{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,13]],"date-time":"2026-02-13T17:26:34Z","timestamp":1771003594908,"version":"3.50.1"},"reference-count":28,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2004,8,10]],"date-time":"2004-08-10T00:00:00Z","timestamp":1092096000000},"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":[[2004,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p><jats:bold>Background and Aim:\u2002<\/jats:bold>  <jats:italic>Helicobacter pylori<\/jats:italic> infection causes hypergastrinemia. This study aimed to determine the association between serum gastrin and the severity of <jats:italic>H.\u2003pylori<\/jats:italic>\u2010related gastric histology.<\/jats:p><jats:p><jats:bold>Methods:\u2002<\/jats:bold> A total of 458 dyspeptic patients were included in this study after the absence of gastric malignancy was confirmed using endoscopy. The gastric specimens of each patient were collected from the antrum and corpus for the analysis of <jats:italic>H.\u2003pylori<\/jats:italic>\u2010related histology changes by updated Sydney's system. Before endoscopy, the fasting blood samples were collected for gastrin analysis.<\/jats:p><jats:p><jats:bold>Results:\u2002<\/jats:bold> The <jats:italic>H.\u2003pylori<\/jats:italic>\u2010infected patients had higher gastrin levels than those without infection (<jats:italic>P\u2003=<\/jats:italic>\u20030.01). Gastrin levels were related to <jats:italic>H.\u2003pylori<\/jats:italic> density and acute and chronic inflammation scores in the corpus mucosa (<jats:italic>P\u2003&lt;<\/jats:italic>\u20030.05), but not in the antral mucosa (<jats:italic>P\u2003=<\/jats:italic>\u2003NS). Gastrin levels were also not related to the presence of gastric atrophy. Multivariate regression showed that the gastrin level was only related to acute corpus inflammation. However, in the patients without infection, the gastrin level was also associated with acute corpus inflammation. Nevertheless, the patients with denser <jats:italic>H.\u2003pylori<\/jats:italic> infection were more likely to have acute corpus gastritis than those with lighter <jats:italic>H.\u2003pylori<\/jats:italic> infection, and thus presented with higher gastrin levels (<jats:italic>P\u2003&lt;<\/jats:italic>\u20030.05).<\/jats:p><jats:p><jats:bold>Conclusions:\u2002<\/jats:bold> The increased level of gastrin of serum after <jats:italic>H.\u2003pylori<\/jats:italic> infection was associated with acute inflammation in the gastric corpus mucosa, but not in the antral mucosa. Denser <jats:italic>H.\u2003pylori<\/jats:italic> infection causes more severe corpus gastritis and thus may lead to a higher fasting level of gastrin of serum.<\/jats:p>","DOI":"10.1111\/j.1440-1746.2004.03416.x","type":"journal-article","created":{"date-parts":[[2004,8,10]],"date-time":"2004-08-10T09:38:46Z","timestamp":1092130726000},"page":"988-993","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Hypergastrinemia after <i>Helicobacter pylori<\/i> infection is associated with bacterial load and related inflammation of the oxyntic corpus mucosa"],"prefix":"10.1111","volume":"19","author":[{"given":"CHIAO\u2010HSIUNG","family":"CHUANG","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"BOR\u2010SHYANG","family":"SHEU","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"HSIAO\u2010BAI","family":"YANG","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"AI\u2010WEN","family":"KAO","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"HSIU\u2010CHI","family":"CHENG","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"WEI\u2010JEN","family":"YAO","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2004,8,10]]},"reference":[{"key":"e_1_2_6_2_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1440-1746.2000.02347.x"},{"key":"e_1_2_6_3_2","doi-asserted-by":"publisher","DOI":"10.3109\/00365529509096340"},{"key":"e_1_2_6_4_2","doi-asserted-by":"publisher","DOI":"10.1097\/00000478-199610000-00001"},{"key":"e_1_2_6_5_2","first-page":"959","article-title":"Helicobacter pylori infection is the major risk factor for atrophic gastritis","volume":"91","author":"Kawaguchi H","year":"1996","journal-title":"Am. 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