title: Serum interferon-inducible protein 10 levels predict hepatitis B s antigen seroclearance in patients with chronic hepatitis B.
abstract: BACKGROUND
  Hepatitis B s antigen (HBsAg) seroclearance is regarded as the optimal virological end-point.
  
  
  OBJECTIVE
  To investigate the dynamic changes in serum cytokine levels around the time of HBsAg seroclearance.
  
  
  METHODS
  This was a case-control study. Consecutive patients with chronic hepatitis B (CHB) who lost HBsAg were matched with those remained positive for HBsAg with same age, gender, HBeAg status and presence of cirrhosis in 1:2 ratio. Relevant serum cytokines [interleukin (IL)-2, IL-3, IL-4, IL-7, IL-9, IL-10, IL-12, IL-15, IL-21 interferon-γ, tumour necrosis factor-α (TNF-α), granulocyte macrophage colony-stimulating factor (GM-CSF) and interferon-inducible protein 10 (IP-10)] were assayed at the time (Year 0) and 3 years before (Year -3) HBsAg seroclearance.
  
  
  RESULTS
  Seventy-one and 142 CHB patients who did and did not achieve HBsAg seroclearance were included. Mean age was 48 ± 11 years; 76% were male, 20% had positive HBeAg, 99 (46%) patients received anti-viral therapy, and mean baseline HBV DNA was 3.78 ± 2.28 log IU/mL vs. 4.36 ± 2.13 log IU/mL respectively (P = 0.05). In those who achieved HBsAg seroclearance, serum IL-15 and GM-CSF levels decreased significantly from Year -3 to Year 0 (P = 0.017 and 0.05 respectively). When compared to controls, only serum IP-10 level was significantly lower at Year 0 than at Year -3 in patients with HBsAg seroclearance. Lower serum IP-10 level at Year 0 was the only factor associated with HBsAg seroclearance. There was no correlation between serum IP-10 and HBsAg levels around the time of HBsAg seroclearance.
  
  
  CONCLUSIONS
  Lower serum IP-10 level at Year 0 was the only factor associated with HBsAg seroclearance.
authors.affiliation: Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong.|Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong.|State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong.
authors.forename: G L-H
authors.initials: GL
authors.lastname: Wong
authors.affiliation: Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong.|Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong.|State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong.
authors.forename: H L-Y
authors.initials: HL
authors.lastname: Chan
authors.affiliation: Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong.|Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong.|State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong.
authors.forename: H-Y
authors.initials: HY
authors.lastname: Chan
authors.affiliation: Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong.|Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong.|State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong.
authors.forename: C-H
authors.initials: CH
authors.lastname: Tse
authors.affiliation: Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong.|Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong.
authors.forename: A M-L
authors.initials: AM
authors.lastname: Chim
authors.affiliation: Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong.|Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong.
authors.forename: A O-S
authors.initials: AO
authors.lastname: Lo
authors.affiliation: Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong.|Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong.|State Key Laboratory of Digestive Disease, The Chinese University of Hong Kong, Hong Kong.
authors.forename: V W-S
authors.initials: VW
authors.lastname: Wong
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D016207:Cytokines / Q000097:blood* / Q000378:metabolism; D005260:Female; D006509:Hepatitis B / Q000276:immunology; D006514:Hepatitis B Surface Antigens / Q000097:blood* / Q000378:metabolism; D006513:Hepatitis B e Antigens / Q000097:blood; D006515:Hepatitis B virus / Q000276:immunology; D019694:Hepatitis B, Chronic / Q000276:immunology*; D006801:Humans; D016753:Interleukin-10 / Q000378:metabolism; D007378:Interleukins; D008103:Liver Cirrhosis / Q000276:immunology; D008297:Male; D008875:Middle Aged; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D000098546:Interleukin-21
chemical_list: D016207:Cytokines; D006514:Hepatitis B Surface Antigens; D006513:Hepatitis B e Antigens; C508609:IL10 protein, human; D007378:Interleukins; C439524:TNF protein, human; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D000098546:Interleukin-21