{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T00:29:53Z","timestamp":1783470593187,"version":"3.55.0"},"reference-count":47,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2013,8,22]],"date-time":"2013-08-22T00:00:00Z","timestamp":1377129600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Gastro and Hepatol"],"published-print":{"date-parts":[[2013,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background and Aims<\/jats:title><jats:p>Bleeding from esophageal and gastric varices is a fatal event in patients with liver cirrhosis and portal hypertension. However, the effects of <jats:italic><jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>elicobacter pylori<\/jats:italic> (<jats:italic><jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>.\u2009pylori<\/jats:italic>) infection on esophagogastric variceal bleeding are not known. The present study was aimed to elucidate the role of <jats:italic><jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>.\u2009pylori<\/jats:italic> infection in esophagogastric variceal bleeding.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>The subjects were 196 cirrhotic patients who were admitted to the <jats:styled-content style=\"fixed-case\">K<\/jats:styled-content>urume <jats:styled-content style=\"fixed-case\">U<\/jats:styled-content>niversity <jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>ospital to treat their esophagogastric varices consisted of 95 with acute bleeding and 101 with nonbleeding but high risk of bleeding. For the diagnosis of <jats:italic><jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>.\u2009pylori<\/jats:italic> infection, a <jats:sup>13<\/jats:sup>C\u2010urea breath test was used, and serum pepsinogen (<jats:styled-content style=\"fixed-case\">PG<\/jats:styled-content>) I and II levels and the <jats:styled-content style=\"fixed-case\">PG<\/jats:styled-content> I\/II ratio were also measured.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Esophagogastric variceal bleeding was seen in 34.9% (<jats:italic>n<\/jats:italic>\u2009=\u200930) of the <jats:italic><jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>.\u2009pylori<\/jats:italic>\u2010infected patients (<jats:italic>n<\/jats:italic>\u2009=\u200986) and in 59.1% (<jats:italic>n<\/jats:italic>\u2009=\u200965) of the noninfected patients (<jats:italic>n<\/jats:italic>\u2009=\u2009110) (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.0007). There was no significant difference in the infection rate between the bleeding sites of the esophagus and the stomach. The serum <jats:styled-content style=\"fixed-case\">PG<\/jats:styled-content> I and II levels and the <jats:styled-content style=\"fixed-case\">PG<\/jats:styled-content> I\/II ratio were 65.6\u2009ng\/<jats:styled-content style=\"fixed-case\">dL<\/jats:styled-content>, 14.7\u2009ng\/<jats:styled-content style=\"fixed-case\">dL<\/jats:styled-content>, and 4.4, respectively, for the bleeding patients (<jats:italic>n<\/jats:italic>\u2009=\u200995), and 43.7\u2009ng\/<jats:styled-content style=\"fixed-case\">dL<\/jats:styled-content>, 17.7\u2009ng\/<jats:styled-content style=\"fixed-case\">dL<\/jats:styled-content>, and 3.1 for the nonbleeding patients (<jats:italic>n<\/jats:italic>\u2009=\u2009101). Thus, the nonbleeding patients had significantly higher rate of <jats:italic><jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>.\u2009pylori<\/jats:italic> infection and lower acid secretion than bleeding patients (0.001). In addition, multivariate logistic regression analysis showed a significant negative association between <jats:italic><jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>.\u2009pylori<\/jats:italic> infection and esophagogastric variceal bleeding.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>These results suggest that <jats:italic><jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>.\u2009pylori<\/jats:italic> infection has a protective effect against esophagogastric variceal bleeding through the induction of gastric mucosal atrophy and concomitant hypoacidity.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jgh.12221","type":"journal-article","created":{"date-parts":[[2013,4,12]],"date-time":"2013-04-12T10:59:57Z","timestamp":1365764397000},"page":"1444-1449","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Effect of <i><scp>H<\/scp>elicobacter pylori<\/i> 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