Statins may up interstitial lung disease risk in smokers
Washington: Smokers who use statins may be more susceptible to interstitial lung disease (ILD), researchers say.
While some studies have suggested that statins might be beneficial in the treatment of fibrotic lung disease, others have suggested that they may contribute to the progression of pulmonary fibrosis by enhancing secretion of inflammasome-regulated cytokines, and numerous case reports have suggested that statins may contribute to the development of various types of ILD.
`Based on earlier case reports of statin-associated ILD and data suggesting that smoking is associated with the interstitial lung abnormalities (ILA) which underlie ILD, we hypothesized that statins would increase the risk for ILA in a population of smokers,`said George R. Washko MD, MMsC, and Gary M. Hunninghake MD, MPH, of the Division of Pulmonary and Critical Care at Brigham and Women’s Hospital in Boston.
`Accordingly, we evaluated the association between statin use and ILA in a large cohort of current and former smokers from the COPDGene study.
`In addition to the association between statin use and ILA we found in humans, we also demonstrated that statin administration aggravated lung injury and fibrosis in bleomycin-treated mice,` he stated.
Bleomycin has been shown to induce lung inflammation and fibrosis.
After adjustment for a number of covariates, including a history of high cholesterol or coronary artery disease, statin users had a 60 percent increase in the odds of having ILA, compared to subjects not taking statins.
No other positive associations between ILA and cardiovascular medications or disorders were detected.
The association between statin use and ILA was greatest with statins with higher hydrophilicity (readily absorbed or dissolved in water), such as pravastatin, and in higher age groups.
The effects of statins on lung injury and fibrogenesis were also examined in a study in mice, which were pretreated with pravastatin prior to intratracheal bleomycin administration.
But there were some limitations to both studies. Findings in the mouse model were not replicated in human samples. All study subjects were current or former smokers, perhaps limiting the applicability of the results to others.
Cigarette smoking by itself may lead to pulmonary inflammation. Finally, the duration and dosage of statin therapy was not available for the majority of patients.
The findings were published online in the American Thoracic Society``s American Journal of Respiratory and Critical Care Medicine.
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