ABSTRACT
Background: Raised serum uric acid has been reported to be associated with an increased risk of coronary heart disease and is commonly encountered with essential hypertension, even untreated hypertension, and type 2 diabetes, which are in turn associated with coronary heart disease. Aim: To estimate the levels of uric acid in patients with essential hypertension. To correlate the levels of uric acid with the severity of hypertension in newly detected hypertensive patients. To compare the levels of uric acid in hypertensives with that in non hypertensives so as to assess the role of uric acid as a risk factor for hypertension. Materials and Methods: This study was an age and sex matched prospective case control study. Matching for other confounding factors such as diet, alcohol and smoking was also done. The study was conducted during the period from September 2010 to September 2012 after obtaining the clearance from the Institutional Ethics Committee. Inclusion Criteria: Patients of age > 18 years, newly detected patients of essential hypertension and patients with essential hypertension on treatment. Exclusion Criteria: Patients with renal failure. Patients on treatment with drugs altering uric acid levels such as thiazides, loop diuretics, pyrazinamide and allopurinol. Lymphoproliferative or myeloproliferative disorders. Secondary hypertension and pregnancy induced hypertension. The study included a total of 142 patients of which 80 were cases (hypertensives) and 62 were controls (non hypertensives). Results: The range of the serum uric acid in cases was 1.40 to 11.30 mg/dl. In hypertensive males it was found to be from 1.40 to 11.30 mg/dl and in hypertensive females it was found to be from 2.70 to 11.10 mg/dl. The range of the serum uric acid in controls was 1.50 to 6.50 mg/dl. In hypertensive Mudumala Issac Abhilash, NL Varun Mai, K.B.R. Sastry. Raised serum uric acid levels as an independent risk factor for the development of hypertension. IAIM, 2017; 4(11): 37-46. Page 38 males it was found to be from 1.50 to 6.50 mg/dl and in hypertensive females it was found to be from 1.60 to 6.20 mg/dl. Serum uric acid is significantly elevated in hypertensives as compared to normotensive individuals. Serum uric acid can be used probably as an early biochemical marker to determine the severity of hypertension as stage 2 hypertensives had more elevation in serum uric acid levels as compared to other hypertensives. The uric acid levels did not differ significantly between hypertensives with and without treatment. There is a considerable difference in the mean serum uric acid levels between stages 1, 2 and isolated systolic hypertension in the newly detected hypertensives but it is not of a linear correlation The total number of newly detected hypertensives were 39 out of which 13 were diagnosed as stage 1 hypertension, 22 as stage 2 hypertension and 4 as isolated systolic hypertension. The mean of the serum uric acid was 4.20 (1.37) mg/dl, 6.56 (1.40) mg/dl and 4.40 (1.40) in stage 1 hypertension, stage 2 hypertension and isolated systolic hypertension respectively, in newly diagnosed hypertensives. Conclusion: Thus serum uric acid estimation can be used for aiding in the diagnosis of essential hypertension as well as in assessment of the severity.
ABSTRACT
BACKGROUND: Studies in several populations have indicated that genetic variation at the apolipoprotein E structural locus influences atherosclerosis leading to cardiovascular diseases. The possible role of apolipoprotein E polymorphism in the development of essential hypertension has not been sufficiently investigated. In this case-control study, we aimed to determine the significance of association between essential hypertension and apolipoprotein E genotypes. In addition, apolipoprotein E genotypes were correlated with serum lipid levels in order to understand the possible interaction between the specific genotype and the lipid profiles that can contribute to hypertension. METHODS AND RESULTS: The apolipoprotein E genotypes were assayed in 185 patients and 200 controls by polymerase chain reaction followed by enzymatic digestion with Hha I. Using logistic regression analysis, the multivariate-adjusted odds of hypertension were calculated. The incidence of epsilon4 allele was found to be significantly higher in patients (12.16%) than in controls (5.75%, chi2=10.87; p<0.05) and also in patients with positive family history (16.7%) as compared to negative family history (8.87%, chi2 = 8.45; p<0.1). Further, it was observed that carriers of epsilon4 allele have twice as much risk (p<0.05) for developing hypertension as compared to carriers of other alleles. Patients with epsilon4 allele had significantly higher levels of total cholesterol and low-density lipoprotein- cholesterol as compared to epsilon4 allele non-carriers (p<0.05). The adjusted odds ratios for epsilon4 and epsilon2 alleles versus epsilon3 allele were 2.2 (95% confidence interval 1.2 to 3.8, p<0.05) and 1.2 (95% CI, 0.75 to 1.77, p<0.514), respectively. CONCLUSIONS: Our study revealed a strong association of apolipoprotein E locus with hypertension and lipid profile. However, large population-based studies are needed to understand the exact role played by the locus in causing the condition.