title: A decline in hepatitis B virus surface antigen (hbsag) predicts clearance, but does not correlate with quantitative hbeag or HBV DNA levels.
abstract: BACKGROUND
  The elimination of hepatitis B virus surface antigen (HBsAg) is the final goal of hepatitis B treatment, but is rarely achieved. As quantitative assays for HBsAg recently became available, we have investigated whether quantitative HBsAg measurements can substitute for hepatitis B virus (HBV) DNA quantification in treatment monitoring.
  
  
  METHODS
  Within this study, 23 liver transplant patients and 18 heart transplant recipients were retrospectively analysed. Patients had been treated with famciclovir and/or lamivudine, in addition some had also received adefovir in cases of lamivudine resistance. Quantitative HBsAg and hepatitis B virus e antigen (HBeAg) levels were determined with the Architect assay. HBV DNA levels were determined with different assays available at given time points.
  
  
  RESULTS
  We did not find a significant correlation between either HBsAg or HBeAg and HBV DNA levels - both in treated and untreated patients. More importantly, there was no significant concordance between an increase or decrease of HBsAg or HBeAg with HBV DNA. However, the curve and decline of quantitative HBsAg enabled prediction of eventual viral clearance. Eight patients showed a 2 log10 drop of HBsAg levels and eight patients demonstrated a reduction of HBsAg levels below 100 IU/ml; five patients fulfilled both criteria. Three of those five cleared HBsAg and became positive for antibodies against HBsAg.
  
  
  CONCLUSIONS
  Quantitative HBsAg and HBeAg cannot substitute for HBV DNA quantification during the assessment of antiviral therapy; however, the decline of HBsAg does predict eventual HBsAg clearance. A 2 log10 drop to below 100 IU/ml is associated with a high likelihood of HBsAg clearance.
authors.affiliation: Abteilung Gastroenterologie, Hepatologie und Endokrinologie, Medizinische Hochschule Hannover, Hannover, Germany.
authors.forename: Johannes
authors.initials: J
authors.lastname: Wiegand
authors.forename: Heiner
authors.initials: H
authors.lastname: Wedemeyer
authors.forename: Andrea
authors.initials: A
authors.lastname: Finger
authors.forename: Benjamin
authors.initials: B
authors.lastname: Heidrich
authors.forename: Jens
authors.initials: J
authors.lastname: Rosenau
authors.forename: Gerd
authors.initials: G
authors.lastname: Michel
authors.forename: C Thomas
authors.initials: CT
authors.lastname: Bock
authors.forename: Michael P
authors.initials: MP
authors.lastname: Manns
authors.forename: Hans L
authors.initials: HL
authors.lastname: Tillmann
mesh_terms: D015075:2-Aminopurine / Q000031:analogs & derivatives / Q000627:therapeutic use; D000998:Antiviral Agents / Q000627:therapeutic use*; D004279:DNA, Viral / Q000097:blood*; D000077595:Famciclovir; D005260:Female; D016027:Heart Transplantation / Q000009:adverse effects; D006509:Hepatitis B / Q000188:drug therapy* / Q000821:virology; D006514:Hepatitis B Surface Antigens / Q000097:blood*; D006513:Hepatitis B e Antigens / Q000097:blood*; D006515:Hepatitis B virus / Q000187:drug effects*; D006801:Humans; D019259:Lamivudine / Q000627:therapeutic use; D016031:Liver Transplantation / Q000009:adverse effects; D008297:Male; D011237:Predictive Value of Tests; D016896:Treatment Outcome
chemical_list: D000998:Antiviral Agents; D004279:DNA, Viral; D006514:Hepatitis B Surface Antigens; D006513:Hepatitis B e Antigens; D019259:Lamivudine; D015075:2-Aminopurine; D000077595:Famciclovir