Sys Rev Pharm 2021;12(1):301-305 A multifaceted review journal in the field of pharmacy 301 Systematic Reviews in Pharmacy Vol 12, Issue 1, January 2021 Role Of Soluble Endoglin In The Diagnosis Of Preeclampsia Severity In Iraqi Women Lamyaa Taha Muhammed 1 , Eham Amer Ali * 2 , Ban Hadi Hameed 3 1 Ministry of Health/Medical City/ National Center for Educational Laboratories. /Iraq 2 Ass.Prof. Department of Chemistry and Biochemistry/College of Medicine/Mustansiriyah University/ Iraq 3 Ass. Prof. F I C O G. in Gynecology and Obstetrics, AL Yarmouk Teaching Hospital, Mustansiriyah university \ College of medicine, Iraq Corresponding Author: ABSTRACT Background: Preeclampsia is a multiorgan disorder and characterized by an imbalance in angiogenic factors, including soluble endoglin (sEng). Till now, the relationship between serum levels of sEng with the severity of preeclampsia is not fully elucidated. The study aimed to clarify the precision of serum soluble endoglin (sEng) in the diagnosis of preeclampsia. Materials and Methods: A case–control study has been conducted in the Department of Obstetrics and Gynaecology and clinical biochemistry department, Al-Yarmouk Teaching Hospital, college of medicine/ Mustansiriyah university, Baghdad-Iraq for six months duration. A total of 130 subjects were enrolled. Among them, 40 subjects of non-severe preeclampsia patients (Group 1), 40 of severe preeclampsia (Group 2), and 50 healthy pregnant normotensive women served as controls. Levels were estimated by enzyme-linked immunosorbent assay technique (ELISA) in both cases and controls. Results: There are no significant differences in age among the three groups with a mean age of controls (27.62 ± 4.76), non-severe PE (27.72 ± 5.99), and severe PE (27.90 ± 5.34) years with (p > 0.05). Similarly, no significant differences between non-severe PE and severe PE groups regarding gestational age when compared to the control group (p < 0.691). Mean level of sEng was the highest in severe preeclampsia group (4.04 ± 2.60 ng/mL) as compared to non-severe group (1.63 ± 0.41) and in controls (0.11 ± 0.28) with p-value (p< 0.001). The results showed that the area-under-the-curve (AUC) of serum soluble Endoglin in cases compared with control was (1.00) with a confidence interval (95% CI). The sensitivity and specificity for sEng in PE groups were (100%). On the other hand, compared with the control group, PE groups showed significantly higher creatinine, blood urea, uric acid, ALT, and AST (p < 0.001). Platelet, hemoglobin, PCV, PT, and PTT showed a significant decrease when compared to control at p-value (p = < 0.001) for the first three, (p = 0.001) for PT and low significant for the last (p = 0.03). sEng levels were moderately correlated with platelets (r = 0.312), (p<0.05) in non-severe preeclampsia also, it correlated moderately but negatively with ALT (r = -0.324) and AST (r = - 0.363), (p<0.05) in severe group. Soluble Endoglin levels were strongly correlated with systolic and diastolic blood pressure with a correlation coefficient in non-severe cases with systolic BP was (r = 0.471), diastolic BP (r = 0.313) while in severe cases of PE, for systolic BP was (r= 0.773) and diastolic BP (r= 0.632) and it was statistically significant (P < 0.001). In conclusion, soluble endoglin (sEng) can be considered as a novel biomarker for the diagnosis and prediction of severity of preeclampsia. Keywords: Soluble Endoglin, diagnosis, prediction, preeclampsia. Correspondence: Eham Amer Ali 2Ass.Prof. Department of Chemistry and Biochemistry/College of Medicine/Mustansiriyah University/ Iraq *Corresponding author: Eham Amer Ali email-address: eham.ali@uomustansiriyah.edu.iq INTRODUCTION Preeclampsia (PE) is a pregnancy-specific disease. It is described by new-onset abnormal high blood pressure and proteinuria after 20 weeks of gestation which is associated with placental hypo-perfusion. Preeclampsia is one of the major causes of restricted fetal growth, and in severe cases, dysfunction can advance into multiorgan maternal affection or even mortality of both the mother and her fetus [1]. Approximately 5-10% of pregnancies worldwide are influenced by preeclampsia [2]. Globally the disease occurs in 2–8% of pregnancies which accounting for approximately 16% of maternal mortality in developing countries [3]. The accurate pathogenesis of preeclampsia remains "controversial", while any damage in coagulation-fibrinolysis systems [4] and abnormal stimulation for immune responses and inflammation are often mentioned [5]. There are different mechanisms which may participate in the dysfunction of endothelial cells and hypoxia with poor perfusion of the placenta. Consequently, this leads to an imbalance of angiogenic factors, a state of excessive oxidative stress, the release of antiangiogenic proteins, and other inflammatory mediators [6]. Measurements of pro-and anti-angiogenic factors in the serum of preeclampsia patients mainly [placental growth factor PIGF], [soluble vascular endothelial growth factor receptor-1, sFlt-1] and [soluble fms-like tyrosine kinase-1] is crucial because of the high prevalence of preeclampsia and seriousness. Additionally, these markers are tested as a diagnostic as well as study their ability for predicting the development of PE severity [7,8]. The regulation of placental vasculature is by the essential role of angiogenesis factors and their cellular receptors. In this process, successful placentation is achieved through the regulation between anti-angiogenic and pro-angiogenic influences. Therefore, an imbalance in this equilibrium leads to loss of functional organization between vasodilator and vasoactive substances with the possible subsequent resultant preeclampsia disease [9]. Soluble endoglin (sEng) or (CD105) is an antiangiogenic factor. It is a homodimeric transmembrane glycoprotein with a molecular weight of 180 KD located on the "vascular endothelial" cell surface. sENG is a co-receptor for transforming growth factor (TGF-β1 and β3) and is highly expressed on cell membranes of vascular endothelium [10]. Soluble Endoglin has an antiangiogenic effect in preeclampsia by binding to TGF-β1in maternal circulation, then preventing the signaling of TGF-β1 in endothelial cells,