title: Steroid-sparing effects of pentoxifylline in pulmonary sarcoidosis.
abstract: BACKGROUND
  Agents that target pro-inflammatory cytokines may be useful in pulmonary sarcoidosis.
  
  
  OBJECTIVE
  To determine effectiveness of a non-selective cyclic nucleotide phosphodiesterase (PDE) inhibitor, pentoxifylline (POF).
  
  
  METHODS
  Randomized, double-blind, placebo-controlled trial,
  
  
  METHODS
  Clinical Research Center, National Institutes of Health.
  
  
  METHODS
  27 patients with biopsy-confirmed pulmonary sarcoidosis receiving prednisone.
  
  
  METHODS
  Placebo or POF (1200-2000 mg/day) for 10 months, as prednisone was tapered.
  
  
  METHODS
  Primary endpoints: sustained improvement in two or more pulmonary function parameters, or a combination of one pulmonary function parameter and dyspnea.
  
  
  RESULTS
  Except for one patient, primary endpoints were not reached in POF-treated patients. Therefore, a post hoc analysis was performed. The observed relative risk reduction for flares associated with POF treatment was 54.9% (95% CI 0.21, 0.89) and the absolute risk reduction was 50.6% (95% CI 0.22, 0.80). Compared to placebo treatment, in the POF group, the mean prednisone dose was lower at 8 and 10 months (p = 0.007 and 0.01 respectively), and there was a trend towards less prednisone usage over the entire study period (p = 0.053), as determined by cumulative change analysis.
  
  
  CONCLUSIONS
  Although our exploratory post hoc analysis suggested that POF reduced flares and had steroid-sparing effects, given the study limitations, definitive conclusions cannot be drawn regarding the efficacy of POF in pulmonary sarcoidosis. In addition, gastrointestinal side-effects, at the doses used, would seem to limit the use of POF in treating pulmonary sarcoidosis. Overall, however, this trial may provide a basis for using more specific, better-tolerated, PDE inhibitors in future clinical trials.
authors.affiliation: Translational Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892-1434, USA.
authors.forename: M K
authors.initials: MK
authors.lastname: Park
authors.lastname: Fontana
authors.forename: H
authors.initials: H
authors.lastname: Babaali
authors.forename: L I
authors.initials: LI
authors.lastname: Gilbert-McClain
authors.forename: M
authors.initials: M
authors.lastname: Stylianou
authors.forename: J
authors.initials: J
authors.lastname: Joo
authors.forename: J
authors.initials: J
authors.lastname: Moss
authors.forename: V C
authors.initials: VC
authors.lastname: Manganiello
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001706:Biopsy; D004305:Dose-Response Relationship, Drug; D004311:Double-Blind Method; D005260:Female; D005540:Forced Expiratory Flow Rates / Q000187:drug effects; D006801:Humans; D006976:Hypertension, Pulmonary / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D010431:Pentoxifylline / Q000008:administration & dosage / Q000627:therapeutic use*; D010726:Phosphodiesterase Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D012129:Respiratory Function Tests; D016896:Treatment Outcome; D055815:Young Adult
chemical_list: D010726:Phosphodiesterase Inhibitors; D010431:Pentoxifylline