Hypovascular tumors developed into hepatocellular carcinoma at a high rate despite the elimination of hepatitis C virus by direct-acting antivirals
Background and aims Direct-acting antivirals (DAAs) against hepatitis C virus (HCV) exert high anti-HCV activity and are expected to show anti-inflammatory effects associated with HCV elimination. Furthermore, hepatocellular carcinoma (HCC) is known to dedifferentiate from hypovascular tumors, such...
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| Veröffentlicht in: | PloS one 2020-08, Vol.15 (8), p.e0237475 |
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| creator | Tabu, Kazuaki Mawatari, Seiichi Oda, Kohei Kumagai, Kotaro Inada, Yukiko Uto, Hirofumi Saisyoji, Akiko Hiramine, Yasunari Hashiguchi, Masafumi Tamai, Tsutomu Hori, Takeshi Fujisaki, Kunio Imanaka, Dai Kure, Takeshi Taniyama, Ohki Toyodome, Ai Ijuin, Sho Sakae, Haruka Sakurai, Kazuhiro Moriuchi, Akihiro Kanmura, Shuji Ido, Akio Kanda, Tatsuo |
| description | Background and aims Direct-acting antivirals (DAAs) against hepatitis C virus (HCV) exert high anti-HCV activity and are expected to show anti-inflammatory effects associated with HCV elimination. Furthermore, hepatocellular carcinoma (HCC) is known to dedifferentiate from hypovascular tumors, such as dysplastic nodules or well-differentiated HCC, to hypervascular tumors. We therefore explored whether or not DAAs can suppress the growth and hypervascularization of hypovascular tumors. Methods We enrolled 481 patients with HCV genotype 1 infection who were treated with Daclatasvir and Asunaprevir therapy. Of these, 29 patients had 33 hypovascular tumors, which were confirmed by contrast-enhanced MRI or CT before therapy. We prospectively analyzed the cumulative incidence of HCC, i.e. the growth or hypervascularization of hypovascular tumors, and compared the HCC development rates between patients with hypovascular tumors and those without any tumors. Results The mean size of the hypovascular tumors was 11.3 mm. Twenty seven of 29 patients who achieved an SVR had 31 nodules, 19 of 31 nodules (61.3%) showed tumor growth or hypervascularization, and 12 (38.7%) nodules showed no change or improvement. The cumulative incidence rates of tumor growth or hypervascularization were 19.4% at 1 year, 36.0% at 2 years, 56.6% at 3 years, and 65.3% at 4 years. Among the patients who achieved a sustained virologic response, the cumulative HCC development rates of patients with hypovascular tumors was significantly higher than in those without any tumors. A Cox proportional hazard analysis showed that a history of HCC therapy, the presence of a hypovascular tumor, and AFP >4.6 ng/mL at the end of treatment were independent risk factors for HCC development. Conclusion Hypovascular tumors developed into HCC at a high rate despite the elimination of HCV by DAAs. As patients with hypovascular tumors were shown to have a high risk of HCC development, they should undergo strict HCC surveillance. |
| doi_str_mv | 10.1371/journal.pone.0237475 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_plos_</sourceid><recordid>TN_cdi_plos_journals_2434078683</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A632403005</galeid><doaj_id>oai_doaj_org_article_77e19cc7fd2f44569864b15ba39951ef</doaj_id><sourcerecordid>A632403005</sourcerecordid><originalsourceid>FETCH-LOGICAL-c669t-4d5228cdf180222633c64f517e7e334e8c396378f89400aaaca3204c73d26d733</originalsourceid><addsrcrecordid>eNqNk9-LEzEQxxdRvLP6HwgGhAMfWrNJNtl9EY6iXuHgwF-vYZqd7absbtYkW-zf4T9seq1yBQXJw4SZz3wzGWay7GVOFzlX-dutm_wA3WJ0Ay4o40qo4lF2mVeczSWj_PGD-0X2LIQtpQUvpXyaXXCmKqpYeZn9vNmPbgfBTB14Eqfe-UBq3GHnRqyJHaIjLY4QncGuu4cMeGMH1wOBSIC0dtMSDxFTWhhtsrFFgp3t7QDRuoG45ihhow1kSXbWT4Gs96S2Hk2cg4l22BAYok0h6MLz7EmTDL442Vn29cP7L8ub-e3dx9Xy-nZupKziXNQFY6Wpm7ykjDHJuZGiKXKFCjkXWBpeSa7KpqwEpQBggDMqjOI1k7XifJa9OuqOnQv61M-gmeCCqlKWB2J1JGoHWz1624PfawdW3zuc32jw0ZoOtVKYV8aopmaNEIWsSinWebEGXlVFjk3Send6bVr3WBscYvrsmeh5ZLCt3ridVoIVpZJJ4PVJwLvvE4b4j5JP1AZSVXZoXBIzvQ1GX0vOBOWHMZhli79Q6dTYW5MmqrHJf5bw5iwhMRF_xA1MIejV50__z959O2evHrAtQhfb4LrpMDjhHBRH0HgXgsfmT-dyqg8L8bsb-rAQ-rQQ_Be_qv4B</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2434078683</pqid></control><display><type>article</type><title>Hypovascular tumors developed into hepatocellular carcinoma at a high rate despite the elimination of hepatitis C virus by direct-acting antivirals</title><source>Public Library of Science (PLoS) Journals Open Access</source><source>DOAJ Directory of Open Access Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><creator>Tabu, Kazuaki ; Mawatari, Seiichi ; Oda, Kohei ; Kumagai, Kotaro ; Inada, Yukiko ; Uto, Hirofumi ; Saisyoji, Akiko ; Hiramine, Yasunari ; Hashiguchi, Masafumi ; Tamai, Tsutomu ; Hori, Takeshi ; Fujisaki, Kunio ; Imanaka, Dai ; Kure, Takeshi ; Taniyama, Ohki ; Toyodome, Ai ; Ijuin, Sho ; Sakae, Haruka ; Sakurai, Kazuhiro ; Moriuchi, Akihiro ; Kanmura, Shuji ; Ido, Akio ; Kanda, Tatsuo</creator><contributor>Kanda, Tatsuo</contributor><creatorcontrib>Tabu, Kazuaki ; Mawatari, Seiichi ; Oda, Kohei ; Kumagai, Kotaro ; Inada, Yukiko ; Uto, Hirofumi ; Saisyoji, Akiko ; Hiramine, Yasunari ; Hashiguchi, Masafumi ; Tamai, Tsutomu ; Hori, Takeshi ; Fujisaki, Kunio ; Imanaka, Dai ; Kure, Takeshi ; Taniyama, Ohki ; Toyodome, Ai ; Ijuin, Sho ; Sakae, Haruka ; Sakurai, Kazuhiro ; Moriuchi, Akihiro ; Kanmura, Shuji ; Ido, Akio ; Kanda, Tatsuo ; Kanda, Tatsuo</creatorcontrib><description>Background and aims Direct-acting antivirals (DAAs) against hepatitis C virus (HCV) exert high anti-HCV activity and are expected to show anti-inflammatory effects associated with HCV elimination. Furthermore, hepatocellular carcinoma (HCC) is known to dedifferentiate from hypovascular tumors, such as dysplastic nodules or well-differentiated HCC, to hypervascular tumors. We therefore explored whether or not DAAs can suppress the growth and hypervascularization of hypovascular tumors. Methods We enrolled 481 patients with HCV genotype 1 infection who were treated with Daclatasvir and Asunaprevir therapy. Of these, 29 patients had 33 hypovascular tumors, which were confirmed by contrast-enhanced MRI or CT before therapy. We prospectively analyzed the cumulative incidence of HCC, i.e. the growth or hypervascularization of hypovascular tumors, and compared the HCC development rates between patients with hypovascular tumors and those without any tumors. Results The mean size of the hypovascular tumors was 11.3 mm. Twenty seven of 29 patients who achieved an SVR had 31 nodules, 19 of 31 nodules (61.3%) showed tumor growth or hypervascularization, and 12 (38.7%) nodules showed no change or improvement. The cumulative incidence rates of tumor growth or hypervascularization were 19.4% at 1 year, 36.0% at 2 years, 56.6% at 3 years, and 65.3% at 4 years. Among the patients who achieved a sustained virologic response, the cumulative HCC development rates of patients with hypovascular tumors was significantly higher than in those without any tumors. A Cox proportional hazard analysis showed that a history of HCC therapy, the presence of a hypovascular tumor, and AFP >4.6 ng/mL at the end of treatment were independent risk factors for HCC development. Conclusion Hypovascular tumors developed into HCC at a high rate despite the elimination of HCV by DAAs. As patients with hypovascular tumors were shown to have a high risk of HCC development, they should undergo strict HCC surveillance.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0237475</identifier><identifier>PMID: 32790728</identifier><language>eng</language><publisher>San Francisco: Public Library of Science</publisher><subject>Antiviral agents ; Antiviral drugs ; Biology and life sciences ; Control ; Daclatasvir ; Development and progression ; Environmental science ; Gastroenterology ; Genotypes ; Hazard assessment ; Hepatitis ; Hepatitis C ; Hepatitis C virus ; Hepatocellular carcinoma ; Hepatology ; Hospitals ; Infections ; Inflammation ; Internal medicine ; Lifestyles ; Liver cancer ; Liver diseases ; Magnetic resonance imaging ; Medicine and Health Sciences ; Nodules ; Patient outcomes ; Patients ; Research and Analysis Methods ; Risk analysis ; Risk factors ; Therapy ; Tumors ; University graduates ; Viruses</subject><ispartof>PloS one, 2020-08, Vol.15 (8), p.e0237475</ispartof><rights>COPYRIGHT 2020 Public Library of Science</rights><rights>2020 Tabu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2020 Tabu et al 2020 Tabu et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c669t-4d5228cdf180222633c64f517e7e334e8c396378f89400aaaca3204c73d26d733</citedby><cites>FETCH-LOGICAL-c669t-4d5228cdf180222633c64f517e7e334e8c396378f89400aaaca3204c73d26d733</cites><orcidid>0000-0002-3847-1065</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7425876/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7425876/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23847,27903,27904,53769,53771,79346,79347</link.rule.ids></links><search><contributor>Kanda, Tatsuo</contributor><creatorcontrib>Tabu, Kazuaki</creatorcontrib><creatorcontrib>Mawatari, Seiichi</creatorcontrib><creatorcontrib>Oda, Kohei</creatorcontrib><creatorcontrib>Kumagai, Kotaro</creatorcontrib><creatorcontrib>Inada, Yukiko</creatorcontrib><creatorcontrib>Uto, Hirofumi</creatorcontrib><creatorcontrib>Saisyoji, Akiko</creatorcontrib><creatorcontrib>Hiramine, Yasunari</creatorcontrib><creatorcontrib>Hashiguchi, Masafumi</creatorcontrib><creatorcontrib>Tamai, Tsutomu</creatorcontrib><creatorcontrib>Hori, Takeshi</creatorcontrib><creatorcontrib>Fujisaki, Kunio</creatorcontrib><creatorcontrib>Imanaka, Dai</creatorcontrib><creatorcontrib>Kure, Takeshi</creatorcontrib><creatorcontrib>Taniyama, Ohki</creatorcontrib><creatorcontrib>Toyodome, Ai</creatorcontrib><creatorcontrib>Ijuin, Sho</creatorcontrib><creatorcontrib>Sakae, Haruka</creatorcontrib><creatorcontrib>Sakurai, Kazuhiro</creatorcontrib><creatorcontrib>Moriuchi, Akihiro</creatorcontrib><creatorcontrib>Kanmura, Shuji</creatorcontrib><creatorcontrib>Ido, Akio</creatorcontrib><creatorcontrib>Kanda, Tatsuo</creatorcontrib><title>Hypovascular tumors developed into hepatocellular carcinoma at a high rate despite the elimination of hepatitis C virus by direct-acting antivirals</title><title>PloS one</title><description>Background and aims Direct-acting antivirals (DAAs) against hepatitis C virus (HCV) exert high anti-HCV activity and are expected to show anti-inflammatory effects associated with HCV elimination. Furthermore, hepatocellular carcinoma (HCC) is known to dedifferentiate from hypovascular tumors, such as dysplastic nodules or well-differentiated HCC, to hypervascular tumors. We therefore explored whether or not DAAs can suppress the growth and hypervascularization of hypovascular tumors. Methods We enrolled 481 patients with HCV genotype 1 infection who were treated with Daclatasvir and Asunaprevir therapy. Of these, 29 patients had 33 hypovascular tumors, which were confirmed by contrast-enhanced MRI or CT before therapy. We prospectively analyzed the cumulative incidence of HCC, i.e. the growth or hypervascularization of hypovascular tumors, and compared the HCC development rates between patients with hypovascular tumors and those without any tumors. Results The mean size of the hypovascular tumors was 11.3 mm. Twenty seven of 29 patients who achieved an SVR had 31 nodules, 19 of 31 nodules (61.3%) showed tumor growth or hypervascularization, and 12 (38.7%) nodules showed no change or improvement. The cumulative incidence rates of tumor growth or hypervascularization were 19.4% at 1 year, 36.0% at 2 years, 56.6% at 3 years, and 65.3% at 4 years. Among the patients who achieved a sustained virologic response, the cumulative HCC development rates of patients with hypovascular tumors was significantly higher than in those without any tumors. A Cox proportional hazard analysis showed that a history of HCC therapy, the presence of a hypovascular tumor, and AFP >4.6 ng/mL at the end of treatment were independent risk factors for HCC development. Conclusion Hypovascular tumors developed into HCC at a high rate despite the elimination of HCV by DAAs. As patients with hypovascular tumors were shown to have a high risk of HCC development, they should undergo strict HCC surveillance.</description><subject>Antiviral agents</subject><subject>Antiviral drugs</subject><subject>Biology and life sciences</subject><subject>Control</subject><subject>Daclatasvir</subject><subject>Development and progression</subject><subject>Environmental science</subject><subject>Gastroenterology</subject><subject>Genotypes</subject><subject>Hazard assessment</subject><subject>Hepatitis</subject><subject>Hepatitis C</subject><subject>Hepatitis C virus</subject><subject>Hepatocellular carcinoma</subject><subject>Hepatology</subject><subject>Hospitals</subject><subject>Infections</subject><subject>Inflammation</subject><subject>Internal medicine</subject><subject>Lifestyles</subject><subject>Liver cancer</subject><subject>Liver diseases</subject><subject>Magnetic resonance imaging</subject><subject>Medicine and Health 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Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tabu, Kazuaki</au><au>Mawatari, Seiichi</au><au>Oda, Kohei</au><au>Kumagai, Kotaro</au><au>Inada, Yukiko</au><au>Uto, Hirofumi</au><au>Saisyoji, Akiko</au><au>Hiramine, Yasunari</au><au>Hashiguchi, Masafumi</au><au>Tamai, Tsutomu</au><au>Hori, Takeshi</au><au>Fujisaki, Kunio</au><au>Imanaka, Dai</au><au>Kure, Takeshi</au><au>Taniyama, Ohki</au><au>Toyodome, Ai</au><au>Ijuin, Sho</au><au>Sakae, Haruka</au><au>Sakurai, Kazuhiro</au><au>Moriuchi, Akihiro</au><au>Kanmura, Shuji</au><au>Ido, Akio</au><au>Kanda, Tatsuo</au><au>Kanda, Tatsuo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hypovascular tumors developed into hepatocellular carcinoma at a high rate despite the elimination of hepatitis C virus by direct-acting antivirals</atitle><jtitle>PloS one</jtitle><date>2020-08-13</date><risdate>2020</risdate><volume>15</volume><issue>8</issue><spage>e0237475</spage><pages>e0237475-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Background and aims Direct-acting antivirals (DAAs) against hepatitis C virus (HCV) exert high anti-HCV activity and are expected to show anti-inflammatory effects associated with HCV elimination. Furthermore, hepatocellular carcinoma (HCC) is known to dedifferentiate from hypovascular tumors, such as dysplastic nodules or well-differentiated HCC, to hypervascular tumors. We therefore explored whether or not DAAs can suppress the growth and hypervascularization of hypovascular tumors. Methods We enrolled 481 patients with HCV genotype 1 infection who were treated with Daclatasvir and Asunaprevir therapy. Of these, 29 patients had 33 hypovascular tumors, which were confirmed by contrast-enhanced MRI or CT before therapy. We prospectively analyzed the cumulative incidence of HCC, i.e. the growth or hypervascularization of hypovascular tumors, and compared the HCC development rates between patients with hypovascular tumors and those without any tumors. Results The mean size of the hypovascular tumors was 11.3 mm. Twenty seven of 29 patients who achieved an SVR had 31 nodules, 19 of 31 nodules (61.3%) showed tumor growth or hypervascularization, and 12 (38.7%) nodules showed no change or improvement. The cumulative incidence rates of tumor growth or hypervascularization were 19.4% at 1 year, 36.0% at 2 years, 56.6% at 3 years, and 65.3% at 4 years. Among the patients who achieved a sustained virologic response, the cumulative HCC development rates of patients with hypovascular tumors was significantly higher than in those without any tumors. A Cox proportional hazard analysis showed that a history of HCC therapy, the presence of a hypovascular tumor, and AFP >4.6 ng/mL at the end of treatment were independent risk factors for HCC development. Conclusion Hypovascular tumors developed into HCC at a high rate despite the elimination of HCV by DAAs. As patients with hypovascular tumors were shown to have a high risk of HCC development, they should undergo strict HCC surveillance.</abstract><cop>San Francisco</cop><pub>Public Library of Science</pub><pmid>32790728</pmid><doi>10.1371/journal.pone.0237475</doi><tpages>e0237475</tpages><orcidid>https://orcid.org/0000-0002-3847-1065</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2020-08, Vol.15 (8), p.e0237475 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_2434078683 |
| source | Public Library of Science (PLoS) Journals Open Access; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Antiviral agents Antiviral drugs Biology and life sciences Control Daclatasvir Development and progression Environmental science Gastroenterology Genotypes Hazard assessment Hepatitis Hepatitis C Hepatitis C virus Hepatocellular carcinoma Hepatology Hospitals Infections Inflammation Internal medicine Lifestyles Liver cancer Liver diseases Magnetic resonance imaging Medicine and Health Sciences Nodules Patient outcomes Patients Research and Analysis Methods Risk analysis Risk factors Therapy Tumors University graduates Viruses |
| title | Hypovascular tumors developed into hepatocellular carcinoma at a high rate despite the elimination of hepatitis C virus by direct-acting antivirals |
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