Risk factors for development of hepatocellular carcinoma in patients with chronic hepatitis C after sustained response to interferon

Ikeda, Masafumi; Fujiyama, Shigetoshi; Tanaka, Motohiko; Sata, Michio; Ide, Tatsuya; Yatsuhashi, Hiroshi; Watanabe, Hiroshi

doi:10.1007/s00535-004-1519-2

Cited by 127 publications

(138 citation statements)

References 38 publications

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“…[17][18][19]30 The present data support this recommendation. Except for the two cases of HCC, none of the patients with SVR in the present series presented any evidence of progression of liver disease assessed clinically and biochemically by routine tests (serum aminotransferases and liver function tests).…”

Section: Table 2 Patient Characteristics and Laboratory Features Of supporting

confidence: 79%

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Long-term follow-up of patients with chronic hepatitis C with sustained virologic response to interferon

Ferreira¹,

Carneiro²,

Souza³

et al. 2010

Braz J Infect Dis

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Background and aim:The durability of the sustained virologic response (SVR) in patients with chronic hepatitis C after treatment and the ideal follow-up time for these patients remains undefi ned. The objective of the study was to evaluate the durability of the virologic response in patients with chronic hepatitis C followed up for at least 12 months after SVR at HCFMRP-USP. Methods: The study was conducted on 174 patients with chronic hepatitis C treated with different antiviral regimens who had achieved SVR. Qualitative serum HCV-RNA was determined by the commercial kit (COBAS AMPLICOR HCV, v2.0). Results: There was predominance of male (73%) with a mean age of 45.6 ± 10 years. Liver cirrhosis was present in 16.1% of the study subjects. Mean follow-up time after SVR was 47 months (12-156 months). Twenty-two patients received monotherapy with interferon; 94 received interferon plus ribavirin, and 58 received pegylated interferon plus ribavirin. A total of 134 patients (77.0%) received one treatment course, 29 (16.7%) received two courses, and 11 (6.3%) received three courses. The distribution of HCV genotypes was: genotype 1 (40.2%), genotype 3 (40.8%) and genotype 2 (10.3%). Genotype was undetermined in 8.7% of cases. None of the 174 patients had recurrence of HCV infection. Two cirrhotic patients developed hepatocellular carcinoma (HCC) during follow-up. Conclusions: Among patients with SVR there was no recurrence of HCV infection or evidence of liver disease progression in any patient followed up for a mean of 47 months after SVR, except for patients with advanced hepatic disease before treatment, who may develop HCC despite SVR. Therefore, one can assume that SVR is associated with long term good prognosis.

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Section: Table 2 Patient Characteristics and Laboratory Features Of supporting

confidence: 79%

“…11 However, even though SVR prevents progression of liver disease to cirrhosis, there is a risk of developing HCC in patients who already have cirrhosis at the time of treatment initiation. [16][17][18][19]29,30 The effects of HCV-RNA, even at low levels, on carcinogenesis have not been fully clarifi ed and more detailed studies are needed.…”

Section: Discussionmentioning

confidence: 99%

Long-term follow-up of patients with chronic hepatitis C with sustained virologic response to interferon

Ferreira¹,

Carneiro²,

Souza³

et al. 2010

Braz J Infect Dis

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“…P revious reports indicated that amino acid (aa) substitutions at position 70 in the hepatitis C virus (HCV) core region in patients infected with HCV genotype 1b (HCV-1b) are pretreatment predictors of poor virological response to antiviral therapy (1,2) and also affect hepatocarcinogenesis, regardless of treatment response (3-7). In particular, hepatocellular carcinoma (HCC) still occurs even after eradication of HCV RNA by antiviral therapy (8)(9)(10)(11)(12), and substitutions of aa70 at the start of antiviral therapy also affect hepatocarcinogenesis following eradication of HCV RNA (13).…”

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confidence: 99%

Impact of Mutations at Amino Acid 70 in Hepatitis C Virus (HCV) Genotype 1b Core Region on Hepatocarcinogenesis following Eradication of HCV RNA

et al. 2015

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bThe impact of the HCV genotype 1b core amino acid (aa) 70 mutant on the cumulative rate of hepatocellular carcinoma following eradication of HCV RNA by antiviral therapy was investigated with the Q-Invader assay. Multivariate analysis based on 649 patients indicated that a core aa70 Q-Invader mutant level >20% is a predictor of hepatocellular carcinoma. P revious reports indicated that amino acid (aa) substitutions at position 70 in the hepatitis C virus (HCV) core region in patients infected with HCV genotype 1b (HCV-1b) are pretreatment predictors of poor virological response to antiviral therapy (1, 2) and also affect hepatocarcinogenesis, regardless of treatment response (3-7). In particular, hepatocellular carcinoma (HCC) still occurs even after eradication of HCV RNA by antiviral therapy (8-12), and substitutions of aa70 at the start of antiviral therapy also affect hepatocarcinogenesis following eradication of HCV RNA (13).Recently, Tadokoro et al. (14) reported the results of a comparative quantitative analysis of aa70 substitution in the HCV-1b core region by the real-time PCR monitoring Invader reaction (Q-Invader assay; BML, Inc., Saitama, Japan). This highly sensitive assay (based on the Q-Invader technology using mutant-specific primers) was developed to determine the relative ratio of the aa70 mutant (glutamine/histidine) to the aa70 wild-type (arginine) virus. The assay in that study (14) detected a minor type plasmid that constituted only 1% of a mixture of plasmids containing wild-type and mutant sequences. In this study, we evaluated the associations between core aa70 Q-Invader mutant levels at the start of antiviral therapy and HCC following eradication of HCV RNA.Among 5,023 consecutive patients infected with HCV in whom antiviral therapy (interferon monotherapy, interferon plus ribavirin combination therapy, or triple therapy of NS3/4A protease inhibitor plus peginterferon plus ribavirin) was initiated between February 1987 and June 2013 at Toranomon Hospital, 2,121 patients infected with a single genotype of HCV-1b, -2a, or -2b were selected for this retrospective study. All patients achieved sustained virological response, defined as negative HCV RNA at 24 weeks after cessation of antiviral therapy, based on HCV RNA qualitative analysis (Amplicor; Roche Diagnostics, Manheim, Germany) or by the Cobas TaqMan HCV test (Roche Diagnostics, Tokyo, Japan), and they were free of HCC before and during interferon therapy. The cumulative rate of HCC was calculated using the Kaplan-Meier technique; differences between the HCC rate curves were tested using the log-rank test. The period between the end of antiviral therapy and the diagnosis of HCC was used for group-based statistical analysis of HCC. Stepwise Cox regression analysis (multivariate analysis) was used to determine independent factors associated with HCC. This study protocol was in compliance with the Good Clinical Practice guidelines and the 1975 Declaration of Helsinki, and it was approved by the institutional review board at Toranomon ...

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“…In a study of veterans who received IFN-based treatment for HCV and achieved a sustained virological response (SVR), indicative of HCV cure, El-Serag, et al found that black patients had an increased risk of developing HCC compared to whites HR of 1.4 but the increase was not statistically significant [p=0.31] [23]. Many of the studies on post-SVR HCC were done in Japan [24,25] and data are limited on risk factors for post-SVR HCC in direct acting antiviral (DAA) users.…”

Section: Potential Contributors To the Elevated Hcc Risk And Higher Mmentioning

confidence: 99%

Worse Outcomes among African Americans with Liver Cancer: What Might Cause the Disparity?

Ad¹

2017

Austin J Gastroenterol

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Liver cancer remains an important cause of cancer mortality in the United States. Incidence of hepatocellular carcinoma (HCC), the most common histological cell type of liver cancer, has increased over the past 30 years. The statistics are particularly worrisome for African Americans. Their incidence of HCC far surpasses that of other races, particularly whites. Additionally, mortality for African Americans with HCC is also far worse. In a review of the literature, we found a stepwise progression of variables that may contribute to this observation. African Americans have the highest observed rates of infection with chronic hepatitis and are offered treatment less often for hepatitis C virus. The progression to cirrhosis is slower, which may complicate HCC surveillance. Regardless, they receive surveillance either biochemical or radiographic at a lower rate than patients of other races. Further, African Americans present at a more advanced stage and are referred for curative therapy less often. When African Americans do receive therapy, their outcomes are worse. Additional investigation is warranted as to whether differences in tumor biology may also play a role.

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Risk factors for development of hepatocellular carcinoma in patients with chronic hepatitis C after sustained response to interferon

Abstract: This study suggests that the risk of development of HCC is not completely eliminated in sustained responders to IFN. These findings may be useful in determining a follow-up strategy after a sustained response to IFN.

Cited by 127 publications

References 38 publications

Long-term follow-up of patients with chronic hepatitis C with sustained virologic response to interferon

Long-term follow-up of patients with chronic hepatitis C with sustained virologic response to interferon

Impact of Mutations at Amino Acid 70 in Hepatitis C Virus (HCV) Genotype 1b Core Region on Hepatocarcinogenesis following Eradication of HCV RNA

Worse Outcomes among African Americans with Liver Cancer: What Might Cause the Disparity?

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