Stem Cell Research Group, Department of Research in Sexual and Reproductive Health Research, Gorgas Memorial Institute for Health Studies, Avenida Justo Arosemena y Calle 35, Panama City, Republic of Panama.
Ministry of Health, Panama City, Republic of Panama.
BMC Pregnancy Childbirth. 2024 Apr 25;24(1):319. doi: 10.1186/s12884-024-06530-y.
Intrauterine fetal demise is a recognized complication of coronavirus disease 2019 in pregnant women and is associated with histopathological placental lesions. The pathological mechanism and virus-induced immune response in the placenta are not fully understood. A detailed description of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-induced inflammation in the placenta during fetal demise is crucial for improved clinical management.
We report the case of a 27-week gestation SARS-CoV-2-asymptomatic unvaccinated pregnant woman without comorbidities or other risk factors for negative pregnancy outcomes with a diagnosis of intrauterine fetal demise. Histopathological findings corresponded to patterns of subacute inflammation throughout the anatomic compartments of the placenta, showing severe chorioamnionitis, chronic villitis and deciduitis, accompanied by maternal and fetal vascular malperfusion. Our immunohistochemistry results revealed infiltration of CD68 macrophages, CD56 Natural Killer cells and scarce CD8 T cytotoxic lymphocytes at the site of placental inflammation, with the SARS-CoV-2 nucleocapsid located in stromal cells of the chorion and chorionic villi, and in decidual cells.
This case describes novel histopathological lesions of inflammation with infiltration of plasma cells, neutrophils, macrophages, and natural killer cells associated with malperfusion in the placenta of a SARS-CoV-2-infected asymptomatic woman with intrauterine fetal demise. A better understanding of the inflammatory effects exerted by SARS-CoV-2 in the placenta will enable strategies for better clinical management of pregnant women unvaccinated for SARS-CoV-2 to avoid fatal fetal outcomes during future transmission waves.
宫内胎儿死亡是 COVID-19 孕妇的一种公认并发症,与胎盘组织病理学损伤有关。胎盘的病理机制和病毒诱导的免疫反应尚未完全阐明。详细描述胎儿死亡期间胎盘内严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)诱导的炎症对于改善临床管理至关重要。
我们报告了一例 27 周妊娠、SARS-CoV-2 无症状、未接种疫苗、无合并症或其他导致妊娠不良结局的危险因素的孕妇,诊断为宫内胎儿死亡。组织病理学发现与胎盘各解剖部位的亚急性炎症模式相对应,表现为严重的绒毛膜羊膜炎、慢性绒毛膜炎和蜕膜炎,并伴有母体和胎儿血管灌注不良。我们的免疫组织化学结果显示,胎盘炎症部位有 CD68 巨噬细胞、CD56 自然杀伤细胞和罕见的 CD8 T 细胞浸润,SARS-CoV-2 核衣壳位于绒毛膜和绒毛的间质细胞以及蜕膜细胞中。
本病例描述了一例无症状 SARS-CoV-2 感染孕妇的胎盘炎症的新型组织病理学损伤,伴有浆细胞、中性粒细胞、巨噬细胞和自然杀伤细胞浸润,以及胎盘灌注不良。更好地了解 SARS-CoV-2 在胎盘内引起的炎症作用,将有助于制定更好的临床管理策略,避免未来传播波中未接种 SARS-CoV-2 疫苗的孕妇发生致命的胎儿结局。