Certain Inhaled Corticosteroids Linked to Increased Pneumonia Risk in COPD

For patients with chronic obstructive pulmonary disease (COPD), inhaled corticosteroid (ICS) use was associated with an increased risk of pneumonia, according to the results of a recently published meta-analysis. 

In order to clarify the results of a recent report examining the association between ICS use and the risk of pneumonia in COPD patients, the study authors searched PubMed, the Cochrane Library, Clinical Trials.gov, and Embase for randomized controlled trials (RCTs) published between February and June of 2019. Twenty-five RCTs (N=49,982 patients) that compared pneumonia risk in COPD patients using ICS- versus non-ICS therapy (ie, long-acting beta agonists, long-acting muscarinic antagonists, or placebo) were included in the analysis.

The study authors reported that ICS use in COPD patients was not only found to increase the risk of pneumonia (RR 1.59; 95% CI: 1.33, 1.90; I²=51%), but was also associated with an increased risk of severe pneumonia (based on pooled results from 5 studies: RR 2.17; 95% CI: 1.47, 3.22;  I²=29%). “The results of subgroup analysis based on doses of ICS were consistent with the above,” the study authors reported. They added, “However, subgroup analyses based on types of ICS revealed that fluticasone therapy was associated with an increased risk of pneumonia but not budesonide.” Additionally, it was noted that pneumonia risk was not found to be increased in patients taking medium- and low-doses of budesonide.

According to the results of this meta-analysis, for patients with COPD, ICS use was associated with an increased risk of pneumonia compared with non-ICS therapy. It was found, however, that these results only pertained to fluticasone-containing ICS, not budesonide-containing ICS. While it is unclear as to why certain ICS affect pneumonia risk more than others, the study authors noted that it has been previously reported that  “fluticasone could suppress effectively innate immunoresponse to bacterial triggers in alveolar macrophages” and that this effect “could be up to tenfold greater than that of budesonide in the human airway/lungs.”

For more information visit sciencedirect.com.

This article originally appeared on MPR