Placental Findings in Postpartum Preeclampsia: A Comparative Retrospective Study

Abstract

Objective Preeclampsia is a multifactorial placental disease that can occur after delivery. The pathophysiology of postpartum preeclampsia remains unknown. The objective was to describe placental findings in postpartum preeclampsia. Study Design This is a case–control study, comparing the placental histologic findings in four groups of 30 patients with postpartum preeclampsia, early-onset preeclampsia, late-onset preeclampsia, and normotensive controls. Results Placentas of postpartum preeclampsia had a mean placental weight not different from that of late-onset preeclampsia at a similar gestational age (479.0 ± 152.7 vs. 521.3 ± 144.1 g, p = 0.07); they showed a higher rate of acute deciduitis of 42.4% than early preeclampsia (5.7%, p < 0.01) or in controls (3.2%, p < 0.01); 18.2% had decidual arteriolopathy, with no significant difference with other groups. These placentas had fewer villous infarcts as compared with early preeclampsia (9.1 vs. 62.9%, p < 0.01) and less accelerated maturation of villi (24.2 vs. 74.3%, p < 0.01). Conclusion There were no significant differences for decidual arteriolopathy and villous infarcts among postpartum preeclampsia, late-onset preeclampsia, and the controls. This suggests that postpartum preeclampsia is more of a maternal disease in which the placenta may act as a priming effect in predisposed mothers and becomes clinically apparent after delivery.

Predictive biomarkers and initial analysis of maternal immune alterations in postpartum preeclampsia reveal an immune-driven pathology

“…We additionally found that the maternal-fetal interface holds signs of prenatal changes, supporting a previous suggestion that the placenta may act as a primer in predisposed individuals ( 58 ). This included elevated heme-oxygenase and confirmed our previous finding of elevated CD163+ cells, which could be leveraged in the identification of women who develop PPPE.…”

Total daily energy expenditure has declined over the past three decades due to declining basal expenditure, not reduced activity expenditure

“…23,24 Preexisting maternal cardiovascular risk factors for postpartum preeclampsia are similar to those for antepartum preeclampsia and both conditions share the finding of an antiangiogenic imbalance in the maternal circulation. 25,26 Postpartum preeclampsia challenges the paradigm that removing the placenta at birth cures HDP and brings into question the role of the placenta as the undisputed trigger for HDP. 27 Postpartum preeclampsia is often underdiagnosed, as BP monitoring in the fourth trimester is not universally recommended for women without HDP and only infrequently undertaken after HDP.…”

Setting a stage: Inflammation during preeclampsia and postpartum

“…Lastly, there are rare cases where patients develop a PE phenotype after delivery, which is known as PP-PE. Patients with PP-PE have similar placental vasculopathies that resemble LOPE by demonstrating a similar role for placenta dysfunction (Ditisheim et al, 2020;Hauspurg and Jeyabalan, 2022). But, more studies are needed to elucidate the mechanisms that induce postpartum PE.…”