{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,5]],"date-time":"2026-11-05T02:11:01Z","timestamp":1793844661013,"version":"4.6.1"},"reference-count":37,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2024,9,21]],"date-time":"2024-09-21T00:00:00Z","timestamp":1726876800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2024,9,21]],"date-time":"2024-09-21T00:00:00Z","timestamp":1726876800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100016168","name":"Ludwig Boltzmann Gesellschaft","doi-asserted-by":"publisher","award":["LBG_KFG_22_32"],"award-info":[{"award-number":["LBG_KFG_22_32"]}],"id":[{"id":"10.13039\/501100016168","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Aliment Pharmacol Ther"],"published-print":{"date-parts":[[2025,1]]},"abstract":"<jats:title>Summary<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background and Aims<\/jats:title>\n                    <jats:p>We aimed to characterise insulin\u2010like growth factor\u20101 (IGF\u20101) signalling in patients with advanced chronic liver disease (ACLD).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Consecutive patients undergoing hepatic venous pressure gradient [HVPG] measurement were prospectively included. Clinical stages were defined as follows: probable ACLD (pACLD): liver stiffness \u226510\u2009kPa and HVPG \u22645\u2009mmHg, S0: mild PH (HVPG 6\u20139\u2009mmHg), S1: clinically significant PH (CSPH), S2: CSPH with varices, S3: past variceal bleeding, S4: past\/current non\u2010bleeding hepatic decompensation and S5: further decompensation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      In total, 269 patients were included; 105 were compensated (pACLD:\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200918; S0:\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200930; S1:\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200920; S2:\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200937), and 164 were decompensated (S3:\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200911; S4:\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200989; S5:\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200964). Median levels of IGF\u20101 decreased with progressive cirrhosis (from pACLD: 88.5\u2009ng\/mL to S5: 51.0\u2009ng\/mL;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001). Patients with CSPH had significantly lower IGF\u20101 levels (63.5\u2009ng\/mL vs. 81.0\u2009ng\/mL;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.001). IGF\u20101 showed an independent negative association with body mass index (BMI; aB: \u22121.56;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001), enhanced liver fibrosis (ELF) test (aB: \u22128.43;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001), MELD (aB: \u22121.13;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.042) and age (per 10\u2009years; aB: \u22126.87;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001). IGF\u20101 exhibited an excellent AUROC (0.856) for the prediction of liver\u2010related death at 6\u2009months of follow\u2010up. Lower IGF\u20101 (per 10\u2009ng\/mL) was linked to higher risk of (further) decompensation (0.90; 95% CI: 0.83\u20130.98;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.016), acute\u2010on\u2010chronic liver failure (ACLF; asHR: 0.80; 95% CI: 0.68\u20130.93;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.004) and liver\u2010related death (asHR: 0.76; 95% CI: 0.63\u20130.91;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.004).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Decreased levels of IGF\u20101 reflect impaired hepatic function and fibrogenesis in patients with cirrhosis, which seems particularly relevant in obesity since low IGF\u20101 was independently linked to high BMI. Lower IGF\u20101 in cirrhosis predicts decompensation, ACLF and liver\u2010related death.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/apt.18289","type":"journal-article","created":{"date-parts":[[2024,9,21]],"date-time":"2024-09-21T04:10:37Z","timestamp":1726891837000},"page":"88-98","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Insulin\u2010like growth factor\u20101 in cirrhosis is linked to hepatic dysfunction and fibrogenesis and predicts liver\u2010related mortality"],"prefix":"10.1111","volume":"61","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3398-6120","authenticated-orcid":false,"given":"Lukas","family":"Hartl","sequence":"first","affiliation":[{"name":"Division of Gastroenterology and Hepatology, Department of Medicine III Medical University of Vienna  Vienna Austria"},{"name":"Vienna Hepatic Hemodynamic Lab, Division of Gastroenterology and Hepatology, Department of Medicine III Medical University of Vienna  Vienna Austria"},{"name":"Clinical Research Group MOTION, Division of Gastroenterology and Hepatology, Department of Medicine III Medical University of Vienna  Vienna Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2587-1385","authenticated-orcid":false,"given":"Michael","family":"Schwarz","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology, Department of Medicine III Medical University of Vienna  Vienna Austria"},{"name":"Vienna Hepatic Hemodynamic Lab, Division of Gastroenterology and Hepatology, Department of Medicine III Medical University of Vienna  Vienna Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8181-9146","authenticated-orcid":false,"given":"Benedikt","family":"Simbrunner","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology, Department of Medicine III 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