肺炎衣原体感染对冠心病发病影响的临床观察

目的 研究肺炎衣原体(Cpn)感染与冠心病(CHD)的关系.方法 应用酶联免疫吸附试验(ELISA)测定冠心病组(120例)和对照组(111例)血清Cpn特异性抗体IgM、IgG及IgA,同时应用免疫浊度法测定冠心病组(97例)和对照组(95例)血清C-反应蛋白(CRP)含量.结果 冠心病组血清Cpn抗体IgG和/或IgA阳性率及IgG和IgA滴度明显高于对照组(均P<0.05);急性心肌梗死(AMI)、不稳定型心绞痛(UAP)及慢性冠心病(CCHD)患者血清Cpn抗体IgG及IgA滴度均分别高于对照组(均P<0.05);冠心病组Cpn抗体IgM阳性率及滴度与对照组无明显差异;IgG和/或IgA及CRP均为阳性组的冠心病发生率明显增高;多元回归分析显示Cpn慢性感染与冠心病发病呈正相关(P=0.045),Cpn慢性感染与冠心病其他危险因素间无相关性.结论Cpn慢性感染可作为冠心病的独立危险因素,炎症反应的发生可能是Cpn慢性感染导致动脉粥样硬化的关键环节.     

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。     

肺炎衣原体感染与慢性阻塞性肺疾病关系的研究

目的　探讨肺炎衣原体感染在慢性阻塞性肺疾病 (COPD)发病中的作用。方法　实验分 2部分 ,(1)动物实验 :雄性Wistar大鼠 4 0只 ,分为A、B、C、D组 ,每组 10只 ,除D组外分别予香烟烟雾吸入和 (或 )经气管滴入肺炎衣原体菌液。 6周后测肺功能 ,行肺部病变病理评分及PCR检测肺部肺炎衣原体感染情况。 (2 )临床研究 :用PCR测COPD患者 (17例 )及健康对照者 (19例 )肺脏肺炎衣原体DNA ,同时测血清肺炎衣原体IgG及IgA抗体。结果　 (1)B组和C组大鼠肺组织肺炎衣原体DNAPCR阳性率分别为 88 9%和 80 0 %。B组大鼠肺组织病理改变主要为炎性细胞浸润及小气道平滑肌增生 ,病理及肺功能改变均较A组显著 ;C组主要病理改变为气道壁炎性细胞浸润及平滑肌增生较明显 ,与D组比较差异有显著性 ,肺功能与D组比较无明显差异。 (2 )COPD患者血清IgG抗体阳性率为 82 4 % ,IgA为 5 8 8% ,均明显高于健康对照者 (P值均 <0 0 5 ) ;PCR检测患者肺组织肺炎衣原体DNA均为阴性。结论　肺炎衣原体感染与COPD无直接关系 ,即单纯肺炎衣原体感染不能引起COPD的发病 ,但它可在吸烟所致病变的基础上加重COPD的病理改变及气流阻塞。     

慢性阻塞性肺病患者肺炎衣原体感染临床分析

目的 调查慢性肺炎衣原体（Cpn）感染和慢性阻塞性肺病（COPD）之间可能的相关性.方法 选取来我院就诊的COPD急性加重期患者60例,COPD稳定期患者40例,以及同期来院参加健康体检的老年人50例（对照组）,测定其第一秒用力呼气容积（FEV1）、用力肺活量（FVC）和圣乔治呼吸问卷（SGRQ）评分.用ELISA法检测Cpn抗体（IgA,IgG和IgM）.结果 COPD急性加重期患者的Cpn-IgM抗体检出率显著高于对照组（P＜0.01）,COPD急性加重期组和COPD稳定期组Cpn-IgA和IgG抗体的检出率均显著高于对照组（P＜0.01）.阿奇霉素治疗后所有COPD患者的临床症状均有显著改善：SGRQ记分和FEV1占预计值％显著增加,仅COPD急性加重期患者Cpn-IgM滴度显著下降（P＜0.01）.结论 慢性Cpn感染可能是COPD发展的危险因素.     

Chlamydia pneumoniae infection and acute exacerbation of chronic obstructive pulmonary disease (COPD)

The objective of the study was to investigate the possible association of Chlamydia pneumoniae (Cpn) in acute exacerbations of chronic obstructive pulmonary disease (COPD) patients. Thirty-eight acutely exacerbated COPD patients and 17 healthy smokers were enrolled in the study, as the study and control groups respectively. Nasopharyngeal swabs and paired serum samples for antibody testing of Cpn (microimmunofluorescence--MIF) were obtained from all subjects. Sputum cultures of COPD patients were also performed. No pathogenic bacteria were isolated from nasopharyngeal swabs in any subject. Serologic evidence of recent Cpn infection was observed in 13 (34%) COPD patients and in one (5%) control subject. The prevalence of Cpn IgG and IgM antibodies representing acute infection were significantly higher in COPD patients than in control subjects (P < 0.05 and P < 0.01 respectively). Prevalence of IgA antibodies and IgG pre-existing antibodies did not show any difference (P > 0.05). Microbiologic culture of the sputa yielded potentially pathogenic micro-organisms in 23 of 38 (60%) COPD patients. Alpha-haemolytic streptococcus (35%), Niesseria spp. (31%) and Candida spp. (9.5%) were most prominent micro-organisms in positive cultures. Although a high prevalence of IgG antibodies against Cpn was detected, it was the sole causative agent in only four (10%) patients. We conclude that a remarkable number of COPD patients (34%) are acutely infected with Cpn and it may either be the sole causative agent or frequently a co-agent in acute exacerbations.     

Increased fibrinogen levels are associated with persistentChlamydia pneumoniaeinfection in unstable coronary artery disease

Aim Increased levels of acute phase proteins, e.g. fibrinogen, arerelated to a poor outcome in unstable coronary artery disease,but the cause of inflammation is unknown. We therefore investigatedthe prevalence of persistent Chlamydia pneumoniae infection,and its relationship to inflammation in this condition. Methods and Results In 256 patients participating in the FRISC trial, evaluatingthe effects of dalteparin (a low molecular weight heparin) inunstable angina or non-Q wave myocardial infarction, Chlamydiapneumoniae IgA antibody titres and levels of fibrinogen, C-reactiveprotein and troponin T were determined at inclusion. IncreasedC. pneumoniae IgA antibody titres were significantly more commonin the patients (36%) than in a reference popu-lation of similarage (19%); P<0·001. Raised titres were associatedwith male gender, increasing age, smoking, and elevated concentrationsof fibrinogen, C-reactive protein and troponin T. The associationbetween persistent C. pneumoniae infection and increased fibrinogenlevels was independent of other risk factors evaluated in multivariateanalysis (P=0·009). Conclusion Persistent C. pneumoniae infection is common in unstable coronaryartery disease. The independent association between increasedC. pneumoniae IgA antibody titres and fibrinogen levels indicatesthat chronic infection could be of importance for disease activity.     

Detection of Chlamydia pneumoniae on cytospin preparations from bronchoalveolar lavage in COPD patients and in lung tissue from advanced emphysema

Chronic obstructive pulmonary disease (COPD) is associated with smoking but other etiological factors contribute. Chlamydia pneumoniae is an obligate intracellular bacterium causing both acute and chronic respiratory tract infections. Studies have revealed an association between chronic C. pneumoniae infection and COPD, asthma and lung cancer but there have been difficulties detecting C. pneumoniae in the bronchial tree. Cytospin slides prepared from bronchoalveolar lavage (BAL) fluid from 14 patients with COPD, 10 healthy smokers (S) and 7 non smokers (NS) were analyzed with a fluorescein isothiocyanate labeled monoclonal antibody to C. pneumoniae. Lung tissue from 24 patients with advanced emphysema who had undergone lung volume reduction surgery (LVRS) was examined with immunohistochemistry for C. pneumoniae. Archived serum samples for detection of specific C. pneumoniae antibodies by microimmunofluorescence were available for 30 of the BAL subjects and 11 of LVRS patients. C. pneumoniae elementary body like structures were found in 29% of cytospin specimens from COPD patients, 14% of NS and 10% of HS. C. pneumoniae was detected in lung tissue in 8%. COPD patients had higher titres of IgG and IgA than NS and S. There was no association between occurrence of C. pneumoniae in BAL fluid and antibody titres. In conclusion, the assays used for detection of C. pneumoniae in lung tissue are feasible, and could be adapted in adequately powered studies to further confirm an association between C. pneumoniae infection and COPD.     

Serology of Chlamydia pneumoniae in patients with chronic cough

OBJECTIVE AND BACKGROUND: Chronic cough is one of the more common respiratory symptoms. Controversy exists as to whether Chlamydia infection is associated with chronic cough. As such, the association of chronic cough with serological evidence of Chlamydia pneumoniae (C. P) infection and a systemic inflammatory marker was assessed. METHODS: Thirty-seven patients who visited Kangwon National University Hospital for chronic cough between September 2003 and August 2004 and 37 age-matched healthy controls were evaluated for C. P. antibodies and C-reactive protein. Chronic infection was defined as an IgG or IgA titre between 1:64 and 1:512, and acute infection was defined as IgM=1:16 or IgG titre of=1:512 or IgA=1:512. A nasopharyngeal swab was evaluated for C. P. DNA using the polymerase chain reaction. RESULTS: The median duration of cough was 3 months (1-240). Nineteen patients (49%) and 19 controls had titres consistent with chronic infection, and the titre difference was not significant (P=0.592). Nine patients and two controls had titres consistent with acute infection (24.3% vs. 5.4%). Acute infection was significantly more prevalent in the patients with chronic cough (P=0.023). There was no difference in the C-reactive protein value (0.13 vs. 0.14, P=0.84). Three patients were positive for C. P. DNA. CONCLUSION: Acute Chlamydia infection was more prevalent in patients with chronic cough, whereas chronic Chlamydia infection was not. There was no elevation of a systemic inflammatory marker in patients with chronic cough.     

Serum IgG and IgA antibodies to Chlamydia pneumoniae and severity of emphysema

OBJECTIVE: Chronic Chlamydia pneumoniae infection has been identified serologically in patients with COPD. The aim of this study was to examine whether the severity of emphysema is related to elevated antibody titres against C. pneumoniae. METHODOLOGY: We measured antibody titres against C. pneumoniae using ELISA, and assessed the severity of emphysema by the percentage of low attenuation area (%LAA) using high resolution (HR) CT in patients with COPD and in non-smoking control subjects. RESULTS: The mean %LAA was 2.2% in non-smoking controls (n = 28) and 13.3% in COPD patients (n = 94). COPD patients with a high IgG antibody index to C. pneumoniae (> or =2.0, n = 42) had a significantly higher %LAA (16.8%) than those with a low IgG index (<2.0, n = 52) (10.6%, P = 0.01). In addition, COPD patients with a high IgA antibody index (> or =2.0, n = 46) had a significantly higher %LAA (15.9%) than those with a low IgA index (<2.0, n = 48) (10.9%, P = 0.048). COPD patients with a high IgA antibody index also had a significantly lower %DLco than that associated with a low IgA index (68.1% and 80.3%, respectively, P = 0.007). There were no significant differences in age, smoking index or FEV(1)/FVC between these groups. CONCLUSION: These results suggest that high antibody titres against C. pneumoniae are linked with the severity of emphysema on high resolution CT and decreased diffusing capacity to carbon monoxide.     

Definition, epidemiology and natural history of COPD.

Chronic obstructive pulmonary disease (COPD) is the fifth cause of morbidity and mortality in the developed world and represents a substantial economic and social burden. Patients experience a progressive deterioration up to end-stage COPD, characterised by very severe airflow limitation, severely limited and declining performance status with chronic respiratory failure, advanced age, multiple comorbidities and severe systemic manifestations/complications. COPD is frequently underdiagnosed and under-treated. Today, COPD develops earlier in life and is less gender specific. Tobacco smoking is the major risk factor for COPD, followed by occupation and air pollution. Severe deficiency for alpha(1)-antitrypsin is rare; several phenotypes are being associated with elevated risk for COPD in the presence of risk factor exposure. Any patient presenting with cough, sputum production or dyspnoea should be assessed by standardised spirometry. Continued exposure to noxious agents promotes a more rapid decline in lung function and increases the risk for repeated exacerbations, eventually leading to end-stage disease. Without major efforts in prevention, there will be an increasing proportion of end-stage patients who can live longer through long-term oxygen therapy and assisted ventilation, but with elevated suffering and huge costs. Smoking prevention and smoking cessation are the most important epidemiological measurements to counteract chronic obstructive pulmonary disease epidemics.     

Disparate innate immune responses to persistent and acute Chlamydia pneumoniae infection in chronic obstructive pulmonary disease

RATIONALE: Chlamydia pneumoniae (Cpn) infection may play a role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Few data are available comparing persistent and acute infection of this pathogen in the human respiratory tract. OBJECTIVES: To study Cpn-induced innate immune responses in lung tissue from patients with COPD and control subjects ex vivo and in vitro. METHODS: Cpn detection was done by nested polymerase chain reaction, in situ hybridization, and immunohistochemistry ex vivo in unstimulated tissue and in vitro using an acute Cpn infection model. As main endpoints for the assessment of early cellular responses, nuclear factor (NF)-kappaB activation and CXC chemokine ligand (CXCL)-8 expression were evaluated. The role of Toll-like receptors (TLRs) as recognition molecules in Cpn-induced innate responses was tested by blocking experiments. MEASUREMENTS AND MAIN RESULTS: Fifteen percent of patients with COPD were chronically infected with Cpn in contrast to 0% of control subjects (p < 0.05). There were no differences in CXCL-8 and NF-kappaB expression between infected and noninfected COPD tissue ex vivo. In contrast, acute in vitro infection induced an intense innate immune response including up-regulation of TLR2. Blocking experiments demonstrated the predominant role of TLR2 in induction of the early immune response, whereas no influence on chlamydial infection rates was observed. CONCLUSIONS: Acute in vitro infection of human lung tissue with Cpn elicited a marked innate response via TLR2, whereas chronic chlamydial infection in patients with COPD was not associated with enhanced cellular activation. These findings suggest different roles of Cpn during acute and chronic stages of pulmonary infection.     

Severe chronic obstructive pulmonary disease: association with marginal bone loss in periodontitis

An association between chronic marginal periodontitis and chronic obstructive pulmonary disease (COPD) has been suggested. The aim of this study was to investigate whether chronic marginal periodontitis is more prevalent in very severe COPD than in other very severe respiratory diseases, and whether periodontitis in COPD is related to risk factors for periodontitis that are often present in COPD subjects. Orthopantomograms were collected from 130 patients with COPD and 50 patients with non-COPD evaluated for lung transplantation. Chronic marginal periodontitis was defined as a general marginal bone level > or = 4 mm. The prevalence of periodontitis was 44% in the COPD group vs. 7.3% in the non-COPD group. All oral measurements differed significantly between the groups. The difference in mean marginal bone level remained statistically significant when adjusting for age, gender and pack years smoked. In logistic regression analysis mean marginal bone level > or = 4 mm was identified as a factor significantly associated with severe COPD. This study demonstrates that chronic marginal periodontitis is common in patients with severe COPD. The high prevalence of periodontitis in COPD patients appears to be independent of possible risk factors for periodontitis such as age, pack years smoked, body mass index, use of corticosteroids and bone mineral density.     

The association study of Apolipoprotein E polymorphisms and chronic obstructive pulmonary disease in the Chinese population: A case-control study

Chronic obstructive pulmonary disease (COPD) patients have increased cardiovascular morbidity and mortality. Apolipoprotein E (ApoE) is involved in chronic inflammation which is the common characteristic of emphysema and cardiovascular disease. ApoE polymorphisms are associated with cardiovascular disorders and atherosclerosis. There is no report about the association between ApoE polymorphism and COPD.A total of 480 COPD patients and 322 controls who were unrelated Chinese Han individuals were enrolled. Rs429358 and rs7412 were genotyped and the associations between ApoE polymorphisms and COPD risk were analyzed by logistic regression analysis. Online software SHEsis were applied to perform linkage disequilibrium (LD) and haplotypes analysis. The interactions of ApoE and environmental factor on COPD susceptibility was analyzed by software MDR3.0.2.No significant association was found between rs429358, rs7412 and COPD under different genetic models. Rs429358 and smoking formed the best model in the MDR analysis. The frequency of E2/E2 phenotype was the lowest in 2 groups. E3/E3 was the most common phenotype, accounting for 69.8% of COPD patients and 68.9% of controls. No statistically difference was identified between the cases and controls under different phenotypes.This was the first genetic association study between ApoE and COPD. No positive association was found in the Chinese Han population. Rs429358 and smoking status existed significant interaction, indicating that both of ApoE and smoking may be involved in the development of COPD disease.     

Chronic obstructive pulmonary disease in non-smokers

Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality worldwide. Tobacco smoking is established as a major risk factor, but emerging evidence suggests that other risk factors are important, especially in developing countries. An estimated 25–45% of patients with COPD have never smoked; the burden of non-smoking COPD is therefore much higher than previously believed. About 3 billion people, half the worldwide population, are exposed to smoke from biomass fuel compared with 1·01 billion people who smoke tobacco, which suggests that exposure to biomass smoke might be the biggest risk factor for COPD globally. We review the evidence for the association of COPD with biomass fuel, occupational exposure to dusts and gases, history of pulmonary tuberculosis, chronic asthma, respiratory-tract infections during childhood, outdoor air pollution, and poor socioeconomic status.     

Elevated antibody levels against Chlamydia pneumoniae, human HSP60 and mycobacterial HSP65 are independent risk factors in myocardial infarction and ischaemic heart disease

The relative significance of traditional risk factors, chronic infections and autoimmune processes in the development of acute myocardial infarction (AMI) has not been fully elucidated. We compared serum IgG antibody titres to various pathogens, i.e. Chlamydia pneumoniae (Cpn), cytomegalovirus (CMV) and herpes simplex virus type 1 (HSV-1), and to the potential autoantigens human heat shock protein 60 (hHSP60) and mycobacterial heat shock protein 65 (mHSP65), in serum samples obtained from patients 3-48 h after AMI (n = 40) or stable effort angina (SEA, n = 43), and from controls (n = 46). The strongest association was observed between AMI and the elevated level of hHSP60 antibodies. The association between AMI and the level of Cpn antibodies was also significant. High levels of hHSP60 and Cpn antibodies represented independent risk factors for the development of AMI, but the simultaneous presence of high levels of antibodies to Cpn and hHSP60 suggested a joint effect on the relative risk of AMI (OR = 12.0-21.1). The antibody titres to mHSP65 were higher in the SEA group than in the controls, and the simultaneous presence of high levels of Cpn and mHSP65 antibodies meant an increased risk among the SEA patients. The antibody titres to CMV or HSV-1 were similar in the three groups. In conclusion, these results demonstrate associations of AMI with high levels of anti-hHSP60 and anti-Cpn antibodies, and of SEA with the level of anti-mHSP65 antibodies, these being independent risk factors.     

Does chronic Chlamydia pneumoniae infection increase the risk of myocardial injury? Insights from patients with non-ST-elevation acute coronary syndromes

Background Cumulative evidence suggests a positive association between Chlamydia pneumoniae (Cpn) infection and risk of future coronary events among patients with stable coronary artery disease. However, its prognostic role in unstable coronary syndromes is less well defined. Because Cpn immunoglobulin A (IgA) may be a more reliable indicator of chronic infection than immunoglobulin G (IgG), we speculated that in patients with non-ST-elevation acute coronary syndromes (ACS), this marker might serve as a more useful prognostic tool. Accordingly, we evaluated plasma samples acquired at presentation in 178 patients with ACS for a possible association between Cpn IgA titer and biochemical evidence of myocardial injury. Methods Cpn IgG (positive if ≥1:32), and IgA titers (positive if ≥1:16) were measured by use of the microimmunofluorescence technique in 70 patients with ACS in whom myocardial injury developed associated with their presenting events (elevated CK-MB and/or troponin I); and in 108 patients with ACS without such injury. The odds ratios (ORs) for myocardial injury associated with consecutive antibody titers were determined for each of Cpn IgG and IgA. Multiple logistic regression was applied to adjust for key baseline characteristics. Results Median age of subjects was 64 years; 63% were male and 33% were smokers. The median antibody titers among those with and without myocardial injury respectively were as follows: IgG (1:128 vs 1:128), IgA (1:32 vs <1:16, P = .2). The adjusted ORs for myocardial injury associated with consecutive IgA titers were as follows: IgA ≥1:16, adjusted OR 1.49 (P = .22); ≥1:32, OR 1.95 (P = .04); ≥1:64, OR 1.37 (P = .38); ≥1:128, OR 0.77 (P = .55). No significant trend was found for any IgG titer. Conclusions Among patients with non-ST-elevation ACS, a Cpn IgA ≥1:32 at presentation was associated with a significantly higher risk of myocardial injury complicating the presenting event. (Am Heart J 2002;144:987-94.)     

肺炎衣原体感染与呼吸系统疾病的血清学相关性研究

目的　探讨肺炎衣原体 (Chlamydia Pneumoniae,CPn)感染与呼吸系统常见疾病的相关性。方法　采用间接免疫荧光法检测 CPn特异性抗体 Ig A、Ig G、Ig M。结果　肺癌组、慢性阻塞性肺疾病 (COPD)组和支气管哮喘组的既往感染率与慢性感染率明显高于自发性气胸组和健康献血员对照组 (P<0 .0 5 ) ;而肺癌组、COPD组和支气管哮喘组之间以及自发性气胸组和健康献血员对照组之间的感染率则无统计学意义 (P>0 .0 5 )。结论　 CPn血清特异性抗体 Ig A、Ig G的升高与肺癌、COPD和支气管哮喘相关 ,CPn感染可能参与了其发病机制。     

Productive cough is an independent risk factor for the development of COPD in former smokers

Background and objective: It has yet to be determined whether the presence of productive cough is a risk factor for the development of COPD. The aim of the present study was to obtain more information on this potential association in Japanese men. Methods: Seven hundred and eighty‐three men with normal spirometry who did not have respiratory disease were recruited. The subjects were divided into three groups: group A, non‐smokers; group B, those with a positive smoking history without productive cough; and group C, those with a positive smoking history and productive cough. The incidence rates of COPD were compared among the three groups and the relative risks for the development of COPD were assessed. Results: During the mean follow‐up period of 33.6 ± 20.4 months, 19 (2.4%) subjects developed COPD. The incidence rate of COPD was significantly higher in group C than in group B (10.1 vs 2.2%, P = 0.003). A multivariate analysis of data for all subjects, current smokers and former smokers revealed that productive cough was an independent risk factor for the development of COPD in all subjects and former smokers but not in current smokers. Conclusions: Productive cough was an independent risk factor for the development of COPD in Japanese men. In particular, former smokers who complain of this symptom should be regarded as being at high risk for the development of COPD. The data suggested that stage 0 disease, as defined in the Global Initiative for Chronic Obstructive Lung Disease 2001 guidelines, is relevant for the identification of subjects at risk of developing COPD.     

What can genetics tell us about the cause of fixed airflow obstruction?

Chronic obstructive pulmonary disease (COPD) is a major cause of chronic morbidity and mortality worldwide with smoking being the most important risk factor of the disease. However, lung function and COPD are known to also have a genetic component and a deeper knowledge of the genetic architecture of the disease could lead to further understanding of predisposition to COPD and also to development of new therapeutic interventions. Genetic linkage studies and candidate gene association studies have not provided evidence to convincingly identify the genes underlying lung function or COPD. However, recent large genome-wide association studies (GWAS) including tens of thousands of individuals have identified 26 variants at different loci in the human genome that show robust association with quantitative lung function measures in the general population. A growing number of these variants are being shown to be associated with COPD. Following the identification of these new lung function loci, the challenge now lies in refining the signals to identify the causative variants underlying the association signals and relating these signals to the molecular pathways that underlie lung function.     

慢性阻塞性肺疾病患者肺炎衣原体感染的研究

目的 探讨肺炎衣原体感染与慢性阻塞性肺疾病（COPD）的相关性。方法 选择61例COPD急性加重期患者,35例COPD稳定期患者,26名正常对照者,采用微量免疫荧光法测定血清肺炎衣原体特异性抗体IgA,IgM,IgG,套式聚俣酶链反应检测痰中的肺炎衣原体DNA。结果 COPD急性加重期患者的急性肺炎衣原体的感染率为31．1％,明显高于COPD稳定期和且（P＜0．05）。COPD急性加重期组和稳定期组的慢性肺炎衣原体感染率分别为21．3％和31．4％,明显高于对照组（P均＜0．05）,同时IgA的几何平均滴度在COPD急性加重期中最高（20．5）,COPD稳定期组中次之（10．8）,对照组最低（3．6）,三组间差异有显著性（P＜0．05）。结论 急性肺炎衣原体感染为COPD急性加重的一个重要诊因,慢性肺炎衣原体感染可能参与COPD的发病机制。