In the Journals

HCC incidence occurred in patients undergoing monotherapy for HBV

In a retrospective cohort study, incidence of hepatocellular carcinoma occurred over time among adults with chronic hepatitis B virus infection being treated with entecavir or tenofovir, according to study data.

“In particular, long-term monotherapy with one of the current first-line nucleoside analogues, entecavir or tenofovir disoproxil fumarate, results in maintained virological remission in [greater than] 95% of patients, often achieves regression of the histological lesions of cirrhosis and prevents or reverses hepatic decompensation,” the researchers wrote. “However, hepatocellular carcinoma may still develop in chronic hepatitis B patients, particularly those with cirrhosis, even when they achieve maintained virological remission under long-term therapy with [nucleoside analogues].”

Researchers followed 1,666 Caucasian patients with chronic HBV undergoing entecavir or tenofovir therapy for 39 months to determine the predictors and incidence rates of hepatocellular carcinoma (HCC). They also tested whether three HCC risk scores —GAG-HCC, CU-HCC and REACH-B — are accurate in detecting and measuring HCC among these types of patients. Sixty-seven percent of patients with chronic HBV did not have cirrhosis, 39% had compensated cirrhosis and 3% had decompensated cirrhosis.

Seventy-one patients developed HCC with an incidence rate of 1.37 (95% CI, 1.09-1.73). After onset of entecavir or tenofovir therapy, the likelihood of developing HCC among these patients was 1.3% at 1 year, 3.4% at 3 years and 8.7% at 5 years. In patients without cirrhosis, cumulative HCC incidence rates were 0.6% at 1 year, 1.4% at 3 years and 3.7% at 5 years. For patients with compensated cirrhosis, incidence rates were 2.1% at 1 year, 4.9% at 3 years and 17.5% at 5 years, and 9.1% at 1 year, 26.7% at 3 years and 36.3% at 5 years for patients with decompensated cirrhosis (P < .001 for all).

Low platelet levels and older age were independent predictors for HCC in the overall population, and in the subgroups of patients with or without cirrhosis, according to the research. However, liver disease severity was an independent predictor of HCC only among the total population and patients with cirrhosis.   

GAG-HCC, CU-HCC and REACH-B risk scores were associated with HCC development in univariable analysis, but not in multivariable analysis, and were not highly predictable, according to data.

“The findings of this large multicenter retrospective study in Caucasian patients with [chronic HBV] indicate that HCC may still develop under effective long-term [entecavir] or [tenofovir] therapy, with the HCC risk being higher in patients with more advanced liver disease,” the researchers wrote.

Disclosure: Relevant financial disclosures were not provided by researchers.

In a retrospective cohort study, incidence of hepatocellular carcinoma occurred over time among adults with chronic hepatitis B virus infection being treated with entecavir or tenofovir, according to study data.

“In particular, long-term monotherapy with one of the current first-line nucleoside analogues, entecavir or tenofovir disoproxil fumarate, results in maintained virological remission in [greater than] 95% of patients, often achieves regression of the histological lesions of cirrhosis and prevents or reverses hepatic decompensation,” the researchers wrote. “However, hepatocellular carcinoma may still develop in chronic hepatitis B patients, particularly those with cirrhosis, even when they achieve maintained virological remission under long-term therapy with [nucleoside analogues].”

Researchers followed 1,666 Caucasian patients with chronic HBV undergoing entecavir or tenofovir therapy for 39 months to determine the predictors and incidence rates of hepatocellular carcinoma (HCC). They also tested whether three HCC risk scores —GAG-HCC, CU-HCC and REACH-B — are accurate in detecting and measuring HCC among these types of patients. Sixty-seven percent of patients with chronic HBV did not have cirrhosis, 39% had compensated cirrhosis and 3% had decompensated cirrhosis.

Seventy-one patients developed HCC with an incidence rate of 1.37 (95% CI, 1.09-1.73). After onset of entecavir or tenofovir therapy, the likelihood of developing HCC among these patients was 1.3% at 1 year, 3.4% at 3 years and 8.7% at 5 years. In patients without cirrhosis, cumulative HCC incidence rates were 0.6% at 1 year, 1.4% at 3 years and 3.7% at 5 years. For patients with compensated cirrhosis, incidence rates were 2.1% at 1 year, 4.9% at 3 years and 17.5% at 5 years, and 9.1% at 1 year, 26.7% at 3 years and 36.3% at 5 years for patients with decompensated cirrhosis (P < .001 for all).

Low platelet levels and older age were independent predictors for HCC in the overall population, and in the subgroups of patients with or without cirrhosis, according to the research. However, liver disease severity was an independent predictor of HCC only among the total population and patients with cirrhosis.   

GAG-HCC, CU-HCC and REACH-B risk scores were associated with HCC development in univariable analysis, but not in multivariable analysis, and were not highly predictable, according to data.

“The findings of this large multicenter retrospective study in Caucasian patients with [chronic HBV] indicate that HCC may still develop under effective long-term [entecavir] or [tenofovir] therapy, with the HCC risk being higher in patients with more advanced liver disease,” the researchers wrote.

Disclosure: Relevant financial disclosures were not provided by researchers.