BACKGROUND: High-sensitivity C-reactive protein (hs-CRP) is a sensitive inflammatory marker suggested for cardiovascular risk stratification. This study aimed to assess the potential genetic determinants for serum hs-CRP levels in a cohort with well-controlled nondiabetic hypertension. MATERIALS AND METHODS: Ethnic Chinese nondiabetic hypertensive patients were enrolled in Taiwan. They received comprehensive evaluation including history taking, physical check-up, blood pressure (BP) measurement, 24-h ambulatory BP monitoring and blood sampling. Serum hs-CRP levels were determined. CRP genotyping was performed in two stages. In the first stage, 4 single-nucleotide polymorphisms (SNPs) of CRP including rs1572970, rs2794520, rs3093077 and rs2808630 were investigated in the 400 participants. In the second stage, only SNPs significant in the first stage were selected for complete genotyping in the whole population. RESULTS: Total 915 consecutive patients (40·9 ± 7·3 years, 68·3% male) completed the study. Two of the 4 SNPs including rs1572970 and rs3093077 were correlated to hs-CRP levels in the whole population. Stepwise multiple linear regression indicated that age (P = 0·001), body mass index (P < 0·001), waist-hip ratio (P = 0·032), smoking habits (P = 0·001), night-time systolic BP (P = 0·040), total cholesterol (P = 0·005) and CRP rs3093077 polymorphism (P < 0·001) were independently associated with serum hs-CRP levels. Overall, genetic correlates explained 2·4%, BMI explained 11·9% and all other clinical correlates explained 4·8% of interindividual variability in serum hs-CRP level. CONCLUSION: C-reactive protein genotype contributed limitedly to serum hs-CRP levels in subjects with well-controlled hypertension, suggesting the impacts of clinical rather than genetic determinants to serum hs-CRP levels for cardiovascular risk stratification in this intermediate-risk Taiwanese cohort.
BACKGROUND: High-sensitivity C-reactive protein (hs-CRP) is a sensitive inflammatory marker suggested for cardiovascular risk stratification. This study aimed to assess the potential genetic determinants for serum hs-CRP levels in a cohort with well-controlled nondiabetic hypertension. MATERIALS AND METHODS: Ethnic Chinese nondiabetic hypertensivepatients were enrolled in Taiwan. They received comprehensive evaluation including history taking, physical check-up, blood pressure (BP) measurement, 24-h ambulatory BP monitoring and blood sampling. Serum hs-CRP levels were determined. CRP genotyping was performed in two stages. In the first stage, 4 single-nucleotide polymorphisms (SNPs) of CRP including rs1572970, rs2794520, rs3093077 and rs2808630 were investigated in the 400 participants. In the second stage, only SNPs significant in the first stage were selected for complete genotyping in the whole population. RESULTS: Total 915 consecutive patients (40·9 ± 7·3 years, 68·3% male) completed the study. Two of the 4 SNPs including rs1572970 and rs3093077 were correlated to hs-CRP levels in the whole population. Stepwise multiple linear regression indicated that age (P = 0·001), body mass index (P < 0·001), waist-hip ratio (P = 0·032), smoking habits (P = 0·001), night-time systolic BP (P = 0·040), total cholesterol (P = 0·005) and CRP rs3093077 polymorphism (P < 0·001) were independently associated with serum hs-CRP levels. Overall, genetic correlates explained 2·4%, BMI explained 11·9% and all other clinical correlates explained 4·8% of interindividual variability in serum hs-CRP level. CONCLUSION: C-reactive protein genotype contributed limitedly to serum hs-CRP levels in subjects with well-controlled hypertension, suggesting the impacts of clinical rather than genetic determinants to serum hs-CRP levels for cardiovascular risk stratification in this intermediate-risk Taiwanese cohort.