Twelve-month endoscopic and histological analysis following proton-pump inhibitor-based triple therapy in Helicobacter pylori-positive patients with gastric ulcers

Abstract

Objective. To evaluate endoscopic and histological findings after Helicobacter pylori eradication therapy in gastric ulcer (GU) patients after 12 months' follow-up. Material and methods. A total of 401 GU patients were randomized to receive either twice-daily (b.i.d.) esomeprazole 20 mg+amoxicillin 1000 mg+clarithromycin 500 mg (EAC) for 1 week followed by placebo for 3 weeks, EAC followed by once-daily (o.d.) esomeprazole 20 mg for 3 weeks or esomeprazole 20 mg b.i.d. plus placebo antibiotics for 1 week followed by esomeprazole 20 mg o.d. for 3 weeks. Endoscopy with biopsy was performed at baseline, after treatment and at 6 and 12 months' follow-up (healed patients). Results. Endoscopic abnormalities, particularly in the stomach, were common at baseline and remained similar during follow-up, regardless of ulcer status and treatment. Helicobacter gastritis was present (antrum or corpus) in ≈ 20% of patients following eradication therapy (versus ≈ 80% with esomeprazole alone); these effects were sustained during follow-up. Similar trends were observed for other histological variables (granulocyte and lymphoplasmocytic cell infiltration, replacement of gastric surface cells by regenerative epithelium, and mucous depletion). No changes in atrophy or intestinal metaplasia were observed. Eighteen gastric cancer cases were detected: 11 at baseline endoscopy, and seven during treatment and follow-up. Conclusions. Endoscopic abnormalities are common in GU patients and persist after proton-pump inhibitor-based triple therapy for H. pylori eradication, which is associated with large, sustained improvements in histological variables. Follow-up endoscopy and histology may be necessary, even in patients with apparently non-malignant GU, to improve the detection rate of gastric malignancy in populations with a high prevalence of gastric cancer.

Key Words::

• Eradication therapy
• esomeprazole
• gastric ulcer
• Helicobacter pylori
• histology

Acknowledgements

This study was supported by AstraZeneca, the manufacturer of esomeprazole. We are indebted to the HELIX study investigators for their contribution to the study. We thank Claire Byrne from inScience Communications (a Wolters Kluwer business), who provided medical writing support funded by AstraZeneca.

M. S. has received financial support from AstraZeneca for lecture fees, travel expenses and registration fees. P. M. has received research funding and acts as an occasional consultant to AstraZeneca and Nycomed. K. T. has received financial support from Roche (registration fees), AstraZeneca (lecture fees and travel expenses) and Abbott (lecture fees). B. C. Y. W. has received lecture fees and travel expenses from AstraZeneca, Eisai and Olympus, and is an advisory board member for Pfizer, Eisai and AstraZeneca. M. G., S. E., M. W. and P. N. are employees of AstraZeneca. The following have no competing interests: Z. T., L. E., E. B., P. D. and L. H.

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