Literature DB >> 16042957

Alcohol abuse and acute lung injury: epidemiology and pathophysiology of a recently recognized association.

David M Guidot1, C Michael Hart.   

Abstract

Alcohol is the most commonly used and abused drug in the United States. The deleterious health effects of alcohol can be attributed both to its acute intoxicating effects, which result in temporary impairment of judgment and motor skills, and to its more chronic and toxic effects on the liver, pancreas, heart, and brain, all of which may result in irreversible organ damage. Although recognized for more than a century as a major risk factor for pneumonia, alcohol abuse was until recently perceived to have no significant effects on lung structure and/or function. However, within the past decade, epidemiologic studies have revealed that alcohol abuse independently increases the risk of acute respiratory distress syndrome (ARDS) two- to fourfold in patients with sepsis or trauma and may play a role in ARDS pathogenesis in as many as half of all patients with the syndrome. Although alcohol abuse alone does not cause acute lung injury, it renders the lung susceptible to dysfunction in response to the inflammatory stresses of sepsis, trauma, and other clinical conditions recognized to cause ARDS. Recent investigations in both animal models of chronic ethanol ingestion and in human subjects with a history of alcohol abuse have explored this previously unrecognized connection between alcohol and acute lung injury and have uncovered multiple derangements, which we now characterize as the "alcoholic lung." This review summarizes the epidemiologic association between alcohol abuse and acute lung injury and the recent experimental findings that are unraveling the underlying pathophysiology.

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Year:  2005        PMID: 16042957     DOI: 10.2310/6650.2005.53506

Source DB:  PubMed          Journal:  J Investig Med        ISSN: 1081-5589            Impact factor:   2.895


  32 in total

1.  Understanding the drug treatment community's ambivalence towards tobacco use and treatment.

Authors:  Kimber P Richter; Jamie J Hunt; A Paula Cupertino; Susan Garrett; Peter D Friedmann
Journal:  Int J Drug Policy       Date:  2012-01-26

2.  ABO blood type A is associated with increased risk of ARDS in whites following both major trauma and severe sepsis.

Authors:  John P Reilly; Nuala J Meyer; Michael G S Shashaty; Rui Feng; Paul N Lanken; Robert Gallop; Sandra Kaplan; Maximilian Herlim; Nathaniel L Oz; Isabel Hiciano; Ana Campbell; Daniel N Holena; Muredach P Reilly; Jason D Christie
Journal:  Chest       Date:  2014-04       Impact factor: 9.410

3.  Exhaled Nitric Oxide Levels Among Adults With Excessive Alcohol Consumption.

Authors:  Majid Afshar; Jill A Poole; Guichan Cao; Ramon Durazo; Richard C Cooper; Elizabeth J Kovacs; Joseph H Sisson
Journal:  Chest       Date:  2016-02-19       Impact factor: 9.410

4.  Ethanol suppresses phagosomal adhesion maturation, Rac activation, and subsequent actin polymerization during FcγR-mediated phagocytosis.

Authors:  John Karavitis; Eva L Murdoch; Cory Deburghgraeve; Luis Ramirez; Elizabeth J Kovacs
Journal:  Cell Immunol       Date:  2012-02-13       Impact factor: 4.868

5.  Glutathione attenuates ethanol-induced alveolar macrophage oxidative stress and dysfunction by downregulating NADPH oxidases.

Authors:  Samantha M Yeligar; Frank L Harris; C Michael Hart; Lou Ann S Brown
Journal:  Am J Physiol Lung Cell Mol Physiol       Date:  2014-01-17       Impact factor: 5.464

6.  Zinc supplementation restores PU.1 and Nrf2 nuclear binding in alveolar macrophages and improves redox balance and bacterial clearance in the lungs of alcohol-fed rats.

Authors:  Ashish J Mehta; Pratibha C Joshi; Xian Fan; Lou Ann S Brown; Jeffrey D Ritzenthaler; Jesse Roman; David M Guidot
Journal:  Alcohol Clin Exp Res       Date:  2011-03-29       Impact factor: 3.455

7.  PPARγ ligands regulate NADPH oxidase, eNOS, and barrier function in the lung following chronic alcohol ingestion.

Authors:  Matthew C Wagner; Samantha M Yeligar; Lou Ann Brown; C Michael Hart
Journal:  Alcohol Clin Exp Res       Date:  2011-07-18       Impact factor: 3.455

8.  Nicotinic acetylcholine receptors are sensors for ethanol in lung fibroblasts.

Authors:  Jeffrey D Ritzenthaler; Susanne Roser-Page; David M Guidot; Jesse Roman
Journal:  Alcohol Clin Exp Res       Date:  2013-02-19       Impact factor: 3.455

9.  Na,K-ATPase expression is increased in the lungs of alcohol-fed rats.

Authors:  Jeffrey S Otis; Patrick O Mitchell; Corey D Kershaw; Pratibha C Joshi; David M Guidot
Journal:  Alcohol Clin Exp Res       Date:  2008-03-13       Impact factor: 3.455

10.  Chronic ethanol ingestion increases nitric oxide production in the lung.

Authors:  John A Polikandriotis; Heidi L Rupnow; Lou Ann Brown; C Michael Hart
Journal:  Alcohol       Date:  2007-08       Impact factor: 2.405

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