Authors: Choi IJ et al. Summary: Patients who had undergone endoscopic resection of early gastric cancer or high-grade adenoma were randomised to receive antibiotics for Helicobacter pylori eradication (evaluable n=194) or placebo (evaluable n=202); median follow-up was 5.9 years. Compared with placebo, a smaller proportion of the H. pylori eradication group developed metachronous gastric cancer (7.2% vs. 13.4% [p=0.03]), and a greater proportion of the subgroup of participants with available data (n=327) experienced histological improvement from baseline in the atrophy grade at the gastric corpus lesser curvature (48.4% vs. 15.0% [p<0.001]). The mild adverse event rate was higher in the H. pylori eradication group than the placebo group (42.0% vs. 10.2% [p<0.001]), but there were no serious adverse events reported.
Comment: H. pylori is well known to be associated with gastric cancer and high-grade adenomas. Gastric cancer in and of itself has high mortality, high symptom burden and is difficult to treat as diagnosis usually is at a late stage. Widespread screening for H. pylori and treatment of incident cases in countries with high rates of H. pylori such as those of Southeast Asia have been considered, with prevention of a case of gastric cancer for every 125 patients treated for H. pylori (N Engl J Med 2018;378:1154–6). In N Engl J Med, Choi et al. report results of a randomised placebo-controlled trial with a median follow up of 5.9 years. In this, it was found that H. pylori eradication was effective in the prevention of metachronous (i.e. identified at 1 year) gastric cancer (hazard ratio 0.50) after selective endoscopic removal of early-stage disease. (In this trial, a gastric cancer was defined as ‘metachronous’ if it was detected on endoscopy at 1-year follow-up or later.) One of the most important findings of this study, however, is the improvement in atrophic gastritis in almost 50% of patients in the treatment arm, compared with 15% in the placebo arm, suggesting that eradication of H. pylori may remove the inflammatory stimulus for carcinogenesis.
Reference: N Engl J Med 2018;378:1085–95