David Sean P, Strong David R, Munafò Marcus R, Brown Richard A, Lloyd-Richardson Elizabeth E, Wileyto Paul E, Evins Eden A, Shields Peter G, Lerman Caryn, Niaura Raymond
Brown University Center for Primary Care and Prevention, Primary Care Genetics and Translational Research Center, Memorial Hospital of Rhode Island, Pawtucket, RI 02860, USA.
Nicotine Tob Res. 2007 Dec;9(12):1251-7. doi: 10.1080/14622200701705027.
We analyzed pooled data from two comparable randomized placebo-controlled clinical trials of bupropion pharmacotherapy for smoking cessation for which data on DRD2 Taq1A genotype were available. A total of 722 smokers across the two trials were randomized to 10 weeks of sustained-release bupropion hydrochloride or placebo. General estimating equation analysis demonstrated a significant gene x drug interaction (B = 0.87, SE = 0.34, p = .009). Smokers with the A2/A2 genotype using bupropion were more than three times as likely, relative to placebo, to be abstinent at end of treatment (35.2% vs. 15.1%; OR = 3.25, 95% CI 2.00-5.28) and at 6 months of follow-up (26.7% vs. 12.2%; OR = 2.81, 95% CI 1.66-4.77), which was attenuated by 12 months (16.3% vs. 10.7%; OR = 1.70, 95% CI 0.95-3.05). We found no significant benefit of bupropion relative to placebo on smoking cessation outcomes at any time point in participants with A1/A1 or A1/A2 genotypes. These data suggest that bupropion may be effective for smoking cessation only in a subgroup of smokers with the DRD2 Taq1 A2/A2 genotype.
我们分析了两项可比的随机安慰剂对照临床试验的汇总数据,这两项试验均为安非他酮药物疗法戒烟试验,且可获得多巴胺D2受体基因(DRD2)Taq1A基因型的数据。两项试验共有722名吸烟者被随机分为两组,分别接受为期10周的盐酸安非他酮缓释剂或安慰剂治疗。一般估计方程分析显示基因与药物之间存在显著的相互作用(B = 0.87,标准误 = 0.34,p = 0.009)。与安慰剂相比,携带A2/A2基因型且使用安非他酮的吸烟者在治疗结束时戒烟的可能性是其3倍多(35.2% 对15.1%;优势比 = 3.25,95% 置信区间2.00 - 5.28),在6个月随访时也是如此(26.7% 对12.2%;优势比 = 2.81,95% 置信区间1.66 - 4.77),但在12个月时这种差异有所减弱(16.3% 对10.7%;优势比 = 1.70,95% 置信区间0.95 - 3.05)。我们发现,对于携带A1/A1或A1/A2基因型的参与者,在任何时间点,安非他酮相对于安慰剂在戒烟效果上均无显著益处。这些数据表明,安非他酮可能仅对携带DRD2 Taq1 A2/A2基因型的吸烟者亚组戒烟有效。