Barbiturates and lung cancer: a re-evaluation.
Barbiturates and lung cancer: a re-evaluation.
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巴比妥类药物和肺癌：重新评估。
DOI：
10.1093/ije/28.3.375
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发表时间：
1999
影响因子：
7.7
通讯作者：
Habel,LA
中科院分区：
文献类型：
--
作者：
Friedman,GD;Habel,LA
背景：巴比妥类药物，特别是苯巴比妥，在动物实验中已被证明是一种肿瘤促进剂，并且在我们筛选药物可能致癌作用的队列随访研究中发现其与肺癌风险增加相关。经过十六年的跟踪研究，我们可以对这种关联进行更详细的评估。方法：总共有 10,213 名 Kaiser Permanente 医疗保健计划订户在 1969 年至 1973 年间从其旧金山药房接受巴比妥类药物的随访，直至 1992 年，每两年将他们的肺癌发病率与基于整个药房队列的经验 (143,594) 的预期进行比较。大约一半巴比妥类使用者的吸烟习惯数据可用于在观察/预期分析和 Cox 比例风险分析中调整吸烟情况。结果：最初升高的标准发病率为1.55（95% CI：1.25-1.91），随访3-7年逐渐下降，随访11-15年后稳定在1.3左右。这种相对风险随着时间的推移而降低的趋势在从不吸烟者中更为明显，但由于人数较少，他们最初的超额风险在统计上并不显着。根据配发的处方数量观察到剂量反应趋势。对吸烟的分析控制减少了这种关联或剂量反应趋势，但并未消除这种关联。大多数从不吸烟者的巴比妥相关病例是女性，主要的组织学类型是腺癌。结论：这些长达 23 年随访的结果并不是结论性的，因为患肺癌的从不吸烟者人数仍然很少。然而，他们加强和完善了先前对巴比妥类药物与肺癌关联的观察，这可能无法通过吸烟的混淆来完全解释。随着时间的推移，过度风险的减少与肿瘤促进作用是一致的。对从不吸烟者的研究结果表明，这种可能对女性腺癌的影响可能最大。
BACKGROUND: Barbiturates, particularly phenobarbital, have been shown to be a tumour promoter in animal experiments and were found to be associated with increased risk of lung cancer in our cohort follow-up study to screen pharmaceuticals for possible carcinogenic effects. Sixteen more years of follow-up have accumulated permitting a more detailed evaluation of this association. METHODS: In all, 10,213 subscribers of the Kaiser Permanente Medical Care Program who received barbiturates between 1969 and 1973 from its San Francisco pharmacy were followed up through 1992 and their incidence of lung cancer at biennial intervals was compared with what was expected based on the experience of the entire pharmacy cohort (143,594). Smoking-habit data were available on about half of the barbiturate users and were used to adjust for cigarette smoking in both the observed/expected analysis and in Cox proportional hazards analysis. RESULTS: The initially elevated standard morbidity ratio of 1.55 (95% CI: 1.25-1.91) with 3-7 years of follow-up gradually decreased and stabilized at about 1.3 after 11-15 years of follow-up. This trend for diminishing relative risk over time was more pronounced among the never smokers but their initial excess risk was not statistically significant due to small numbers. A dose-response trend was observed, based on the number of prescriptions dispensed. Analytical control for cigarette smoking reduced but did not eliminate either the association or the dose-response trend. Most of the barbiturate-associated cases in never smokers were women and the predominant histological type was adenocarcinoma. CONCLUSIONS: These findings from up to 23 years of follow-up are not conclusive because of the continuing small number of never smokers who developed lung cancer. However, they strengthen and refine previous observations of a barbiturate-lung cancer association, which is probably not fully explained by confounding by cigarette smoking. The diminution of excess risk over time is consistent with a tumour promoter effect. Findings among the never smokers suggest that this possible effect may be greatest on adenocarcinomas in women.
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