Browsing by Author "Abindau, E."
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Item Effects of factor v Leiden polymorphism on the pathogenesis and outcomes of preeclampsia(BMC Medical Genetics, 2019-11-27) Ababio, G.K.; Adu-Bonsaffoh, K.; Abindau, E.; Narh, G.; Tetteh, D.; Botchway, F.; Morvey, D.; Neequaye, J.; Quaye, I.K.Background: Factor V Leiden polymorphism is a well-recognized genetic factor in the etiology of preeclampsia. Considering that Ghana is recording high incidence of preeclampsia, we examined if factor V Leiden is a contributory factor to its development and pregnancy outcomes. Methods: STROBE consensus checklist was adopted to recruit eighty-one (81) consenting subjects after ethical clearance. Subjects were followed up till delivery to obtain outcomes of PE. Routine blood chemistry and proteinuria were done on all samples. Factor V Leiden was characterized by polymerase chain reaction and restriction fragment length polymorphism (RFLP). The data was captured as protected health information (PHI) and analyzed with SPSS version 22. Results: Overall allelic frequencies found in FVL exon 10 were 0.67 and 0.33 for G and A alleles respectively. The FVL mutation was more in PE and hypertensive patients. Increased white blood cells, increased uric acid and a three – fold increment of AST / ALT ratio was observed in PE cases when stratified by FVL exons (exon 8 and 10). Significant differences were also observed between FVL and age, systolic blood pressure (SBP), diastolic blood pressure (DBP), liver enzymes, white blood cells (wbc), hemoglobin levels. Conclusion: FVL mutation allele frequency was 0.33, a first report. The mutation was associated with increased uric acid, liver enzymes and blood cell indices suggestive of acute inflammation.Item An evaluation of serum leptin dynamics in Preeclampsia at the Korle-Bu Teaching Hospital(University of Ghana, 2016-07) Abindau, E.Background: Preeclampsia is a peculiar human pregnancy condition with heightened immune response, oxidative stress, hypoxia and reduced angiogenesis. These features of preeclampsia which are influenced by leptin which causes endothelial dysfunction; the main pathology of this condition. Hypertension, which is a diagnostic marker of preeclampsia, is also associated with increased leptin level. This implicates leptin in preeclampsia pathogenesis. Data from Caucasians and Asians show higher leptin level in preeclamptic subjects and also leptin as a contributory factor to preeclamsia severity but such data is non-existent in the Ghanaian population. Aim: To determine and correlate maternal serum leptin levels in normotensive pregnant and preeclamptic women and to relate these to the gestational age of delivery and birthweight. Methodology: The study used a case control study design and recruited 144 consenting participants. Blood samples were drawn for hematological and biochemical analysis. Maternal serum obtained from the blood samples were used for leptin Quantification by ELISA. Results: There was no significant difference in the leptin level between both cases and controls or the mild and severe preeclampsia cases with p>0.05. There was no correlation between leptin level and blood pressure for the controls, cases, mild preeclampsia and severe preeclampsia. The birth weight of cases was significantly higher than that of the controls. Conclusion: Preeclampsia pathogenesis and severity in Ghanaian patients is not associated with maternal circulating leptin levels.