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We identified profiles of liver fibrosis evolution in coinfected patients undergoing tenofovir (TDF).<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We included 169 HIV\u2010HBV\u2010coinfected patients on TDF\u2010based antiretroviral therapy. Virological and clinical data were obtained at TDF\u2010initiation and every 6\u201012\u00a0months. From data on non\u2010invasive liver fibrosis assessments collected yearly (FibroTest\u00ae), we established clusters of individuals with similar liver fibrosis evolution using group\u2010based trajectory models.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Four profiles of liver fibrosis evolution were established from a median follow\u2010up of 7.6\u00a0years (IQR\u00a0=\u00a03.1\u201013.1): low fibrosis with no progression (29.6%, profile A), low fibrosis with progression (22.5%, profile B), moderate fibrosis with high fluctuation (39.6%, profile C), and cirrhosis with no regression (8.3%, profile D). When compared to profile A, baseline HBeAg\u2010positive status was associated with profiles B (<jats:italic>P<\/jats:italic>\u00a0=\u00a0.007) and C (<jats:italic>P<\/jats:italic>\u00a0=\u00a0.004), older age with profiles C (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a0.001) and D (<jats:italic>P<\/jats:italic>\u00a0=\u00a0.001), exposure to second\u2010generation protease inhibitors with profile C (<jats:italic>P<\/jats:italic>\u00a0=\u00a0.004), and CD4<jats:sup>+<\/jats:sup> &lt;500\/mm<jats:sup>3<\/jats:sup> at the last visit with profiles C (<jats:italic>P<\/jats:italic>\u00a0=\u00a0.02) and D (<jats:italic>P<\/jats:italic>\u00a0=\u00a0.002). Incident liver\u2010related events occurred in profiles other than A (B, n\u00a0=\u00a01\/38; C, n\u00a0=\u00a06\/67; D, n\u00a0=\u00a03\/14) and all five cases of hepatocellular carcinoma occurred in profiles C (n\u00a0=\u00a02) and D (n\u00a0=\u00a03).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>TDF\u2010treated HIV\u2010HBV coinfected individuals do not seem to benefit from comparable levels of liver fibrosis regression as in HBV mono\u2010infection. Liver\u2010related morbidity occurs mainly in those with fluctuating or consistently high fibrosis levels.<\/jats:p><\/jats:sec>","DOI":"10.1111\/liv.15019","type":"journal-article","created":{"date-parts":[[2021,7,23]],"date-time":"2021-07-23T13:39:31Z","timestamp":1627047571000},"page":"2874-2884","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Profiles of liver fibrosis evolution during long\u2010term tenofovir treatment in HIV\u2010positive patients coinfected with hepatitis B"],"prefix":"10.1111","volume":"41","author":[{"given":"Lorenza N. 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