Fluticasone propionate and increased risk of pneumonia in COPD: is it PAFR-dependent?

• Published in: International journal of chronic obstructive pulmonary disease 2017-01, Vol.12, p.3425-3427
• Main Author: Sohal, Sukhwinder Singh
• Format: Article
• Language: English
• Subjects: Bacterial infections; Chronic obstructive lung disease; Chronic obstructive pulmonary disease; Complications and side effects; COPD; Dosage and administration; Drug dosages; Drug therapy; Environmental health; Fluticasone; fluticasone propionate; ICS; Letter; Lung diseases; PAFR; Pathogens; Pneumonia; Risk factors; Sleep; Steroids; Streptococcus infections; Viral infections
• ISSN: 1178-2005; 1176-9106; 1178-2005
• DOI: 10.2147/COPD.S154897

Authors’ reply Christer Janson,1 Georgios Stratelis,1,2 Anna Miller-Larsson,3 Tim W Harrison,4 Kjell Larsson5 1Respiratory, Allergy and Sleep Research Unit, Department of Medical Sciences, Uppsala University, Uppsala, 2Respiratory, Inflammation and Autoimmunity, AstraZeneca Nordic, Södertälje, 3Respiratory GMed, AstraZeneca Gothenburg, Mölndal, Sweden; 4Nottingham Respiratory Research Unit, City Hospital Campus, University of Nottingham, Nottingham, UK; 5Lung and Airway Research, National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden We thank Dr Sohal for his interest in our recently published manuscript discussing the scientific rationale for the possible inhaled corticosteroid (ICS) intraclass difference in the risk of pneumonia in COPD. His own work on platelet-activating factor receptor (PAFR) expression on airway epithelial cells in COPD patients shows a trend toward increased expression of PAFR by 6-month treatment with fluticasone propionate (FP), suggesting an increased rate of pneumococcal adhesion with FP, and hence the possible development of infection or pneumonia.1 This supports in part the work by Heijink et al2 that we cited in our paper.2 View the original article by Janson et al