title: Effect of central obesity, low high-density lipoprotein cholesterol and C-reactive protein polymorphisms on C-reactive protein levels during treatment with Rosuvastatin (10 mg Daily).
abstract: Plasma levels of high-sensitivity C-reactive protein (hsCRP) are an important predictor of cardiovascular disease, and achievement of lower targets of hsCRP with rosuvastatin treatment was associated with improved cardiovascular outcomes. The aim of this study was to examine whether hsCRP levels were related to genetic variants and traditional cardiovascular risk factors in Chinese patients treated with rosuvastatin 10 mg/day. The relations were analyzed between on-treatment plasma hsCRP concentrations and cardiovascular risk factors and 14 single-nucleotide polymorphisms in CRP and other candidate genes. In 281 patients with a median plasma hsCRP level of 0.81 mg/L (interquartile range 0.46 to 1.86), higher hsCRP levels were significantly associated with female gender, greater waist circumference (WC), having diabetes, higher triglycerides, and lower high-density lipoprotein (HDL) cholesterol. Three single-nucleotide polymorphisms (rs1205, 3872G>A and rs2808630, 5237A>G in CRP and rs1169288, I27L in HNF1A) were independently associated with hsCRP levels before and after adjustment for other variables. WC and the CRP rs1205 polymorphism showed the strongest relations with hsCRP, and in multiple regression analysis, gender, WC, diabetes, triglycerides, HDL cholesterol, and the 3 genetic variants explained 35.5% of the variance in hsCRP levels. The 2 CRP polymorphisms, female gender, higher WC, and lower HDL cholesterol were associated with risk for having CRP concentrations ≥ 1 mg/L. In conclusion, central obesity, low HDL cholesterol, and CRP polymorphisms are major determinants of higher hsCRP levels in Chinese patients receiving treatment with rosuvastatin.
authors.affiliation: Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong SAR, China.
authors.forename: Miao
authors.initials: M
authors.lastname: Hu
authors.forename: Michael H K
authors.initials: MH
authors.lastname: Lee
authors.forename: Valiant W L
authors.initials: VW
authors.lastname: Mak
authors.forename: Brian
authors.initials: B
authors.lastname: Tomlinson
mesh_terms: D000368:Aged; D002097:C-Reactive Protein / Q000235:genetics* / Q000378:metabolism; D002681:China / Q000453:epidemiology; D008076:Cholesterol, HDL / Q000097:blood*; D003327:Coronary Disease / Q000453:epidemiology / Q000235:genetics* / Q000517:prevention & control; D004247:DNA / Q000235:genetics*; D004305:Dose-Response Relationship, Drug; D005260:Female; D005464:Fluorobenzenes / Q000008:administration & dosage*; D005838:Genotype; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage; D015994:Incidence; D008297:Male; D008875:Middle Aged; D009391:Nephelometry and Turbidimetry; D056128:Obesity, Abdominal / Q000097:blood* / Q000150:complications / Q000235:genetics; D011110:Polymorphism, Genetic; D011743:Pyrimidines / Q000008:administration & dosage*; D012307:Risk Factors; D000068718:Rosuvastatin Calcium; D013449:Sulfonamides / Q000008:administration & dosage*
chemical_list: D008076:Cholesterol, HDL; D005464:Fluorobenzenes; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011743:Pyrimidines; D013449:Sulfonamides; D000068718:Rosuvastatin Calcium; D002097:C-Reactive Protein; D004247:DNA