{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,7,27]],"date-time":"2024-07-27T21:57:07Z","timestamp":1722117427668},"reference-count":19,"publisher":"Walter de Gruyter GmbH","issue":"3","license":[{"start":{"date-parts":[[2017,9,1]],"date-time":"2017-09-01T00:00:00Z","timestamp":1504224000000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/3.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2017,9,30]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec id=\"j_jtim-2017-0028_s_006_w2aab3b7b8b1b6b1aab1c17b1Aa\">\n                  <jats:title id=\"d248999e15382_w2aab3b7b8b1b6b1aab1c17b1aAa\">Objective<\/jats:title>\n                  <jats:p>To elucidate the mechanism of an increase in the albumin levels by daclatasvir (DCV)\/asunaprevir (ASV) therapy, we assessed the factors associated with an increase in the albumin levels.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec id=\"j_jtim-2017-0028_s_007_w2aab3b7b8b1b6b1aab1c17b2Aa\">\n                  <jats:title id=\"d248999e15390_w2aab3b7b8b1b6b1aab1c17b2aAa\">Methods<\/jats:title>\n                  <jats:p>We retrospectively analyzed 125 patients with chronic hepatitis C virus (HCV) infection, treated with DCV\/ASV from November 2014 to January 2016.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec id=\"j_jtim-2017-0028_s_008_w2aab3b7b8b1b6b1aab1c17b3Aa\">\n                  <jats:title id=\"d248999e15398_w2aab3b7b8b1b6b1aab1c17b3aAa\">Results<\/jats:title>\n                  <jats:p>Albumin levels significantly increased from 4.0 \u00b1 0.4 g\/dL at baseline to 4.2 \u00b1 0.4 g\/dL at 24 weeks after the end of treatment (EOT) (<jats:italic>P<\/jats:italic> &lt; 0.0001) in 108 patients with SVR. Patients with SVR were divided into three groups according to their baseline albumin levels: group A, \u2265 4 g\/dL; group B, 3.6\u20133.9 g\/dL; and group C, \u2264 3.5 g\/dL. The increase in albumin levels from baseline to at 24 weeks after EOT was significantly larger in group C (0.5 \u00b1 0.5 g\/dL, <jats:italic>P<\/jats:italic> &lt; 0.0001) and group B (0.2 \u00b1 0.4 g\/dL, <jats:italic>P<\/jats:italic> = 0.0059) than in group A (0.0 \u00b1 0.3 g\/dL). Multivariate analysis showed that aspartate transaminase (AST) levels was the only factor associated with \u2265 0.3 g\/dL increase in albumin levels in groups B and C (<jats:italic>P<\/jats:italic> = 0.0305). An increase in albumin levels was significantly correlated with a decrease in AST levels (<jats:italic>r<\/jats:italic> = 0.4729, <jats:italic>P<\/jats:italic> = 0.0119).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec id=\"j_jtim-2017-0028_s_009_w2aab3b7b8b1b6b1aab1c17b4Aa\">\n                  <jats:title id=\"d248999e15425_w2aab3b7b8b1b6b1aab1c17b4aAa\">Conclusion<\/jats:title>\n                  <jats:p>DCV\/ASV therapy resulted in an increase in albumin levels in SVR patients, which was significantly correlated with a decrease in AST levels. It is probable that the reduction of inflammation, but not by reduction of fibrosis, mainly caused an increase in albumin levels.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1515\/jtim-2017-0028","type":"journal-article","created":{"date-parts":[[2017,10,10]],"date-time":"2017-10-10T10:01:12Z","timestamp":1507629672000},"page":"148-154","source":"Crossref","is-referenced-by-count":2,"title":["Increase in albumin by daclatasvir\/asunaprevir therapy is correlated with decrease in aspartate transaminase"],"prefix":"10.1515","volume":"5","author":[{"given":"Toshiki","family":"Kan","sequence":"first","affiliation":[{"name":"Department of Liver, Biliary Tract and Pancreas Diseases , Fujita Health University , Aichi 470-1192 , Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Senju","family":"Hashimoto","sequence":"additional","affiliation":[{"name":"Department of Liver, Biliary Tract and Pancreas Diseases , Fujita Health University , Aichi 470-1192 , Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Naoto","family":"Kawabe","sequence":"additional","affiliation":[{"name":"Department of Liver, Biliary Tract and Pancreas Diseases , Fujita Health University , Aichi 470-1192 , Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Takuji","family":"Nakano","sequence":"additional","affiliation":[{"name":"Department of Liver, Biliary Tract and Pancreas Diseases , Fujita Health University , Aichi 470-1192 , Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kazunori","family":"Nakaoka","sequence":"additional","affiliation":[{"name":"Department of Liver, Biliary Tract and Pancreas Diseases , Fujita Health University , Aichi 470-1192 , Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kentaro","family":"Yoshioka","sequence":"additional","affiliation":[{"name":"Department of Liver, Biliary Tract and Pancreas Diseases , Fujita Health University , Aichi 470-1192 , Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"374","published-online":{"date-parts":[[2017,9,30]]},"reference":[{"key":"2023042508120841211_j_jtim-2017-0028_ref_001_w2aab3b7b8b1b6b1ab1b5b1Aa","doi-asserted-by":"crossref","unstructured":"Niederau C, Lange S, Heintges T, Erhardt A, Buschkamp M, Hurter D, et al. 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