title: Large fragment pre-S deletion and high viral load independently predict hepatitis B relapse after liver transplantation.
abstract: Hepatitis B virus (HBV) associated end-stage liver diseases are the leading causes of liver transplantation (LT) in Taiwan. Relapse of hepatitis B occurs after LT, raising the risk of graft failure and reducing patient survival. Although several oral antiviral agents have been approved for anti-HBV treatment, lamivudine (LAM) remained to be the most widely used preventive regimen in Taiwan. While several clinical predictors have been identified for hepatitis B relapse, the predictive roles of the histopathological characteristics in liver explants as well as the genotypic features of the viruses in pre-LT serum samples have not been assessed. Between September 2002 and August 2009, 150 consecutive hepatitis B surface antigen (HBsAg) positive patients undergoing LT were included for outcome analysis following assessment of the clinicopathological and virological factors prior to LT. Kaplan-Meier analyses discovered that pre-operative LAM treatment ≤3 months; membranous distribution and higher expression of tissue HBsAg in liver explants; preoperative viral load ≥10(6) copies/ml; and presence of large fragment (>100 base pairs) pre-S deletion (LFpreSDel) correlated significantly with hepatitis B relapse. Multivariate Cox regression analysis showed that the presence of LFpreSDel (P = 0.001) and viral load ≥10(6) copies/mL (P = 0.023) were independent predictors for hepatitis B relapse. In conclusion, besides high viral load, LFpreSDel mutation is an important independent predictor for hepatitis B relapse after LT. More aggressive preventive strategies should be applied for patients carrying these risk factors.
authors.affiliation: Division of Liver and Transplantation Surgery, Department of General Surgery, Chang Gung Memorial Hospital, Taoyuan, Taiwan.
authors.forename: Ting-Jung
authors.initials: TJ
authors.lastname: Wu
authors.forename: Tse-Ching
authors.initials: TC
authors.lastname: Chen
authors.forename: Frank
authors.initials: F
authors.lastname: Wang
authors.forename: Kun-Ming
authors.initials: KM
authors.lastname: Chan
authors.forename: Ruey-Shyang
authors.initials: RS
authors.lastname: Soong
authors.forename: Hong-Shiue
authors.initials: HS
authors.lastname: Chou
authors.forename: Wei-Chen
authors.initials: WC
authors.lastname: Lee
authors.forename: Chau-Ting
authors.initials: CT
authors.lastname: Yeh
mesh_terms: D018572:Disease-Free Survival; D006509:Hepatitis B / Q000473:pathology / Q000517:prevention & control / Q000628:therapy* / Q000821:virology*; D006515:Hepatitis B virus / Q000235:genetics*; D006801:Humans; D007150:Immunohistochemistry; D008099:Liver / Q000473:pathology / Q000821:virology; D016031:Liver Transplantation; D015999:Multivariate Analysis; D011379:Prognosis; D016016:Proportional Hazards Models; D012008:Recurrence; D017384:Sequence Deletion / Q000235:genetics*; D016896:Treatment Outcome; D014759:Viral Envelope Proteins / Q000235:genetics*; D019562:Viral Load / Q000235:genetics*
chemical_list: C096362:L protein, hepatitis B virus; D014759:Viral Envelope Proteins