Department of Clinical Science and Education, Unit of Obstetrics and Gynecology, Karolinska Institute, Södersjukhuset Hospital, Stockholm, Sweden.
Department of Laboratory Medicine, Karolinska University Hospital Huddinge, Huddinge, Sweden.
Acta Obstet Gynecol Scand. 2020 Dec;99(12):1649-1656. doi: 10.1111/aogs.13941. Epub 2020 Jul 3.
The prevalence of obesity in pregnancy is increasing worldwide. Maternal obesity increases risks of severe fetal and neonatal complications. The underlying pathophysiological mechanisms are unclear. One possible contributing factor could be chronic fetal hypoxia. The aim of this study was to compare placentas from women with and without obesity with respect to placental lesions, which could reflect compensatory mechanisms in response to chronic fetal hypoxia as well as lesions possibly leading to chronic fetal hypoxia. In addition, levels of erythropoietin in cord blood were compared between offspring of lean and obese women.
This cohort study included 180 women with uneventful, full-term, singleton pregnancies, out of which 91 lean women had a body mass index (BMI) of 18.5-24.9 kg/m and 89 women had obesity (BMI ≥30 kg/m ). Women were recruited at Södersjukhuset between 16 October 2018 and 2 December 2019. Placentas were investigated by two senior perinatal pathologists, who were blinded for maternal BMI. Cord blood was analyzed for levels of erythropoietin.
Levels of erythropoietin in cord blood increased with maternal BMI (P = .01, β = 0.97, 95% CI 0.27-1.68). There was no difference between placentas of obese and lean women in number of placental lesions reflecting chronic fetal hypoxia or in lesions that could possibly lead to chronic fetal hypoxia.
This study of term and uneventful pregnancies demonstrated a positive association between maternal obesity and concentrations of erythropoietin in cord blood at birth. This finding supports the hypothesis of chronic fetal hypoxia as a risk factor for complications in the pregnancies of obese women. There were no differences in lesions associated with hypoxia between placentas of obese and lean women.
肥胖在妊娠中的流行率正在全球范围内增加。母体肥胖增加了严重胎儿和新生儿并发症的风险。潜在的病理生理机制尚不清楚。一个可能的促成因素可能是慢性胎儿缺氧。本研究的目的是比较肥胖和非肥胖妇女的胎盘,以了解胎盘病变,这些病变可能反映了对慢性胎儿缺氧的代偿机制,以及可能导致慢性胎儿缺氧的病变。此外,还比较了瘦妇女和肥胖妇女的脐带血中促红细胞生成素的水平。
这项队列研究纳入了 180 名无并发症、足月、单胎妊娠的妇女,其中 91 名瘦妇女的体重指数(BMI)为 18.5-24.9kg/m,89 名妇女肥胖(BMI≥30kg/m)。这些妇女是在 2018 年 10 月 16 日至 2019 年 12 月 2 日期间在 Södersjukhuset 招募的。两名资深围产病理学家对胎盘进行了检查,他们对产妇 BMI 不知情。分析脐带血中促红细胞生成素的水平。
脐带血中促红细胞生成素的水平随产妇 BMI 的增加而升高(P=0.01,β=0.97,95%CI 0.27-1.68)。肥胖妇女和瘦妇女的胎盘病变数量、反映慢性胎儿缺氧的病变或可能导致慢性胎儿缺氧的病变之间无差异。
这项对足月和无并发症妊娠的研究表明,肥胖母亲与出生时脐带血中促红细胞生成素浓度之间存在正相关。这一发现支持了慢性胎儿缺氧作为肥胖妇女妊娠并发症的危险因素的假说。肥胖和瘦妇女的胎盘与缺氧相关的病变没有差异。