{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,18]],"date-time":"2026-05-18T12:09:23Z","timestamp":1779106163664,"version":"3.51.4"},"reference-count":26,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[2013,2,1]],"date-time":"2013-02-01T00:00:00Z","timestamp":1359676800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["AIDS Research and Human Retroviruses"],"published-print":{"date-parts":[[2013,2]]},"abstract":"<jats:p>\n                    To evaluate the course of liver fibrosis, 328 HIV-hepatitis C virus (HCV)-coinfected patients (210 HCV treated and 118 HCV untreated) were followed-up for 38\u201342 months. Liver fibrosis was assessed by biopsy or elastometry at baseline and by elastometry afterward, in addition to other noninvasive indexes. A combined liver stiffness stage (LSS) was established and evaluated over time. Eighty patients had sustained virological response (SVR) and 130 had treatment failure (TF) after a standard course of peginterferon-ribavirin therapy. LSS decreased significantly in all fibrosis indexes during HCV therapy in treated patients, but the improvement persisted only in those with SVR. At the end of study, median elastometry values suffered variations of \u221229%, \u22125.0%, and +15.4% in SVR, TF, and untreated patients, respectively. Likewise, LSS worsened in 2.5%, 33.1%, and 39% of these groups, respectively: [OR (95% CI) 19.3 (4.4\u2013119),\n                    <jats:italic toggle=\"yes\">p<\/jats:italic>\n                    &lt;0.001] for TF vs. SVR; [24.9 (5.6\u2013154),\n                    <jats:italic toggle=\"yes\">p<\/jats:italic>\n                    &lt;0.001] for no therapy vs. SVR; and [1.29 (0.74\u20132.3),\n                    <jats:italic toggle=\"yes\">p<\/jats:italic>\n                    =0.40] for no therapy vs. TF. LSS improved in 53.8%, 19.2%, and 5.9% of these groups, respectively: [4.88 (2.51\u20139.53),\n                    <jats:italic toggle=\"yes\">p<\/jats:italic>\n                    &lt;0.001] for SVR vs. TF; 18.4 (7.17\u201349.4),\n                    <jats:italic toggle=\"yes\">p<\/jats:italic>\n                    &lt;0.001 for SVR vs. no therapy; and 3.78 (1.47\u201310.1),\n                    <jats:italic toggle=\"yes\">p<\/jats:italic>\n                    =0.003 for TF vs. no therapy. Independent predictive factors of LSS improvement or worsening were as follows: alcohol abuse [OR (95% CI) 0.48 (0.20\u20130.99),\n                    <jats:italic toggle=\"yes\">p<\/jats:italic>\n                    =0.047] and [2.45 (1.19\u20135.03),\n                    <jats:italic toggle=\"yes\">p<\/jats:italic>\n                    =0.016], respectively; SVR [27.7 (6.41\u2013168),\n                    <jats:italic toggle=\"yes\">p<\/jats:italic>\n                    &lt;0.001] and [0.15 (0.07\u20130.31),\n                    <jats:italic toggle=\"yes\">p<\/jats:italic>\n                    &lt;0.001], respectively; and lower baseline CD4 counts [1.92 (1.08\u20133.45),\n                    <jats:italic toggle=\"yes\">p<\/jats:italic>\n                    =0.026] and [0.31 (0.15\u20130.63),\n                    <jats:italic toggle=\"yes\">p<\/jats:italic>\n                    =0.001], respectively. SVR was usually associated with regression of noninvasive liver fibrosis markers, whereas TF and HCV-untreated patients experienced poorer outcomes.\n                  <\/jats:p>","DOI":"10.1089\/aid.2012.0108","type":"journal-article","created":{"date-parts":[[2012,6,27]],"date-time":"2012-06-27T11:43:09Z","timestamp":1340797389000},"page":"215-222","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":9,"title":["Course of Liver Fibrosis in HIV-Hepatitis C Virus-Coinfected Patients Depending on the Response to Hepatitis C Therapy"],"prefix":"10.1177","volume":"29","author":[{"given":"Jos\u00e9-Antonio","family":"Cart\u00f3n","sequence":"first","affiliation":[{"name":"Oviedo University School of Medicine","place":["Spain"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Julio","family":"Collazos","sequence":"additional","affiliation":[{"name":"Hospital de Gald\u00e1cano","place":["Spain"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bel\u00e9n","family":"de la Fuente","sequence":"additional","affiliation":[{"name":"Hospital de Cabue\u00f1es","place":["Spain"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"V\u00edctor","family":"Asensi","sequence":"additional","affiliation":[{"name":"Oviedo University School of Medicine","place":["Spain"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2013,2,1]]},"reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jhep.2011.02.023"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1002\/hep.23744"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2893.2009.01087.x"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jhep.2010.07.033"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.3851\/IMP1708"},{"key":"e_1_3_3_7_2","first-page":"504","article-title":"Hepatic elastography. 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