Does COPD risk vary by ethnicity? A retrospective cross-sectional study.
Does COPD risk vary by ethnicity? A retrospective cross-sectional study.
复制标题
DOI：
10.2147/copd.s96391
复制
发表时间：
2016
影响因子：
2.8
通讯作者：
White P
中科院分区：
文献类型：
--
作者：
Gilkes A;Ashworth M;Schofield P;Harries TH;Durbaba S;Weston C;White P
据报道，黑人和亚洲人患COPD的风险较低，这引发了认知能力较差或易感性降低的问题。我们在控制吸烟的情况下，评估了不同种族人群中COPD的患病率和严重程度。一项回顾性横断面研究，使用伦敦常规收集的初级保健数据。对不同种族人群的COPD患病率、严重程度（1秒用力呼气量[FEV 1]预测值的百分比）、吸烟状况和治疗进行比较，调整年龄、性别、吸烟、剥夺和实践聚集。在47个全科诊所的358，614名患者中，47.6%为白色，20%为黑人，5%为亚洲人。COPD的患病率总体为1.01%，白人为1.55%，黑人为0.58%，亚洲人为0.78%。与白人相比，黑人（调整的比值比[OR]，0.44; 95%置信区间[CI]，0.39-0.51）和亚洲人（0.82; CI，0.68-0.98）发生COPD的可能性较小。黑人COPD患者目前吸烟的可能性较低（OR，0.56; CI，0.44-0.71），而从不吸烟的可能性较高（OR，4.9; CI，3.4-7.1）。无论种族如何，具有相似疾病严重程度的患者的治疗相似，除了在黑人COPD患者中处方的长效毒蕈碱拮抗剂较少（OR，0.53; CI，0.42-0.68）。黑人种族是肺功能较差的预测因子（%预测FEV 1：B系数，-7.6; P<0.0001），当使用种族特异性预测FEV 1值时，未观察到这种效应。在调整黑人较低的吸烟率后，伦敦的黑人患COPD的可能性是白人的一半。观察到的差异可能是由于吸烟方式的种族差异或COPD易感性的种族差异。
Lower risk of COPD has been reported in black and Asian people, raising questions of poorer recognition or reduced susceptibility. We assessed prevalence and severity of COPD in ethnic groups, controlling for smoking. A retrospective cross-sectional study using routinely collected primary care data in London. COPD prevalence, severity (% predicted forced expiratory volume in 1 second [FEV1]), smoking status, and treatment were compared between ethnic groups, adjusting for age, sex, smoking, deprivation, and practice clustering. Among 358,614 patients in 47 general practices, 47.6% were white, 20% black, and 5% Asian. Prevalence of COPD was 1.01% overall, 1.55% in whites, 0.58% in blacks, and 0.78% in Asians. COPD was less likely in blacks (adjusted odds ratio [OR], 0.44; 95% confidence interval [CI] 0.39–0.51) and Asians (0.82; CI, 0.68–0.98) than whites. Black COPD patients were less likely to be current smokers (OR, 0.56; CI, 0.44–0.71) and more likely to be never-smokers (OR, 4.9; CI, 3.4–7.1). Treatment of patients with similar disease severity was similar irrespective of ethnic origin, except that long-acting muscarinic antagonists were prescribed less in black COPD patients (OR, 0.53; CI, 0.42–0.68). Black ethnicity was a predictor of poorer lung function (% predicted FEV1: B coefficient, −7.6; P<0.0001), an effect not seen when ethnic-specific predicted FEV1 values were used. Black people in London were half as likely as whites to have COPD after adjusting for lower smoking rates in blacks. It seems likely that the differences observed were due either to ethnic differences in the way cigarettes were smoked or to ethnic differences in susceptibility to COPD.