Response to rebuttal: Meta-analysis of the relationship of factor V Leiden and intrauterine growth restriction – based on solid evidence?

2005 ◽  
Vol 94 (07) ◽  
pp. 231-232
Author(s):  
John Attia ◽  
Tracy Dudding
2003 ◽  
Vol 105 (3) ◽  
pp. 279-285 ◽  
Author(s):  
Dietmar SCHLEMBACH ◽  
Ernst BEINDER ◽  
Juergen ZINGSEM ◽  
Ute WUNSIEDLER ◽  
Matthias W. BECKMANN ◽  
...  

This study was conducted to investigate the association of maternal and/or fetal factor V Leiden (FVL) and G20210A prothrombin mutation with HELLP syndrome. FVL and G20210A prothrombin mutation were determined using PCR. Sixty-three pregnant women, 36 of them diagnosed with HELLP syndrome, were included in the study. Overall, 68 children were born as a result of these pregnancies and blood sampling was possible in 28 out of 39 children from HELLP patients and 25 out of 29 children from the control women. The prevalence of a maternal FVL was elevated 2-fold in HELLP patients compared with the control women [six out of 36 (16.7%) compared with two out of 27 (7.4%); P=0.282]. None of the HELLP patients and only one woman in the control group was found to be positive for the G20210A prothrombin mutation (P=0.251). The fetal carrier frequency was four out of 28 compared with three out of 25 for FVL (P=0.811), and two out of 28 compared with one out of 25 for G20210A prothrombin mutation (P=0.629). Intrauterine growth restriction (IUGR) was significantly higher in fetuses found to be positive for a thrombophilic mutation (P=0.022). IUGR occurred in seven out of ten fetuses with a thrombophilic mutation compared with 11 out of 43 in fetuses without a mutation. The prevalence of FVL, but not of the G20210A prothrombin mutation, seems to be elevated in women with HELLP syndrome. A fetal thrombophilic mutation does not contribute significantly to the clinical features of the HELLP syndrome. Our results demonstrate a fetal contribution to IUGR. Fetal thrombophilic mutations may lead to placental microthrombosis, which consecutively could lead to a disturbed fetoplacental blood flow and thus cause growth restriction.


Author(s):  
Hossein Dalili ◽  
Fatemeh Sadat Nayeri ◽  
Seyed Reza Mirjalili ◽  
Seyyed Nasrollah Hossein ◽  
Alireza Abdollahi ◽  
...  

Introduction: Intrauterine growth restriction is a multifaceted problem and is associated with a significant increase in the level of morbidity and perinatal mortality. According to some studies, failure of the placenta is responsible for the most cases of intrauterine growth restriction. The aim of this study was to evaluate the placental pathologic changes in the intrauterine growth restriction (IUGR) samples and compare them with normal cases.   Methods: A study population consisted of 60 intrauterine growth restriction neonates and 60 normalized neonates born at Tehran Imam Khomeini Hospital between June 2016 and July 2017. The placenta was weighed, immediately after delivery, and the umbilical cord was separated, then stored in 10% formalin and sent for pathological examination as soon as possible. Data collection was performed according to the following items: the pathologist's report, the results of the infants' examination, and the data in the neonatal cases.   Results: The intrauterine growth restriction group showed a high frequency of placenta infarction (P < 0.001), inflammation of the villous (P < 0.001), villous fibrosis (P = 0.044), villous vascularization disorder (P = 0.001), prevalence of chorioamnionitis (P = 0.027), prevalence of Syncytiotrophoblastic knots (P < 0.001) and placental necrosis (P = 0.048) than normal group. However, the mean weight of the placenta (P < 0.001), the length and width of the macroscopic placenta changes was less (P < 0.001).   Conclusion: The results of the current study showed that a major part of the macroscopic and histological changes are detectable in the intrauterine growth restriction samples, which are considerably more common than normal, although they are not pathognomonic, but in the future, more accurate results can be obtained from more extensive studies.


2020 ◽  
Vol 19 ◽  
pp. 127-130
Author(s):  
Jeske J.K. van Diemen ◽  
Jeske M. Bij de Weg ◽  
Arda Arduç ◽  
Olivier Veraart ◽  
David Mager ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document