title: Risk of peptic ulcer hospitalizations in users of NSAIDs with gastroprotective cotherapy versus coxibs.
abstract: OBJECTIVE
  The primary strategies to reduce the risk of serious gastropathy caused by traditional nonsteroidal anti-inflammatory drugs (NSAIDs) are use of a coxib or concurrent use of a proton pump inhibitor or double-dose histamine-2 receptor antagonist. However, the relative clinical effectiveness of these therapeutic alternatives is understudied.
  
  
  METHODS
  We studied peptic ulcer hospitalizations in a cohort of Tennessee Medicaid enrollees between 1996 and 2004. To decrease potential "channeling" bias, the study included only new episodes of prescribed NSAID or coxib use and controlled for multiple baseline risk factors for upper gastrointestinal disease. There were 234,010 and 48,710 new episodes of NSAID and coxib use, respectively, with 363,037 person-years of follow-up and 1223 peptic ulcer hospitalizations.
  
  
  RESULTS
  Current users of NSAIDs with no gastroprotective cotherapy had an adjusted incidence of peptic ulcer hospitalizations of 5.65 per 1000 person-years, 2.76 (95% confidence interval, 2.35-3.23) times greater than that for persons not currently using either NSAIDs or coxibs. This risk was reduced by 39% (16%-56%, 95% CI) for current users of NSAIDs with gastroprotective cotherapy and 40% (23%-54%) for current users of coxibs without such cotherapy. Concurrent users of NSAIDs and proton pump inhibitors had a 54% (27%-72%) risk reduction, very similar to the 50% (27%-66%) reduction for concurrent users of proton pump inhibitors and coxibs.
  
  
  CONCLUSIONS
  These findings suggest that coprescribing a proton pump inhibitor with an NSAID is as effective as use of a coxib for reducing the risk of NSAID-induced gastropathy.
authors.affiliation: Division of Pharmacoepidemiology, Department of Preventive Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37212, USA. wayne.ray@vanderbilt.edu
authors.forename: Wayne A
authors.initials: WA
authors.lastname: Ray
authors.forename: Cecilia P
authors.initials: CP
authors.lastname: Chung
authors.forename: C Michael
authors.initials: CM
authors.lastname: Stein
authors.forename: Walter E
authors.initials: WE
authors.lastname: Smalley
authors.forename: Kathi
authors.initials: K
authors.lastname: Hall
authors.forename: Patrick G
authors.initials: PG
authors.lastname: Arbogast
authors.forename: Marie R
authors.initials: MR
authors.lastname: Griffin
mesh_terms: D000328:Adult; D000368:Aged; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects* / Q000627:therapeutic use; D000897:Anti-Ulcer Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy; D015331:Cohort Studies; D052246:Cyclooxygenase 2 Inhibitors / Q000627:therapeutic use*; D004305:Dose-Response Relationship, Drug; D004359:Drug Therapy, Combination; D005260:Female; D041981:Gastrointestinal Tract / Q000187:drug effects; D006635:Histamine H2 Antagonists / Q000627:therapeutic use; D006760:Hospitalization / Q000706:statistics & numerical data; D006801:Humans; D015994:Incidence; D008297:Male; D008875:Middle Aged; D010003:Osteoarthritis / Q000188:drug therapy; D010437:Peptic Ulcer / Q000139:chemically induced / Q000453:epidemiology* / Q000517:prevention & control* / Q000628:therapy; D054328:Proton Pump Inhibitors; D012307:Risk Factors
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000897:Anti-Ulcer Agents; D052246:Cyclooxygenase 2 Inhibitors; D006635:Histamine H2 Antagonists; D054328:Proton Pump Inhibitors