title: Anti-acid treatment and disease progression in idiopathic pulmonary fibrosis: an analysis of data from three randomised controlled trials.
abstract: BACKGROUND
  Abnormal acid gastro-oesophageal reflux is common in patients with idiopathic pulmonary fibrosis (IPF) and is considered a risk factor for development of IPF. Retrospective studies have shown improved outcomes in patients given anti-acid treatment. The aim of this study was to investigate the association between anti-acid treatment and disease progression in IPF.
  
  
  METHODS
  In an analysis of data from three randomised controlled trials, we identified patients with IPF assigned to receive placebo. Case report forms had been designed to prospectively obtain data about diagnosis and treatment of abnormal acid gastro-oesophageal reflux in each trial. The primary outcome was estimated change in forced vital capacity (FVC) at 30 weeks (mean follow-up) in patients who were and were not using a proton-pump inhibitor or histamine-receptor-2 (H2) blocker.
  
  
  RESULTS
  Of the 242 patients randomly assigned to the placebo groups of the three trials, 124 (51%) were taking a proton-pump inhibitor or H2 blocker at enrolment. After adjustment for sex, baseline FVC as a percentage of predicted, and baseline diffusing capacity of the lung for carbon monoxide as a percentage of predicted, patients taking anti-acid treatment at baseline had a smaller decrease in FVC at 30 weeks (-0·06 L, 95% CI -0·11 to -0·01) than did those not taking anti-acid treatment (-0·12 L, -0·17 to -0·08; difference 0·07 L, 95% CI 0-0·14; p=0·05).
  
  
  CONCLUSIONS
  Anti-acid treatment could be beneficial in patients with IPF, and abnormal acid gastro-oesophageal reflux seems to contribute to disease progression. Controlled clinical trials of anti-acid treatments are now needed.
  
  
  BACKGROUND
  National Institutes of Health.
authors.affiliation: Department of Medicine, University of California, San Francisco, San Francisco, CA, USA.
authors.forename: Joyce S
authors.initials: JS
authors.lastname: Lee
authors.affiliation: Department of Medicine, University of California, San Francisco, San Francisco, CA, USA.
authors.forename: Harold R
authors.initials: HR
authors.lastname: Collard
authors.affiliation: Duke Clinical Research Institute, Durham, NC, USA.
authors.forename: Kevin J
authors.initials: KJ
authors.lastname: Anstrom
authors.affiliation: Department of Medicine, University of Michigan, Ann Arbor, MI, USA.
authors.forename: Fernando J
authors.initials: FJ
authors.lastname: Martinez
authors.affiliation: Department of Medicine, University of Chicago, Chicago, IL, USA.
authors.forename: Imre
authors.initials: I
authors.lastname: Noth
authors.affiliation: Duke Clinical Research Institute, Durham, NC, USA.
authors.forename: Rhonda S
authors.initials: RS
authors.lastname: Roberts
authors.affiliation: Duke Clinical Research Institute, Durham, NC, USA.
authors.forename: Eric
authors.initials: E
authors.lastname: Yow
authors.affiliation: Department of Medicine, University of Washington, Seattle, WA, USA. Electronic address: graghu@uw.edu.
authors.forename: Ganesh
authors.initials: G
authors.lastname: Raghu
mesh_terms: D000368:Aged; D018450:Disease Progression; D005260:Female; D005764:Gastroesophageal Reflux / Q000150:complications / Q000188:drug therapy; D006635:Histamine H2 Antagonists / Q000627:therapeutic use*; D006801:Humans; D054990:Idiopathic Pulmonary Fibrosis / Q000150:complications* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D054328:Proton Pump Inhibitors / Q000627:therapeutic use*; D016896:Treatment Outcome; D014797:Vital Capacity / Q000502:physiology
chemical_list: D006635:Histamine H2 Antagonists; D054328:Proton Pump Inhibitors