Sixty studies (with 66 treatment arms) comprising a total of 4,329 patients were included in the review.
H. pylori eradication improved ulcer healing by 15 to 20%, regardless of diagnoses (GU, DU or PU). The OR was 2.7 (95% CI: 1.3, 5.4, p<0.01) for GU, 5.1 (95% CI: 4, 6.5, p<0.0001) for DU, and 6.6 (95% CI: 4.1, 10.6, p<0.0001) for PU.
Gastric acid suppression by normal or high doses of antisecretory drugs combined with H. pylori treatment provides better results (11% difference) only if therapy fails. Normal and high doses of antisecretory drugs gave ORs of 4.4 (95% CI: 3.3, 5.8, p<0.0001) and 6.5 (95% CI: 3.8, 10.9, p<0.0001), respectively, for all ulcer types.
The results from prolonged acid suppression treatment (extending the initial eradication phase) revealed that only those patients who had prolonged acid inhibition in initially normal or high doses, and who had had eradication failure at the end of evaluation, had an increase in PU healing (approximately 15% difference). The subgroup of patients remaining infected, who had had eradication therapy with missing acid suppression, had no benefit from subsequent prolonged acid inhibition. If the infection was cured by using high-dose acid suppression (mainly dual therapy), ulcer healing was 13% lower in H. pylori-negative patients, if not supported by additional prolonged acid suppression. The ulcer healing rate, however, was still better (20% benefit) than in those patients in whom the infection was not cured.
PU healing rates were better in patients successfully treated for H. pylori, regardless of the time point considered (range: 13 to 25%).
There was a positive correlation between PU healing and H. pylori eradication (correlation coefficient, r=0.539, p<0.0001). This relationship also existed for studies with no prolonged acid inhibition after initial eradication (r=0.667, p<0.001).