Association of hyperhomocysteinemia and MTHFR C677T gene polymorphism in Essential hypertensive patients

Abstract

Essential hypertension contributes 90 to 95 per cent Homocysteine levels acts as predictors of end organ damage in EH by causing arteriolar constriction renal dysfunction and increased sodium reabsorption increased arterial stiffness Homocysteine also induces smooth muscle cell migration and proliferation thus reducing elasticity of vessel wall homocysteine activates matrix metallo proteinases which degrade collagen and elastin leading to imbalance of elastin collagen ratio cause vascular dysfunction Studies are lacking involving a larger sample size and role of endothelial biomarkers in essential hypertension based on the above lacunae the aim of the study was to find out the association of homocysteine with essential hypertension and the MTHFR C677T polymorphism in EHT The objectives of the study were assessing the alterations in endothelial biomarkers inflammatory marker oxidative stress markers along with homocysteine levels This case control study involved 3 groups The results of our study indicate that alterations in endothelial and other biomarkers are associated with the occurrence of hypertension as well as end organ damage in essential hypertensives The genetic study reveals the susceptibility of CT genotype to hypertension and onset of end organ damage EMPs act as mirror of endothelial dysfunction The percentage of EMPs was found to be higher in hypertension Oxidative stress and Hhcy biologically plausible Accordingly oxidative stress might one day be considered as a novel therapeutic target for the therapy of essential hypertension EMP levels as integrative markers of vascular competence may offer new perspectives to assess vascular risk and to monitor treatment efficacy newline newline newline