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Hepatitis B surface antigen loss and clinical outcomes between HBeAg‐negative cirrhosis patients who discontinued or continued nucleoside analogue therapy
Author(s) -
Hung C.H.,
Wang J.H.,
Lu S.N.,
Hu T.H.,
Lee C.M.,
Chen C.H.
Publication year - 2017
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.12683
Subject(s) - medicine , entecavir , gastroenterology , cirrhosis , hbeag , hepatocellular carcinoma , hbsag , decompensation , nucleoside analogue , hepatitis b , incidence (geometry) , hepatitis b virus , immunology , virus , lamivudine , nucleoside , stereochemistry , chemistry , physics , optics
Summary We investigated the incidence and predictors of post‐treatment hepatitis B virus ( HBV ) relapse and hepatitis B surface antigen ( HB sAg) loss. After cessation of nucleoside analogue (NA) treatment in hepatitis B e antigen (HBeAg)‐negative patients with cirrhosis. The rates of HB sAg loss and hepatocellular carcinoma ( HCC ) development in HB eAg‐negative patients with cirrhosis who continued NA treatment were compared with those who discontinued treatment. Patients with compensated cirrhosis who had discontinued NA treatment for at least 12 months (discontinuing group; n=73) and patients who continued entecavir treatment for at least 4 years (continuing group; n=158) were recruited. Serum HB sAg levels were analysed at the end of treatment (discontinuing group) or at 2.5‐3 years of treatment (continuing group). In the discontinuing group, the 6‐year cumulative incidence of post‐treatment virological relapse and HB sAg loss were 56.3% and 46.7%, respectively. The end‐of‐treatment HB sAg level of 300 IU/mL was a cut‐off value for subsequent post‐treatment HB sAg loss and sustained response. In the continuing group, HB sAg loss occurred in five of 158 patients. Cox regression analysis showed that HB sAg levels in the discontinuing group were independent predictors for HB sAg loss in all patients and 104 propensity score ( PS )‐matched patients. There was no significant difference in HCC development between the groups in all patients and 104 PS ‐matched patients. Two patients experienced post‐treatment alanine aminotransferase flare with hepatic decompensation, and neither of them died after retreatment. In conclusion, HB eAg‐negative patients with cirrhosis who discontinued NA treatment might have a higher rate of HB sAg loss and their risk of developing HCC did not increase compared with those who continued entecavir treatment.