{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T17:24:55Z","timestamp":1789925095674,"version":"4.0.1"},"reference-count":44,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2018,1,29]],"date-time":"2018-01-29T00:00:00Z","timestamp":1517184000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100006483","name":"AbbVie","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100006483","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100004326","name":"Bayer","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100004326","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002336","name":"Daiichi Sankyo Company","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100002336","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100005564","name":"Gilead Sciences","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100005564","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100009947","name":"Merck Sharp and Dohme","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100009947","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Aliment Pharmacol Ther"],"published-print":{"date-parts":[[2018,4]]},"abstract":"Summary<\/jats:title>Background<\/jats:title>Elevated plasma von Willebrand factor antigen (vWF<\/jats:styled-content>) has been shown to indicate the presence of clinically significant portal hypertension, and thus, predicts the development of clinical events in patients with cirrhosis.<\/jats:p><\/jats:sec>Aim<\/jats:title>To investigate the impact of bacterial translocation and inflammation on vWF<\/jats:styled-content>, as well as the association between vWF<\/jats:styled-content> and procoagulant imbalance. Moreover, we assessed whether vWF<\/jats:styled-content> predicts complications of cirrhosis, independent of the severity of portal hypertension.<\/jats:p><\/jats:sec>Methods<\/jats:title>Our study population comprised 225 patients with hepatic venous pressure gradient (HVPG<\/jats:styled-content>)\u00a0\u2265\u00a010\u00a0mm Hg without active bacterial infections or hepatocellular carcinoma.<\/jats:p><\/jats:sec>Results<\/jats:title>vWF<\/jats:styled-content> correlated with markers of bacterial translocation (lipopolysaccharide\u2010binding protein [LBP<\/jats:styled-content>; \u03c1\u00a0=\u00a00.201; P<\/jats:italic>\u00a0=\u00a00.021]), inflammation (interleukin 6 [IL<\/jats:styled-content>\u20106; \u03c1\u00a0=\u00a00.426; P\u00a0<\/jats:italic><\u00a00.001] and C\u2010reactive protein [CRP<\/jats:styled-content>; \u03c1\u00a0=\u00a00.249; P\u00a0<\/jats:italic><\u00a00.001]), and procoagulant imbalance (factor VIII<\/jats:styled-content>\/protein C ratio; \u03c1\u00a0=\u00a00.507; P\u00a0<\/jats:italic><\u00a00.001). Importantly, the associations between vWF<\/jats:styled-content> and these parameters were independent of HVPG.<\/jats:p>Moreover, vWF<\/jats:styled-content> (per 10%) independently predicted variceal bleeding (hazard ratio [HR<\/jats:styled-content>]: 1.08 [95% confidence interval (95% CI<\/jats:styled-content>): 1.01\u20101.16]; P<\/jats:italic>\u00a0=\u00a00.023), requirement of paracentesis (HR<\/jats:styled-content>: 1.05 [95% CI<\/jats:styled-content>: 1.01\u20101.1]; P<\/jats:italic>\u00a0=\u00a00.023) and bacterial infections (HR<\/jats:styled-content>: 1.04 [95% CI<\/jats:styled-content>: 1\u20101.09]; P<\/jats:italic>\u00a0=\u00a00.04) including spontaneous bacterial peritonitis (HR<\/jats:styled-content>: 1.09 [95% CI<\/jats:styled-content>: 0.999\u20101.18]; P<\/jats:italic>\u00a0=\u00a00.053) on a trend\u2010wise level. After backward elimination, vWF<\/jats:styled-content> (HR<\/jats:styled-content>: 1.05 [95% CI<\/jats:styled-content>: 1.02\u20101.08]; P<\/jats:italic>\u00a0=\u00a00.003) and CRP<\/jats:styled-content> (per 10\u00a0mg\/L; HR<\/jats:styled-content>: 1.53 [95% CI<\/jats:styled-content>: 1.14\u20102.05]; P<\/jats:italic>\u00a0=\u00a00.005) remained in the final model for transplant\u2010free mortality. Finally, the independent prognostic value of vWF<\/jats:styled-content>\/CRP<\/jats:styled-content> groups for mortality was confirmed by competing risk analysis.<\/jats:p><\/jats:sec>Conclusion<\/jats:title>Our results demonstrate that vWF<\/jats:styled-content> is not only a marker of portal hypertension but also independently linked to bacterial translocation, inflammation and procoagulant imbalance, which might explain its HVPG<\/jats:styled-content>\u2010independent association with most clinical events. Prognostic groups based on vWF<\/jats:styled-content>\/CRP<\/jats:styled-content> efficiently discriminate between patients with a poor 5\u2010year survival and patients with a favourable prognosis.<\/jats:p><\/jats:sec>","DOI":"10.1111\/apt.14522","type":"journal-article","created":{"date-parts":[[2018,1,29]],"date-time":"2018-01-29T21:28:29Z","timestamp":1517261309000},"page":"980-988","source":"Crossref","is-referenced-by-count":105,"title":["Von Willebrand factor indicates bacterial translocation, inflammation, and procoagulant imbalance and predicts complications independently of portal hypertension severity"],"prefix":"10.1111","volume":"47","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2330-0017","authenticated-orcid":false,"given":"M.","family":"Mandorfer","sequence":"first","affiliation":[{"name":"Division of Gastroenterology and Hepatology Department of Internal Medicine III Medical University of Vienna Vienna 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