mines the outcome after OLT in patients on high dose HBIg Hepatitis B virus (HBV) infection of the liver graft is a major prophylaxis. (HEPATOLOGY 1997;26:478-484.) complication after orthotopic liver transplantation (OLT) for HBV-related cirrhosis. A high viral load before OLT is a known risk factor, whereas the relevance of precore mutants Recurrent hepatitis B virus (HBV) infection of the liver of HBV is a subject of controversy. The aim of this study was graft (HBV recurrence) is the main cause of morbidity and to correlate the pretransplantation viral load and a pretransmortality after orthotopic liver transplantation (OLT) in paplantation infection with precore mutant HBV (pmHBV) or tients with end-stage, chronic hepatitis B. Long-term (inwildtype HBV (wtHBV) with allograft damage, graft failure, definite), high-dose immunoprophylaxis with anti-hepatitis and survival after OLT. Sixty-nine patients with HBV cirrhosis B surface (HBs) hyperimmunoglobulins (HBIg) proved effecunderwent OLT under high dose immunoprophylaxis with tive in reducing the incidence of HBV recurrence. Two anti-hepatitis B surface (HBs) hyperimmunoglobulins (HBIg). well-known risk factors for recurrent HBV infection are a A pretransplantation infection with pmHBV and wtHBV was high preoperative viremia (a high serum level of HBV DNA) detected by polymerase chain reaction (PCR) and direct seand the proof of preoperative HBV replication (detectable quencing in 30 patients each (pmHBV and wtHBV group). hepatitis B virus e antigen [HBeAg]). Therefore, patients with Nine of 69 patients were PCR-negative (noHBV group). Medetectable preoperative HBV replication are considered undian pretransplantation levels of HBV DNA assessed by hysuitable for transplantation (''EUROHEP'' Consensus Report bridization assay were 42 pg/mL for pmHBV and 54 pg/mL from 1994 9 ). Precore mutants of the hepatitis B virus for wtHBV patients. HBV recurred in 17 of 30 (57%) of (pmHBV) can be associated with high rates of HBV graft pmHBV and in 14 of 30 (47%) of wtHBV patients and graft infection, graft failure and mortality after OLT, and with failure occurred in 6 of 30 (20%) of pmHBV and 7 of 30 fibrosing cholestatic hepatitis (FCH). [11][12][14][15][16] In these viruses, (23%) of wtHBV patients. Neither HBV recurrence nor graft most frequently a translational stop codon (nt. 1896 G-A) failure occurred in patients in whom no HBV DNA could be in the distal precore-gene 17 and less frequently mutations in detected by PCR using primers flanking the HBV precore the precore start codon 18 abolish the synthesis of HBeAg. region (noHBV) patients. Allograft damage assessed by histol-However, in previous studies on patients outside the liver ogy activity index (HAI) scoring was median 6 for pmHBV transplantation setting, an infection with pmHBV was not and 7 for wtHBV patients. Cumulative survival after 5 years necessarily associated with severe, acute, or chronic hepatitis was 72% for pmHBV, 74% for wtHBV, and 100% for noHBV but was also found in chronic carriers without hepatitis. 19,20 patients. In this study, we provide evidence that pretrans-The clinical impact of pmHBV as a risk factor for a poor plantation viral load, but not infection with pmHBV, deteroutcome after OLT would be considerable because pmHBV are the most frequent mutants of HBV worldwide.
The aim of our study was to examine whether a preopera-Abbreviations: HBV, hepatitis B virus; OLT, orthotopic liver transplantation; Hbs, tive infection with pmHBV or wildtype HBV (wtHBV) influhepatitis B surface; HBIg, anti-HBs hyperimmunoglobulins; HBeAg/, seropositive for ences the rate of HBV recurrence, the severity of graft hepatihepatitis B virus e antigen; pmHBV, precore mutant HBV; FCH, fibrosing cholestatic tis, the occurrence of FCH, the rate of graft failure, and the hepatitis; wtHBV, wildtype HBV; HBsAg, hepatitis B surface antigen; HDV, hepatitis survival in a large group of patients with end-stage chronic delta virus; HCV, hepatitis C virus; HBe, hepatitis B e core; PCR, polymerase chain reaction; HAI, histology activity index; noHBV, patients in whom no HBV DNA could hepatitis B. We compared the relative amount of HBV viremia be detected by PCR using primers flanking the HBV precore region.