There Is No Reason to Delay Helicobacter pylori Eradication after Treatment for Upper Gastrointestinal Bleeding

Correspondence to: Sun-Young Lee Department of Internal Medicine, Konkuk University School of Medicine, 120 Neungdong-ro, Gwangjin-gu, Seoul 143-729, Korea Tel: +82-2-2030-7505, Fax: +82-2-2030-7748, E-mail: [email protected] pISSN 1976-2283 eISSN 2005-1212 http://dx.doi.org/10.5009/gnl14499 Helicobacter pylori is a major cause of peptic ulcer disease (PUD) recurrence, and thus eradication is essential for the treatment of PUD patients with H. pylori infection. Although revised guidelines on H. pylori infection differ between countries due to differences in national health insurance systems, H. pylori eradication is recommended for PUD in the Korean, Japanese, and Chinese guidelines. Data from the Cochrane database show that H. pylori eradication is more effective than antisecretory therapy for preventing recurrent PUD-associated bleeding. Consequently, all patients should be tested for H. pylori infection after hemostasis for PUD-associated bleeding, and eradication should be performed in H. pylori-positive patients. However, there is no evidence regarding the optimal timing of H. pylori eradication in these subjects. In a Taiwanese study by Drs. Chang and Hu reported in this issue of Gut and Liver, H. pylori eradication within 120 days (i.e., early H. pylori eradication therapy) was significantly associated with reduced complicated recurrent PUD in patients with bleeding control. Using the Taiwan National Health Insurance Research Database, those authors found that patients in the late H. pylori eradication therapy group (i.e., H. pylori eradication after 120 days) who were admitted and treated for PUD-associated bleeding in Taiwan between 2000 and 2010 had a higher rate of complicated recurrent PUD. That study is the first large-sized comparison between early and late timing of H. pylori eradication therapy in PUD after bleeding control. Chang and Hu analyzed possible confounding factors from various viewpoints. They excluded patients under the age of 20 years, those with prior gastrectomies or vagotomies, those with cerebral vascular disease, liver cirrhosis, or chronic kidney disease, and those diagnosed with gastric cancer or ZollingerEllison syndrome. With regard to medications, patients were defined as users of proton pump inhibitors (PPIs), histamine 2 (H2)-blockers, aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), cyclooxygenase 2-specific inhibitors, steroids, clopidogrel, ticlopidine, and warfarin. In a recent study of 522 PUD patients with upper gastrointestinal bleeding, rebleeding was more frequent in patients on aspirin medication and after endoscopic hemostasis lasting longer than 13.5 minutes. Notably, in the study by Chang and Hu, the proportion of patients who used PPIs, H2 blockers, or NSAIDs was significantly lower in the early eradication group than in the late eradication group. The authors explained that participants taking PPIs or H2 blockers may have higher risk of PUD-associated bleeding, but this issue requires further clarification. Interestingly, of the significant factors, late H. pylori eradication therapy was an independent risk factor for rehospitalization on multivariate analysis. On the other hand, time delays of more than 1 year did not increase the risk of complicated recurrent PUD. With regard to the diagnosis for H. pylori infection, patients with upper gastrointestinal bleeding frequently exhibit falsenegative findings on H. pylori infection. Furthermore, testing for H. pylori is affected by concomitant medications such as NSAIDs, aspirin, or PPIs. These finding might be attributable to the low percentage of patients who underwent eradication in that study, only 2,463 patients of the 12,686 patients hospitalized with PUD-associated bleeding underwent H. pylori eradication. Neither second look endoscopy nor C-urea breath test was performed to confirm H. pylori status in patients who were initially negative for H. pylori by diagnostic testing. Moreover, the diagnosis of H. pylori infection in the study of Chang and Hu was based on the results of a rapid urease test or histologi-