{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T21:06:27Z","timestamp":1791234387361,"version":"4.1.0"},"reference-count":38,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2016,1,7]],"date-time":"2016-01-07T00:00:00Z","timestamp":1452124800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Aliment Pharmacol Ther"],"published-print":{"date-parts":[[2016,3]]},"abstract":"<jats:title>Summary<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Recent animal studies have shown that platelets directly activate hepatic stellate cells to promote liver fibrosis, whereas anti\u2010platelet agents decrease liver fibrosis. It is unknown whether platelet inhibition by aspirin prevents liver fibrosis in humans.<\/jats:p><\/jats:sec><jats:sec><jats:title>Aim<\/jats:title><jats:p>To examine the association between aspirin use and liver fibrosis among adults with suspected chronic liver disease.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We conducted a cross\u2010sectional analysis using data from the National Health and Nutrition Examination Survey <jats:styled-content style=\"fixed-case\">III<\/jats:styled-content>. We identified 1856 individuals with suspected chronic liver disease (<jats:styled-content style=\"fixed-case\">CLD<\/jats:styled-content>). The degree of liver fibrosis was determined using four validated fibrosis indices and a composite index.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The use of aspirin was associated with a significantly lower composite liver fibrosis index calculated from <jats:styled-content style=\"fixed-case\">FIB<\/jats:styled-content>4, <jats:styled-content style=\"fixed-case\">APRI<\/jats:styled-content>, Forns and <jats:styled-content style=\"fixed-case\">NFS<\/jats:styled-content> [0.24 standard deviation (s.d.) units lower; 95% <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content> \u22120.42 to \u22120.06, <jats:italic>P<\/jats:italic> = 0.009]. The association of aspirin with lower fibrosis scores was significantly larger among those with suspected <jats:styled-content style=\"fixed-case\">CLD<\/jats:styled-content> compared to those without (\u22120.23 vs. \u22120.03 s.d. units; <jats:italic>P<\/jats:italic> interaction = 0.05). The negative association between aspirin use and lower fibrosis index was consistent across all four fibrosis indices (<jats:italic>P<\/jats:italic> = 0.002\u20130.08) in individuals with chronic viral hepatitis, suspected alcoholic liver disease and <jats:styled-content style=\"fixed-case\">NASH<\/jats:styled-content>. In comparison, no negative associations with liver fibrosis were seen with ibuprofen in parallel analyses.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>The use of aspirin was associated with significantly lower indices of liver fibrosis among <jats:styled-content style=\"fixed-case\">US<\/jats:styled-content> adults with suspected chronic liver diseases. Aspirin and other anti\u2010platelet drugs warrant further investigation for the prevention and treatment of liver fibrosis.<\/jats:p><\/jats:sec>","DOI":"10.1111\/apt.13515","type":"journal-article","created":{"date-parts":[[2016,1,10]],"date-time":"2016-01-10T09:15:10Z","timestamp":1452417310000},"page":"734-743","source":"Crossref","is-referenced-by-count":99,"title":["Aspirin use is associated with lower indices of liver fibrosis among adults in the United States"],"prefix":"10.1111","volume":"43","author":[{"given":"Z. Gordon","family":"Jiang","sequence":"first","affiliation":[{"name":"Division of Gastroenterology and Hepatology Department of Medicine Beth Israel Deaconess Medical Center Harvard Medical School Boston MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L.","family":"Feldbr\u00fcgge","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology Department of Medicine Beth Israel Deaconess Medical Center Harvard Medical School Boston MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E. B.","family":"Tapper","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology Department of Medicine Beth Israel Deaconess Medical Center Harvard Medical School Boston MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Y.","family":"Popov","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology Department of Medicine Beth Israel Deaconess Medical Center Harvard Medical School Boston MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T.","family":"Ghaziani","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology Department of Medicine Beth Israel Deaconess Medical Center Harvard Medical School Boston MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"N.","family":"Afdhal","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology Department of Medicine Beth Israel Deaconess Medical Center Harvard Medical School Boston MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S. C.","family":"Robson","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology Department of Medicine Beth Israel Deaconess Medical Center Harvard Medical School Boston MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K. 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