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. 2017 Nov;96(46):e8696.
doi: 10.1097/MD.0000000000008696.

Dynamic noninvasive markers predict hepatocellular carcinoma in chronic hepatitis C patients without sustained virological response after interferon-based therapy: Prioritize who needs urgent direct-acting antiviral agents

Chao-Min Huang  1 , Tsung-Hui Hu, Kuo-Chin Chang, Po-Lin Tseng, Sheng-Nan Lu, Chien-Hung Chen, Jing-Houng Wang, Chuan-Mo Lee, Ming-Chao Tsai, Ming-Tsung Lin, Yi-Hao Yen, Chao-Hung Hung, Chung-Lung Cho, Cheng-Kun Wu
Affiliations

Dynamic noninvasive markers predict hepatocellular carcinoma in chronic hepatitis C patients without sustained virological response after interferon-based therapy: Prioritize who needs urgent direct-acting antiviral agents

Chao-Min Huang et al. Medicine (Baltimore). 2017 Nov.

Abstract

Some patients with hepatitis C virus (HCV) infections who fail to achieve sustained virological responses (SVRs) after interferon (IFN) therapy do not develop hepatocellular carcinoma (HCC). Risk stratification of these patients may help identify those who would benefit most from treatment with direct-acting antivirals (DAAs).A total of 552 HCV-infected patients with non-SVR status were enrolled. Laboratory data before and after IFN treatment were analyzed to determine the relationship of changes in serum markers with development of HCC during the 7-year study period.HCC developed in 93 patients. The risk factors for HCC were pre-existing liver cirrhosis, low hemoglobin level at baseline, low pretreatment platelet count, high post-treatment alpha-fetoprotein (AFP) level (≥15 ng/mL), and high post-treatment Fibrosis 4 (FIB4) index (>3.25). For patients without pre-existing cirrhosis, those with high post-treatment AFP level and FIB4 index had the highest risk of HCC (1 year: 6.7%; 3 years: 10.9%; 5 years: 29.7%), followed by those with high post-treatment AFP level and low post-treatment FIB4 index (5 years: 25%), and those with low post-treatment AFP level and high post-treatment FIB4 index (1 year: 3.7%; 3 years: 5.2%; 5 years: 10.6%). The risk was even lower for patients with low post-treatment AFP level and FIB4 index (1 year: 0%; 3 years: 0.4%; 5 years: 2.5%). None of the patients with FIB4 indexes consistently below 1.45 developed HCC.The combined use of post-treatment AFP level and FIB4 index was useful for risk stratification of HCV-infected patients with non-SVR status after IFN therapy. These data may help clinicians to identify patients who most urgently need DAA treatment.

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Conflict of interest statement

The authors have no conflicts of interest to disclose.

Figures

Figure 1
Figure 1
Effect of pretreatment and post-treatment AFP level (A and B) and pretreatment and post-treatment platelet count (C and D) on HCC development in HPC patients without SVRs after IFN therapy (n = 552). AFP = alpha-fetoprotein, HCC = hepatocellular carcinoma, HPC = hepatitis C, IFN = interferon, SVRs = sustained virological responses.
Figure 2
Figure 2
Effect of pretreatment and post-treatment APRI (E and F) and pretreatment and post-treatment FIB4 index (G and H) on HCC development in HPC patients without SVRs after IFN therapy (n = 552). APRI = Aminotransferase-to-Platelet Ratio Index, FIB4 = Fibrosis 4, HCC = hepatocellular carcinoma, HPC = hepatitis C, IFN = interferon, SVRs = sustained virological responses.
Figure 3
Figure 3
Effect of changes in pretreatment and post-treatment AFP level (A), platelet count (B), APRI (C), and FIB4 index (D) on HCC development in HPC patients without SVRs after IFN therapy (n = 552). AFP = alpha-fetoprotein, APRI = Aminotransferase-to-Platelet Ratio Index, FIB4 = Fibrosis 4, HCC = hepatocellular carcinoma, HPC = hepatitis C, IFN = interferon, SVRs = sustained virological responses.
Figure 4
Figure 4
Effect of the combined use of post-treatment AFP level and FIB4 index on development of HCC in patients without SVRs after IFN therapy in those with pre-existing liver cirrhosis (A) and without pre-existing liver cirrhosis (B) (n = 552). AFP = alpha-fetoprotein, FIB4 = Fibrosis 4, HCC = hepatocellular carcinoma, IFN = interferon, SVRs = sustained virological responses.
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References

    1. Thevenot T, Regimbeau C, Ratziu V, et al. Metaanalysis of interferon randomized trials in the treatment of viral hepatitis C in naive patients: 1999 update. J Viral Hepat 2001;8:48–62. - PubMed
    1. Morgan TR, Ghany MG, Kim HY, et al. Outcome of sustained virological responders with histologically advanced chronic hepatitis C. Hepatology 2010;52:833–44. - PMC - PubMed
    1. Morgan RL, Baack B, Smith BD, et al. Eradication of hepatitis C virus infection and the development of hepatocellular carcinoma: a meta-analysis of observational studies. Ann Intern Med 2013;158:329–37. - PubMed
    1. Wu CK, Chang KC, Hung CH, et al. Dynamic α-fetoprotein, platelets and AST-to-Platelet Ratio Index predict hepatocellular carcinoma in chronic hepatitis C patients with sustained virological response after antiviral therapy. J Antimicrob Chemother 2016;71:1943–7. - PubMed
    1. Poynard T, Moussalli J, Munteanu M, et al. Slow regression of liver fibrosis presumed by repeated biomarkers after virological cure in patients with chronic hepatitis C. J Hepatol 2013;59:675–83. - PubMed