6年间气道高反应性对重度吸烟者慢性阻塞性肺疾病发病的影响

目的探讨气道高反应性对重度吸烟者慢性阻塞性肺疾病（COPD）发病的影响。方法1996年，对456名慢性呼吸症状和重度心脑血管病的重度吸烟者（FVC≥15包／年）进行调查，询问吸烟史，测量气道反应性、第一秒用力呼气量（FEV1）、用力肺活量（FVC）。2002年对其中259人再次进行呼吸功能测量，以及COPD发病情况。结果调整年龄、性别、身高、吸烟包／年、吸烟种类（无过滤嘴、有过滤嘴、混吸）、戒烟和基线FEV1后，气道高反应性（AHR，PC20 FEV1〈8mg／ml）加快了FEV1（β=19．2ml／yr，P=0．003），FVC（β=20．6ml／yr，P=0．012）和FEV1／FVC（β=0．4％／yr，P=0．008）的1996-2002年间的下降速度。对基线无COPD者进行亚组分析发现，气道高反应性者6年后COPD发病危险显著增加，调整调整年龄、性别、身高、吸烟影年、吸烟种类（无过滤嘴、有过滤嘴、混吸）、戒烟和基线FEV1后，OR值为5．6（95％可信区间：1．1-28．2）。结论气道高反应性在吸烟引起的COPD发病过程中起着重要作用，气道反应性测定有助于吸烟易感者的早期发现。     

慢性阻塞性肺疾病支气管舒张试验47例临床分析

目的探讨支气管舒张试验不同结果的慢性阻塞性肺疾病(COPD)患者的临床特点。方法对2007年4月至2008年1月上海交通大学医学院附属新华医院呼吸内科住院的47例COPD患者进行肺功能及支气管舒张试验的检查,并收集患者相关临床资料,对于不同的支气管舒张试验结果进行比较分析。结果舒张试验阳性组的COPD患者吸烟史明显少于阴性组(P<0.05),而血清IgE则明显高于阴性组(P<0.05)。阳性组用力肺活量(FVC)改善率、第一秒钟用力呼气容积(FEV1)改善率、功能残气量(FRC)、75%肺活量时的最大呼气流量(MEF75%)改善率、50%肺活量时的最大呼气流量(MEF50%)改善率均高于阴性组(P<0.05),其中尤以FEV1改善率、MEF75%改善率、MEF50%改善率明显(P<0.01)。不同分级的COPD患者舒张试验的结果差异有统计学意义(P<0.05)。结论吸烟是影响COPD患者支气管舒张试验结果的一个因素。支气管舒张试验阳性的COPD患者具有更高的血清IgE水平,可能存在气道高反应性。舒张试验阳性的COPD患者气流受限的小气道的改善不明显,可能是以大中气道的改善为主。轻-中度的COPD患者更具有的气流受限的可逆性。     

慢性阻塞性肺疾病患者痰液炎症细胞计数与分类及其意义

目的探讨炎症细胞在慢性阻塞性肺疾病(COPD)发病机制中的作用。方法对受试者痰液进行炎症细胞计数与分类检查,并与肺功能指标作相关分析。结果COPD组痰液细胞总数、中性粒细胞计数(Neu)及百分比(Neu%)、嗜酸性粒细胞计数(Eos)、淋巴细胞计数(Lym)明显高于健康吸烟者(HS组)和健康不吸烟者(HNS组)(P<0.01);嗜酸性粒细胞百分比(Eos%)高于HNS组(P<0.01);淋巴细胞百分比(Lym%)高于HS组(P<0.01)。HS组痰液细胞总数、Neu及Neu%、Eos及Eos%均明显高于HNS组(P<0.05~0.01)。在COPD组,痰液Neu%与一秒钟用力呼气容积占预计值百分比(FEV1占预计值%)、一秒钟用力呼气容积/用力肺活量(FEV1/FVC)呈显著负相关(r’s=-0.734、-0.735,P<0.01)。结论多种炎症细胞尤其是中性粒细胞参与了COPD气道炎症反应的发生并导致气流阻塞的形成。     

COPD和哮喘患者支气管舒张实验用力肺活量和呼气容积的变化

目的 探讨COPD和哮喘患者支气管舒张实验用力肺活量和呼气容积变化.方法 随机选取COPD急性加重期78例和哮喘急性发作期64例,采用支气管舒张实验比较COPD和哮喘患者实验前后用力肺活量(FVC)、一秒用力呼气容积(FEV1)的增加量和增加率.结果 支气管舒张实验后,COPD患者的用力肺活量(FVC)的增加量191 ml,较舒张前增加12.93%,而一秒用力呼气容积(FEV1)的增加量63 ml,较舒张前增加10.01%;哮喘患者的用力肺活量(FVC)的增加量363 ml,较舒张前增加15.34%,而一秒用力呼气容积(FEV1)的增加量289 ml,较舒张前增加23.57%.结论 COPD患者支气管舒张试验后用力肺活量的增加幅度大于呼气容积的增加幅度,而哮喘患者正好相反,因此用力肺活量可鉴别COPD和哮喘患者病情的客观指标.     

第三秒用力呼气容积/用力肺活量下降在早期轻度气道功能障碍中的临床意义

目的探讨第三秒用力呼气容积(FEV3)/用力肺活量(FVC)在早期轻度气道功能障碍中的临床意义。方法收集294例肺功能检查患者并分为3组。正常组164例,第一秒用力呼气容积(FEV1)/FVC、FEV3/FVC均正常; FEV3组39例,仅FEV3/FVC降低,但FEV1/FVC正常; FEV1组91例,FEV1/FVC降低。比较各组一般资料及肺功能指标。结果①正常组平均年龄及吸烟比例显著小于FEV3组(P<0. 05); FEV3组与FEV1组相比,平均年龄及吸烟比例差异无统计学意义(P>0. 05)。②FEV3组与正常组相比及FEV1组与FEV3组相比,FEV1%pred、FEV1/FVC较低,肺总量(TLC)、残气量(RV)、RV/TLC较高,一氧化碳弥散量(DLCO)较低,差异均有统计学意义(P<0. 05)。结论 FEV3/FVC检测应作为肺功能检测的常规检查,仅FEV3/FVC下降可能是早期判断轻度气道功能障碍的指标。     

慢性阻塞性肺疾病患者血清MMP-9检测及意义

目的探讨基质金属蛋白酶-9（MMP-9）在慢性阻塞性肺疾病（COPD）气道炎症发生、发展过程中的作用。方法采用ELISA法测定56例COPD患者（观察组）急性加重期（56例）及稳定期（52例）血清MMP-9水平,并与50例同期健康体检者（对照组）比较,对MMP-9表达与第一秒用力呼气容积占预计值的百分比（FEV1%）、一秒钟用力呼气容积占用力肺活量的百分比（FEV1/FVC）%、残气量与肺总量之比（RV/TLC）%行相关性分析。结果 COPD急性加重期及稳定期患者血清MMP-9水平均明显高于对照组（P〈0.01,P〈0.05）,且与FEV1%呈负相关（r=-0.712,P〈0.05）,与（RV/TLC）%呈正相关（r=0.691,P〈0.05）。结论 MMP-9参与了COPD气道炎症的发生、发展;检测血清MMP-9水平有助于判断COPD病情及预后。     

测定慢性阻塞性肺疾病患者6s用力呼气容积的意义

目前判断气流受限的常用肺功能指标是时间肺活量,包括:第1秒用力呼气容积(FEV1)和1 s率(FEV1与用力呼气容积比值)的降低来确定的。气道阻塞患者呼气时间可明显延长,最长可达20 s或以上,但呼气时间过长会使患者出现过度通气,导致头晕、呼吸困难、肢体麻木,甚至危及性命,尤其慢性阻塞性肺疾病(COPD)患者多见于老年人,体质较差,容易出现并发症。6 s呼气容积(FEV6)是指最大吸气至肺总量位后6 s之内快速呼出气量。由于呼气时间相对较短,患者比较容易接受,不良反应少。本文就COPD患者肺功能指标用力肺活量(FVC)与FEV6及FEV1/FVC与FEV1/FEV6进行相关性分析。     

气道高反应性在COPD和哮喘的比较

目的探讨慢性阻塞性肺疾病(chronic obstructive pulmonary diseases,COPD)和支气管哮喘(简称哮喘)患者在组胺支气管激发试验中气道高反应性(airwayhyperresponsiveness,AHR)的不同。方法将我院2008～2010年间诊断为COPD和哮喘的并经随访一年处于稳定期的患者共80例,其中COPD组39例,哮喘组41例,均行支气管组胺激发试验,观察FEF25%～75%/FVC(肺活量为25%～75%时最大呼气流量与用力肺活量的比值)在两组患者的变化。结果 COPD组FEF25%～75%和FEF25%～75%/FVC均明显低于哮喘组(P值均<0.01);以激发试验阳性的两组患者为对象分别进行简单相关分析,在COPD组和哮喘组中FEF25%～75%/FVC与Log10DRS呈负相关(r分别为-0.510和-0.466,P<0.05),与PD20FEV1呈正相关(r分别为0.518和0.487,P<0.05),说明相对于肺容积而言,气道容积越小,气道收缩性越强,反应性越高。随后在以气道收缩性指标Log10DRS为因变量,以年龄、体表面积、FEV1%及FEF25%～75%/FVC为自变量进行线性回归分析,在COPD组FEV1%对Log10DRS较FEF25%～75%/FVC影响大(P<0.05),而哮喘组不存在这情况。结论在COPD中AHR患者并不少见,其发生机制与哮喘是不同的。     

肥胖对气道反应性的影响

目的探讨肥胖是否与气道反应性增高有关及是否存在性别差异。方法选择中南大学湘雅二医院肺功能室2003年1月至2006年6月激发试验阳性的气道高反应性患者1180例,分析其体重指数(BMI)与肺功能的相关性;与吸入药物后第一秒用力呼气容积(FEV1)下降百分率达对照值20%时的药物浓度(PC20FEV1)的相关性;并进一步分析男、女患者BMI与PC20FEV1的相关性。结果BMI与用力肺活量(FVC)、FEV1、PC20FEV1均呈负相关(r分别为-0.735,-0.645和-0.044,P均(0.05)。男性患者BMI与PC20FEV1无相关性(P(0.05),女性患者BMI与PC20FEV1呈负相关(r=-0.044,P(0.05)。结论肥胖与肺功能降低及气道反应性增高可能相关,这种影响在女性患者中更明显。成年女性气道反应性较成年男性高。     

出生体重、孕周对学龄儿童肺功能的影响

目的研究出生体重、孕周与学龄儿童肺功能测定指标之间的关系。方法测定35名6～9岁低出生体重儿的身高、体重、肺功能,调查孕周以及被动吸烟情况,并与年龄、性别配对的正常出生体重儿童进行比较。结果(1)低出生体重组儿童的用力肺活量(FVC)、一秒钟用力呼气容积(FEV     

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     

Isocapnic cold air challenge in patients with COPD: are there any predisposing factors?

Cold air hyperventilation is an indirect challenge (cold air challenge, CACh) with high specificity and low sensitivity in defining asthmatic subjects. A small proportion of chronic obstructive pulmonary disease (COPD) patients present with positive CACh. The aim of this prospective study was to investigate the presence of factors related to cold air challenge (CACh) in COPD patients. Factors examined were FEV(1), FEV(1)/FVC, reversibility after bronchodilation, eosinophils in induced sputum, bronchial hyperresponsiveness to methacholine and the spirometric response to tiotropium compared to placebo. We studied 92 consecutive COPD patients in order to retrieve 15 CACh positive + patients. Fifteen COPD patients with negative CACh [CACh(-)], randomly selected from the initial group, were added in order to retrieve a group of 30 patients. Spearman's correlation coefficient was used in order to evaluate possible significant correlations between CACh values and study parameters. Sixteen percent of our subjects presented CACh+. CACh values were repeatable with an intraclass correlation coefficient between the two measurements 0.980 (95% CI 0.940-0.993). The only significant correlation observed was between Delta FEV(1) after CACh [Delta(C)FEV(1)] and trough FEV(1) values post tiotropium inhalation (r(2) = 0.62, p < 0.0001). When we analyzed the response to tiotropium in the 2 separate groups we found that patients with CACh+ presented significantly lower values of trough FEV(1) compared to those with CACh(-). In conclusion, a small proportion of COPD patients present with bronchial hyperresponsiveness to CACh. The only parameter related to CACh + in our study was a smaller bronchodilating effect of tiotropium.     

Underdiagnosis and undertreatment of COPD in primary care settings

OBJECTIVE: The aim of this study was to improve the detection of COPD in a primary care setting and to evaluate the subsequent management of these patients by general practitioners. METHODOLOGY: A two-step protocol was followed: patients were screened for airway obstruction and their subsequent management status reviewed. Screening spirometry was performed in 56 primary care settings (23 hospitals and 33 general practices). Inclusion criteria for screening subjects were: (i) > or =40-year-old smokers (both current and past smokers) and/or (ii) > or =40-year-old patients with respiratory symptoms of chronic cough and sputum. Patients with a previously diagnosed respiratory disease were excluded. In the second part of the study, the diagnosis and the subsequent management status of subjects with airway obstructive changes (FEV1/FVC <70%) were sought from their physician using a questionnaire 2 months after detection. RESULTS: A total of 1168 patients were screened, with 128 not analysed because of incomplete data, leaving 1040 patients. The percentages of current smokers, ex-smokers, and non-smokers among all analysed subjects were 41.7%, 29.8% and 28.5%, respectively. Airway obstructive changes (FEV1/FVC <70%) were found in 27.0% (n = 281) of all analysed subjects. Questionnaires for 194 subjects (with positive screening tests) were sent back by the participating physicians. Eighty-one per cent (n = 158) of the 194 subjects had COPD and 13.4% (n = 26) had asthma. Sixty-one per cent (n = 96) of the subjects with moderate to severe COPD according to international guidelines (FEV1 <80% predicted). However, 31.3% (n = 30) did not receive any clinical intervention (smoking cessation advice and/or drug administration). CONCLUSIONS: Screening spirometry in outpatients in a primary care setting can identify many COPD patients. However, COPD management appears to be poor in Japan.     

Airway mucosal inflammation in COPD is similar in smokers and ex-smokers: a pooled analysis.

Bronchial biopsy specimens from chronic obstructive pulmonary disease (COPD) patients demonstrate increased numbers of CD8+ T-lymphocytes, macrophages and, in some studies, neutrophils and eosinophils. Smoking cessation affects the rate of forced expiratory volume in one second (FEV(1)) decline in COPD, but the effect on inflammation is uncertain. Bronchial biopsy inflammatory cell counts were compared in current and ex-smokers with COPD. A pooled analysis of subepithelial inflammatory cell count data from three bronchial biopsy studies that included COPD patients who were either current or ex-smokers was performed. Cell count data from 101 subjects, 65 current smokers and 36 ex-smokers, were analysed for the following cell types: CD4+ and CD8+ T-lymphocytes, CD68+ (monocytes/macrophages), neutrophil elastase+ (neutrophils), EG2+ (eosinophils), mast cell tryptase+ and cells mRNA-positive for tumour necrosis factor-alpha. Current smokers and ex-smokers were similar in terms of lung function, as measured by FEV(1) (% predicted), forced vital capacity (FVC) and FEV(1)/FVC. The results demonstrate that there were no significant differences between smokers and ex-smokers in the numbers of any of the inflammatory cell types or markers analysed. It is concluded that, in established chronic obstructive pulmonary disease, the bronchial mucosal inflammatory cell infiltrate is similar in ex-smokers and those that continue to smoke.     

Mast cell numbers in airway smooth muscle and PC20AMP in asthma and COPD

INTRODUCTION: Most patients with asthma and many patients with COPD show bronchial hyperresponsiveness to adenosine (BHR(AMP)). BHR(AMP) may be caused by release of mast cell histamine, which induces smooth muscle contraction. AIM OF THE STUDY: To evaluate whether mast cell numbers in airway smooth muscle are increased in patients with asthma and COPD compared to their age-matched controls, and whether mast cell numbers are correlated with BHR(AMP). PATIENTS: Twenty-two non-smoking subjects with asthma (age 31yr, FEV(1): 89% pred, PC(20)AMP: 2.7mg/ml), 18 ex-smoking subjects with COPD (age 62yr, FEV(1): 58% pred, PC(20)AMP: 52.4mg/ml). METHODS: Snap-frozen bronchial biopsies were immunostained with anti-mast cell tryptase and anti-desmin antibodies. Mast cell number was expressed as the number of tryptase positive cells per area of smooth muscle. RESULTS: There were no significant differences in mast cell number between patients with asthma, COPD, and their respective age-matched healthy controls. Furthermore, there was no significant correlation between mast cell number and FEV(1) or PC(20)AMP in any of the groups. Surprisingly, the mast cell number was negatively correlated with reversibility to salbutamol in COPD patients (rho -0.47, P<0.05). CONCLUSION: Mast cell numbers in central airway smooth muscle apparently do not contribute importantly to bronchial hyperresponsiveness to adenosine.     

Prevalence and nature of bronchial hyperresponsiveness in subjects with chronic obstructive pulmonary disease

The prevalence, nature, and severity of bronchial hyperresponsiveness in subjects with chronic obstructive pulmonary disease (COPD) is not known. To determine these factors, a 1 in 4 random sample of adults attending the Busselton population survey was studied. Subjects answered a modified Medical Research Council questionnaire and had spirometric function tested. They were defined as having COPD or asthma from the questionnaire. Bronchial responsiveness to histamine was measured using the rapid method, and results in the subjects with COPD were compared with those in asthmatic subjects with abnormal lung function. Fifty-nine subjects with COPD had a histamine inhalation test, and of these, 27 had bronchial hyperresponsiveness (BHR) (PD20FEV1 less than 3.9 mumol). The position of the dose response curves of the subjects with COPD overlapped considerably with those obtained from the 17 asthmatics. The geometric mean values for PD20FEV1 for these 2 groups were significantly different (p less than 0.001). There was a good correlation between FEV1/FVC and PD20FEV1 values in the subjects with COPD but not in the asthmatic subjects. Pretreatment with 600 micrograms of aerosolized fenoterol significantly improved the PD20FEV1 values in 11 subjects with COPD (1.26 to 6.16 mumol; p less than 0.001). The results suggest that approximately half the subjects with COPD in a general population have BHR but this BHR has different characteristics from that occurring in asthmatic subjects.     

Regular physical activity modifies smoking-related lung function decline and reduces risk of chronic obstructive pulmonary disease: a population-based cohort study

RATIONALE: We have previously reported that regular physical activity reduces risk of chronic obstructive pulmonary disease (COPD) exacerbation. We hypothesized that higher levels of regular physical activity could reduce the risk of COPD by modifying smoking-related lung function decline. OBJECTIVE: To estimate the longitudinal association between regular physical activity and FEV(1) and FVC decline and COPD risk. METHODS: A population-based sample (n = 6,790) was recruited and assessed with respect to physical activity, smoking, lung function, and other covariates, in Copenhagen in 1981-1983, and followed until 1991-1994. Mean level of physical activity between baseline and follow-up was classified into "low," "moderate," and "high." FEV(1) and FVC decline rates were expressed as milliliters per year. COPD was defined as FEV(1)/FVC < or = 70%. Adjusted associations between physical activity and FEV(1) and FVC decline, and COPD incidence, were obtained using linear and logistic regression, respectively. RESULTS: Active smokers with moderate and high physical activity had a reduced FEV(1) and FVC decline compared with those with low physical activity (relative change of +2.6 and +4.8 ml/yr of FEV(1), P-for-trend = 0.006, and +2.6 and +7.7 ml/yr of FVC, P-for-trend < 0.0001, for the moderate and high physical activity group, respectively), after adjusting for all potential confounders and risk factors of lung function decline. Active smokers with moderate to high physical activity had a reduced risk of developing COPD as compared with the low physical activity group (odds ratio, 0.77; p = 0.027). CONCLUSIONS: This prospective study shows that moderate to high levels of regular physical activity are associated with reduced lung function decline and COPD risk among smokers.     

Subepithelial immunopathology of the large airways in smokers with and without chronic obstructive pulmonary disease.

Previous work has shown an increase in CD8+ T-cells, neutrophils and eosinophils in small airway subepithelium in smokers. The authors have now investigated whether similar changes occur in the large airways. Immunohistochemistry on frozen sections of bronchial biopsies were obtained at bronchoscopy in 11 nonsmokers, eight asymptomatic smokers and 11 smokers with chronic bronchitis and chronic obstructive pulmonary disease (COPD). There was an increase in the number of CD8+ cells infiltrating the bronchial subepithelium in the COPD group compared to the asymptomatic smokers (305 (109-400) versus 92 (41-550) cells x mm(-2), p=0.030). There was a negative correlation between the number of CD8+ cells and the forced expiratory volume in one second (FEV1) %predicted (p=0.005, r=-0.62), and a positive correlation between the number of CD8+ cells and the number of pack years smoked (p=0.017, r=0.42). There was a negative correlation between the activated/total eosinophils ratio and the FEV1 % pred (p=0.017, r=-0.51). There was a negative correlation between pack years smoked and the number of neutrophils (p=0.022, r=-0.36). Smokers who develop chronic obstructive pulmonary disease have increased numbers of CD8+ T-cells in large airways when compared to asymptomatic smokers. Airway obstruction was associated with an increase in the proportion of eosinophils that were activated.     

Interleukin-17 in sputum correlates with airway hyperresponsiveness to methacholine

BACKGROUND: Interleukin-17 (IL-17) is a novel cytokine secreted by activated human memory CD4+ T cells. In vivo IL-17 recruits neutrophils into the airways via the release of CXC chemokines (interleukin-8) from bronchial epithelial cells. Since neutrophils are implicated in pathogenesis of chronic obstructive pulmonary disease (COPD) chronic bronchitis (CB) and asthma, we hypothesized that there would be increased concentration of IL-17 in the airways of these patients. To test this hypothesis, we measured levels of IL-17 in induced sputum of COPD patients, chronic bronchitis and asthmatics and compared them with healthy controls. METHODS: Levels of IL-17 in induced sputum were measured via ELISA method in 19 COPD, 16 CB, 10 asthma and 11 control subjects. Airway responsiveness to methacholine was performed in people with FEV1 higher than 70% of predicted. RESULTS: There were no significant differences in IL-17 levels between control group and the other groups. However, levels of IL-17 in sputum of COPD patients were significantly lower than in asthma (P=0.004) and in CB (P=0.01) groups. Medians and (ranges) were as follows: asthma--37.6 pg/ml (18.8-55.7 pg/ml), CB 293 pg/ml (18.8-49.7 pg/ml) and COPD 24.6 pg/ml (0-34.1 pg/ml). Comparison of healthy control subjects (PC20 > 8 mg/ml) to a group with bronchial hyperreactivity, which consisted of asthmatics and CB patients, whose PC20 was less than 8 mg/ml, revealed that levels of IL-17 were significantly increased in the second group (P=0.02). Also, levels of IL-17 were significantly increased (P=0.02) in the asthmatic patients with bronchial hyperreactivity compared to healthy subjects. Moreover levels of IL-17 in sputum of all studied subjects correlated negatively with PC20 (r=-0.51, P=0.002). CONCLUSIONS: According to our results IL-17 is probably not involved in pathogenesis of stable COPD, but it may play a role in people with airway hyperresponsiveness.     

Maternal and personal cigarette smoking synergize to increase airflow limitation in adults

Susceptibility of the lungs to cigarette smoke is poorly understood. It is not known whether maternal smoking increases chronic obstructive pulmonary disease (COPD) risk. In 1998 we reported an inverse association between maternal smoking (prerecorded) and FEV(1) in adults. Because FEV(1) and FVC are strongly correlated, it is unclear whether the association in question reflects a link with lung volume, airflow limitation, or both. We extended our original analysis to investigate whether maternal and personal smoking synergize to increase airflow limitation. We estimated residual FEV(1) to express FEV(1) variation that was not associated with FVC. Maternal smoking was inversely associated with FVC and FEV(1) irrespective of personal smoking. It was inversely associated with FEV(1)/FVC, forced midexpiratory flow rates (FEF(25-75) [mean forced expiratory flow during the middle half of the FVC], FEF(25-75)/FVC), and residual FEV(1) in current smokers but not in never or former smokers (heterogeneity p = 0.016, 0.024, 0.021, and 0.016, respectively). We tested the clinical relevance of findings in ever smokers without asthma: 10 cigarettes/day maternal smoking increased prevalent COPD by 1.7 (95% confidence interval: 1.2-2.5) after adjustment for covariates. Maternal smoking impairs lung volume irrespective of personal smoking and appears to synergize with personal smoking to increase airflow limitation and COPD.