{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,11]],"date-time":"2026-06-11T13:04:36Z","timestamp":1781183076725,"version":"3.54.1"},"reference-count":49,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2026,5,22]],"date-time":"2026-05-22T00:00:00Z","timestamp":1779408000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,5,22]],"date-time":"2026-05-22T00:00:00Z","timestamp":1779408000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Liver International"],"published-print":{"date-parts":[[2026,6]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background and Aims<\/jats:title>\n                    <jats:p>Portal\u2010hypertensive gastropathy (PHG) is considered a potential cause of chronic bleeding and anaemia in patients with advanced chronic liver disease (ACLD) and might represent an endoscopic reflection of an impaired gut\u2010liver axis associated with portal hypertension. The clinical significance of PHG in patients with ACLD undergoing routine endoscopies remains understudied.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>PHG was classified as absent, mild, or severe in prospectively recruited ACLD patients undergoing routine endoscopy (i.e., variceal screening) in the absence of acute bleeding between Q2\/2017\u2010Q3\/2023. PHG severity was correlated with liver disease severity, systemic inflammation, anaemia, and development of non\u2010variceal bleeding, decompensation or liver\u2010related death during follow\u2010up.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Among 324 patients included in the study, 68 (21%) had no PHG, 190 (58.6%) mild, and 66 (20.4%) severe PHG. Increasing PHG severity was associated with higher MELD (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001), hepatic venous pressure gradient (HVPG,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001), presence of varices (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.001), and elevated IL\u20106 levels (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001). Iron deficiency anaemia occurred at similar frequencies in patients with mild (24.2%) and severe PHG (31.8%). PHG evaluation was not confounded by the presence of histological gastritis or proton pump inhibitor use. During a median follow\u2010up of 17.6\u2009months, severe PHG was not associated with an increased risk of non\u2010variceal gastrointestinal bleeding, transfusion\u2010dependent anaemia, or bacterial infections. Severe PHG was associated with a higher incidence of hepatic decompensation and liver\u2010related mortality (HR\u2009=\u20091.64;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.015). However, severe PHG was not an independent risk factor for hepatic decompensation and liver\u2010related death (aHR: 1.12;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.727) when adjusted for portal hypertension (HVPG; aHR: 1.07;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.007) and liver dysfunction (MELD; aHR: 1.05;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.123).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>In stable patients with ACLD undergoing routine endoscopy, the presence and severity of PHG reflect portal hypertension, liver disease severity, and systemic inflammation. However, PHG does not represent an independent risk factor for liver disease progression when adjusted for established markers of portal hypertension and hepatic dysfunction.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Trial Registration<\/jats:title>\n                    <jats:p>NCT03267615<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/liv.70700","type":"journal-article","created":{"date-parts":[[2026,5,23]],"date-time":"2026-05-23T04:30:37Z","timestamp":1779510637000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["The Link of Portal\u2010Hypertensive Gastropathy to Anaemia, Systemic Inflammation and Disease Progression in Cirrhosis"],"prefix":"10.1111","volume":"46","author":[{"given":"Nikolaus","family":"Pfisterer","sequence":"first","affiliation":[{"name":"Division of Gastroenterology and Hepatology, Department of Medicine III Medical University of Vienna  Vienna Austria"},{"name":"Hepatic Hemodynamic Laboratory Medical University of Vienna  Vienna Austria"},{"name":"Klinik Landstrasse 4. 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