From Tommy's Maternal and Fetal Health Research Centre, St. Mary's Hospital, Division of Developmental Biology & Medicine, Faculty of Biology, Medicine & Health, University of Manchester, Manchester, United Kingdom (Kerby, Baker, Heazell, Sharps).
The Department of Paediatric and Perinatal Pathology, Royal Manchester Children's Hospital, Manchester University Hospitals NHS Foundation Trust, Manchester, United Kingdom (Batra).
Arch Pathol Lab Med. 2021 Jan 1;145(1):82-89. doi: 10.5858/arpa.2019-0524-OA.
CONTEXT.—: Women with diabetes have increased stillbirth risk. Although the underlying pathophysiological processes are poorly understood, stillbirth is frequently related to abnormal placental structure and function.
OBJECTIVE.—: To investigate placental morphology and cellular characteristics in the placentas of women with diabetes who had stillbirths and stillbirths of unexplained cause.
DESIGN.—: Placentas from women with uncomplicated live births, live births in women with diabetes, unexplained stillbirths, and stillbirths related to diabetes (n = 10/group) underwent clinical histopathologic assessment and were also investigated using immunohistochemical staining to quantify syncytial nuclear aggregates, proliferation, trophoblast area, vascularization, T cells, placental macrophages (Hofbauer cells), and the receptor for advanced glycation end products.
RESULTS.—: Ki67+ cells were decreased in unexplained stillbirths compared with live births in women with diabetes. Both stillbirth groups had increased cytokeratin 7+/nuclear area compared with controls. Blood vessels/villi were decreased in unexplained stillbirth compared with live births from women with diabetes. Compared with uncomplicated controls, CD163+ macrophages were increased in live births in women with diabetes and unexplained stillbirths, and further increased in stillbirths related to diabetes. There was no change in CD3+ T cells or syncytial nuclear aggregates. Receptor for advanced glycation end products-positive cells were decreased in both stillbirth groups compared with diabetes-related live births. Co-localization of receptor for advanced glycation end products in macrophages was increased in both stillbirth groups compared with live birth groups.
CONCLUSIONS.—: Stillbirths related to diabetes exhibit placental phenotypic differences compared with live births. Further investigation of these parameters may provide understanding of the pathologic mechanisms of stillbirth and aid the development of stillbirth prevention strategies.
患有糖尿病的女性死胎风险增加。尽管潜在的病理生理过程尚不清楚，但死胎通常与异常的胎盘结构和功能有关。
研究患有糖尿病和不明原因死胎的女性的胎盘形态和细胞特征。
对无并发症的活产、糖尿病活产、不明原因死产和与糖尿病相关的死产（每组 10 例）的胎盘进行临床组织病理学评估，并通过免疫组织化学染色进行研究，以定量检测合胞核聚集物、增殖、滋养层面积、血管化、T 细胞、胎盘巨噬细胞（Hofbauer 细胞）和晚期糖基化终产物受体。
与糖尿病活产相比，不明原因死产的 Ki67+细胞减少。两组死胎的角蛋白 7+/核面积均高于对照组。与糖尿病活产相比，不明原因死产的血管/绒毛减少。与无并发症的对照组相比，糖尿病活产和不明原因死产的 CD163+巨噬细胞增加，而与糖尿病相关的死产则进一步增加。CD3+T 细胞或合胞核聚集物无变化。与糖尿病相关的活产相比，两组死胎的晚期糖基化终产物受体阳性细胞均减少。与活产组相比，两组死胎的晚期糖基化终产物受体在巨噬细胞中的共定位增加。
与糖尿病相关的死胎与活产相比表现出胎盘表型差异。进一步研究这些参数可能有助于了解死胎的病理机制，并为预防死胎策略的发展提供帮助。
