Hypovascular tumors developed into hepatocellular carcinoma at a high rate despite the elimination of hepatitis C virus by direct-acting antivirals.
<h4<Background and aims</h4<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 hypova...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Kazuaki Tabu [verfasserIn] Seiichi Mawatari [verfasserIn] Kohei Oda [verfasserIn] Kotaro Kumagai [verfasserIn] Yukiko Inada [verfasserIn] Hirofumi Uto [verfasserIn] Akiko Saisyoji [verfasserIn] Yasunari Hiramine [verfasserIn] Masafumi Hashiguchi [verfasserIn] Tsutomu Tamai [verfasserIn] Takeshi Hori [verfasserIn] Kunio Fujisaki [verfasserIn] Dai Imanaka [verfasserIn] Takeshi Kure [verfasserIn] Ohki Taniyama [verfasserIn] Ai Toyodome [verfasserIn] Sho Ijuin [verfasserIn] Haruka Sakae [verfasserIn] Kazuhiro Sakurai [verfasserIn] Akihiro Moriuchi [verfasserIn] Shuji Kanmura [verfasserIn] Akio Ido [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2020 |
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| Übergeordnetes Werk: |
In: PLoS ONE - Public Library of Science (PLoS), 2007, 15(2020), 8, p e0237475 |
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| Übergeordnetes Werk: |
volume:15 ; year:2020 ; number:8, p e0237475 |
| Links: |
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| DOI / URN: |
10.1371/journal.pone.0237475 |
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| Katalog-ID: |
DOAJ078686989 |
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| 245 | 1 | 0 | |a 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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| 520 | |a <h4<Background and aims</h4<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.<h4<Methods</h4<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.<h4<Results</h4<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.<h4<Conclusion</h4<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. | ||
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| 700 | 0 | |a Kohei Oda |e verfasserin |4 aut | |
| 700 | 0 | |a Kotaro Kumagai |e verfasserin |4 aut | |
| 700 | 0 | |a Yukiko Inada |e verfasserin |4 aut | |
| 700 | 0 | |a Hirofumi Uto |e verfasserin |4 aut | |
| 700 | 0 | |a Akiko Saisyoji |e verfasserin |4 aut | |
| 700 | 0 | |a Yasunari Hiramine |e verfasserin |4 aut | |
| 700 | 0 | |a Masafumi Hashiguchi |e verfasserin |4 aut | |
| 700 | 0 | |a Tsutomu Tamai |e verfasserin |4 aut | |
| 700 | 0 | |a Takeshi Hori |e verfasserin |4 aut | |
| 700 | 0 | |a Kunio Fujisaki |e verfasserin |4 aut | |
| 700 | 0 | |a Dai Imanaka |e verfasserin |4 aut | |
| 700 | 0 | |a Takeshi Kure |e verfasserin |4 aut | |
| 700 | 0 | |a Ohki Taniyama |e verfasserin |4 aut | |
| 700 | 0 | |a Ai Toyodome |e verfasserin |4 aut | |
| 700 | 0 | |a Sho Ijuin |e verfasserin |4 aut | |
| 700 | 0 | |a Haruka Sakae |e verfasserin |4 aut | |
| 700 | 0 | |a Kazuhiro Sakurai |e verfasserin |4 aut | |
| 700 | 0 | |a Akihiro Moriuchi |e verfasserin |4 aut | |
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| 700 | 0 | |a Akio Ido |e verfasserin |4 aut | |
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10.1371/journal.pone.0237475 doi (DE-627)DOAJ078686989 (DE-599)DOAJ77e19cc7fd2f44569864b15ba39951ef DE-627 ger DE-627 rakwb eng Kazuaki Tabu verfasserin aut Hypovascular tumors developed into hepatocellular carcinoma at a high rate despite the elimination of hepatitis C virus by direct-acting antivirals. 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <h4<Background and aims</h4<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.<h4<Methods</h4<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.<h4<Results</h4<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.<h4<Conclusion</h4<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. Medicine R Science Q Seiichi Mawatari verfasserin aut Kohei Oda verfasserin aut Kotaro Kumagai verfasserin aut Yukiko Inada verfasserin aut Hirofumi Uto verfasserin aut Akiko Saisyoji verfasserin aut Yasunari Hiramine verfasserin aut Masafumi Hashiguchi verfasserin aut Tsutomu Tamai verfasserin aut Takeshi Hori verfasserin aut Kunio Fujisaki verfasserin aut Dai Imanaka verfasserin aut Takeshi Kure verfasserin aut Ohki Taniyama verfasserin aut Ai Toyodome verfasserin aut Sho Ijuin verfasserin aut Haruka Sakae verfasserin aut Kazuhiro Sakurai verfasserin aut Akihiro Moriuchi verfasserin aut Shuji Kanmura verfasserin aut Akio Ido verfasserin aut In PLoS ONE Public Library of Science (PLoS), 2007 15(2020), 8, p e0237475 (DE-627)523574592 (DE-600)2267670-3 19326203 nnns volume:15 year:2020 number:8, p e0237475 https://doi.org/10.1371/journal.pone.0237475 kostenfrei https://doaj.org/article/77e19cc7fd2f44569864b15ba39951ef kostenfrei https://doi.org/10.1371/journal.pone.0237475 kostenfrei https://doaj.org/toc/1932-6203 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_34 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_235 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2020 8, p e0237475 |
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10.1371/journal.pone.0237475 doi (DE-627)DOAJ078686989 (DE-599)DOAJ77e19cc7fd2f44569864b15ba39951ef DE-627 ger DE-627 rakwb eng Kazuaki Tabu verfasserin aut Hypovascular tumors developed into hepatocellular carcinoma at a high rate despite the elimination of hepatitis C virus by direct-acting antivirals. 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <h4<Background and aims</h4<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.<h4<Methods</h4<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.<h4<Results</h4<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.<h4<Conclusion</h4<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. Medicine R Science Q Seiichi Mawatari verfasserin aut Kohei Oda verfasserin aut Kotaro Kumagai verfasserin aut Yukiko Inada verfasserin aut Hirofumi Uto verfasserin aut Akiko Saisyoji verfasserin aut Yasunari Hiramine verfasserin aut Masafumi Hashiguchi verfasserin aut Tsutomu Tamai verfasserin aut Takeshi Hori verfasserin aut Kunio Fujisaki verfasserin aut Dai Imanaka verfasserin aut Takeshi Kure verfasserin aut Ohki Taniyama verfasserin aut Ai Toyodome verfasserin aut Sho Ijuin verfasserin aut Haruka Sakae verfasserin aut Kazuhiro Sakurai verfasserin aut Akihiro Moriuchi verfasserin aut Shuji Kanmura verfasserin aut Akio Ido verfasserin aut In PLoS ONE Public Library of Science (PLoS), 2007 15(2020), 8, p e0237475 (DE-627)523574592 (DE-600)2267670-3 19326203 nnns volume:15 year:2020 number:8, p e0237475 https://doi.org/10.1371/journal.pone.0237475 kostenfrei https://doaj.org/article/77e19cc7fd2f44569864b15ba39951ef kostenfrei https://doi.org/10.1371/journal.pone.0237475 kostenfrei https://doaj.org/toc/1932-6203 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_34 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_235 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2020 8, p e0237475 |
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10.1371/journal.pone.0237475 doi (DE-627)DOAJ078686989 (DE-599)DOAJ77e19cc7fd2f44569864b15ba39951ef DE-627 ger DE-627 rakwb eng Kazuaki Tabu verfasserin aut Hypovascular tumors developed into hepatocellular carcinoma at a high rate despite the elimination of hepatitis C virus by direct-acting antivirals. 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <h4<Background and aims</h4<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.<h4<Methods</h4<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.<h4<Results</h4<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.<h4<Conclusion</h4<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. Medicine R Science Q Seiichi Mawatari verfasserin aut Kohei Oda verfasserin aut Kotaro Kumagai verfasserin aut Yukiko Inada verfasserin aut Hirofumi Uto verfasserin aut Akiko Saisyoji verfasserin aut Yasunari Hiramine verfasserin aut Masafumi Hashiguchi verfasserin aut Tsutomu Tamai verfasserin aut Takeshi Hori verfasserin aut Kunio Fujisaki verfasserin aut Dai Imanaka verfasserin aut Takeshi Kure verfasserin aut Ohki Taniyama verfasserin aut Ai Toyodome verfasserin aut Sho Ijuin verfasserin aut Haruka Sakae verfasserin aut Kazuhiro Sakurai verfasserin aut Akihiro Moriuchi verfasserin aut Shuji Kanmura verfasserin aut Akio Ido verfasserin aut In PLoS ONE Public Library of Science (PLoS), 2007 15(2020), 8, p e0237475 (DE-627)523574592 (DE-600)2267670-3 19326203 nnns volume:15 year:2020 number:8, p e0237475 https://doi.org/10.1371/journal.pone.0237475 kostenfrei https://doaj.org/article/77e19cc7fd2f44569864b15ba39951ef kostenfrei https://doi.org/10.1371/journal.pone.0237475 kostenfrei https://doaj.org/toc/1932-6203 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_34 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_235 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2020 8, p e0237475 |
| allfieldsGer |
10.1371/journal.pone.0237475 doi (DE-627)DOAJ078686989 (DE-599)DOAJ77e19cc7fd2f44569864b15ba39951ef DE-627 ger DE-627 rakwb eng Kazuaki Tabu verfasserin aut Hypovascular tumors developed into hepatocellular carcinoma at a high rate despite the elimination of hepatitis C virus by direct-acting antivirals. 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <h4<Background and aims</h4<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.<h4<Methods</h4<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.<h4<Results</h4<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.<h4<Conclusion</h4<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. Medicine R Science Q Seiichi Mawatari verfasserin aut Kohei Oda verfasserin aut Kotaro Kumagai verfasserin aut Yukiko Inada verfasserin aut Hirofumi Uto verfasserin aut Akiko Saisyoji verfasserin aut Yasunari Hiramine verfasserin aut Masafumi Hashiguchi verfasserin aut Tsutomu Tamai verfasserin aut Takeshi Hori verfasserin aut Kunio Fujisaki verfasserin aut Dai Imanaka verfasserin aut Takeshi Kure verfasserin aut Ohki Taniyama verfasserin aut Ai Toyodome verfasserin aut Sho Ijuin verfasserin aut Haruka Sakae verfasserin aut Kazuhiro Sakurai verfasserin aut Akihiro Moriuchi verfasserin aut Shuji Kanmura verfasserin aut Akio Ido verfasserin aut In PLoS ONE Public Library of Science (PLoS), 2007 15(2020), 8, p e0237475 (DE-627)523574592 (DE-600)2267670-3 19326203 nnns volume:15 year:2020 number:8, p e0237475 https://doi.org/10.1371/journal.pone.0237475 kostenfrei https://doaj.org/article/77e19cc7fd2f44569864b15ba39951ef kostenfrei https://doi.org/10.1371/journal.pone.0237475 kostenfrei https://doaj.org/toc/1932-6203 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_34 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_235 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2020 8, p e0237475 |
| allfieldsSound |
10.1371/journal.pone.0237475 doi (DE-627)DOAJ078686989 (DE-599)DOAJ77e19cc7fd2f44569864b15ba39951ef DE-627 ger DE-627 rakwb eng Kazuaki Tabu verfasserin aut Hypovascular tumors developed into hepatocellular carcinoma at a high rate despite the elimination of hepatitis C virus by direct-acting antivirals. 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <h4<Background and aims</h4<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.<h4<Methods</h4<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.<h4<Results</h4<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.<h4<Conclusion</h4<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. Medicine R Science Q Seiichi Mawatari verfasserin aut Kohei Oda verfasserin aut Kotaro Kumagai verfasserin aut Yukiko Inada verfasserin aut Hirofumi Uto verfasserin aut Akiko Saisyoji verfasserin aut Yasunari Hiramine verfasserin aut Masafumi Hashiguchi verfasserin aut Tsutomu Tamai verfasserin aut Takeshi Hori verfasserin aut Kunio Fujisaki verfasserin aut Dai Imanaka verfasserin aut Takeshi Kure verfasserin aut Ohki Taniyama verfasserin aut Ai Toyodome verfasserin aut Sho Ijuin verfasserin aut Haruka Sakae verfasserin aut Kazuhiro Sakurai verfasserin aut Akihiro Moriuchi verfasserin aut Shuji Kanmura verfasserin aut Akio Ido verfasserin aut In PLoS ONE Public Library of Science (PLoS), 2007 15(2020), 8, p e0237475 (DE-627)523574592 (DE-600)2267670-3 19326203 nnns volume:15 year:2020 number:8, p e0237475 https://doi.org/10.1371/journal.pone.0237475 kostenfrei https://doaj.org/article/77e19cc7fd2f44569864b15ba39951ef kostenfrei https://doi.org/10.1371/journal.pone.0237475 kostenfrei https://doaj.org/toc/1932-6203 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_34 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_235 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2020 8, p e0237475 |
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Kazuaki Tabu @@aut@@ Seiichi Mawatari @@aut@@ Kohei Oda @@aut@@ Kotaro Kumagai @@aut@@ Yukiko Inada @@aut@@ Hirofumi Uto @@aut@@ Akiko Saisyoji @@aut@@ Yasunari Hiramine @@aut@@ Masafumi Hashiguchi @@aut@@ Tsutomu Tamai @@aut@@ Takeshi Hori @@aut@@ Kunio Fujisaki @@aut@@ Dai Imanaka @@aut@@ Takeshi Kure @@aut@@ Ohki Taniyama @@aut@@ Ai Toyodome @@aut@@ Sho Ijuin @@aut@@ Haruka Sakae @@aut@@ Kazuhiro Sakurai @@aut@@ Akihiro Moriuchi @@aut@@ Shuji Kanmura @@aut@@ Akio Ido @@aut@@ |
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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.<h4<Methods</h4<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.<h4<Results</h4<The mean size of the hypovascular tumors was 11.3 mm. 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Kazuaki Tabu |
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Kazuaki Tabu misc Medicine misc R misc Science misc Q 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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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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Kazuaki Tabu Seiichi Mawatari Kohei Oda Kotaro Kumagai Yukiko Inada Hirofumi Uto Akiko Saisyoji Yasunari Hiramine Masafumi Hashiguchi Tsutomu Tamai Takeshi Hori Kunio Fujisaki Dai Imanaka Takeshi Kure Ohki Taniyama Ai Toyodome Sho Ijuin Haruka Sakae Kazuhiro Sakurai Akihiro Moriuchi Shuji Kanmura Akio Ido |
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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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Hypovascular tumors developed into hepatocellular carcinoma at a high rate despite the elimination of hepatitis C virus by direct-acting antivirals. |
| abstract |
<h4<Background and aims</h4<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.<h4<Methods</h4<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.<h4<Results</h4<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.<h4<Conclusion</h4<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. |
| abstractGer |
<h4<Background and aims</h4<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.<h4<Methods</h4<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.<h4<Results</h4<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.<h4<Conclusion</h4<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_unstemmed |
<h4<Background and aims</h4<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.<h4<Methods</h4<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.<h4<Results</h4<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.<h4<Conclusion</h4<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. |
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Seiichi Mawatari Kohei Oda Kotaro Kumagai Yukiko Inada Hirofumi Uto Akiko Saisyoji Yasunari Hiramine Masafumi Hashiguchi Tsutomu Tamai Takeshi Hori Kunio Fujisaki Dai Imanaka Takeshi Kure Ohki Taniyama Ai Toyodome Sho Ijuin Haruka Sakae Kazuhiro Sakurai Akihiro Moriuchi Shuji Kanmura Akio Ido |
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Seiichi Mawatari Kohei Oda Kotaro Kumagai Yukiko Inada Hirofumi Uto Akiko Saisyoji Yasunari Hiramine Masafumi Hashiguchi Tsutomu Tamai Takeshi Hori Kunio Fujisaki Dai Imanaka Takeshi Kure Ohki Taniyama Ai Toyodome Sho Ijuin Haruka Sakae Kazuhiro Sakurai Akihiro Moriuchi Shuji Kanmura Akio Ido |
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