[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.
Cheng
X
X
Cardiopulmonary Circulation Division, Fu Wai Hospital, CAMS & PUMC, Beijing 100037.
Wu
Y
Y
Li
J
J
D002681:China / Q000453:epidemiology; D005260:Female; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D008297:Male; D010446:Peptide Fragments / Q000378:metabolism; D011347:Procollagen / Q000378:metabolism; D029424:Pulmonary Disease, Chronic Obstructive / Q000453:epidemiology* / Q000209:etiology / Q000378:metabolism; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects*; D000515:alpha 1-Antitrypsin / Q000378:metabolism
D007074:Immunoglobulin G; D010446:Peptide Fragments; D011347:Procollagen; D000515:alpha 1-Antitrypsin; C041876:procollagen Type III-N-terminal peptide; D007073:Immunoglobulin E