Incidence of hepatocellular carcinoma in chronic hepatitis B patients receiving nucleos(t)ide therapy: A systematic review

Papatheodoridis, George V.; Lampertico, Pietro; Manolakopoulos, Spilios; Lok, Anna S.

doi:10.1016/j.jhep.2010.02.035

Cited by 414 publications

(348 citation statements)

References 45 publications

(257 reference statements)

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“…This finding could be related to improvements in the control of viral replication with potent medications (entecavir and tenofovir), which has prevented the progression of liver disease to more advanced stages of fibrosis and has prevented decompensation in already cirrhotic patients. HBV-related carcinogenesis develops independently of the onset of cirrhosis; therefore, antiviral treatments such as nucleo(t)side analogs, which may result in the regression of fibrosis or prevent clinical decompensation, often fail to prevent HCC, especially in Asian and African countries [30] . A randomized study conducted by Liaw et al [31] demon- strated that lamivudine therapy for a median of 32 mo resulted in a decrease in the incidence of HCC in patients with advanced fibrosis, but not in patients with decompensated liver disease.…”

Section: Discussionmentioning

confidence: 99%

Liver transplantation for hepatitis B virus: Decreasing indication and changing trends

Al–Hamoudi¹

2015

WJG

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Section: Discussionmentioning

confidence: 99%

Liver transplantation for hepatitis B virus: Decreasing indication and changing trends

Al–Hamoudi¹

2015

WJG

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“…Several large population-based and international studies have reveal that antiviral therapy could reduce the incidence of hepatic failure, cirrhosis, HCC, and mortality in CHB patients without alcoholism [33][34][35][36][37][38][39][40].…”

Section: Treatment In Patients With Concomitant Hbv Infection and Alcmentioning

confidence: 99%

Treatment and Prognosis of Hepatitis B Virus Concomitant with Alcoholism

Lin¹,

Lin²,

Yang³

2017

Advances in Treatment of Hepatitis C and B

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Hepatitis B virus (HBV) infection is a global disease worldwide. The Asia-Pacific regionhas a high prevalence of viral hepatitis, and Taiwan is a region of high prevalence of chronic hepatitis B (CHB) with increasing alcoholic liver disease. We have investigated the prognosis and treatment of patients with concomitant hepatitis B virus (HBV) infection and alcoholism. The 10-year cumulative incidence of hepatocellular carcinoma (HCC) is much higher in patients with concomitant alcoholism and HBV infection than in those with alcoholism or HBV infection alone. Treatment with antiviral therapy and abstinence may be started in patients with decompensated cirrhosis and compensated cirrhosis with high HBV DNA. In pre-cirrhotic cases, treatment with antiviral therapy and abstinence may be started in patients with persistently elevated ALT levels and high HBV DNA, and significant fibrosis with minimal elevated or normal ALT levels and mild high HBV DNA. Treatment with antiviral therapy and abstinence reduces the incidence of HCC in patients with concomitant HBV infection and alcoholism. In conclusion, patients with concomitant HBV infection and alcoholism have high incidence of cirrhosis, HCC, and mortality. Treatment with antiviral therapy and abstinence may be started to reduce the incidence of cirrhosis, HCC, and mortality in these patients.

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“…At least from the theoretically point of view, the inhibition of viral replication could decrease the cumulative incidence of HCC, considering that HBV DNA levels have been identified as an independent risk factor for HCC occurrence [8]. Thus, there have been published some studies which established that long-term treatment with potent NUCs have been linked to the reduction of the incidence of HCC [19,20]. On the opposite, the risk of HCC could not be eliminated with any available treatments because of the truncated sequences of HBs genes integrated in the DNA of the infected hepatocytes, which is believed to be associated with carcinogenesis.…”

Section: Antiviral Treatment Strategy With Available Options: Peg-ifnmentioning

confidence: 99%

Response-Guided Therapy Based on the Combination of Quantitative HBsAg and HBV DNA Kinetics in Chronic Hepatitis B Patients

Gheorghiță¹,

Căruntu²

2017

Advances in Treatment of Hepatitis C and B

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Chronic hepatitis B (CHB) remains a difficult-to-treat disease because no current treatments provide an optimal virological and immunological control, there is a high rate of relapse following any antiviral therapy, and there are no identified clinical useful treatment stopping rules, especially in hepatitis B e antigen (HBeAg)-negative patients treated with nucleoside or nucleotide analogues (NUCs). Taking into account the limited options of antiviral drugs, the response-guided therapy seems to be the best approach for optimization of treatment response. Hepatitis B surface antigen (HBsAg) can be considered a surrogate marker of HBV immune control during antiviral therapy, regardless of virological response reflected by serum HBV DNA. Thus, the decrease of HBV DNA level represents a reduction of viral replication, while serum HBsAg decline signifies a reduction of messenger RNA translation. The most important on-treatment predictors of the antiviral treatment response, especially Peg-IFN α-2a, are the quantitative HBsAg and HBV DNA evolution during therapy. A combination of no HBsAg decline and <2 log10 IU/mL decrease of HBV DNA seems to be a predictor of nonresponse in European HBeAg-negative patients with genotype D. The reduction of HBsAg levels during NUCs treatment in HBeAg-positive patients may identify cases with subsequent HBeAg or HBsAg loss.

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Incidence of hepatocellular carcinoma in chronic hepatitis B patients receiving nucleos(t)ide therapy: A systematic review

Cited by 414 publications

References 45 publications

Liver transplantation for hepatitis B virus: Decreasing indication and changing trends

Liver transplantation for hepatitis B virus: Decreasing indication and changing trends

Treatment and Prognosis of Hepatitis B Virus Concomitant with Alcoholism

Response-Guided Therapy Based on the Combination of Quantitative HBsAg and HBV DNA Kinetics in Chronic Hepatitis B Patients

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