Background: Pregnancies with a macrosomic fetus comprise a subgroup of high‐risk pregnancies. There is uncertainty in the clinical management and outcomes of such pregnancies. Aim: We sought to examine clinical management and maternal and fetal outcomes in pregnancies with macrosomic infants at Royal Brisbane and Women's Hospital (RBWH). Methods: Data from 276 macrosomic births (weighing ≥ 4500 g) and 294 controls (weighing 3250–3750 g) delivered during 2002–2004 at RBWH were collected from the hospital database. Univariate and logistic regression analyses were performed for maternal risk factors and maternal and neonatal outcomes that were associated with fetal macrosomia. Results: Macrosomia was more than two times likely in women with body mass index (BMI) of > 30 kg/m2 (odds ratio (OR) 2.41, 95% confidence interval (CI) 1.26–4.61) and in male infant sex (OR 2.05, 95% CI 1.35–3.12), and four times more likely in gestation of > 40 weeks (OR 3.93, 95% CI 1.99–7.74). Maternal smoking reduced the risk of fetal macrosomia (OR 0.27, 95% CI 0.14–0.51). Macrosomia was associated with nearly two times higher risk of emergency caesarean section (OR 1.75, 95% CI 1.02–2.97) and maternal hospital stay of > 3 days (OR 1.66, 95% CI 1.11–2.50), and four times higher risk of shoulder dystocia (OR 4.08, 95% CI 1.62–10.29). Macrosomic infants were twice as likely to have resuscitation (OR 2.21, 95% CI 1.46–3.34) and intensive care nursery admission (OR 1.89, 95% CI 1.03–3.46). Conclusion: Macrosomia was associated with an increased risk of adverse maternal and neonatal health outcomes. Optimal management strategies of macrosomic pregnancies need evaluation.
SummaryThere are controversies in reports on the association of the angiotensinogen (AGT ) gene polymorphisms with the risk of developing pre-eclampsia (PE). We performed a meta-analysis to examine the association between the AGT polymorphisms and PE risk: M235T (31 studies involving 2555 patients and 6114 controls) and T174M (six studies involving 681 patients and 2076 controls). For the M235T polymorphism, the TT genotype increased the PE risk as compared to the MM genotype (odds ratio 1.61, 95% confidence intervals 1.22-2.14, P = 0.001). When stratified by ethnicity, the TT genotype remained significantly associated with higher PE risk in Caucasians and Mongolians but not in Africans. Similar results were also obtained under all three genetic models of the M235T polymorphism. For the T174M polymorphism, no significant association was found in the comparisons (MT vs. TT and MM vs. TT) and under any genetic models. The analysis excluding the highly significant Hardy-Weinberg equilibrium-violating studies and sensitivity analysis further strengthened the validity of these associations. No publication bias was observed in this study. This meta-analysis demonstrates that the AGT M235T polymorphism is significantly associated with PE whereas the T174M polymorphism is not.
Two meta-analysis of genome wide association studies identified two variants at adenylate cyclase 5 (ADCY5) associated with type 2 diabetes mellitus, fasting and 2-hour glucose in non-pregnant individuals of European descent. The objective of our study was to explore the role of common variants in ADCY5 on gestational glycemic traits, including plasma glucose, insulin values, β cell function and insulin resistance in the fasted state as well as plasma glucose 1 hour after a 50-gram glucose challenge test among Chinese Han women. Homoeostasis model assessment (HOMA) was used to quantify β cell function (HOMA1-β and HOMA2-β) and insulin resistance (HOMA1-IR and HOMA2-IR). Thirty-five single nucleotide polymorphisms (SNPs) in ADCY5 were genotyped in 929 unrelated Chinese Han women with singleton pregnancies. Three SNPs (rs6797915, rs9856662 and rs9875803) displayed evidence for association with plasma glucose 1 hour after a 50-gram glucose challenge test (P = 0.042, 0.018 and 0.018, respectively), one (rs6777397) displayed evidence for association with HOMA1-β (P = 0.014), and one (rs6762009) displayed evidence for association with HOMA1-IR (P = 0.033). These results provide additional insight into the effects of genetic variation within ADCY5 in glucose metabolism, especially during pregnancy and in non-European descent populations. OPEN ACCESS Citation: Lin R, Yuan Z, Zhang C, Ju H, Sun Y, Huang N, et al. (2020) Common genetic variants in ADCY5 and gestational glycemic traits. PLoS ONE 15(3): e0230032. https://doi.org/10.
Previous studies suggest that leptin (LEP) has an important role in glucose metabolism in the nonpregnant state. During pregnancy, circulating maternal concentrations of leptin rise significantly, mainly due to increased secretion of leptin from maternal adipose tissue and placenta. This study aimed to analyze the impact of maternal and fetal common LEP variants on glucose homeostasis in the pregnant state. Several glycemic traits, including fasting plasma glucose, fasting plasma insulin (FPI), and plasma glucose 1 hour after a 50-g oral glucose load, were measured in 1,112 unrelated Chinese Han pregnant women at 24–28 weeks gestation. Homeostatic model assessment (HOMA) was used to assess beta cell function (HOMA1-β and HOMA2-β) and insulin resistance (HOMA1-IR and HOMA2-IR).The relationships between glycemic traits and 12 LEP variants were determined. After applying the Bonferroni correction, we detected that (1) maternal rs10954173 and fetal rs10244329 were associated with maternal FPI although the effect of fetal rs10244329 may be not independent of maternal rs10244329, and (2) maternal rs12537573 was associated with maternal FPI and HOMA2-IR. This study provides genetic evidence that both maternal and fetal LEP polymorphisms may affect maternal glucose metabolism in pregnancy.
Recent studies suggested that maternal and placental leptin receptor (LEPR) may be involved in maternal glucose metabolism in pregnancy. To identify maternal and fetal LEPR common variants influencing gestational glycemic traits, we performed association study of 24-28-week maternal fasting glucose, glucose 1 hour after the consumption of a 50-g oral glucose load, fasting insulin and indices of beta-cell function (HOMA-β) and insulin resistance (HOMA-IR) in 1,112 unrelated women and their children. Follow-up of 36 LEPR loci identified 3 maternal loci (rs10889567, rs1137101 and rs3762274) associated with fasting glucose, these 3 fetal loci associated with fasting insulin and HOMA1-IR, as well as these 3 maternal-fetal loci combinations associated with HOMA2-β. We also demonstrated association of maternal locus rs7554485 with HOMA2-β and HOMA2-IR, maternal locus rs10749754 with fasting glucose, fetal locus rs10749754 with HOMA2-IR. However, these associations were no longer statistically significant after Bonferroni correction. In conclusion, our results first revealed multiple associations between maternal and fetal LEPR common variants and gestational glycemic traits. These associations did not survive Bonferroni correction. These corrections are overly conservative for association studies. We therefore believe the influence of these nominally significant variants on gestational glycometabolism will be confirmed by additional studies.
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