Serum HBV DNA significantly decreased from week 0-24 in patients treated with entecavir.
Both tenofovir alafenamide (TAF) and entecavir (ETV) are safe and effective at treating hepatitis B virus (HBV) reactivation.
A team, led by Kento Inada, Department of Gastroenterology and Hepatology, Musashino Red Cross Hospital, examined the efficacy and safety of TAF for hepatitis B virus reactivation.
HBV reactivation is classified as the reactivation of HBV DNA during cytotoxic or immunosuppressive therapy in patients who were previously treated for hepatitis B virus infections.
The reactivations can be asymptomatic but are commonly followed by a clinical flare characterized by a substantial increase in serum transaminase levels and histologic evidence of active inflammation, which could lead to fatal hepatic failure.
After HBV infects the host cells, the covalently closed circular DNA is stable in the infected cells and serves as a template for viral replication.
Tenofovir alafenamide was designed to have greater plasma stability compared to tenofovir disoproxil fumarate.
However, there is little known about the administration of tenofovir alafenamide for either the prevention or treatment of hepatitis B virus reactivation.
In the study, the investigators examined 77 patients treated with either entecavir (n = 66) and tenofovir alafenamide (n = 11) as a prophylaxis against or treatment of HBV reactivation during chemotherapy or immune suppression therapy between January 2010 and June 2020.
Baseline levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), HBeAg, HBsAg, HBV core antibody (HBcAb), HBsAb, serum HBV DNA, creatinine, and estimated glomerular filtration rate (eGFR) were measured at baseline.
The investigators also quantified HBV DNA by real-time polymerase chain reaction (Roche) and HBeAg and HBV genotypes were confirmed by commercially available enzyme immunoassay kits.
The investigators assessed antiviral effects and safety and used Student's t-test or the Mann–Whitney U-test to analyze the changes in continuous variables.
They also used Fisher’s exact test for analyses of categorical variables.
The team found at week 24 the antiviral effects on patients receiving either treatment were similar in terms of reduction of HBV DNA (−2.83 ± 1.45log IU/mL vs −3.05 ± 2.47log IU/mL; P = 0.857). There was also similar results of achieving undetectable levels of HBV DNA (78.8 vs 90.9%; P = 0.681) between the 2 cohorts.
Also, serum HBV DNA significantly decreased from week 0-24 in patients treated with entecavir (3.27 ± 1.72/0.43 ± 0.94 Log IU/mL, at week 0/24, respectively, P < 0.001) and tenofovir alafenamide (3.34 ± 2.98/0.29 ± 0.96 Log IU/mL at week 0/24, respectively, P = 0.005).
The safety was also similar between the 2 groups.
The investigators did not see significant differences in the decrease in estimated glomerular filtration rate (eGFR) between the entecavir and tenofovir alafenamide treatment groups (−0.62 ± 11.2 mL/min/1.73 m2 vs −3.67 ± 13.2 mL/min/1.73 m2; P = 0.291).
There was also no significant decrease in the eGFR of patients who received entecavir (70.7 ± 21.6/70.1 ± 20.7 mL/min/1.73 m2, at week 0/24, respectively, P = 0.865) or tenofovir alafenamide (72.2 ± 19.0/68.6 ± 18.2 mL/min/1.73 m2, at week 0/24, respectively, P = 0.185).
In the tenofovir alafenamide group, 2 patients were treated for de novo hepatitis, 1 patient was treated for HBV reactivation with serum HBV DNA elevation, and the remaining 8 patients took tenofovir alafenamide for prophylaxis against HBV reactivation.
“In conclusion, TAF and ETV are safe and effective against HBV reactivation,” the authors wrote. “TAF may lead to better outcomes due to its accessibility and better patient adherence.”
The study, “Tenofovir alafenamide for prevention and treatment of hepatitis B virus reactivation and de novo hepatitis,” was published online in the Journal of Gastroenterology and Hepatology.