{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,27]],"date-time":"2025-12-27T07:24:01Z","timestamp":1766820241827,"version":"3.40.5"},"reference-count":30,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2019,6,14]],"date-time":"2019-06-14T00:00:00Z","timestamp":1560470400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Gastro and Hepatol"],"published-print":{"date-parts":[[2019,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background and Aim<\/jats:title><jats:p>The nuclear farnesoid X receptor (FXR) regulates critical pathways of hepatic metabolism, inflammation, and gut mucosal barrier. Thus, we investigated the association of FXR\u2010single nucleotide polymorphism (SNPs) with hepatic decompensation and liver\u2010related mortality in patients with advanced chronic liver disease.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Two FXR\u2010SNPs (<jats:italic>rs56163822<\/jats:italic> G\u00a0&gt;\u00a0T and <jats:italic>rs35724<\/jats:italic> G\u00a0&gt;\u00a0C) were genotyped in a cohort of 402 prospectively characterized patients with hepatic venous pressure gradient (HVPG) \u2265\u00a06\u00a0mmHg.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Only 19 patients (4.7%) harbored a <jats:italic>rs56163822<\/jats:italic> T\u2010allele and had less pronounced liver disease as indicated by lower Child\u2013Pugh score (CPS, 6\u00a0\u00b1\u00a01 <jats:italic>vs<\/jats:italic> 7\u00a0\u00b1\u00a02 points, <jats:italic>P<\/jats:italic>\u00a0=\u00a00.034) and higher albumin levels (38.9\u00a0\u00b1\u00a04.9 <jats:italic>vs<\/jats:italic> 35.9\u00a0\u00b1\u00a05.9\u00a0g\/L, <jats:italic>P<\/jats:italic>\u00a0=\u00a00.026). In contrast, <jats:italic>n<\/jats:italic>\u00a0=\u00a0267 (66.4%) patients harbored minor <jats:italic>rs35724<\/jats:italic> allele (G\/C or C\/C) and had more advanced liver disease, as indicated by a higher model of end\u2010stage liver disease (11\u00a0\u00b1\u00a04 <jats:italic>vs<\/jats:italic> 10\u00a0\u00b1\u00a03, <jats:italic>P<\/jats:italic>\u00a0=\u00a00.016), while other baseline characteristics were similar across FXR\u2010SNP genotypes. In compensated CPS\u2010A patients, the <jats:italic>rs35724<\/jats:italic> minor allele was independently protective for the development of ascites (adjusted hazard ratio [aHR]\u00a0=\u00a00.411, 95% confidence interval (95% CI): 0.191\u20130.885; <jats:italic>P<\/jats:italic>\u00a0=\u00a00.023) and tended to reduce the risk of hepatic decompensation (aHR\u00a0=\u00a00.625, 95% CI: 0.374\u20131.044, <jats:italic>P<\/jats:italic>\u00a0=\u00a00.072) in multivariate analyses. Of note, transplant\u2010free survival was longer in patients with <jats:italic>rs35724<\/jats:italic> minor allele and HVPG\u00a0\u2265\u00a010\u00a0mmHg (at 5\u00a0years: 68.2% <jats:italic>vs<\/jats:italic> 55.8%, <jats:italic>P<\/jats:italic>\u00a0=\u00a00.047) and those with HVPG\u00a0\u2265\u00a016\u00a0mmHg (63.3% <jats:italic>vs<\/jats:italic> 44.0%, <jats:italic>P<\/jats:italic>\u00a0=\u00a00.021). After adjusting for established risk factors, the <jats:italic>rs35724<\/jats:italic> minor allele was independently associated with reduced liver\u2010related mortality in the overall cohort (aHR\u00a0=\u00a00.658, 95% CI: 0.434\u20130.998, <jats:italic>P<\/jats:italic>\u00a0=\u00a00.049), in compensated CPS\u2010A patients (aHR\u00a0=\u00a00.488, 95% CI: 0.252\u20130.946, <jats:italic>P<\/jats:italic>\u00a0=\u00a00.034), in patients with HVPG\u00a0\u2265\u00a010\u00a0mmHg (aHR\u00a0=\u00a00.547, 95% CI: 0.346\u20130.864, <jats:italic>P<\/jats:italic>\u00a0=\u00a00.010), and in patients with HVPG\u00a0\u2265\u00a016\u00a0mmHg (aHR\u00a0=\u00a00.519, 95% CI: 0.307\u20130.878, <jats:italic>P<\/jats:italic>\u00a0=\u00a00.014).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>The FXR\u2010SNP <jats:italic>rs35724<\/jats:italic> was associated with a reduced risk for development of ascites and liver\u2010related mortality in patients with advanced chronic liver disease.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jgh.14700","type":"journal-article","created":{"date-parts":[[2019,5,7]],"date-time":"2019-05-07T00:53:08Z","timestamp":1557190388000},"page":"2164-2172","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Impact of farnesoid X receptor single nucleotide polymorphisms on hepatic decompensation and mortality in cirrhotic patients with portal hypertension"],"prefix":"10.1111","volume":"34","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0411-166X","authenticated-orcid":false,"given":"Georg","family":"Semmler","sequence":"first","affiliation":[{"name":"Division of Gastroenterology and Hepatology, Department of Internal Medicine III Medical University of Vienna  Vienna Austria"},{"name":"Vienna Hepatic Hemodynamic Lab Medical University of Vienna  Vienna 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Internal Medicine III Medical University of Vienna  Vienna Austria"},{"name":"Vienna Hepatic Hemodynamic Lab Medical University of Vienna  Vienna Austria"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1813-5769","authenticated-orcid":false,"given":"Rafael","family":"Paternostro","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology, Department of Internal Medicine III Medical University of Vienna  Vienna Austria"},{"name":"Vienna Hepatic Hemodynamic Lab Medical University of Vienna  Vienna Austria"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3901-4111","authenticated-orcid":false,"given":"Theresa","family":"Bucsics","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology, Department of Internal Medicine III Medical University of Vienna  Vienna Austria"},{"name":"Vienna Hepatic Hemodynamic Lab Medical University of 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