Bioequivalence of clopidogrel hydrogen sulfate tablets in healthy Chinese volunteers.

We aimed to evaluate the bioequivalence of clopidogrel in healthy Chinese volunteers after administration of a single oral dose. We administered a single oral dose of 75 mg clopidogrel (test and reference) to 32 healthy Chinese volunteers according to an open, randomized, crossover design. The concentration of clopidogrel acid (carboxylic metabolite of clopidogrel) in the plasma was determined using liquid chromatography-tandem mass spectrometry (LC-MS/MS). Bioequivalence of the test and reference preparations were calculated using analysis of variance and one-sided t-test by using the DAS 2.0 software. The pharmacokinetic parameters of the test and reference preparations were as follows: peak plasma concentration (Cmax), 1351.101 ± 654.955 ng/mL and 1184.652 ± 607.713 ng/mL; area under the curve, 2642.017 ± 1093.848 ng·h/mL and 2780.666 ± 1283.100 ng·h/mL; and time to reach Cmax (Tmax), 0.789 ± 0.318 h and 0.953 ± 0.633 h, respectively. The relative bioavailability of the formulation was 101.7 ± 35.3%, which indicated that the test preparation was bioequivalent to the reference drug.

Positive association between PPARD rs2016520 polymorphism and coronary heart disease in a Han Chinese population.

PPARD encodes peroxisome proliferator-activated re-ceptor delta, which has been shown to play an important role in control-ling lipid metabolism and atherosclerosis. In this case-control study, we explored the relationship between PPARD rs2016520 polymorphism and coronary heart disease (CHD) in a Han Chinese population. A to-tal of 657 CHD cases and 640 controls were included in the associa-tion study. rs2016520 polymorphism genotyping was performed using the melting temperature-shift polymerase chain reaction method. The PPARD rs2016520-G allele reduced CHD risk by 17.9% (χ(2) = 5.061, P = 0.025, OR = 0.821, 95%CI = 0.692-0.975). Furthermore, a signifi-cant difference in CHD risk was observed for the PPARD rs2016520 polymorphism in the dominant model (AG + GG vs AA: χ(2) = 4.751, degrees of freedom (df) = 1, P = 0.029, OR = 0.784, 95%CI = 0.631- 0.976). Analysis by age suggested that the G-allele decreased CHD risk by 14.8% in ages greater than 65 years (χ(2) = 4.446, P = 0.035, OR = 0.852, 95%CI = 0.684-1.060). In contrast, meta-analysis of PPARD rs2016520 among 3732 cases and 5042 controls revealed no associa-tion between PPARD rs2016520 and CHD (P = 0.19). We found that the PPARD rs2016520-GG genotype decreased CHD risk in a Han Chinese population. Moreover, we found an association between serum high-density lipoprotein cholesterol level and PPARD rs2016520 in senior individuals aged ≥ 65 years. The meta-analysis revealed no association between PPARD rs2016520 and CHD, suggesting ethnic differences in the association between the PPARD locus and CHD.