pylori eradication, even in the absence of gastroprotective treatment selleck compound [7]. Despite these findings, further studies are needed to confirm
whether this strategy is a (cost-) effective therapy to reduce ulcer bleeding in high-risk aspirin users. A prospective 10-year cohort study from Hong Kong assessed whether testing for H. pylori in aspirin users with a high ulcer risk would reduce the long-term incidence of ulcer bleeding [8]. The investigators divided patients into three different cohorts. The first included H. pylori-positive aspirin users with a PUB history in whom H. pylori had been eradicated (n = 249). The second group consisted of H. pylori-negative aspirin users with a PUB history (n = 118). The third group, assigned as average-risk cohort, included aspirin users without a history of ulcers (n = 537). The incidence of ulcer bleeding (per 100 patient-years) in the H. pylori-eradicated cohort (OR 0.97; 95% CI 0.53–1.80) was similar to the average-risk cohort (OR 0.66; 95% CI 0.38–0.99). On the other hand, the H. pylori-negative cohort had a high incidence of recurrent bleeding (OR 5.22; 95% CI learn more 3.04–8.96). This confirms that the long-term incidence of recurrent ulcer bleeding with aspirin use is low after H. pylori eradication despite a history
of ulcer bleeding. Aspirin users without current or past H. pylori infection who develop ulcer bleeding, however, have a high risk of recurrent bleeding. Tests for H. pylori infection can be used to assign high-risk aspirin MCE users to groups that require different gastroprotective strategies, in particular, patients with a positive
test for H. pylori should receive anti-H. pylori therapy followed by confirmation of eradication. Their need for long-term gastroprotective therapy depends on the success of H. pylori eradication and concomitant use of drugs that can cause bleeding. However, H. pylori-negative patients should receive adequate gastroprotective co-therapy if they have a history of ulcer because they are prone to ulcer bleeding with aspirin use. Gastroesophageal reflux disease (GERD) is a highly prevalent condition in the general population. Although it has previously been suggested that H. pylori eradication may cause both reflux symptoms and erosive esophagitis, the existence of such an association remains largely unsubstantiated. A meta-analysis of 10 trials in which data of patients treated for H. pylori infection were compared to those receiving placebo concluded that the post-treatment incidence of reflux symptoms (17 vs 22.6%) and erosive esophagitis (5 vs 5.1%) was similar between both groups [9]. A further subanalysis revealed a significantly lower incidence of GERD symptoms in the eradicated versus noneradicated group (13.8 vs 24.9%) (OR 0.55; 95% CI 0.35–0.87, p = .01). Overall, these data suggest that H.
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