Rate of progression of CT-quantified emphysema in male current and ex-smokers: a follow-up study

Abstract

BackgroundLittle is known about the factors associated with CT-quantified emphysema progression in heavy smokers. The objective of this study was to investigate the effect of length of smoking cessation and clinical / demographical factors on the rate of emphysema progression and FEV1-decline in male heavy smokers.Methods3,670 male smokers with mean (SD) 40.8 (17.9) packyears underwent chest CT scans and pulmonary function tests at baseline and after 1 and 3 years follow-up. Smoking status (quitted ≥5, ≥1-<5, <1 years or current smoker) was noted. Rate of progression of emphysema and FEV1-decline after follow-up were assessed by analysis of variance adjusting for age, height, baseline pulmonary function and emphysema severity, packyears, years in study and respiratory symptoms. The quitted ≥5 group was used as reference.ResultsMedian (Q1-Q3) emphysema severity,<-950 HU, was 8.8 (5.1 – 14.1) and mean (SD) FEV1 was 3.4 (0.73) L or 98.5 (18.5) % of predicted. The group quitted ‘>5 years’ showed significantly lower rates of progression of emphysema compared to current smokers, 1.07% and 1.12% per year, respectively (p<0.001). Current smokers had a yearly FEV1-decline of 69 ml, while subjects quit smoking >5 years had a yearly decline of 57.5 ml (p<0.001).ConclusionQuit smoking >5 years significantly slows the rate of emphysema progression and lung function decline.Trial registrationRegistered at http://www.trialregister.nl with trial number ISRCTN63545820.

Immune-mediated inflammation in the pathogenesis of emphysema: insights from mouse models

“…The administration of elastase inhibitors has a protective effect only when given immediately before or immediately after elastase challenge–they are not effective even if given 4 hours after the insult (Gudapaty, et al, 1985, Kleinerman, et al, 1980, Stone, et al, 1981). The persistent emphysematous change in this animal model thus may have similarities with observations in humans with emphysema, where the emphysema continues to progress even after stopping smoking (Mohamed Hoesein, et al, 2013, Rutgers, et al, 2000). The mechanism of these chronic progressive changes is not clear, but it suggests that host endogenous responses triggered by an acute injury to the lung epithelium/endothelium may be sufficient to trigger a chronic non-resolving, self-perpetuating cycle of inflammation and lung damage.…”

Tiotropium Attenuates Virus-Induced Pulmonary Inflammation in Cigarette Smoke-Exposed Mice

“…Worldwide, approximately 65 million people suffer from chronic obstructive pulmonary disease (COPD), a major health and economic burden and one of the leading causes of premature death in both current and former smokers ( Stockley et al, 2009 ; Dance, 2012 ; Mohamed Hoesein et al, 2013 ). Generally, COPD is associated with increased neutrophil numbers and high levels of pro-inflammatory cytokines, such as tumor necrosis factor- α (TNF- α ), interleukin (IL)-6, IL-8, interferon- γ (IFN- γ ), and IL-1 β in the airways ( Barnes, 2008 ).…”

Urinary desmosine is associated with emphysema severity and frequent exacerbation in patients with COPD

“…In the latest report on COPD and desmosines, although measured in plasma, no significant correlation was found between the level of desmosines and progression of emphysema for 3 years . We believe that 3 years may be a too short period to differentiate between group changes in emphysema severity indices, because the rate of emphysema progression is slow (approximately only 1% per year in a follow‐up study of male smokers) . Therefore, a longer follow‐up period is required to evaluate longitudinal changes of emphysema severity in subgroups of COPD patients.…”