慢性肺炎衣原体感染是慢性阻塞性肺病（COPD）的危险因子

目的研究慢性Cpn感染和慢性阻塞性肺病（COPD）之间可能的相关性。方法观察组为年龄在58岁以上的轻度至重度的COPD患者165例和年龄、性别匹配的80例对照组，并测定其FEVl、FVC和圣乔治呼吸问卷（SGRQ）计分。用直接免疫荧光（DIF）法检测外周血单核细胞（PBMC）中的肺炎衣原体特异性抗原（Cpn—Ag），同时用间接微量免疫荧光（MIF）法检测Cpn抗体（IgA，IgG和IgM）。结果观察组Cpn的感染率为63．0％（104／165），对照组15．0％（12／80）。代表急性感染的Cpn—Ag和Cpn-IgM抗体的检出率观察组亦显著高于对照组（P〈O．001），代表慢性感染的Cpn—IgA和IgG抗体的检出率观察组也显著高于对照组（P％0．001）。阿奇霉素治疗后观察组病人的临床症状均有显著改善：SGRQ记分和FEV。／FVC（％）显著增加，与此同时观察组只有Cpn—IgM滴度显著下降（P〈O．001）。慢性Cpn感染与吸烟及较高的年龄有关但与性别无关。结论慢性Cpn感染可能是COPD发展的独立危险因素。

Chronic Chlamydia pneumoniae infection is a risk factor of COPD

To investigate the possible relationship between chronic Cpn infection and chronic obstructive pulmonary disaease （COPD）. The observation group was comprised of 165 patients with moderate to severe COPD（over age 58 years） and 80 subjects relative to age and sex-matched controls with measurement of forced expiratory volume in one second （FEV1）, forced vital capacity （FVC）, St. Georges Respiratory Questionnaire （SGRQ） score. The human peripheral blood mononuclear cells （PBMC） were separated. The Chlamydia pneumoniae-antigen （Cpn-Ag） was detected by direct immunofluorescence （DIF） method. We measured antibodies against C. pneumoniae using microimmunofluorescence technique （MIF）. The infection rates of Cpn were 63.0% （103/165） in observation group and 15.0% （12/80） in control,respectively. The prevalences of Cpn-A and Cpn-IgM representing acute infection were significantly higher in observation group than in control （P-（0. 001）, the preva lences of Cpn-IgA and Cpn-IgG representing chronic infection were significantly higher in observation group than in control （P d0. 001）. After azithromycin treatment, the patient＇s clinical symptoms of observation group are improved markely. SGRQ scores and FEVI/FVC（%） were increased significantly, and meanwhile, only the titer of Cpn-IgM was decreased significantly （P-~0. 001）. Chronic infection was associated with smoking and higher age, but no gender difference was observed. The re sults suggest that chronic Cpn infection may be an independent risk factor for the development of COPD.