Adiponectin and resistin in essential hypertension: association with cardiovascular disease

Hypertension is a well established risk factor for vascular diseases, with wide ranging implications on morbidity and mortality. High prevalence of arterial hypertension in obese humans seems to suggest that adipose tissue may influence blood pressure. Adiponectih and resistin, an adipocyte-derived proteins, may play roles in the development of atherosclerotic vascular disease. The present study was aimed to study adiponectin and resistin levels in essential hypertension [EH] and their association with development of cardiovascular disease [CVD]. Thirty EH patients were subclassified into two groups; 17 EH patients without CVD and 13 EH patients with CVD. 15 apparently healthy subjects were studied as control group. All participants were subjected to the following laboratory investigations: fasting glucose, insulin, calculation of homeostatic model assessment-insulin resistance [HOMA-IR], lipid profile, high sensitivity CRP [hs-CRP]. Adiponectin and resistin were done by ELISA technique. Adiponectin was significantly decreased in both EH groups compared to controls and in EH patients with CVD compared to those without CVD. Hypoadiponectinemia was associated with significant increased risk of hypertension [OR 7.3, 95% CI 1.2-42.8] and CVD [OR 7.6, 95% CI 1.2-48.0], where OR is odds ratio and CI is confidence interval. Resistin was significantly increased in EH patients with CVD compared to those without CVD and control groups, while no significant difference in resistin was found between EH patients without CVD and controls. Hyperresistinemia was significantly associated with increased risk of CVD [OR 6.4, 95% CI 1.2-34.6] in hypertensive patients. Hypoadiponectinemia and hyperresistenemia were correlated with other risk factors of CVD as elevated blood pressure, atherogenic lipid profile and hs-CRP. Decreased adiponectin and increased resistin were associated with CVD in EH patients. Therapeutic strategies that maintain higher adiponectin and lower resistin may be helpful to lower cardiovascular risk in those patients

Insulin resistance and its fibrogenic effect in chronic hepatitis C virus patients: role of tumor necrosis factor alpha activation

Insulin resistance [IR] is one of the extrahepatic complications that occur in chronic hepatitis C virus infection [HCV], and is claimed as one of the fibrogenic factors which cause more rapid fibrosis progression. We examined the effect of HCV infection on insulin resistance states, and the possible link between IR, tumor necrosis factor-alpha [TNF-alpha] activation and development of hepatic fibrosis. Thirty patients with chronic hepatitis C infection divided into 2 groups according to presence or absence of fibrosis, 15 apparently healthy volunteer and 15 patients with hepatic fibrosis due to causes other than HCV were studied. Laboratory assessment of liver functions, fasting glucose, insulin levels, homeostasis model assessment of insulin resistance [HOMA-IR] and soluble tumor necrosis factor receptors 2 [sTNFR2] were done. HOMA-IR and sTNFR2 levels were significantly increased in patients with chronic HCV without fibrosis as compared with healthy control [p<0.01, p<0.001, respectively], and in patients with HCV induced fibrosis compared to HCV patients without fibrosis [p<0.001], and non HCV fibrosis [p<0.001, p< 0.05, respectively]. HOMA-IR was significantly correlated with sTNFR2 and fibrosis stage [p< 0.001]. IR was associated with increased risk of developing hepatic fibrosis in chronic HCV infection [OR 8.0, 95% CI 1.5-42]. Insulin resistance can be induced by chronic HCV infection per se and is correlated to fibrosis stages. Its fibrogenic role may be mediated by TNF-alpha activation