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עמוד בית
Wed, 16.10.24

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February 2014
Itai Gat, Mordechai Dulitzki, Eyal Schiff, Eyal Sivan and Michal J. Simchen
Background: Homozygous carriers of factor V Leiden (FVL) have an up to 80-fold increased risk of venous thrombosis, but the risk of obstetric complications in FVL homozygosity is unclear.

Objectives:
To compare obstetric and thromboembolic complications among factor V Leiden (FVL) homozygous and heterozygous carriers treated with prophylactic dose anticoagulation during pregnancy.

Methods:
In this retrospective case-control study we performed a chart review for the years 2004–2010 of homozygous and heterozygous FVL carriers who were treated with low molecular weight heparin (LMWH) at a dose of 0.6 mg/kg/day during pregnancy. Adverse outcomes included thromboembolic and obstetric complications. A composite adverse obstetric outcome was defined as the presence of at least one of the following: late intrauterine fetal demise, severe intrauterine growth restriction (< 5th percentile), preeclampsia, placental abruption. Pregnancy outcomes of homozygous and heterozygous FVL carriers were compared.

Results:
We compared the pregnancies of 13 homozygous FVL women with those of 82 heterozygous FVL carriers. Thromboembolic events occurred only in heterozygous FVL controls. Gestational age and birth weight were similar. The composite adverse obstetric outcome rate was higher for homozygous compared with heterozygous FVL carriers (23.1% vs. 11%, respectively), although not statistically significant. A trend for prematurity among homozygous FVL patients was evident, with 2/13 women (15.3%) in the homozygous FVL group giving birth before 34 weeks gestation, compared with only 2/82 (2.3%) in the heterozygous group.

Conclusions:
Pregnancy outcome was similar for homozygous and heterozygous FVL carriers on LMWH thromboprophylaxis. The overall likelihood of thromboembolic complications was low. Thromboprophylaxis may decrease the risk for placental and thromboembolic complications in homozygous FVL patients to a similar level as in heterozygotes.
January 2006
M. Koren-Michowitz, N. Rahimi-Levene, Y. Volcheck, O. Garach-Jehoshua and A. Kornberg.
December 2005
V. Yehezkely-Schildkraut, M. Kutai, Y. Hugeirat, C. Levin, S. Alon Shalev, G. Mazor, A. Koren.

Background: The cause of cerebral palsy remains unknown in most cases. Factor V Leiden mutation, a common cause of hereditary thrombophilia, has been associated with CP[1].

Objectives: To analyze the prevalence of factor V Leiden (G1691A), prothrombin (G20210A), and methylenetetrahydrofolate reductase (C677T) mutations in children with CP.

Methods: Sixty-one children with CP were studied for the presence of the three gene mutations associated with thrombophilia.

Results: We found that 41% of the children with CP and 33% of the controls carry one or more of the studied mutations (P = 0.348). The prevalence of the factor V mutation was 27.9% in CP and 16.4% in controls (P = 0.127). The frequency of the other two genetic factors was even less significant. The FVL[2] mutation was found in 35% of the Arab CP patients (15/42) and in 22% of the controls from the same population (9/40) (P = 0.067).

Conclusions: Each of the genetic factors studied was shown to be related to CP. Despite the high frequency of FVL among the studied patients, we were unable to prove a significant correlation between FVL and CP, mainly because this factor is frequent in the Arab control group. In this population a trend toward significance can be seen (P = 0.067). Larger studies are needed to validate the significance of these results.






[1] CP = cerebral palsy



[2] FVL = factor V Leiden


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