title: Antacid Therapy and Disease Progression in Patients with Idiopathic Pulmonary Fibrosis Who Received Pirfenidone.
abstract: BACKGROUND
  Gastroesophageal reflux disease is a potential risk factor for idiopathic pulmonary fibrosis (IPF) progression; however, the impact of antacid therapy (AAT) is under debate.
  
  
  OBJECTIVE
  To evaluate the effect of AAT on IPF progression in pirfenidone-treated patients.
  
  
  METHODS
  This post hoc analysis included patients with IPF who received pirfenidone in 3 trials (CAPACITY [PIPF-004/PIPF-006] and ASCEND [PIPF-016]). Pulmonary function, exercise tolerance, survival, hospitalizations, and adverse events (AEs) over 52 weeks were analyzed by baseline AAT use. Disease progression was defined as a decrease in forced vital capacity (FVC) of ≥10%, a decrease in 6-min walking distance of ≥50 m, or death over 1 year.
  
  
  RESULTS
  Of 623 patients, 44% received AAT. No significant differences were found at 52 weeks (AAT versus non-AAT, respectively) in disease progression (24.9 vs. 30.6%; p = 0.12), all-cause mortality rate (2.9 vs. 4.0%; p = 0.47), IPF-related mortality rate (1.1 vs. 2.0%; p = 0.37), all-cause hospitalization rate (16.1 vs. 18.3%; p = 0.48), or mean change in percent FVC (-2.7 vs. -3.1%; p = 0.44). A relative, but not absolute, FVC decline of ≥10% favored AAT (15 vs. 22%; p = 0.03). Severe gastrointestinal AEs (3.7 vs. 0.9%; p = 0.015) and severe pulmonary infections (3.7 vs. 1.1%; p = 0.035) were more frequent with AAT.
  
  
  CONCLUSIONS
  AAT and pirfenidone had outcomes comparable to those of pirfenidone alone in patients with IPF, underscoring the need for prospective trials to elucidate the role of AAT with or without antifibrotic drugs as a treatment for IPF.
authors.affiliation: Center for Interstitial and Rare Lung Diseases, Pneumology and Respiratory Critical Care Medicine, Thoraxklinik, University of Heidelberg, Heidelberg, Germany.
authors.forename: Michael
authors.initials: M
authors.lastname: Kreuter
authors.forename: Paolo
authors.initials: P
authors.lastname: Spagnolo
authors.forename: Wim
authors.initials: W
authors.lastname: Wuyts
authors.forename: Elisabetta
authors.initials: E
authors.lastname: Renzoni
authors.forename: Dirk
authors.initials: D
authors.lastname: Koschel
authors.forename: Francesco
authors.initials: F
authors.lastname: Bonella
authors.forename: Toby M
authors.initials: TM
authors.lastname: Maher
authors.forename: Martin
authors.initials: M
authors.lastname: Kolb
authors.forename: Derek
authors.initials: D
authors.lastname: Weycker
authors.forename: Klaus-Uwe
authors.initials: KU
authors.lastname: Kirchgässler
authors.forename: Ulrich
authors.initials: U
authors.lastname: Costabel
mesh_terms: D000368:Aged; D000863:Antacids / Q000627:therapeutic use; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D002423:Cause of Death; D018450:Disease Progression; D017079:Exercise Tolerance / Q000502:physiology; D005260:Female; D005764:Gastroesophageal Reflux / Q000150:complications / Q000188:drug therapy*; D006635:Histamine H2 Antagonists / Q000627:therapeutic use*; D006760:Hospitalization / Q000706:statistics & numerical data; D006801:Humans; D054990:Idiopathic Pulmonary Fibrosis / Q000150:complications / Q000188:drug therapy* / Q000401:mortality / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009026:Mortality; D054328:Proton Pump Inhibitors / Q000627:therapeutic use*; D011728:Pyridones / Q000627:therapeutic use*; D012129:Respiratory Function Tests; D015996:Survival Rate; D014797:Vital Capacity; D000070857:Walk Test
chemical_list: D000863:Antacids; D000894:Anti-Inflammatory Agents, Non-Steroidal; D006635:Histamine H2 Antagonists; D054328:Proton Pump Inhibitors; D011728:Pyridones; C093844:pirfenidone
keywords: Antacid therapy; Gastroesophageal reflux disease; Idiopathic pulmonary fibrosis; Pirfenidone; Progression-free survival