Viral and Host Responses After Stopping Long-term Nucleos(t)ide Analogue Therapy in HBeAg-Negative Chronic Hepatitis B - Christoph Höner zu Siederdissen1,a,
- Franziska Rinker1,3,a,
- Benjamin Maasoumy1,
- Steffen B. Wiegand1,
- Natalie Filmann4,
- Christine S. Falk2,
- Katja Deterding1,
- Kerstin Port1,
- Carola Mix1,
- Michael P. Manns1,2,3,
- Eva Herrmann4,
- Heiner Wedemeyer1,2,3,
- Anke R. M. Kraft1,3 and
- Markus Cornberg1,3
- 1Department of Gastroenterology, Hepatology and Endocrinology
- 2Institute of Transplant Immunology, IFB-Tx, Hannover Medical School
- 3German Center for Infection Research, partner site Hannover-Braunschweig
- 4Institute of Biostatistics and Mathematical Modeling, Faculty of Medicine, Goethe-University, Frankfurt am Main, Germany
- Correspondence: M. Cornberg, Hannover Medical School, Carl-Neuberg Strasse 1, 30625 Hannover, Germany (cornberg.markus{at}mh-hannover.de).
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Presented in part: European Association for the study of the liver, Vienna, 22-26 April 2015; International Viral Hepatitis Congress, Berlin, 26–28 June 2015. -
↵a C. H. z. S. and F. R. contributed equally to this work.
Abstract This prospective study investigated viral and host markers after stopping long-term therapy with nucleos(t)ide analogues in noncirrhotic patients with hepatitis B e antigen–negative chronic hepatitis B. After stopping therapy, 13 of 15 patients experienced a virological relapse. Rebound of hepatitis B virus DNA and hepatitis B core-related antigen was associated with induction of plasma tumor necrosis factor, interleukin (IL) 10 , IL-12p70, CXCL10 and subsequent decline in hepatitis B surface antigen (HBsAg), with 20% HBsAg loss after long-term follow-up. The peak levels of hepatitis B virus DNA and hepatitis B core-related antigen after cessation of therapy were positively correlated with the level of HBsAg decline at week 48. Thus, stopping or interrupting NA treatment should be further investigated as a strategy to accelerate HBsAg loss.
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发表于 2016-10-29 17:10