Does Reduced α1-Antitrypsin Activity Explain the Link Between Cigarette Smoking and Idiopathic Pulmonary Fibrosis?

CHEST Journal ◽  
2001 ◽  
Vol 120 (1) ◽  
pp. S72-S74
Author(s):  
Edward D. Chan ◽  
Annemarie H. Ralston ◽  
Leland Shapiro
2021 ◽  
pp. 2101372
Author(s):  
Taro Yasuma ◽  
Corina N. D'Alessandro-Gabazza ◽  
Osamu Hataji ◽  
Tetsu Kobayashi ◽  
Esteban C Gabazza

1991 ◽  
Vol 71 (5) ◽  
pp. 1688-1693 ◽  
Author(s):  
D. A. Schwartz ◽  
R. A. Helmers ◽  
C. S. Dayton ◽  
R. K. Merchant ◽  
G. W. Hunninghake

To investigate factors that determine bronchoalveolar lavage (BAL) cellularity in patients with idiopathic pulmonary fibrosis (IPF), we compared BAL cells in patients with IPF (n = 83) to both nonsmoking (n = 111) and smoking (n = 19) normal volunteers. Patients with IPF had higher concentrations of BAL total cells and alveolar macrophages than nonsmoking volunteers and more BAL neutrophils and eosinophils than normal volunteers regardless of smoking status. Among patients with IPF, the numbers of alveolar macrophages, neutrophils, or eosinophils were strongly associated with either smoking status or pack-years of cigarette smoking. In fact, after accounting for cigarette smoking, using multivariate analysis, the only additional factors that were found to be associated with BAL cellularity were age (macrophages and eosinophils) and the percent predicted forced expired volume in 1 s (neutrophils). Additional multivariate models failed to identify a significant relationship between BAL cellularity and either the type of immunosuppressive therapy or other physiological measures of lung function. We conclude that cigarette smoking strongly influences BAL cellularity in patients with IPF. These findings suggest that cigarette smoking may have a role in the pathogenesis of IPF or may adversely affect the prognosis in patients with IPF.


2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Chad K. Oh ◽  
Lynne A. Murray ◽  
Nestor A. Molfino

Idiopathic pulmonary fibrosis (IPF) is a disease of unknown etiology with considerable morbidity and mortality. Cigarette smoking is one of the most recognized risk factors for development of IPF. Furthermore, recent work suggests that smoking may have a detrimental effect on survival of patients with IPF. The mechanism by which smoking may contribute to the pathogenesis of IPF is largely unknown. However, accumulating evidence suggests that increased oxidative stress might promote disease progression in IPF patients who are current and former smokers. In this review, potential mechanisms by which cigarette smoking affects IPF, the effects of cigarette smoking on accelerated loss of lung function in patients with IPF, key genetic studies evaluating the potential candidate genes and gene-environment (smoking) interaction, diagnosis, and treatment with emphasis on recently closed and ongoing clinical trials are presented.


CHEST Journal ◽  
1990 ◽  
Vol 98 (1) ◽  
pp. 71-76 ◽  
Author(s):  
Hubert De Cremoux ◽  
Jean-François Bernaudin ◽  
Philippe Laurent ◽  
Patrick Brochard ◽  
Jean Bignon

1997 ◽  
Vol 155 (1) ◽  
pp. 242-248 ◽  
Author(s):  
K B Baumgartner ◽  
J M Samet ◽  
C A Stidley ◽  
T V Colby ◽  
J A Waldron

1991 ◽  
Vol 144 (3_pt_1) ◽  
pp. 504-506 ◽  
Author(s):  
David A. Schwartz ◽  
Robert K. Merchant ◽  
Richard A. Helmers ◽  
Steven R. Gilbert ◽  
Charles S. Dayton ◽  
...  

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