Is thrombophilia associated with placenta‐mediated complications? A prospective cohort study: comment

Abstract

SW. Is thrombophilia associated with placenta-mediated pregnancy complications? A prospective cohort study. J Thromb Haemost 2014; 12:469-78 and Rodger MA, Langlois NJ. Is thrombophilia associated with placenta-mediated pregnancy complications? A prospective cohort study: reply. This issue, pp 1536-7We read with great interest the article by Rodger et al.[1], who reported a prospective cohort study on the influences of factor V Leiden (FVL) and prothrombin gene mutation (PGM) on placenta-mediated pregnancy complications. Five hundred and seven women carrying FVL and/or PGM were enrolled in the study, and the authors concluded that carriers of FVL or PGM are not at significantly increased risk of pregnancy complications. The authors claimed that previous prospective cohort studies were too underpowered to detect small differences. However, we wish to draw attention to our prospective cohort study, published in 2010, which concerned placenta-mediated pregnancy complications in 491 women with FVL and 1030 controls [2]. Our power calculation was derived from the lowest incidence of placenta-mediated complications (intrauterine growth retardation, incidence 2.5%), and, at 80% power and a 0.05 significance level, at least 430 cases and 860 controls were needed. We drew the same conclusions as Rodger et al. There were no differences in placenta-mediated complications, such as pre-eclampsia, placental abruption, and intrauterine growth retardation, or in prematurity. We chose to express intrauterine growth retardation as birth weight deviation from a reference material as a percentage, thus obtaining a continuous variable, independent of gestational age and sex, which allowed a powerful statistical analysis. We found no significant difference in birth weight deviation between FVL carriers and controls. This is a more exact method for studying growth retardation than comparing the number of neonates with a birth weight under a certain level.The inclusion of our prospective cohort study would have added valuable data for the updated systematic review and meta-analysis of prospective cohort studies examining the association of FVL and PGM with placenta-mediated pregnancy complications [1,3]. This would have given an opportunity to draw stronger final conclusions. The authors have chosen to add only the results from their new study and the results from one other study with 29 FVL carriers [4]. AddendumU Kjellberg and M Hellgren wrote the letter and approved its submission. Disclosure of Conflict of InterestsThe authors state that they have no conflict of interest.

Features of the course of the gestational process with the carriage of genotypes F5L:G(1961)A and F2:G(20210)A and inheritance options

“…Наряду с изучением риска развития ВТЭ последние 20 лет активно исследуется связь мутаций генов белков системы гемостаза, таких как мутация Лейден и мутация гена протромбина, с риском развития гестационных осложнений, определяющих перинатальную заболеваемость и смертность: преэклампсия (ПЭ), задержка роста плода (ЗРП), преждевременная отслойка нормально расположенной плаценты (ПОНРП) и преждевременные роды (ПР) [3][4][5]. Имеющаяся доказательная база патогенетически обоснованной профилактики как тромботических, так и гестационных осложнений у носительниц тромбофилических генотипов позволяет избежать фатальных осложнений во время беременности как со стороны матери, так и плода.…”