38% (27/260) compared to a control group (4.7 % (11/240)).…”

Section: Hereditary Apcr (Factor V Leiden) and Pregnancy Losssupporting

confidence: 56%

“…However, in those studies that do address this, none of them dispute the definite association between acquired APCR and recurrent pregnancy loss. Younis et al (2000) were intrigued with their finding of a higher prevalence of acquired as opposed to hereditary activated protein C resistance in the second trimester. Rai et al (2000), also reported a significantly higher incidence of acquired APCR in women with recurrent first trimester and second trimester losses 8.8% (80/904) and 8.7%(18/207), compared to a control group of parous women 3.3%(5/150).…”

Section: Acquired Apcr and Pregnancy Lossmentioning

confidence: 99%

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Inherited and Acquired Thrombophilia in Pregnancy

Dawood¹

2011

Thrombophilia

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Section: Hereditary Apcr (Factor V Leiden) and Pregnancy Losssupporting

confidence: 56%

Section: Acquired Apcr and Pregnancy Lossmentioning

confidence: 99%

Inherited and Acquired Thrombophilia in Pregnancy

Dawood¹

2011

Thrombophilia

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“…In a subgroup of patients with 3 or more pregnancy losses and no successful pregnancies, the prevalence of the mutation was 9% OR 2.6, 95% CI, 1-6.7. Younis et al [108]. evaluated APCR and the FV Leiden mutation in women with first trimester recurrent embryonic loss, in women with second trimester loss and controls.…”

Section: Prevalence Of Inherited Thrombophilias In First and Second Tmentioning

confidence: 99%

Thrombophilia and pregnancy

Brenner¹

2005

Eur J Clin Investigation

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Pregnancy is hypercoagulable state. The field of thrombophilia; the tendency to thrombosis, has been developed rapidly and has been linked to many aspects of pregnancy. It is recently that severe pregnancy complications such as severe preeclampsia intrauterine growth retardation abruptio placentae and stillbirth has been shown to be associated with thrombophilia. Recurrent miscarriage and has also been associated with thrombophilia. Finally, thromboembolism in pregnancy as in the non-pregnant state is linked to thrombophilia. In this review all aspects of thrombophilia in pregnancy are discussed, and also all prophylactic and therapeutic implications.Thrombophilias are inherited or acquired conditions which predispose an individual to thromboembolism. Deficiencies of protein S C and antithrombin are rare and each of them is found in about 3% of patients with thrombosis. Recently, three important inherited thrombophilias were discovered which are responsible of the majority of thromboembolic events in patients with otherwise no apparent risk for thrombosis. Resistance to activated protein C caused by an adenine 506 guanine (A506G) mutation in factor V (factor V Leiden) has been linked with an increased risk for venous thromboembolism [1][2][3]. Heterozygosity for the factor V (FV) Leiden mutation is found in about 5% of the population and the mutation is responsible of 20-30% of venous thromboembolism events. A recently described guanine 20210 adenine mutation in prothrombin is associated with higher plasma prothrombin concentrations and increased risk for venous thromboembolism [4] and cerebral-vein thrombosis [5]. Homozygosity for the cytosine 677 thymine (C677T) mutation in methylenetetrahydrofolate reductase (MTHFR) results in decreased synthesis of 5-methyltetrahydrofolate, the primary methyl donor in the conversion of homocysteine to methionine and the resulting increase in plasma homocysteine concentrations is a risk factor for thrombosis [6,7]. The mutation is responsible for reduced MTHFR activity and is the most frequent cause of mild hyperhomocysteinemia and can be found in 5-15% of the population.Homocysteine is an independent risk factor for atherosclerosis, stroke, peripheral vascular disease and cardiovascular diseases [8,9]. Homocysteine concentrations are affected by nutrition. A deficiency in folate, B-6, and/or B-I2 causes elevation of homocysteine. Homocysteine concentrations are also affected by genetics such as cystathionine beta-synthase deficiency (10) and C677T MTHFR gene mutation [7]. Hyperhomocysteinemia promotes vascular damage by several mechanisms. Many of the endothelial vascular changes associated with hyperhomocysteinemia can be found in preeclampsia [11][12][13][14][15]. thrombophilia is substantially increased. The risk of VTE in pregnant women may be further amplified by the type of underlying genetic predisposition, like, homozygosity for a mutation, the presence of multiple mutations (multigenic defects) or thrombophilic anomalies [16][17][18][19].Thrombophilia and ad...

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“…Multiple studies [14,15,16,17] have shown that thrombophilias increase the risk of recurrent first-and secondtrimester pregnancy losses through placental bed thrombosis. To date, meta-analyses of relatively small case-control studies have demonstrated a small but significant increase (OR 1.5-4.0) in embryonic and fetal loss, abruption, intrauterine growth restriction and preeclampsia in association with inherited thrombophilias [18,19] Prospective cohort studies have similarly supported a minor contribution of inherited thrombophilias on perinatal outcomes [20,21].…”

Section: Introductionmentioning

confidence: 99%