胸部低剂量CT定量指标与肺气流受限的相关性分析

目的 探讨胸部低剂量CT(LDCT)定量指标和肺气流受限及其严重程度的相关性,建立初步相关模型.方法 纳入2008年7月至2012年2月在我院同步完成LDCT和肺功能检查的48例40岁以上有吸烟史的患者,对LDCT定量指标和肺功能指标进行相关性分析,并结合年龄、性别等因素建立回归模型.通过绘制受试者工作特征曲线(ROC曲线)确定对气流受限的判断作用最佳的LDCT定量指标.结果 经调整年龄、性别及BMI校正后,EV和El与FEV1、FEV1％ pred、FEV1/FVC和TLC％ pred呈负相关(P＜0.05).但与RV/TLC％ pred则无明显相关性(P＞0.05);确定最佳回归模型为FEV1/FVC％=94.17+25.31×性别(gender)-0.58×年龄(age)-l0.84×In(El(％));FEV1％ pred=141.76-0.78×年龄(age)-14.07×In(EI(％)).经ROC曲线确定对气流受限的判断作用最佳的LDCT定量指标为El.结论 El可用于判别有无气流受限,通过回归方程计算可估测气流受限和肺气肿严重程度.LDCT有望用于COPD的早期诊断.     

Rapid Fall in Lung Density Following Smoking Cessation in COPD

Introduction: Whether smoking-induced lung inflammation subsides after smoking cessation is currently a matter of debate. We used computed tomography (CT) to evaluate the effect of smoking cessation on lung density in patients with COPD. Material and methods: Thirty-six patients quit smoking out of 254 current smokers with COPD who were followed with annual CT and lung function tests (LFT) for 2–4 years as part of a randomised placebo-controlled trial of the effect of inhaled budesonide on CT-lung density. Lung density was expressed as the 15th percentile density (PD15) and relative area of emphysema below -910 HU (RA-910). From the time-trends in the budesonide and placebo groups the expected CT-lung densities at the first visit after smoking cessation were calculated by linear regression and compared to the observed densities. Results: Following smoking cessation RA-910 increased by 2.6% (p = 0.003) and PD15 decreased by ?4.9 HU (p = 0.0002). Furthermore, changes were larger in the budesonide group than the placebo group (PD15: ?7.1 vs ?2.8 HU. RA-910 3.7% vs 1.7%). These differences were, however, not statistically significant. The LFT parameters (FEV₁ and diffusion capacity) were not significantly influenced by smoking cessation. Conclusion: Inflammation partly masks the presence of emphysema on CT and smoking cessation results in a paradoxical fall in lung density, which resembles rapid progression of emphysema. This fall in density is probably due to an anti-inflammatory effect of smoking cessation.     

Sildenafil for Chronic Obstructive Pulmonary Disease: A Randomized Crossover Trial

Abstract

Rationale: Pulmonary hypertension with exercise is common in chronic obstructive pulmonary disease (COPD) and may contribute to exercise limitation in this disease. We aimed to determine the effects of treatment with sildenafil on exercise capacity in patients with COPD and emphysema. Methods: We performed a randomized, double-blind, placebo-controlled 2-period crossover trial of sildenafil thrice daily in ten adults with COPD and emphysema on CT scan without pulmonary hypertension. We randomized study participants to 4 weeks of sildenafil (or placebo) followed by a 1-week washout and then 4 weeks of placebo (or sildenafil). The 2 primary outcomes were the 6-minute walk distance and oxygen consumption at peak exercise. Results: Sildenafil had no effect on 6-minute walk distance (placebo-corrected difference = -7.8 m, 95% confidence interval, -23.2 to 7.5 m, p = 0.35) or oxygen consumption at peak exercise (placebo-corrected difference = -0.1 ml/kg/min, 95% confidence interval -2.1 to 1.8 ml/kg/min, p = 0.89). Sildenafil increased the alveolar-arterial oxygen gradient (p = 0.02), worsened symptoms (p = 0.04), and decreased quality-of-life (p = 0.03). Adverse events were more frequent while receiving sildenafil (p = 0.005). Conclusions: Routine sildenafil administration did not have a beneficial effect on exercise capacity in patients with COPD and emphysema without pulmonary hypertension. Sildenafil significantly worsened gas exchange at rest and quality of life. (clinicaltrials.gov NCT00104637).     

不同分级慢性阻塞性肺疾病患者胸部定量CT变化的研究

目的 通过分析不同分级慢性阻塞性肺疾病(COPD)稳定期患者胸部定量CT的变化及其与肺功能和症状评分的相关性,探讨其能否做为评估COPD严重程度的方法之一.方法 研究对象为山西医科大学附属大医院呼吸科门诊的90例COPD患者,均行肺功能及胸部定量CT检查,症状评估采用MMRC问卷.根据2011年版GOLD综合评估的方法分为A、B、C和D四组.分别对各组肺功能、胸部定量CT肺气肿评估指标LAA％及症状评分进行相关性分析.结果 ①肺功能:FEV1％pred、VC、DL Adj、FEF75分别在A、B、C和D四组间差异有统计学意义(F分别为59.83,18.56,14.39,16.06,P值均＜0.05);且C、D组均分别小于A和B组,差异均有统计学意义(P值均＜0.05);A、B组间及C、D组间差异均无统计学意义(P值均＞0.05).RV,RV/TLC在A、B、C和D四组间差异无统计学意义(P值均＞0.05).②胸部定量CT:LAA％在CT阈值分别-1 024～-970、-960、-950、-940、-930、-920、-910 HU值下均为一致结果.在-i 024～-910 HU下,A、B、C和D四组间LAA％差异有统计学意义(F=20.22,P＜0.05),两两比较,C和D组LAA％分别大于A和B组,差异均有统计学意义(P值均＜0.05),B组大于A组,差异均有统计学意义(P＜0.05),C组与D组差异无统计学意义(P＞0.05).③相关性:(a)LAA％与肺功能各指标:在-1 024～-910 HU下LAA％与FEV1％ pred、FEF75、DL Adj均呈显著负相关,(r分别为-0.686,-0.509,-0.481,均P＜0.01);与RV和RV/TLC无相关性(P=0.34).(b)LAA％与症状评分:在-1 024～-910 HU下LAA％与MMRC呈显著正相关,(r=0.570,P＜0.01).(c)症状评分与肺功能各项指标:MMRC与FEV1％ pred、FEF75及DL Adj呈显著负相关(r分别为-0.493,-0.330,-0.267,前两者P值均＜0.01,后者P＜0.05).结论 肺气肿可能为A、B两组患者临床症状出现差异的原因之一.COPD患者气流受限严重程度、小气道功能和弥散功能的改变及症状评分与胸部定量CT肺气肿严重程度相关.对于GOLD肺功能分级轻中度以下(FEV1％pred≥50％)的COPD患者,胸部定量CT LAA％评估肺气肿严重程度优于肺功能.胸部定量CT可以做为评估COPD严重程度的方法之一.     

Retroperitoneal and mediastinal emphysema as a complication of colonoscopy

Retroperitoneal and mediastinal emphysema as a complication of colonoscopy, though infrequent, may occur. It is important to realize that this can be a benign clinical condition that will resolve with conservative management. A case of retroperitoneal emphysema after routine colonoscopy is reported with a review of literature and a brief discussion.     

Airway inflammation and peribronchiolar attachments in the lungs of nonsmokers,current and ex-smokers

to determine the effect of smoking cessation on the number and type of inflammatory cells in the walls of the small airways, we examined the lungs of 13 lifetime nonsmokers, 25 patients who had stopped smoking for at least 6 months, and 49 current smokers. We found that, compared to nonsmokers, both ex-smokers and current smokers had significantly increased numbers of total inflammatory cells and polymorphonuclear leukocytes in the walls of the membranous, but not the respiratory bronchioles. These differences were found even when there was no emphysema present in the gross lung specimen, and current and ex-smokers were matched with the nonsmokers for age. The current and ex-smokers had similar numbers and types of inflammatory cells in the airway wall, and in both current and ex-smokers there was no difference in inflammatory cell number or type when the groups were subdivided based on emphysema score less than or greater than 5. Analysis of peribronchiolar alveolar attachments showed an increase in percentage of alveoli destroyed associated with an increased interalveolar distance in both the current and ex-smokers, which did not change with the presence of emphysema. Pulmonary function was similar in the current and ex-smokers, and the group with emphysema showed greater functional abnormalities compared to the group with little or no emphysema. We conclude that the cigarette smoking habit induces a stereotypical inflammatory response in the small airways. This inflammatory response does not abate after smoking cessation, and in this cross-sectional study, appears to be independent of the presence or absence of emphysema, but related to destruction of the peribronchiolar alveolar attachments.