Physiological predictions and the role of IL-10 -819 promoter polymorphism in preeclampsia

Shno Sabah Tahir; Mudhir Sabir Shekha

doi:10.21271/ZJPAS.33.1.1

Authors

Shno Sabah Tahir 1 Department of Biology, College of Science, Salahaddin University-Erbil, 44001 Erbil, Kurdistan-Region, Iraq 3 Research Centre, Salahaddin University-Erbil, 44001 Erbil, Kurdistan-Region, Iraq
Mudhir Sabir Shekha 1 Department of Biology, College of Science, Salahaddin University-Erbil, 44001 Erbil, Kurdistan-Region, Iraq 2 Department of Pathological Analysis, College of Science, Knowledge University, Erbil 074016, Kurdistan-Region of Iraq, Iraq 3 Research Centre, Salahaddin University-Erbil, 44001 Erbil, Kurdistan-Region, Iraq

DOI:

https://doi.org/10.21271/ZJPAS.33.1.1

Keywords:

Physiological markers, IL-10 -819, polymorphism and preeclampsia

Abstract

Preeclampsia is a multisystem pregnancy-specific syndrome that affects some of pregnancies, which remains a leading cause of maternal and perinatal morbidity and mortality worldwide. Preeclampsia primarily provokes life-threatening, especially to the fetus. The aim of this study was to estimate some physiological and biochemical markers of preeclampsia and investigate the association between IL-10 -819 polymorphism and preeclampsia.

A total of 52 pregnant women with preeclampsia and 35 women with normal pregnancy attended the high-risk unit of Erbil Maternity and Pediatric Governmental Hospital, KRG, Iraq, were considered in the present study. During the regular pregnancy check-ups, blood pressure, occurrence of gestational hypertension (early or late onset), preeclampsia, were also documented. Remarkably, serum Urea, Creatinine, Alkaline Phosphatase (ALP) and Mean Platelet Volume (MPV) were significantly increased in preeclampsia patients. In contrast, Direct Bilirubin, Glucose, GPT, GOT and Platelet count were not significant between preeclampsia and control women. Additionally, Mean Arterial Pressure (MAP) and Systolic Blood Pressure (SBP) were significantly elevated. Furthermore, genotyping of IL-10 T-819 C promoter polymorphism was carried out for all participants using a standard Amplification Refractory Mutation System (ARMS) PCR. Genotypic distribution of the control and patient groups were compared with values predicted by Hardy-Weinberg equilibrium using χ² test. Interestingly, there were significant differences in (IL)-10 (-819) T/C genotype distribution frequency between preeclampsia and control groups. Conclusion The present study suggests that the IL-10 T-819 C gene promoter polymorphism might be a major genetic regulator in the etiology of increased risk of preeclampsia.

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