Published online Nov 6, 2018. doi: 10.12998/wjcc.v6.i13.671
Peer-review started: July 24, 2018
First decision: August 30, 2018
Revised: September 5, 2018
Accepted: October 12, 2018
Article in press: October 12, 2018
Published online: November 6, 2018
A 60-year-old individual suffered liver cirrhosis and renal dysfunction, and was infected with multidrug-resistant hepatitis B virus (HBV) before tenofovir alafenamide (TAF) treatment.
He was diagnosed with HBeAg negative compensated liver cirrhosis at admission.
The differential diagnosis included alcoholic cirrhosis and hepatocellular carcinoma.
Laboratory tests showed that HBV DNA peaked to 2.47 log10IU/mL and the estimated glomerular filtration rate declined to < 50 mL/min/1.73 m2 before TAF treatment.
Ultrasonic tests showed liver cirrhosis and splenomegaly at admission.
Hepatocellular carcinoma was diagnosed according to liver pathology during follow-up.
Given the renal insufficiency and lack of full viral suppression under tenofovir disoproxil fumarate, TAF was started at 25 mg per day.
Grossi et al[7] reported the use of TAF as a rescue therapy in a cirrhotic patient with a history of Fanconi syndrome and multi-drug resistance, while in our case, the patient received TAF treatment and hepatocellular carcinoma (HCC) occurred during follow-up.
The pathogenesis of HCC is thought to be multifactorial, and liver cirrhosis is an important risk factor for HCC. Even though a potent NA can maintain HBV suppression, it reduces but does not eliminate the risk of HCC development.
The surveillance for HCC should be continued during TAF treatment.