DAA treatment for HCV raises risk for potential HBV reactivation
Patients with chronic hepatitis C and a current hepatitis B infection have a potential risk for HBV reactivation during direct-acting antiviral therapy, according to the results of a prospective study.
“There is increasing concern regarding hepatitis flare related to HBV reactivation during DAA therapy in [chronic HCV] patients with current or past HCV infections,” the researchers wrote. “The current study demonstrated that there is no impact of HBV exposure on [chronic HCV] treatment with pan-oral DAA in high HBV endemic areas, such as Taiwan, in terms of HCV efficacy. However, we also found that patients still carried the risk of HBV virological reactivation with a clinical hepatitis flare-up during therapy.”
Researchers conducted the study in one tertiary hospital in Taiwan between December 2013 and August 2016 and evaluated 64 chronic HCV patients treated with DAA therapy. Seven patients had current HBV infections (positive hepatitis B surface antigen, or HBsAg) and 57 had past HBV infections (negative HBsAg/positive hepatitis B core antibody, or Anti-HBc). Mean patient age was 63 years and 26.6% were men. Twenty-two patients had liver cirrhosis and four had hepatocellular carcinoma.
Twenty-three patients received Harvoni (ledipasvir/sofosbuvir, Gilead Sciences), 17 received Sovaldi (sofosbuvir, Gilead Sciences) plus ribavirin, 15 received Daklinza (daclatasvir, Bristol-Myers Squibb) and nine received Viekira Pak (paritaprevir/ritonavir/ombitasvir/dasabuvir, AbbVie).
Regarding patients with past HBV infections, two had clinical reactivation at week 4, one at week 8 and one at end of treatment, but no patients had virological reactivation during treatment.
Of the seven patients with a current HBV infection, three patients had detectable pre-treatment HBV DNA levels of 127,998 IU/mL and 16,600 IU/mL and four had no detectable HBV DNA. The patient with detectable HBV DNA of 16,600 IU/mL had a virological and clinical reactivation. Three of the patients without detectable HBV DNA at baseline had virological reactivation. One had HBV DNA reappearance at week 1 and one had reappearance at week 4, while there was an HBV DNA surge in the third patient at week 8 that spontaneously declined to an undetectable level by the end of treatment.
No mortality, liver transplantation or obvious fluctuation of the HBsAg level was observed in any patient. Due to the small sample size, the researchers were unable to analyze the factors associated with HBV reactivation.
“The mechanism through which HBV reactivation occurs remains unknown. Prior studies have demonstrated that hepatitis C virus might suppress hepatitis B virus, but the mechanism remains uncertain,” the researchers wrote. “Although [interferon]-based therapy was effective in the treatment of HBV/HCV dually infected patients, HBV reactivation after HCV eradication has also been reported with IFN-based therapy for HBV/HCV dually infected patients. Interestingly, HBV reactivation was not reported in patients with an occult HBV infection with [pegylated-interferon]-based therapy but was reported in those with pan-oral DAA therapy. The distinct mechanism that was involved was considered but requires further investigation.” – by Talitha Bennett
Disclosure: The researchers report no relevant financial disclosures.