Screening and treatment for infection caused by the gastrointestinal bacterium Helicobacter pylori could substantially reduce the risk of ulcers for patients starting long-term non-steroidal anti-inflammatory drug (NSAID) treatment, conclude authors of a study in this week’s issue of THE LANCET. A meta-analysis also published in this week’s issue confirms both H pylori and NSAIDs as independent risk factors for peptic-ulcer disease.
Whether H pylori increases the risk of ulcers in patients taking NSAIDs is controversial. Francis Chan and colleagues from Prince of Wales Hospital, Hong Kong, hypothesised that eradication of H pylori would reduce the risk of ulcers for patients starting long-term NSAID treatment.
Patients requiring long-term NSAIDs were randomly assigned omeprazole triple therapy (eradication group) or omeprazole with placebo instead of antibiotics (placebo group) for 1 week. All patients were given diclofenac slow release 100 mg daily for 6 months from randomisation. Endoscopy was done at 6 months or if severe dyspepsia or gastrointestinal bleeding occurred. The primary endpoint was the probability of ulcers within 6 months.
Of 210 arthritis patients screened,100 patients were enrolled in the study. H pylori was eradicated in 90% of the eradication group and 6% of the placebo group. Five of 51 eradication-group patients and 15 of 49 placebo-group patients had ulcers. The 6-month probability of ulcers was 12% in the eradication group and 34% in the placebo group. The corresponding 6-month probabilities of complicated ulcers were 4% and 27%, respectively.
A meta-analysis (p 14) by Richard Hunt and colleagues from McMaster University Medical Center, Canada, pooled data from previous studies about H pylori, NSAID use, and peptic-ulcer disease. In 16 studies of 1625 NSAID takers, uncomplicated peptic-ulcer disease was more than twice as likely in patients positive for H pylori than in those negative for H pylori. H pylori infection and NSAID use increased the risk of ulcer bleeding 1.79 and 4.85 fold, respectively. However, the risk of ulcer bleeding increased by a factor of 6.13 when both factors were present.
See also Commentary (p 3).
Contact: Dr Francis K L Chan, Department of Medicine & Therapeutics, Prince of Wales Hospital, 30-32 Ngan Shing Street, Shatin, Hong Kong; T) +852 2632 3126; F) +852 2637 3852; E) fklchan@cuhk.edu.hk
Professor Richard Hunt, Division of Gastroenterology, Department of Medicine, McMaster University Medical Center, Hamilton, Ontario L8N3Z5, Canada; T) +1 905 521 2100 Ext. 73219; E) huntr@mcmaster.ca
The Lancet