The fact that continuous immunosuppression was required to prevent graft rejection in these cases may have accounted for the poor outcome with IFN therapy. No conclusions are warranted from this study about the effectiveness of the therapies that were tried. of HBsAg, something accomplished once in 16 individuals treated with -interferon, by no means in 3 individuals with passive immunization only and once in 4 individuals with no therapy. In individuals with recurrent hepatitis B disease infection, the pace of hepatitis development in the graft appeared to be accelerated, and this was particularly impressive in individuals who underwent multiple retransplantations at gradually shorter intervals. None of them of the individuals who became HBsAg-negative experienced HBeAg preoperatively. How to manage individuals with HBV who undergo transplantation after developing Aldose reductase-IN-1 end-stage chronic disease or fulminant hepatic failure (FHF) has been one of the unanswered questions in hepatology ever since it was recognized that HBV can cause early or later on graft loss (1, 2). Liver substitute transiently lowers the viral titer in the blood, as determined by serial HBsAg screening (1C5). However, the virus is definitely difficult to eradicate, almost ensuring that the viral illness will persist and that recurrent hepatitis will happen and impair the recovery and subsequent health of most recipients (3, 4, 6). Hepatitis B hyperimmune globulin Aldose reductase-IN-1 (HEIG) (5C7), hepatitis Rabbit Polyclonal to Notch 1 (Cleaved-Val1754) B vaccine (HBVx) (5) and -interferon (-IFN) (8) have been administered only or in some combination to such individuals to prevent recurrent HBV illness in the Aldose reductase-IN-1 new liver. The effectiveness of such therapies at clearing either the infection or the antigenemia is not established. This study reports observations on 59 adult individuals who experienced chronic or fulminant HBV illness at the time of liver transplantation. Follow-ups are at least 19 mo. We have compared the programs of those 59 recipients with those of 38 additional individuals with postnecrotic cirrhosis (PNC) who have been HBsAg bad but whose serum experienced anti-HBs, reflecting a earlier HBV illness and presumed subsequent immunity. MATERIALS AND METHODS Case Material From March 1, 1981, to February 28, 1988, 924 consecutive individuals who have been at least 16 yr older were treated with orthotopic liver transplantation in the Presbyterian-University Hospital of the University or college of Pittsburgh. Throughout this time, preoperative testing for HBV illness was routine for those potential recipients. At the time of their transplantation, 38 individuals were found to have anti-HBs but not HBsAg in their serum. They were designated as group 1 (HBV immune control) (Table 1). All 38 of these individuals experienced PNC, and 6 (15.8%) of these 38 had coexisting main liver tumor (PLC). Table 1 Liver transplant recipients with past or present HBV illness = chronic carrier state with little or no evidence of hepatic damage; = acute hepatitis, including examples of fulminant progression; = the transition phase from acute hepatitis to CAH, defined by bridging necrosis and a transition from panlobular to periportal hepatocyte damage; = CAH and = cirrhosis. All histopathological samples were examined by one pathologist who did not know the medical program or end result. Statistical Analysis All data are offered as imply S.D. College students checks and 2 checks were utilized for the statistical analyses. Patient survival was determined using the method of Kaplan-Meier. Comparisons between groups were made by the methods of Breslow and Mantel-Cox using the BMDP statistical software (BMDP Statistical Software, Inc., Los Angeles, CA). RESULTS Patient Survival for 60 Days Consistent with the degree of patient illness, heavy mortality occurred in group 1 and group 2 individuals within 60 days after liver transplantation. Eight individuals (21.1%) died in group 1, and 13 individuals (25.5%) died in group 2, after a mean survival time of 23. 7 24.2 (S.D.) days and 29.8 15.1 (S.D.) days, respectively. The causes of these early deaths are demonstrated in Table 3. No statistical Aldose reductase-IN-1 variations existed between group 1 and.