title: Increasing hepatitis B viral load is associated with risk of significant liver fibrosis in HBeAg-negative but not HBeAg-positive chronic hepatitis B.
abstract: OBJECTIVE
  To evaluate the association between demographical features, serum ALT and HBV DNA and the prevalence of significant fibrosis and inflammation on liver biopsy in patients with chronic hepatitis B.
  
  
  METHODS
  In this cross-sectional study of patients on St Vincent's Hospital HBV database, patients were classified into three groups on the basis of HBeAg status and HBV DNA level and the prevalence of significant (F2/3/4) fibrosis and (A2/3) inflammation in each group was established. Patients were also divided into HBeAg-positive and -negative groups and examined for the prevalence of significant fibrosis/inflammation in the strata of HBV DNA and ALT. Predictors of significant fibrosis and inflammation in HBeAg-positive and -negative patients were examined by logistic regression.
  
  
  RESULTS
  Three hundred and ninety four patients (HBeAg positive=198; HBeAg negative=196) with liver biopsy were identified. Fifty-eight percent of HBeAg-negative patients with HBV DNA >25,000 IU/ml had F2/3/4 fibrosis. HBV DNA and F2/3/4 were positively correlated in HBeAg-negative patients [odds ratio (OR) 1.42, P=0.001] but inversely correlated in HBeAg-positive patients (OR 0.71, P=0.03). HBV DNA was an independent predictor of significant fibrosis in HBeAg negative (P=0.03) but not HBeAg-positive patients. In HBeAg-positive patients, age was the only predictor of significant fibrosis (P=0.001) and ALT the only predictor of significant inflammation (P=0.003). In the whole cohort there was a close positive association between inflammation and fibrosis.
  
  
  CONCLUSIONS
  Increasing levels of HBV DNA are associated with increasing prevalence of significant fibrosis only in patients with HBeAg-negative CHB.
authors.affiliation: Department of Gastroenterology, St Vincent's Hospital, Fitzroy, Vic., Australia. catherine.croagh@svhm.org.au
authors.forename: Catherine M N
authors.initials: CM
authors.lastname: Croagh
authors.forename: Sally J
authors.initials: SJ
authors.lastname: Bell
authors.forename: John
authors.initials: J
authors.lastname: Slavin
authors.forename: Yu X G
authors.initials: YX
authors.lastname: Kong
authors.forename: Robert Y
authors.initials: RY
authors.lastname: Chen
authors.forename: Stephen
authors.initials: S
authors.lastname: Locarnini
authors.forename: Paul V
authors.initials: PV
authors.lastname: Desmond
mesh_terms: D000410:Alanine Transaminase / Q000378:metabolism; D000704:Analysis of Variance; D001706:Biopsy; D003430:Cross-Sectional Studies; D006513:Hepatitis B e Antigens / Q000378:metabolism*; D006515:Hepatitis B virus / Q000502:physiology*; D019694:Hepatitis B, Chronic / Q000453:epidemiology* / Q000473:pathology* / Q000821:virology*; D006801:Humans; D008099:Liver / Q000473:pathology*; D016017:Odds Ratio; D018709:Statistics, Nonparametric; D014739:Victoria / Q000453:epidemiology; D019562:Viral Load / Q000502:physiology*
chemical_list: D006513:Hepatitis B e Antigens; D000410:Alanine Transaminase