Premium
Low incidence of hepatitis B virus reactivation and subsequent hepatitis in patients with chronic hepatitis C receiving direct‐acting antiviral therapy
Author(s) -
Tamori A.,
Abiru S.,
Enomoto H.,
Kioka K.,
Korenaga M.,
Tani J.,
Enomoto M.,
Sugiyama M.,
Masaki T.,
Kawada N.,
Yatsuhashi H.,
Nishiguchi S.,
Mizokami M.
Publication year - 2018
Publication title -
journal of viral hepatitis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 100
eISSN - 1365-2893
pISSN - 1352-0504
DOI - 10.1111/jvh.12840
Subject(s) - medicine , virology , incidence (geometry) , chronic hepatitis , antiviral therapy , hepatitis a virus , hepatitis , hepatitis virus , gastroenterology , virus , physics , optics
Summary To determine the clinical characteristics of hepatitis B virus ( HBV ) reactivation in patients undergoing interferon‐free antihepatitis C virus ( HCV ) therapy, we examined HBV DNA in 25 HBV co‐infected patients and 765 patients with resolved HBV infection during and after treatment with direct‐acting antiviral agents ( DAA s). Among those with HCV genotype 1, asunaprevir plus daclatasvir was administered to 160 patients, sofosbuvir ( SOF ) plus ledipasvir to 438 patients and paritaprevir plus ombitasvir and ritonavir to 25 patients. In total, 167 patients with genotype 2 were treated with SOF plus ribavirin. Three patients with an HBV DNA level ≥2000 IU / mL were treated with entecavir before anti‐ HCV therapy, without reactivation of HBV . In 3 of 22 (12%) HBV surface antigen ( HB sAg)‐positive patients with an HBV DNA level <2000 IU / mL , the viral load increased during treatment. However, hepatitis flare did not occur in these patients. There was no significant difference in clinical history between patients with and without HBV reactivation. Among 765 patients with resolved HBV infection, HBV reactivation occurred in 1 (0.1%) patient after initial resolution, whose HBV DNA level spontaneously decreased after DAA therapy. We compared anti‐ HB s titres at baseline with those at post‐ DAA therapy in 123 patients without HB sAg. There was no significant difference in anti‐ HB s levels between the two points ( P = .79). In conclusion, HBV reactivation was rare in HB sAg‐negative patients treated with DAA therapy. Additionally, hepatitis did not occur in HBV ‐reactivated patients with a baseline HBV DNA level <2000 IU / mL before DAA therapy.