HCC incidence declines with prolonged HBV treatment
medwireNews: The incidence of hepatocellular carcinoma (HCC) in patients with chronic hepatitis B virus (HBV) infection declines significantly after the first 5 years of treatment with the nucleos(t)ide analogs (NA) entecavir and/or tenofovir, researchers report.
This was particularly true for patients with cirrhosis, and “supports the hypothesis that the HCC risk is decreasing […] with prolongation of treatment and maintained inhibition of HBV replication,” George Papatheodoridis (National and Kapodistrian University of Athens, Greece) and study co-authors remark.
They found that 101 (5.2%) of 1951 Caucasian adults (aged 16 years and older) with chronic HBV developed HCC during the first 5 years of therapy with entecavir and/or tenofovir.
By comparison, 17 (1.4%) of 1205 patients without HCC during the first 5 years of therapy subsequently developed it during the next 5 years.
This gave annual HCC incidence rates of 1.22% within and 0.73% after 5 years of therapy, a difference that is statistically significant (p=0.05).
Of note, the annual HCC incidence rates were similar within and after 5 years of therapy among patients without cirrhosis, at 0.49% and 0.47%, respectively, but were significantly higher during the first 5 years, compared with after, among those with cirrhosis, at 3.22% versus 1.57% (p=0.039).
“Whether this observation is related to a low baseline HCC risk in non-cirrhotic [chronic HBV] patients that is not affected by NA therapy or to a type II error due to the low initial HCC risk cannot be easily determined,” Papatheodoridis et al write in Hepatology.
The authors also found that all HCCs diagnosed after 5 years of treatment with NA therapy developed in patients who were older than 50 years at treatment onset.
Furthermore, a baseline age of 50 years or older was a significant independent predictor of late HCC development, at a hazard ratio (HR) of 1.06 (p=0.032).
Other independent predictors of HCC development beyond year 5 were lower platelet levels at baseline (HR=0.99 per 10,000/mm3, p=0.021) and year 5 (HR=0.98 per 10,000/mm3, p=0.004) and liver stiffness of at least 12 kPa at year 5 (HR=4.10, p=0.036).
The researchers speculate that the increased HCC incidence early on could be due, in part, to malignant transformation occurring before the onset of therapeutic intervention. However, when they excluded 23 HCC cases diagnosed during the first year of follow-up the findings were unchanged.
Papatheodoridis and team add that “prolongation of antiviral therapy results in longer inhibition of HBV replication, longer biochemical remission and improvement of hepatic necroinflammation and progressive improvement of hepatic fibrosis, which may all have favorable delayed effects on liver carcinogenesis.”
By Laura Cowen
medwireNews is an independent medical news service provided by Springer Healthcare. © 2017 Springer Healthcare part of the Springer Nature group