Plasma Heme Scavengers Alpha-1-Microglobulin and Hemopexin as Biomarkers in High-Risk Pregnancies.

Grigorios Kalapotharakos,Esa Hämäläinen,Katja Murtoniemi,Bo Åkerström,Stefan R Hansson,Hannele Laivuori,Katri Räikkönen,Eero Kajantie,Pia Villa

doi:10.3389/fphys.2019.00300

Abstract

Women with established preeclampsia (PE) have increased plasma concentration of free fetal hemoglobin. We measured two hemoglobin scavenger system proteins, hemopexin (Hpx) and alpha-1-microglobulin (A1M) in maternal plasma using enzyme-linked immunosorbent assay during the late second trimester of pregnancy in women with high and low risk of developing PE. In total 142 women were included in nested case-control study: 42 women diagnosed with PE and 100 controls (49 randomly selected high-risk and 51 low-risk controls). The concentration of plasma A1M in high-risk controls was higher compared to low-risk controls. Women with severe PE had higher plasma A1M levels compared to women with non-severe PE. In conclusion, the concentration of plasma A1M is increased in the late second trimester in high-risk controls, suggesting activation of endogenous protective system against oxidative stress.

Highlights

Preeclampsia (PE) is a relatively common hypertensive disorder in pregnancy, affecting 4,6% of pregnancies worldwide (Abalos et al, 2013)
The present nested case-control study is a part of the multidisciplinary “Prediction and Prevention of Pre-eclampsia and Intrauterine Growth Restriction” (PREDO) project
Seven women with PE participated in the ASA trial, as well, and were treated with low dose acetylsalicylic acid starting before 14th week of gestation

Summary

Introduction

Preeclampsia (PE) is a relatively common hypertensive disorder in pregnancy, affecting 4,6% of pregnancies worldwide (Abalos et al, 2013). Plasma Heme Scavengers in Preeclampsia placental development is thought to be the initial stage leading to reduced utero-placental perfusion and increased oxidative stress that in turn causes placental damage. Circulating toxic factors derived from the placenta cross the blood-placenta barrier and leak into the maternal circulation where they in turn trigger an inflammatory response and general endothelial damage. As a consequence of that, general organ damage develops, which leads to the typical manifestations of PE after 20th week of gestation, including hypertension, edema and proteinuria. We still lack a full explanation on how placental damage leads to distinct maternal and fetal manifestations that occur either during early pregnancy or late pregnancy, so called early onset PE and late-onset PE. Onset PE is linked to poor placentation while the late-onset is more determined by maternal risk factors such as obesity, diabetes mellitus and chronic hypertension, which are associated with a higher pre-pregnancy level of vascular inflammation (Roberts and Redman, 1993; Ness and Roberts, 1996)

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Conclusion