Nishimura Masaharu
Division of Respiratory Medicine, Hokkaido University Graduate School of Medicine.
Nihon Rinsho. 2003 Dec;61(12):2095-100.
As only a small portion of smokers develop clinically-apparent COPD, there should be some factors relevant to the susceptibility to smoking. Several studies have demonstrated an increased risk of COPD within families of COPD probands. Recent exploratory studies have revealed a number of candidate genes that may influence a person's risk of COPD, including MMP-9, microsomal epoxide hydrolase, glutathione S-transferase, hemeoxygenase, and TNF-alpha. However, the results from other laboratory are often inconsistent, and there have been no genes except alpha 1-antitrypsin, which have been definitely confirmed to explain the susceptibility to smoking in the development of COPD. It is of note that the susceptibility to smoking could be explained also by non-genetic factors such as adenovirus latent infection to the airways.
由于只有一小部分吸烟者会发展为临床明显的慢性阻塞性肺疾病（COPD），所以应该存在一些与吸烟易感性相关的因素。多项研究表明，COPD先证者的家族成员患COPD的风险增加。近期的探索性研究已经揭示了一些可能影响个体患COPD风险的候选基因，包括基质金属蛋白酶-9、微粒体环氧化物水解酶、谷胱甘肽S-转移酶、血红素加氧酶和肿瘤坏死因子-α。然而，其他实验室的结果往往不一致，除了α1-抗胰蛋白酶外，尚无其他基因被明确证实可解释COPD发生过程中对吸烟的易感性。值得注意的是，吸烟易感性也可能由非遗传因素解释，如气道的腺病毒潜伏感染。
