吸烟者慢性阻塞性肺疾病易患因素的研究

目的　通过病例对照研究，探讨吸烟者慢性阻塞性肺疾病（ＣＯＰＤ） 的易患因素。方法病例组为１５４ 例吸烟指数（每日平均吸烟支数×吸烟年数） ≥３００ 、无慢性呼吸道疾病症状的ＣＯＰＤ 患者，其一秒钟用力呼气容积占用力肺活量的比值（ＦＥＶ１／ＦＶＣ）＜ ７０％ ；在同居住地（乡镇）按１：１ 配对选择同年龄（ ±３ 岁） 、同性别的吸烟者（无慢性呼吸道疾病症状， 且ＦＥＶ１／ＦＶＣ≥７５ ％） 作为吸烟对照组；另检查了２３ 名从不吸烟、无慢性呼吸道疾病症状，且ＦＥＶ１／ＦＶＣ≥７５ ％ 者作为正常对照组。做问卷、查体、心电图、Ｘ线胸片、肺功能、支气管反应性及包括α１ 抗胰蛋白酶（α１ＡＴ） 活性、弹性蛋白酶活性、丙二醛（ＭＤＡ）、前胶原Ⅲ肽（ＰⅢＰ）、ＩｇＥ、ＩｇＧ等血清学检查。结果　两组一般情况的均衡性检验无显著性差异，资料有可比性。血清学检查：病例组α１ＡＴ活性明显低于吸烟对照组和正常对照组，差异有非常显著意义（ Ｐ＜ ０－０５） ，后两组间差异无显著意义；病例组与吸烟对照组间ＰⅢＰ及ＩｇＥ无显著性差异，但均高于正常对照组。病例组支气管反应性阳性率为７８ ％ ，ＰＣ２０ 为（１－４ ±１－６）ｇ／Ｌ；吸烟对照组阳性率为２８％ ，Ｐ

Study on susceptible risk factors for COPD in smokers

OBJECTIVE: To explore the susceptible risk factors for COPD in smokers. METHODS: 154 patients with COPD (FEV1/FVC < 70%) were recruited as the case group whose smoking index (average cigarettes a day times smoking years) was > or = 300 and there was no complaint of chronic respiratory symptoms. The control group included 154 smokers pair-matched in age(+/- 3 years) gender, residence, absence of COPD (FEV1/FVC > or = 75%) and respiratory symptoms. 23 never-smoking subjects with FEV1/FVC > or = 75% and no respiratory symptoms served as healthy control. The following parameters were evaluated: questionaire, physical examination, ECG, chest X-ray, lung function test, methacholine provocation test of bronchial responsiveness and serum levels of elastase activity, alpha 1-AT activity, MDA, PIIIP, IgE and IgG. RESULTS: The positive rate of bronchial hyperresponsiveness was 78% in the case group, PC20 = (1.4 +/- 1.6) g/L; but 28% in the matched group were positive, PC20 = (2.7 +/- 2.3) g/L, (P < 0.001). No one was found hyperresponsive in the healthy control group. There were no differences in serum PIIIP and IgE between the case and the control groups, but they were markedly higher than those in the healthy control. Serum alpha 1-AT activity, room condition, occupational exposure, smoking habit (deep inhalation), cigarettes with or without filter tip, parents with bronchitis and(or) emphysema history, brothers or sisters with bronchitis history were correlated with COPD, OR being 2.33, 2.00, 1.64, 1.88, 1.76 and 3.67, respectively. Logistic regression revealed that alpha 1-AT activity, bronchial hyperresponsiveness, room condition and occupational exposure, smoking habit and respiratory disease history in family were related to COPD. CONCLUSIONS: alpha 1-AT deficiency may be a risk factor for COPD susceptible smokers. There may be relationship between bronchial hyperresponsiveness and developing COPD, but whether it is the cause or result of COPD needs further study. Smoking may induce elevation of serum PIIIP and IgE, but both of them are not directly related to COPD. Room condition, occupational exposure, smoking habit, and respiratory disease history in family may be associated with COPD in smokers.