Leon-Garcia Sandra M, Roeder Hilary A, Nelson Katharine K, Liao Xiaoyan, Pizzo Donald P, Laurent Louise C, Parast Mana M, LaCoursiere D Yvette
Department of Reproductive Medicine, University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Department of Pathology, University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Placenta. 2016 Feb;38:33-40. doi: 10.1016/j.placenta.2015.12.006. Epub 2015 Dec 15.
Adverse effects of obesity have been linked to inflammation in various tissues, but studies on placental inflammation and obesity have demonstrated conflicting findings. We sought to investigate the influence of pregravid obesity and fetal sex on placental histopathology while controlling for diabetes and hypertension.
Placental histopathology focusing on inflammatory markers of a cohort of normal weight (BMI = 20-24.9) and obese (BMI ≥ 30) patients was characterized. Demographic, obstetric and neonatal variables were assessed.
192 normal and 231 obese women were included. Placental characteristics associated with obesity and fetal sex independent of diabetes and hypertension were placental disc weight >90(th) percentile, decreased placental efficiency, chronic villitis (CV), fetal thrombosis, and normoblastemia. Additionally, female fetuses of obese mothers had higher rates of CV and fetal thrombosis. Increasing BMI increased the risk of normoblastemia and CV. The final grade and extent of CV was significantly associated with obesity and BMI, but not fetal gender. Finally, CV was less common in large-for-gestation placentas.
Maternal obesity results in placental overgrowth and fetal hypoxia as manifested by normoblastemia; it is also associated with an increased incidence of CV and fetal thrombosis, both more prevalent in female placentas. We have shown for the first time that the effect of maternal obesity on placental inflammation is independent of diabetes and hypertension, but significantly affected by fetal sex. Our data also point to the intriguing possibility that CV serves to normalize placental size, and potentially fetal growth, in the setting of maternal obesity.
肥胖的不良影响与多种组织的炎症有关,但关于胎盘炎症与肥胖的研究结果相互矛盾。我们试图在控制糖尿病和高血压的同时,研究孕前肥胖和胎儿性别对胎盘组织病理学的影响。
对一组体重正常(BMI = 20 - 24.9)和肥胖(BMI≥30)患者的胎盘组织病理学进行研究,重点关注炎症标志物。评估人口统计学、产科和新生儿变量。
纳入了192名体重正常和231名肥胖女性。与肥胖和胎儿性别相关且独立于糖尿病和高血压的胎盘特征包括胎盘盘重量>第90百分位数、胎盘效率降低、慢性绒毛炎(CV)、胎儿血栓形成和幼红细胞血症。此外,肥胖母亲的女胎CV和胎儿血栓形成发生率更高。BMI升高会增加幼红细胞血症和CV的风险。CV的最终分级和程度与肥胖和BMI显著相关,但与胎儿性别无关。最后,CV在大于孕周胎盘的情况中较少见。
母亲肥胖导致胎盘过度生长和幼红细胞血症所表现出的胎儿缺氧;它还与CV和胎儿血栓形成的发生率增加有关,这两者在女性胎盘中更为普遍。我们首次表明,母亲肥胖对胎盘炎症的影响独立于糖尿病和高血压,但受胎儿性别的显著影响。我们的数据还指出了一个有趣的可能性,即在母亲肥胖的情况下,CV有助于使胎盘大小以及潜在的胎儿生长正常化。