Abstract

Angiogenic imbalance contributes to the development of preeclampsia. We evaluated the protein expression of the proangiogenic placental growth factor (PlGF) and transforming growth factor beta 1 (TGF-β1) compared with the anti-angiogenic soluble fms-like tyrosine kinase receptor (sFlt1) and soluble endoglin (sEng) in HIV-infected normotensive and pre-eclamptic pregnancies. Blood was obtained from 110 pregnant women, enrolled in four groups, namely, HIV-negative normotensives (27); HIV-positive normotensives (31); HIV-negative pre-eclamptics (27) and HIV-positive pre-eclamptics (25), and was used to measure PlGF, TGF-β₁, sFlt1 and sEng levels. Increased sFlt1 and sEng levels were associated with the pre-eclamptics (HIV negative and positive) compared with their counterparts. Decreased PlGF levels were observed between the HIV-negative pre-eclamptics versus HIV-negative normotensives, but levels differed significantly (p = 0.02) among the normotensives (HIV negative and positive). TGF-β₁ remained unchanged across all groups. Higher sEng/TGF-β₁ ratios were associated with the pre-eclamptics (HIV negative and positive) compared with their counterparts. This study demonstrated increased sFlt1 and sEng levels in pre-eclamptic compared with normotensive pregnancies, irrespective of the HIV status.

Highlights

  • Blood was obtained from 110 pregnant women, enrolled in four groups, namely, HIV-negative normotensives (27); HIV-positive normotensives (31); HIV-negative pre-eclamptics (27) and HIV-positive pre-eclamptics (25), and was used to measure placental growth factor (PlGF), TGF-β1, sFlt[1] and soluble endoglin (sEng) levels

  • This study demonstrated increased sFlt[1] and sEng levels in pre-eclamptic compared with normotensive pregnancies, irrespective of the HIV status

  • Pre-eclampsia, a clinical syndrome unique to human pregnancy is characterised by new-onset hypertension and proteinuria, which present after the 20th week of gestation.[1,2,3,4]

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Summary

Introduction

Blood was obtained from 110 pregnant women, enrolled in four groups, namely, HIV-negative normotensives (27); HIV-positive normotensives (31); HIV-negative pre-eclamptics (27) and HIV-positive pre-eclamptics (25), and was used to measure PlGF, TGF-β1, sFlt[1] and sEng levels. Pre-eclampsia is reported to be a two-stage disorder, namely, a pre-clinical/asymptomatic, and a clinical stage.[2,7] The first stage is characterised by abnormal placentation leading to a hypoxic placenta, oxidative stress and immune dysregulation, while the second stage is characterised by the placental discharge of soluble factors, such as sFlt[1] and sEng into the maternal circulation, resulting in widespread endothelial dysfunction and the clinical syndrome of hypertension, proteinuria, intrauterine growth restriction (IUGR) and thrombocytopenia.[2,7,8,9,10] Both pre-eclampsia and HIV infection are common conditions in sub-Saharan Africa and major causes of maternal deaths.[11] Recent studies have reported that the persistent infection of HIV-infected individuals contributes to the development of chronic arterial injury and subsequent endothelial damage, atherosclerosis and thrombosis.[12] untreated HIV-infected patients may be prone to endothelial dysfunction.[12] HIV infection seems to affect the mechanisms implicated in the aetiology of pre-eclampsia and IUGR

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