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Clinical Commentary |

COPD: New Lessons From α1-Antitrypsin Deficiency?

Adam Wanner, MD, FCCP
Author and Funding Information

*From the University of Miami Miller School of Medicine, Miami, FL.

Correspondence to: Adam Wanner, MD, FCCP, 1600 NW Tenth Ave, No. 7052, Miami, FL 33136; e-mail: awanner@miami.edu


The author has reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/site/misc/reprints.xhtml).


© 2009 American College of Chest Physicians


Chest. 2009;135(5):1342-1344. doi:10.1378/chest.08-2341
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Approximately 6% of the population has COPD, and COPD has become the fourth leading cause of death in the United States.1 Although the awareness of COPD as a global health problem is growing and although there has been a recent surge in COPD research, spawned by industry and government funding agencies, our understanding of the pathogenetic mechanisms underlying this highly prevalent disease remains fragmentary. As a result, disease-modifying treatment is still elusive. Inhaled smoke, especially cigarette smoke, has been identified as the major cause of COPD, but it is not clear why clinical COPD develops in only a minority of those persons who are exposed to or are exposing themselves to smoke. Genetic predisposition comes to mind as a possible explanation for this phenomenon, and the study of COPD genetics therefore is in full swing.2,3

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