{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T06:31:59Z","timestamp":1790836319745,"version":"4.1.0"},"reference-count":50,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2017,12,28]],"date-time":"2017-12-28T00:00:00Z","timestamp":1514419200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100004191","name":"Novo Nordisk","doi-asserted-by":"publisher","award":["NNF13OC0006561"],"award-info":[{"award-number":["NNF13OC0006561"]}],"id":[{"id":"10.13039\/501100004191","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003035","name":"Aase og Ejnar Danielsens Fond","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100003035","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000329","name":"Novo Nordisk UK Research Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000329","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Gastro and Hepatol"],"published-print":{"date-parts":[[2018,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background and Aim<\/jats:title><jats:p>Decompensated cirrhosis is characterized by disturbed hemodynamics, immune dysfunction, and high risk of infections. Translocation of viable bacteria and bacterial products from the gut to the blood is considered a key driver in this process. Intestinal decontamination with rifaximin may reduce bacterial translocation (BT) and decrease inflammation. A randomized, placebo\u2010controlled trial investigated the effects of rifaximin on inflammation and BT in decompensated cirrhosis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Fifty\u2010four out\u2010patients with cirrhosis and ascites were randomized, mean age 56\u00a0years (\u00b1\u00a08.4), and model for end\u2010stage liver disease score 12 (\u00b1\u00a03.9). Patients received rifaximin 550\u2010mg BD (<jats:italic>n<\/jats:italic>\u00a0=\u00a036) or placebo BD (<jats:italic>n<\/jats:italic>\u00a0=\u00a018). Blood and fecal (<jats:italic>n<\/jats:italic>\u00a0=\u00a015) sampling were conducted at baseline and after 4\u00a0weeks. Bacterial DNA in blood was determined by real\u2010time qPCR 16S rRNA gene quantification. Bacterial composition in feces was analyzed by 16S rRNA gene sequencing.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Circulating markers of inflammation, including tumor necrosis factor alpha, interleukins 6, 10, and 18, stromal cell\u2010derived factor 1\u2010\u03b1, transforming growth factor \u03b2\u20101, and high sensitivity C\u2010reactive protein, were unaltered by rifaximin treatment. Rifaximin altered abundance of bacterial taxa in blood marginally, only a decrease in <jats:italic>Pseudomonadales<\/jats:italic> was observed. In feces, rifaximin decreased bacterial richness, but effect on particular species was not observed. Subgroup analyses on patients with severely disturbed hemodynamics (<jats:italic>n<\/jats:italic>\u00a0=\u00a034) or activated lipopolysaccharide binding protein (<jats:italic>n<\/jats:italic>\u00a0=\u00a037) revealed no effect of rifaximin.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Four weeks of treatment with rifaximin had no impact on the inflammatory state and only minor effects on BT and intestinal bacterial composition in stable, decompensated cirrhosis (NCT01769040).<\/jats:p><\/jats:sec>","DOI":"10.1111\/jgh.13852","type":"journal-article","created":{"date-parts":[[2017,7,3]],"date-time":"2017-07-03T13:13:17Z","timestamp":1499087597000},"page":"307-314","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":56,"title":["Rifaximin has minor effects on bacterial composition, inflammation, and bacterial translocation in cirrhosis: A randomized trial"],"prefix":"10.1111","volume":"33","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4807-1575","authenticated-orcid":false,"given":"Nina","family":"Kimer","sequence":"first","affiliation":[{"name":"Gastro Unit, Medical Division Copenhagen University Hospital Hvidovre  Hvidovre Denmark"},{"name":"Centre of Diagnostic Imaging and Research, Department of Clinical Physiology and Nuclear Medicine Copenhagen University Hospital Hvidovre  Hvidovre Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julie S","family":"Pedersen","sequence":"additional","affiliation":[{"name":"Gastro Unit, Medical Division Copenhagen University Hospital Hvidovre  Hvidovre Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Juliette","family":"Tavenier","sequence":"additional","affiliation":[{"name":"Clinical Research Centre Copenhagen University Hospital Hvidovre  Hvidovre Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeffrey E","family":"Christensen","sequence":"additional","affiliation":[{"name":"Vaiomer SAS  Toulouse France"},{"name":"Institute of Cardiovascular and Metabolic Diseases (I2MC), INSERM U1048  Toulouse France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Troels M","family":"Busk","sequence":"additional","affiliation":[{"name":"Centre of Diagnostic Imaging and Research, Department of Clinical Physiology and Nuclear Medicine Copenhagen University Hospital Hvidovre  Hvidovre Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lise","family":"Hobolth","sequence":"additional","affiliation":[{"name":"Gastro Unit, Medical Division Copenhagen University Hospital Hvidovre  Hvidovre Denmark"},{"name":"Department of Gastroenterology and Hepatology Copenhagen University Hospital Bispebjerg  Bispebjerg Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aleksander","family":"Krag","sequence":"additional","affiliation":[{"name":"Department of 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