tetano
Editor, Senior Moderator
BMC Pregnancy Childbirth
. 2024 Apr 25;24(1):319.
doi: 10.1186/s12884-024-06530-y. Placental inflammation in a fetal demise of a SARS-CoV-2-asymptomatic, COVID-19-unvaccinated pregnant woman: a case-report
Maricarmen Abrego-Navarro[SUP] #[/SUP][SUP] 1 2 [/SUP], Rodrigo Villalobos[SUP] #[/SUP][SUP] 3 [/SUP], Jaime Sanchez[SUP] 4 [/SUP], Deisa Lamela[SUP] 3 [/SUP], Cindy Fu[SUP] 1 [/SUP], Erika Guerrero[SUP] 1 5 [/SUP], Paulino Vigil-De Gracia[SUP] 6 5 [/SUP], Sandra López-Vergès[SUP] #[/SUP][SUP] 7 8 [/SUP], Mairim A Solis[SUP] #[/SUP][SUP] 9 10 [/SUP]
Affiliations
Background: 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.
Case presentation: 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[SUP]+[/SUP] macrophages, CD56[SUP]+[/SUP] Natural Killer cells and scarce CD8[SUP]+[/SUP] 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.
Conclusion: 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.
Keywords: COVID-19 in pregnancy; Fetal vascular malperfusion; Intrauterine fetal demise; Maternal vascular malperfusion; Placental inflammation; Placental pathology; SARS-CoV-2.
. 2024 Apr 25;24(1):319.
doi: 10.1186/s12884-024-06530-y. Placental inflammation in a fetal demise of a SARS-CoV-2-asymptomatic, COVID-19-unvaccinated pregnant woman: a case-report
Maricarmen Abrego-Navarro[SUP] #[/SUP][SUP] 1 2 [/SUP], Rodrigo Villalobos[SUP] #[/SUP][SUP] 3 [/SUP], Jaime Sanchez[SUP] 4 [/SUP], Deisa Lamela[SUP] 3 [/SUP], Cindy Fu[SUP] 1 [/SUP], Erika Guerrero[SUP] 1 5 [/SUP], Paulino Vigil-De Gracia[SUP] 6 5 [/SUP], Sandra López-Vergès[SUP] #[/SUP][SUP] 7 8 [/SUP], Mairim A Solis[SUP] #[/SUP][SUP] 9 10 [/SUP]
Affiliations
- PMID: 38664805
- DOI: 10.1186/s12884-024-06530-y
Background: 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.
Case presentation: 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[SUP]+[/SUP] macrophages, CD56[SUP]+[/SUP] Natural Killer cells and scarce CD8[SUP]+[/SUP] 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.
Conclusion: 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.
Keywords: COVID-19 in pregnancy; Fetal vascular malperfusion; Intrauterine fetal demise; Maternal vascular malperfusion; Placental inflammation; Placental pathology; SARS-CoV-2.