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Author Spotlight: Advancements and Challenges in Hepatitis B Virus Detection
Published on: December 15, 2023
Risk of hepatocellular carcinoma in cirrhotic hepatitis B virus patients during nucleoside/nucleotide analog therapy
Etsuro Orito1, Chitomi Hasebe2, Masayuki Kurosaki3
1Department of Gastroenterology, Japanese Red Cross Nagoya Daini Hospital, Nagoya, Japan.
Aim:
Some patients develop hepatocellular carcinoma (HCC) during nucleoside/nucleotide analog (NA) therapy even if alanine aminotransferase (ALT) or hepatitis B virus (HBV) DNA levels are sufficiently reduced. The aim of this study is to identify the risk factors of development of HCC during NA therapy.
Methods:
Six hundred and two patients were analyzed who were continuously receiving NA for chronic HBV infection. The patients who developed HCC previously or within 1 year of therapy were excluded. In the patients studied, the median duration of therapy was 90 months. A total of 492 patients had chronic hepatitis (CH) and 110 had liver cirrhosis (LC).
Results:
In 602 patients, the rate of normalization of ALT, loss of serum HBV DNA and development of HCC were 90.4%, 55.4%, and 6.1%, respectively. The significant risk factors of development of HCC were LC status and duration of therapy. The annual incidence of HCC in LC patients was 2.53%/year, compared with 0.34%/year in CH patients. When the relation between the incidence of HCC and the response to therapy was evaluated, in patients with normalization of ALT level, loss of HBV DNA by real-time polymerase chain reaction or hepatitis B e-antigen seroconversion, the incidences of HCC was reduced to some extent. However, none of the patients who achieved hepatitis B surface antigen (HBsAg) seroclearance during NA therapy developed HCC.
Conclusion:
LC status was the significant risk factor of development of HCC during NA therapy. However, none of the patients who showed HBsAg seroclearance developed HCC. The ultimate goal of therapy for reduced risk of HCC may be HBsAg seroclearance.
Insights
Hepatocellular carcinoma (HCC) risk during nucleoside/nucleotide analog (NA) therapy is linked to liver cirrhosis and treatment duration. Achieving hepatitis B surface antigen (HBsAg) seroclearance eliminates HCC development risk.
Area of Science:
- Hepatology
- Virology
- Oncology
Background:
- Hepatocellular carcinoma (HCC) can develop during nucleoside/nucleotide analog (NA) therapy for chronic hepatitis B virus (HBV) infection, even with controlled viral load and liver enzymes.
- Identifying risk factors for HCC development during NA therapy is crucial for patient management.
Purpose of the Study:
- To identify risk factors associated with hepatocellular carcinoma (HCC) development in patients undergoing nucleoside/nucleotide analog (NA) therapy for chronic hepatitis B virus (HBV) infection.
- To evaluate the impact of treatment response markers on HCC incidence.
Main Methods:
- Analysis of 602 patients receiving continuous NA therapy for chronic HBV infection.
- Exclusion of patients with prior HCC or HCC within one year of therapy initiation.
- Assessment of risk factors including liver cirrhosis (LC) status, chronic hepatitis (CH) status, and duration of NA therapy.
Main Results:
- The overall incidence of HCC was 6.1% over a median therapy duration of 90 months.
- Significant risk factors for HCC development were identified as liver cirrhosis (LC) status and longer duration of NA therapy.
- Patients with LC had a higher annual HCC incidence (2.53%/year) compared to those with CH (0.34%/year).
- Normalization of ALT, loss of HBV DNA, and HBeAg seroconversion showed some reduction in HCC incidence.
- No HCC cases were observed in patients who achieved hepatitis B surface antigen (HBsAg) seroclearance during NA therapy.
Conclusions:
- Liver cirrhosis (LC) status is a significant risk factor for HCC development during NA therapy.
- Hepatitis B surface antigen (HBsAg) seroclearance during NA therapy is associated with a complete absence of HCC development.
- Achieving HBsAg seroclearance should be the ultimate therapeutic goal to minimize HCC risk in chronic HBV patients.
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