Setting a stage: Inflammation during preeclampsia and postpartum

Abstract

Preeclampsia (PE) is a leading cause of maternal and fetal mortality worldwide. The immune system plays a critical role in normal pregnancy progression; however, inappropriate inflammatory responses have been consistently linked with PE pathophysiology. This inflammatory phenotype consists of activation of the innate immune system, adaptive immune system, and increased inflammatory mediators in circulation. Moreover, recent studies have shown that the inflammatory profile seen in PE persists into the postpartum period. This manuscript aims to highlight recent advances in research relating to inflammation in PE as well as the inflammation that persists postpartum in women after a PE pregnancy. With the advent of the COVID-19 pandemic, there has been an increase in obstetric disorders associated with COVID-19 infection during pregnancy. This manuscript also aims to shed light on the relationship between COVID-19 infection during pregnancy and the increased incidence of PE in these women.

Reducing the Risk of Pre-Eclampsia in Women with Polycystic Ovary Syndrome Using a Combination of Pregnancy Screening, Lifestyle, and Medical Management Strategies

“…Pathological levels of maternal inflammation may result in altered decidual and placental inflammatory responses that affect placental development and function [ 27 , 120 , 161 ]. Inflammatory processes can contribute to, and exacerbate, the effects of insulin resistance and hyperandrogenism [ 1 ].…”

Unraveling the Predictive Power: Placenta Growth Factor and Pregnancy-Associated Plasma Protein A in Pre-eclampsia

“…Placental ischemia and immune imbalance: The intricate interplay between immune cells, such as inflammatory macrophages, dendritic cells, NK cells, and T cells, assumes significance in early-onset pre-eclampsia. In this scenario, these immune cells disrupt the formation of spiral arteries, leading to placental hypoxia [ 35 ]. Late-onset pre-eclampsia presents a different dynamic, where normal spiral artery formation coexists with insufficient perfusion capacity, resulting in placental hypoxia and a reminiscent inflammatory environment akin to early-onset pre-eclampsia [ 35 ].…”

“…In this scenario, these immune cells disrupt the formation of spiral arteries, leading to placental hypoxia [ 35 ]. Late-onset pre-eclampsia presents a different dynamic, where normal spiral artery formation coexists with insufficient perfusion capacity, resulting in placental hypoxia and a reminiscent inflammatory environment akin to early-onset pre-eclampsia [ 35 ]. This intricate connection between immune responses and placental perfusion underscores the multifaceted nature of pre-eclampsia's pathophysiology.…”

“…Memory of inflammation: In a compelling aspect, inflammatory cells from pre-eclampsia retain a memory postpartum, thereby elevating the risk of experiencing pre-eclampsia in subsequent pregnancies [ 35 ]. This phenomenon signifies the persistence of inflammatory alterations beyond the immediate gestational period, emphasizing the long-term implications of inflammatory responses in the recurrence of pre-eclampsia.…”

Experience in using acetylsalicinic acid to prevent the development of preeclampsia

“…Треть всех ПЭ ассоциирована с задержкой развития плода и недоношенностью, что ведет к риску возникновения церебрального паралича, изменению неврологического статуса, гипертензии, почечной дисфункции, инсулинорезистентности, ожирению, сердечно-сосудистой патологии у ребенка [4,5]. Матери, перенесшие ПЭ, в 2-5 раз чаще страдают гипертензией, сердечно-сосудистыми и церебро-сосудистыми заболеваниями [6,7].…”