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Decreasing incidence of symptomatic gastrointestinal ulcers and ulcer complications in patients with rheumatoid arthritis
  1. K S S Steen1,
  2. M T Nurmohamed2,
  3. I Visman3,
  4. M Heijerman3,
  5. M Boers4,
  6. B A C Dijkmans1,
  7. W F Lems5
  1. 1
    Department of Rheumatology, VU University Medical Center, Amsterdam, The Netherlands
  2. 2
    Department of Internal Medicine, VU University Medical Center, Amsterdam, The Netherlands
  3. 3
    Department of Rheumatology, Jan van Breemen Institute, Amsterdam, The Netherlands
  4. 4
    Department of Clinical Epidemiology and Biostatistics, VU University Medical Center, Amsterdam, The Netherlands
  5. 5
    Department of Rheumatology, Slotervaart Hospital, Amsterdam, The Netherlands
  1. K S S Steen, Department of Rheumatology, VU University Medical Center, Boelelaan 1117, 1081 HV, Amsterdam, The Netherlands; k.steen{at}vumc.nl

Abstract

Background: Non-steroidal anti-inflammatory drugs (NSAIDs) frequently cause gastrointestinal (GI) ulcers and complications of ulcers. In 1997 in Amsterdam, the incidence of symptomatic GI events was 2.1% (95% CI 1.0–3.1) in patients with rheumatoid arthritis (RA). We conducted a new prospective, observational study on the symptomatic GI events in our outpatient clinics, and compared the data to a previous study conducted by our group. Over the same time period, a decline of GI events over the last decade was reported for US patients.

Methods: In 2003, three questionnaires were sent to all RA patients in Amsterdam at 4-month intervals, addressing medication use, dyspepsia, and symptomatic GI events in the previous 4 months.

Results: The incidence of GI events in high-risk patients, defined as age ⩾60 and/or history of GI event) using NSAIDs or cyclo-oxygenase 2 specific inhibitors (COXIBs) was 1.2% (95% CI 0.2–2.3), which appears to be substantially lower than the 2.1% observed in 1997; however this difference did not reach statistical significance (p = 0.3). In 64% (95% CI 61–68) of the high-risk patients, acid-suppressive drugs (ie, proton pump inhibitors, prostaglandin analogues or high dose H2 antagonists) were used. In 1997 this percentage was significantly lower at 49% (45–52; p<0.001). The compliance to the Dutch guidelines for prevention of NSAID-related gastropathy was almost 75%, with 64% of the patients using acid-suppressive drugs and 11% using COXIBs.

Conclusion: The present study reveals a decline of NSAID-induced gastrointestinal events, which is similar to the results observed in the US. This is most likely due to a more strict adherence to guidelines for prevention of NSAID gastropathy, and better treatment of rheumatoid arthritis.

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Footnotes

  • Funding: This study was financially supported by an unrestricted grant from AstraZeneca

  • Competing interests: None declared

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