EASL 2018 FRI-319
Durability of HBsAg loss during or after antiviral treatment in a
predominantly middle European collective
G. Teuber1, M. Sprinzl2, D. Hüppe3, R. Heyne4, W.P. Hofmann5,
M. Cornberg6, S. Arne7, J. Petersen8. 1Praxis PD Dr. med. G: Teuber,
Frankfurt/M, Germany; 2UNI-Klinikum, I. Medizinische Klinik, Mainz,
Germany; 3Center of Gastroenterology, Center of Gastroenterology,
Herne, Germany; 4Leberzentrum am Checkpoint, Leberzentrum am
Checkpoint, Berlin, Germany; 5Praxis Wolf Peter Hofmann, Berlin,
Germany; 6Department of Gastroenterology, Hepatology and
Endocrinology, Hannover Medical School, Hannover, Germany;
7Diabetes Zentrum Mergentheim, Diabetes Zentrum Mergentheim, Bad
Mergentheim, Germany; 8IFI-institute for interdisciplinary medicine,
Hamburg, Germany
Email: [email protected]
Background and Aims: Concerning the durability of HBsAg loss
during or after antiviral treatment only a few data are available
indicating a high rate of reactivation with reccurance of HBsAg and/or
HBV-DNA of up to 16% in Asian patients. This may be due to the high
percentage of patients with perinatal infection in these countries.
There are no data from european patients available concerning the
durability of HBsAg loss during or after antiviral treatment and the
impact on further clinical outcome.
Method: In this retrospective german multicentre study,143 patients
with chronic hepatitis B (mean age: 43 ± 13.8 years, 93 males, 50
females) who lost HBsAg during or after antiviral treatment with
peginterferon-α and/or nucleos(t)ides between april 2008 and july
2014 were included. Before antiviral treatment, 15 patients had
established liver cirrhosis and 2/15 hepatocellular carcinoma,
receiving partial liver resection. Primary end pointswere reactivation
with reccurrence of HBsAg Further endpoints were clinical progressive
liver disease, liver transplantation and death.
Results: During the follow-up period (mean: 3.0 ± 2.1 years) a
recurrence of HBsAg was observed in only 3/143 patients (2.1%),
none with previous seroconversion to Anti-HBs. The HBV reactivation
in these patients was not associated with detectable HBV-DNA levels
or a rise in ALT-levels. 2/3 patients had baseline cirrhosis and 1/2
subsequently died due to recurrent multifocal hepatocellular
carcinoma. Among the 140 patients with persisting HBsAg loss, two
initially cirrhotic patients died and one received liver transplantation
all due to hepatocellular carcinoma.
Conclusion: In a predominantly caucasian patient population HBsAg
loss during and/or after antiviral treatment seems to be durable with
low rates of reactivation. Cirrhotic patients, however, have a high risk
for developing hepatocellular carcinoma even after HBsAg loss and
regular surveillance in these patients seems to be mandatory.
