title: Hepatitis B surface antigen (HBsAg) decrease and serum interferon-inducible protein-10 levels as predictive markers for HBsAg loss during treatment with nucleoside/nucleotide analogues.
abstract: BACKGROUND
  Hepatitis B surface antigen (HBsAg) loss is the ultimate goal of antiviral therapy and its prediction may be important for treatment individualization. Quantitative HBsAg (qHBsAg) has been shown to predict response to interferon-α, but few studies have analysed qHBsAg during treatment with nucleoside/nucleotide analogues (NAs). Serum interferon-inducible protein-10 (IP-10) has been associated with treatment response in hepatitis C, but data in chronic hepatitis B are lacking. Here, we aimed to investigate potential factors predictive for HBsAg loss.
  
  
  METHODS
  HBsAg was quantified at multiple time points in 126 patients with chronic HBV infection; 95 received NA treatment for 6-107 months. At an early time point (first 6 months of therapy) and late time point after virological response (VR; HBV DNA<100 IU/ml), we distinguished three patterns of HBsAg decrease: strong decrease (>0.5 log(10)), moderate decrease (10% to 0.5 log(10)) and no decrease (<10%). In addition to conventional biochemical and virological parameters, we analysed serum IP-10 levels in 55 patients.
  
  
  RESULTS
  Early and late HBsAg kinetics did not correlate. Overall, 42% of patients with a strong HBsAg decrease 2 years after VR cleared HBsAg. Importantly, no patient without a late HBsAg decrease >0.5 log(10) cleared HBsAg. By contrast, early HBsAg decrease after 6 months of NA therapy was not associated with HBsAg loss. Baseline serum IP-10 levels were associated with late but not early HBsAg kinetics and were highest in patients with HBsAg loss.
  
  
  CONCLUSIONS
  Monitoring qHBsAg after successful HBV DNA suppression might be useful to identify patients who clear HBsAg, implicating finite NA treatment. The role of IP-10 as predictive marker for HBsAg loss should be further evaluated.
authors: Department of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.
authors: Jerzy
authors: J
authors: Jaroszewicz
authors: Huy
authors: H
authors: Ho
authors: Antoaneta
authors: A
authors: Markova
authors: Katja
authors: K
authors: Deterding
authors: Karsten
authors: K
authors: Wursthorn
authors: Sandra
authors: S
authors: Schulz
authors: Claus-Thomas
authors: CT
authors: Bock
authors: Hans L
authors: HL
authors: Tillmann
authors: Michael P
authors: MP
authors: Manns
authors: Heiner
authors: H
authors: Wedemeyer
authors: Markus
authors: M
authors: Cornberg
mesh_terms: D000328:Adult; D000998:Antiviral Agents / Q000627:therapeutic use*; D054357:Chemokine CXCL10 / Q000097:blood*; D005260:Female; D006514:Hepatitis B Surface Antigens / Q000097:blood*; D006515:Hepatitis B virus / Q000235:genetics; D019694:Hepatitis B, Chronic / Q000175:diagnosis / Q000188:drug therapy* / Q000378:metabolism; D006801:Humans; D007700:Kinetics; D008297:Male; D008875:Middle Aged; D009711:Nucleotides / Q000627:therapeutic use; D011379:Prognosis; D016896:Treatment Outcome; D055815:Young Adult
chemical_list: D000998:Antiviral Agents; D054357:Chemokine CXCL10; D006514:Hepatitis B Surface Antigens; D009711:Nucleotides