Current issues of ACP Journal Club are published in Annals of Internal Medicine


Therapeutics

Helicobacter pylori eradication reduced the risk for ulcers in dyspeptic patients who were about to begin NSAID treatment

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ACP J Club. 2002 Jul-Aug;137:13. doi:10.7326/ACPJC-2002-137-1-013


Source Citation

Chan FK, To KF, Wu JC, et al. Eradication of Helicobacter pylori and risk of peptic ulcers in patients starting long-term treatment with non-steroidal anti-inflammatory drugs: a randomised trial. Lancet. 2002 Jan 5;359:9-13. [PubMed ID: 11809180] (All 2002 articles were reviewed for relevancy, and abstracts were last revised in 2008.)


Abstract

Question

In patients who have Helicobacter pylori infection and dyspepsia or a history of ulcer and who are about to begin nonsteroidal anti-inflammatory drug (NSAID) treatment, does the eradication of H. pylori infection reduce the risk for ulcers?

Design

Randomized {allocation concealed*}†, blinded (investigators, research nurse, and patients),* placebo-controlled trial with 6-month follow-up.

Setting

A family clinic and outpatient clinic in Hong Kong.

Patients

102 patients who required long-term regular NSAID treatment, had a positive result for H. pylori on a urea breath test, and had moderate dyspepsia or a history of endoscopically confirmed peptic ulcers. Exclusion criteria were exposure to NSAIDs (except for aspirin, ≤ 325 mg/d) for > 1 month within the previous 8 weeks; concomitant treatment with steroids, anticoagulants, or antiulcer drugs; substantial renal impairment; previous treatment for H. pylori; or history of gastric surgery or serious ulcer complications. Follow-up was 98% (mean age 63 y, 67% women).

Intervention

Patients were allocated to triple therapy (omeprazole, 20 mg; amoxicillin, 1 g; and clarithromycin, 500 mg) (n = 51) or control therapy (omeprazole, 20 mg, and placebo antibiotics) (n = 51) given twice daily for 1 week.

Main outcome measures

Endoscopically confirmed gastric or duodenal ulcers. A secondary outcome measure was complicated (symptomatic or bleeding) ulcers.

Main results

Analysis was by intention to treat. Fewer patients in the eradication group than in the control group had gastric or duodenal ulcers or complicated ulcers (Table).

Conclusion

In patients who had Helicobacter pylori infection and dyspepsia or a history of ulcer and who began long-term nonsteroidal anti-inflammatory drug treatment, the eradication of H. pylori infection reduced the risk for ulcers.

*See Glossary.

†Information provided by author.

Source of funding: No external funding.

For correspondence: Dr. F.K.L. Chan, Prince of Wales Hospital, Shatin, Hong Kong. E-mail fklchan@cuhk.edu.hk.


Table. Eradication of Helicobacter pylori infection vs no eradication for patients who have dyspepsia or history of ulcer and receive NSAIDs‡

Outcomes at 6 mo Eradication No eradication RRR (95% CI) NNT (CI)
Gastric or duodenal ulcer 9.8% 31% 68% (23 to 87) 5 (3 to 19)
Complicated ulcer 3.9% 24% 84% (41 to 96) 5 (3 to 14)

‡NSAIDs = nonsteroidal anti-inflammatory drugs. Other abbreviations defined in Glossary; RRR, NNT, and CI calculated from data in article.


Commentary

The Hong Kong Prince of Wales Hospital Gastrointestinal Group is to be congratulated on having done several of the pivotal studies investigating whether synergy exists between H. pylori infection and NSAIDs (including aspirin). The study by Chan and colleagues and a recent meta-analysis (1) suggest that synergy does exist. The current study shows that in NSAID-naive patients who either had a history of proven ulcers or moderate dyspepsia, curing H. pylori at the start of NSAID treatment decreased the risk for ulcers at 6 months. The difference in ulcer frequency was clinically important. Although anti–H. pylori treatment offered benefit, I still would recommend NSAID prophylaxis with a proton-pump inhibitor (PPI) in patients with an ulcer history or substantial dyspepsia, given that the prevalence of ulcers was 12% in this group. Most ulcers in such patients starting conventional NSAIDs can be prevented by concomitant therapy with a PPI. Whether cyclooxygenase-2 inhibitors would reduce (i.e., unmask, not necessarily cause) ulcers in patients with H. pylori infection and an ulcer history is not known.

The situation is different for patients taking aspirin because Chan and colleagues previously showed that cure of H. pylori prevented recurrent aspirin-related ulcers but not other NSAID ulcers (2). The risk for ulcers in NSAID users is higher in the first few months of therapy. Gastric adaptation is said to be responsible for this phenomenon, but H. pylori infection now seems a likely culprit for pushing NSAID users over the ulcer threshold.

Sander J.O. Veldhuyzen van Zanten, MD, PhD
Queen Elizabeth II Health Sciences Centre
Halifax, Nova Scotia, Canada


References

1. Huang JQ, Sridhar S, Hunt RH. Role of Helicobacter pylori infection and non-steroidal anti-inflammatory drugs in peptic-ulcer disease: a meta-analysis. Lancet. 2002;359:14-22. [PubMed ID: 11809181]

2. Chan FK, Chung SC, Suen BY, et al. Preventing recurrent upper gastrointestinal bleeding in patients with Helicobacter pylori infection who are taking low-dose aspirin or naproxen. N Engl J Med. 2001;344:967-73. [PubMed ID: 11274623]