高分辨CT测定支气管哮喘患者的气道壁厚度

目的用高分辨CT(highresolutionCT,HRCT)扫描测量支气管哮喘患者段及亚段水平气道壁的厚度。方法用HRCT扫描重、中和轻度哮喘患者36例,分别分为第1组(13例)、第2组(11例)和第3组(12例),并测量能显示支气管横截面的气道壁的内外径、内外腔面积、通过公式计算出气道壁厚度与外径之比(T/D);气道壁面积占气道总横截面积百分比(WA%)。另设第4组为正常对照组(10例)。结果HRCT扫描示中、重度哮喘患者较轻度哮喘患者及正常人气道壁厚度均显著增厚(P<0.05)。结论HRCT可测定气道壁厚度,评估哮喘患者气道重构;中、重度哮喘患者气道壁显著增厚。     

Airway blood flow reactivity in healthy smokers and in ex-smokers with or without COPD

STUDY OBJECTIVES: Cigarette smoking has been associated with impaired endothelium-dependent relaxation responses in the brachial and coronary arteries (endothelial dysfunction). The aim of the present study was to determine whether the airway circulation is also affected and whether pharmacologic treatment has an effect on endothelial function in patients with COPD.Methods and patients: Airway blood flow (Qaw) responses to therapy with inhaled albuterol, which causes endothelium-dependent vasodilation, were measured with a noninvasive soluble-gas-uptake technique in age-matched healthy current smokers (n = 10), healthy ex-smokers (n = 10), ex-smokers with COPD (n = 10), and healthy lifetime nonsmokers. In the ex-smokers with COPD, the albuterol responsiveness measurement was repeated after 4 weeks of treatment with fluticasone/salmeterol and after a drug washout period of 4 or 8 weeks. RESULTS: The mean (+/- SE) baseline Qaw values ranged between 40.7 +/- 3.9 and 50.9 +/- 2.8 microL/min/mL anatomic dead space in the four groups (differences were not significant). The mean FEV(1) was 53.4 +/- 2.3% predicted in the ex-smokers with COPD. Albuterol inhalation increased mean Qaw significantly in lifetime nonsmokers (50.1 +/- 8.3% predicted; p < 0.05) and healthy ex-smokers (37.2 +/- 3.4% predicted; p < 0.05), but not in healthy current smokers (13.9 +/- 3.2% predicted; difference was not significant) and ex-smokers with COPD (9.7 +/- 4.5% predicted; difference was not significant). While fluticasone/salmeterol did not change Qaw significantly, it restored albuterol responsiveness (67.6 +/- 11.1% predicted; p < 0.05) in the ex-smokers with COPD; this effect was no longer seen after the drug washout period. CONCLUSIONS: Cigarette smoking is associated with a blunted vasodilator response to inhaled albuterol in the airway as an expression of endothelial dysfunction, with a partial recovery of albuterol responsiveness after smoking cessation in healthy ex-smokers but not in ex-smokers with COPD. In the latter group, combined glucocorticoid/long-acting beta(2)-adrenergic agonist treatment restores albuterol responsiveness. The role of endothelial dysfunction in the physiopathology of COPD remains to be examined.     

吸烟对慢性阻塞性肺疾病急性加重期患者C-反应蛋白的影响

目的比较吸烟、戒烟及非吸烟慢性阻塞性肺疾病急性加重期(AECOPD)患者血中C-反应蛋白(CRP)的差异及其与血白细胞(WBC)计数的关系,探讨吸烟患者CRP的变化。方法回顾性分析广西医科大学第四附属医院呼吸内科2002年6月至2006年7月间568例AECOPD患者,分为吸烟组(n=156)、戒烟组(n=170)和非吸烟组(n=242),测定血清CRP质量浓度及血WBC计数。结果3组CRP质量浓度的中位数分别为5.7mg/L,5.6mg/L和5.8mg/L,组间比较差异无显著性意义,吸烟暴露对AECOPD患者血清CRP的升高无影响;3组WBC计数中位数分别为8.6×109/L,9.1×109/L和8.5×109/L,组间比较差异无显著性意义,CRP与WBC计数呈正相关(r=0.305,P<0.01)。结论吸烟、戒烟及非吸烟的AECOPD患者CRP均无差异,CRP与吸烟无关,与感染有一定的关系。     

Smoking characteristics: differences in attitudes and dependence between healthy smokers and smokers with COPD

OBJECTIVE: To ascertain the differences in smoking characteristics between a group of smokers with COPD and another group of healthy smokers, both of which were identified in a population-based epidemiologic study. DESIGN AND PARTICIPANTS: This is an epidemiologic, multicenter, population-based study conducted in seven areas of SPAIN: A total of 4,035 individuals, men and women aged 40 to 69 years, who were selected randomly from a target population of 236,412 subjects, participated in the study. INTERVENTIONS: Eligible subjects answered the European Commission for Steel and Coal questionnaire. Spirometry was performed followed by a bronchodilator test when bronchial obstruction was present. The Fagerstr?m questionnaire was used for study of the degree of physical nicotine dependence, and the Prochazka model was followed for analysis of the smoking cessation phase. RESULTS: Of 1,023 active smokers, 153 (15%) met the criteria for COPD. Smokers with COPD were more frequently men (odds ratio [OR], 2.18; 95% confidence interval [CI], 1.21 to 3.95), were > or = 46 years of age (OR, 1.97; 95% CI, 1.18 to 3.31), had a lower educational level (OR, 1.96; 95% CI, 1.23 to 3.14), and had smoked > 30 pack-years (OR, 3.70; 95% CI, 2.42 to 5.65). Smokers with COPD showed a higher dependence on nicotine than healthy smokers (mean [+/- SD] Fagerstr?m test score, 4.77 +/- 2.45 vs 3.15 +/- 2.38, respectively; p < 0.001) and higher concentrations of CO in exhaled air (mean concentration, 19.7 +/- 16.3 vs 15.4 +/- 12.1 ppm, respectively; p < 0.0001). Thirty-four percent of smokers with COPD and 38.5% of smokers without COPD had never tried to stop smoking. CONCLUSIONS: Smokers with COPD have higher tobacco consumption, higher dependence on nicotine, and higher concentrations of CO in exhaled air, suggesting a different pattern of cigarette smoking. Cases of COPD among smokers predominate in men and in individuals with lower educational levels. A significant proportion of smokers have never tried to stop smoking; thus, advice on cessation should be reinforced in both groups of smokers.     

The measurement of exhaled carbon monoxide in healthy smokers and non-smokers

The measurement of exhaled carbon monoxide (CO) level may provide an immediate, non-invasive method of assessing smoking status. The aims of this study were to use a portable CO monitor to compare the exhaled CO levels in established smokers and non-smokers. The exhaled CO levels were measured in 322 subjects (243 healthy smokers, 55 healthy non-smokers, 24 passive smokers) who applied to healthy stand during the spring student activity of Firat University in Elazi?. Exhaled CO concentration was measured using the EC50 Smokerlyser. The mean exhaled CO level was 17.13+/-8.50 parts per million (ppm) for healthy smokers and 3.61+/-2.15 ppm for healthy non-smokers, and 5.20+/-3.38 ppm for passive smokers. There were significant positive correlation between CO levels and daily cigarette consumption, and CO levels and duration of smoking in healthy smokers (r=+0.550, P<0.001, r=+0.265, P<0.001, respectively. Spearman's test). When smokers and non-smokers were looked at as a whole, a cutoff of 6.5 ppm had a sensitivity of 90% and specificity of 83%. In conclusion, exhaled CO level provides an easy, an immediate way of assessing a subject's smoking status.     

Glutathione and nitrite levels in induced sputum at COPD patients and healthy smokers

Objectives

The role of oxidative stress at the pathogenesis of chronic obstructive pulmonary disease (COPD) is known. The aim of this study is to investigate the oxidative stress with sputum induction that is a simple method in COPD patients and healthy smokers.

Methods

Sputum induction was performed in 21 COPD patients (10 stable, 11 acute exacerbations), nine healthy smokers, and ten healthy non-smokers. Glutathione, NO₂^– levels, and cell counts at sputum, and plasma NO₂^– contents were evaluated in all subjects.

Results

Mean sputum glutathione and NO₂^– levels were significantly higher in acute exacerbations with COPD patients than healthy smokers (P=0.007 and P<0.001 respectively), and non-smokers (P<0.001 and P<0.001 respectively). On the other hand, sputum glutathione and NO₂^– levels did not show significant differences between stable and acute exacerbations with COPD patients. Although, sputum glutathione levels were higher in stable COPD patients than healthy smokers’, no statistically significant difference was established. In addition, sputum glutathione levels were significantly higher in healthy smokers than non-smokers (P<0.001).

Conclusions

As a result, we can say that oxidative stress increases not only in COPD patients but also in healthy smokers. In addition, sputum induction that is a simple method can be used to demonstrate to show oxidative stress.     

Airway inflammation and lymphocyte subset analysis in patients with chronic obstructive pulmonary disease and healthy smokers

Chronic airway inflammation is reported to have an important role for the development of chronic obstructive pulmonary disease (COPD), in addition to smoking, genetic and environmental factors. The present study was aimed to investigate whether the airway inflammation differed in subjects with stable COPD and healthy smokers. A total of 35 subjects (18 patients with COPD and 17 healthy smokers) were enrolled in this study. Bronchoalveolar lavage (BAL) was performed via fiberoptic bronchoscope in all subjects and cell counts and profiles and lymphocyte subset were analyzed in BAL fluids. The number of neutrophils in BAL of subjects with stable COPD was significantly higher than that of the healthy smokers (p< 0.001), and the number of macrophages was significantly lower than that of the healthy smokers (p< 0.001). Although CD4+ T:CD8+ T lymphocyte ratio was higher in healty smokers, the difference was not significant (p> 0.05). As a result, the most marked cellular change in BAL of subjects with stable COPD is the increase in neutrophils and decrease in macrophages, suggesting a very important role in the chronic airflow limitation.     

Enthesopathy and tendinopathy in gout: computed tomographic assessment.

OBJECTIVE: To establish if computed tomography (CT) imaging, which has proved helpful in detecting intra-articular tophi in gout, can also be used to document gouty enthesopathy and tendinopathy. METHODS: Three patients with tophaceous gout and clinical involvement of the Achilles tendon (two cases) or patellar tendon (one case) were assessed with CT examination and plain radiographs. RESULTS: In the first two cases, CT images revealed linear or nodular high attenuation opacities within the substance of the Achilles tendons and their calcaneal insertion. In case 3, dense linear opacities were seen within the patellar tendon and within its tibial insertion. No such opacities of the tendons and entheses were seen on standard radiographs of these patients. CONCLUSIONS: CT appears to be the imaging method of choice for demonstrating monosodium urate deposits in entheses and tendons in tophaceous gout.     

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.     

Mean transit time, forced expiratory volume and age in healthy male smokers and non-smokers

We studied 67 healthy males aged 20-30 years, 29 of them non-smokers and 38 smokers. In smokers, forced expiratory volume (FEV), 1 s forced expiratory volume (FEV1) and peak flow (PF) were significantly lower than in non-smokers, while the FEV1/FEV ratio, flows and mean transit time (MTT) compared well. MTT appeared directly related to age and negatively to FEV1/FEV, with no difference between the two groups, but MTT was directly related to FEV in non-smokers and negatively in smokers. Multiple regression analysis, MTT = a + b(FEV)+c(age), showed that parameters b and c were significantly different between smokers and non-smokers and, in the former, parameter b was negative. In non-smokers the effects of age and FEV on MTT were roughly the same, but in smokers MTT was influenced above all by age, probably because MTT measured the effects of continued smoking.     

Determination of left ventricular mass in dogs with rapid-acquisition cardiac computed tomographic scanning

The development of left ventricular hypertrophy in patients with heart disease often has far-reaching clinical implications with respect to overall morbidity and mortality. Approaches used to assess left ventricular mass include electrocardiography, echocardiography, contrast ventriculography, single photon-emission tomography, and conventional computed tomography. However, all of these modalities suffer from some major draw back that precludes widespread application to all patients. In this study we assessed the accuracy of determinations of left ventricular mass in 22 dogs by rapid-acquisition (50 msec) computed axial tomography (RACAT), an ultrafast computed tomographic (CT) instrument. Electrocardiographically triggered, end-diastolic, short-axis cardiac scans were obtained from apex to base during administration of intravenous iodinated contrast. Myocardial edges were determined for each tomographic scan by two methods: the regional half-contour method (the CT density half way between that of the left ventricular myocardium and adjacent ventricular cavities or lung) and "interactive plateau thresholding" of the cardiac borders. Left ventricular mass by RACAT was calculated as the sum of the mass of each individual scan from apex to base (modified Simpson's rule). Postmortem left ventricular mass ranged from 58 to 160 g. The correlation between true left ventricular mass and tomographically determined mass was excellent (r = .99), with the slope and y intercept not statistically different from 1 and 0, respectively. The standard error of the estimate was 4.1 g. Interobserver and intraobserver variability for determining left ventricular mass demonstrated excellent agreement (r = .99 and r = .99, respectively). We conclude that quantitative assessment of left ventricular mass can be accurately and reproducibly performed in dogs by rapid acquisition CT scanning. It is likely that this technique will be readily transferable to the clinical settings and prove to be an important method for quantifying left ventricular mass in patients.     

Similar gene expression profiles in smokers and patients with moderate COPD

Chronic obstructive pulmonary disease (COPD) is characterized by multiple cellular and structural changes affecting the airways, lung parenchyma and vasculature, some of which are also identified in smokers without COPD. The molecular mechanisms underlying these changes remain poorly understood. With the aim of identifying mediators potentially implicated in the pathogenic processes that occur in COPD and their potential relationship with cigarette smoking, we evaluated the mRNA expression of genes involved in inflammation, tissue remodeling and vessel maintenance. Lung tissue samples were obtained from 60 patients who underwent lung resection (nonsmokers, n=12; smokers, n=12; and moderate COPD, n=21) or lung transplant (severe-to-very severe COPD, n=15). PCR arrays containing 42 genes coding for growth factors/receptors, cytokines, metalloproteinases, adhesion molecules, and vessel maintenance mediators were used. Smoking-induced changes include the up-regulation of inflammatory genes (IL-1β, IL-6, IL-8, CCL2, and CCL8) and the decreased expression of growth factor/receptor genes (BMPR2, CTGF, FGF1, KDR and TEK) and genes coding for vessel maintenance factors (EDNRB). All these genes exhibited a similar profile in moderate COPD patients. The up-regulation of MMP1 and MMP9 was the main change associated with COPD. Inflammatory genes as well as the endothelial selectin gene (SELE) were down-regulated in patients with more severe COPD. Clustering analysis revealed a closer relationship between moderate COPD and smokers than between both subsets of COPD patients for this selected set of genes. The study reveals striking similarities between smokers and COPD patients with moderate disease emphasizing the crucial role of cigarette smoking in the genesis of these changes, and provides additional evidence of the involvement of the matrix metalloproteinase's in the remodeling process of the lung in COPD.     

Combined cryptogenic fibrosing alveolitis and emphysema: the value of high resolution computed tomography in assessment

Simple tests of lung function may be misleading in the assessment of patients with interstitial lung disease. Eight patients are described with cryptogenic fibrosing alveolitis (histologically proven in four) with severe breathlessness and low gas transfer (median DLCO 32.4%, range 9.2 to 35.3%, % predicted) in whom lung volumes were preserved [median VC 98.7, range 67.5-131.1%; median TLC 92.5, range 88.1 to 121.2, (% predicted)], and in whom there was no evidence of airflow obstruction [median FEV1/FVC 84.6, range 68-116 (% predicted)]. All were current or ex-heavy smokers. Thoracic high resolution computed tomography revealed upper zone emphysema, the extent of which was not appreciated using conventional chest radiography. The atypical physiological and radiological features can be explained by coincidental cryptogenic fibrosing alveolitis and emphysema and high resolution computed tomography was valuable in the assessment of these patients.