Abstract
The hallmark of preeclampsia (PE) is a shift toward persistent inflammatory response, accompanied by endothelial dysfunction. The driving forces in PE are proinflammatory cytokine and growth factors, in parallel with reduced functionality of anti-inflammatory effectors, like regulatory T cells are observed. Unfortunately, no conclusive mechanism underlying preeclampsia has been identified. For this reason, research on preeclampsia is needed to provide a state of the art understanding of the pathophysiology, identification of new diagnostics tools and the development of targeted therapies. The 68 patients were divided into three groups: gestational hypertension (GH) group (n = 19) and PE group (n = 28) and a control group (n = 21). We have tested a set of 53 cytokines, chemokines and growth factors in preeclampsia and gestational hypertension, and then compared them with normal pregnancies. Using a diagnostic test assessment characteristic parameters (IL-22, MDC/CCL22, IL-2/IL-4 ratio) have been identified and cut-off values have been proposed to diagnose preeclampsia. All parameters had high negative or positive predictive values, above 80%. In conclusion, we have proposed a potential set of immune parameters to diagnose preeclampsia.
Highlights
Preeclampsia (PE) is a common complication during pregnancy, affecting 2–5% of pregnant women
The results were presented according to the study flow diagram (Figure 1), first patients were screen with pregnancy-associated plasma protein A (PAPP-A) and using only valid parameters for PE/gestational hypertension (GH), AUC was calculated to find the markers with high discriminatory capacities (AUC ≥0.7)
We have extensively studied a wide range of serum proteins, mainly cytokines, chemokines and growth factors, as potential markers of preeclampsia
Summary
Preeclampsia (PE) is a common complication during pregnancy, affecting 2–5% of pregnant women. Immune cells such as natural killer cells, dendritic cells, and T regulatory lymphocytes located in the decidua, maintain immunotolerance toward spiral artery remodeling and emerging fetal trophoblast. This local microenvironment plays a role in the maternal immune tolerance towards the fetal allograft, and abnormal placentation can lead to increased placental shedding, exaggerated systemic inflammation and subsequent endothelial dysfunction, the key characteristics of preeclampsia [8, 9]
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