title: Haemoglobin decreases in NSAID users over time: an analysis of two large outcome trials.
abstract: BACKGROUND
  Nonsteroidal anti-inflammatory drugs (NSAIDs) have been associated with clinically significant decreases in haemoglobin dependent and independent of acute bleeding events.
  
  
  OBJECTIVE
  To evaluate the incidence and time to a clinically meaningful decrease in haemoglobin in two double-blind, prospective randomised clinical trials comparing NSAIDs in patients with osteoarthritis (OA) or rheumatoid arthritis (RA).
  
  
  METHODS
  In CLASS, patients with OA/RA who were aged ≥ 18 years and required continuous NSAID treatment were included; patients who were Helicobacter pylori positive and/or using aspirin were not excluded. In contrast, in the CONDOR trial, comparing celecoxib alone to diclofenac sustained release (plus omeprazole), patients were aged ≥ 60 years or ≥ 18 years with a history of gastroduodenal ulcer and were H. pylori negative; aspirin or other anti-platelet users were excluded. To make a parallel post hoc analysis we limited our study to 6 months and the populations to only the non-aspirin users in CLASS and those patients receiving either celecoxib or diclofenac. A decrease in haemoglobin of ≥ 2 g/dL defined the primary end point.
  
  
  RESULTS
  At 6 months, in the CLASS and CONDOR trials, 1.9% and 2.0% of patients treated with celecoxib and 3.3% and 5.7% of patients treated with diclofenac developed a ≥ 2 g/dL decrease in haemoglobin, respectively, [CLASS: odds ratio (OR) 1.80 (95% confidence interval (CI), 1.22-2.65) and CONDOR: OR 2.93 (95% CI, 2.06-4.15), respectively].
  
  
  CONCLUSIONS
  IN these two large, independent trials, clinically-meaningful decreases in haemoglobin ≥ 2 g/dL occurred in a relatively similar fashion over time despite differences in trial designs.
authors.affiliation: Department of Medicine, University of Illinois at Chicago, Chicago, IL 60612, USA. jlgoldst@uic.edu
authors.forename: J L
authors.initials: JL
authors.lastname: Goldstein
authors.forename: F K L
authors.initials: FK
authors.lastname: Chan
authors.forename: A
authors.initials: A
authors.lastname: Lanas
authors.forename: C M
authors.initials: CM
authors.lastname: Wilcox
authors.forename: D
authors.initials: D
authors.lastname: Peura
authors.forename: G H
authors.initials: GH
authors.lastname: Sands
authors.forename: M F
authors.initials: MF
authors.lastname: Berger
authors.forename: H
authors.initials: H
authors.lastname: Nguyen
authors.forename: J M
authors.initials: JM
authors.lastname: Scheiman
mesh_terms: D000328:Adult; D000368:Aged; D000740:Anemia / Q000209:etiology; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage / Q000009:adverse effects*; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000188:drug therapy*; D001241:Aspirin / Q000008:administration & dosage / Q000009:adverse effects; D000068579:Celecoxib; D052246:Cyclooxygenase 2 Inhibitors / Q000008:administration & dosage / Q000009:adverse effects; D004008:Diclofenac / Q000008:administration & dosage / Q000009:adverse effects; D004311:Double-Blind Method; D004359:Drug Therapy, Combination; D005260:Female; D006454:Hemoglobins / Q000378:metabolism*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010003:Osteoarthritis / Q000097:blood / Q000188:drug therapy*; D011446:Prospective Studies; D011720:Pyrazoles / Q000008:administration & dosage / Q000009:adverse effects; D013449:Sulfonamides / Q000008:administration & dosage / Q000009:adverse effects
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D052246:Cyclooxygenase 2 Inhibitors; D006454:Hemoglobins; D011720:Pyrazoles; D013449:Sulfonamides; D004008:Diclofenac; D000068579:Celecoxib; D001241:Aspirin