These results show that immunosuppression with MP inhibits both spontaneous tolerance and rejection of liver allografts in a rat model and question the efficacy of administering MP to all liver allograft recipients from the time of transplantation.

We retrospectively examined 154 adults to ascertain the frequency, site of and pre-disposing factors for biliary strictures after liver transplantation, as well as their management and clinical outcome. Twenty patients (12.5%) were identified with biliary strictures; 16 were non-anastomotic and four were anastomotic strictures. The median time from transplantation to stricture diagnosis was 17 weeks (range 3-366). Of the 16 non-anastomotic strictures, six were intrahepatic, eight hilar and two extrahepatic (donor bile duct). A control group (n = 32) of patients transplanted immediately before and after index cases was used to examine for correlates in patients with non-anastomotic strictures. At the time of diagnosis in the non-anastomotic index cases, there was a higher incidence of: (i) biliary sludge (63 vs 0%; P < 0.001); and (ii) clinical cholangitis (75 vs 0%; P < 0.001) compared with controls. Primary sclerosing cholangitis was more often the diagnosis in index patients with non-anastomotic strictures compared with controls (31 vs 9%; P < 0.05). There were no differences between index patients and controls (non-anastomotic group) in ABO blood group non-identity, cold allograft ischaemia time, use of OKT3 (murine monoclonal antibody to CD3) and hepatic artery thrombosis. Of 15 patients treated with balloon dilatation, seven required stent insertion although none have required surgery. As determined by liver function tests, there was evidence of persisting graft dysfunction in index patients compared with controls (SAP 381 vs 112 U/L, P < 0.001; GGT 529 vs 80 U/L, P < 0.001), but there was no difference in survival during a median follow-up time of 16 months (range: 3-48 months) from stricture diagnosis. In conclusion, biliary strictures tend to occur within 6 months of transplantation and are an important cause of ongoing graft dysfunction. Non-anastomotic strictures were more common in patients requiring transplantation for primary sclerosing cholangitis.

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Objectives To report the experience of the Australian National Liver Transplant Unit with patients with fulminant hepatic failure and to describe the role of liver transplantation. Patients: Twenty‐seven patients presented with acute or subacute fulminant hepatic failure during the period from January, 1986, to March, 1990. Twenty‐two had acute arid five had subacute fulminant hepatic failure. The causes were hepatitis B in 10 patients, presumed non‐A, non‐B {NANB) hepatitis in eight patients, drug‐induced hepatic damage in five patients, and Wilson's disease in four patients. There were 13 males and 14 females. Ages were 2–43 years (mean, 23). Twenty patients (74%) were in grade IV encephalopathy on presentation. Results Six patients (22%) began to improve soon after admission and went on to full recovery. Spontaneous recovery was more frequent in patients with drug‐induced hepatic damage (four patients [80%]) and was less frequent in those with hepatitis B (one patient [10% and NANB hepatitis (one patient [12%. The other 21 patients (78%) were considered for orthotopic liver transplantation. Eight (30%) were judged to be unsuitable and went. on to early death. Thirteen (48%).were suitable for transplantation. Of these five (19%) died before a liver donor became available and eight (30%) received liver grafts and went. on to full recovery. Overall, 14 patients (52%) survived and 13 (48%) died. Patients with Wilson's disease (four [100% were most suitable for orthotopic liver transptantatlon whereas eight (44%) of those with hepatitis B or NANB hepatitis were unsuitable. Of the eight patients receiving liver grafts one. had hepatitis B, three had NANB hepatitis and four had Wilson's disease. Five were in grade IV encephalopathy at the time of operation. The mean waiting time for transplantation was 6.4 days. Five patients received ABO blood group compatible grafts and three received ABO incompatible grafts. Of the latter group, two subsequently required secondary orthotopic liver transplantation with ABO compatible grafts. All eight patients who received transplants are alive and well 3–24 months after the operation. No patient has any neurological sequelae. Conclusions Orthotopic liver transplantation is a preferred option. for patients with fulminant hepatic failure whose condition is not responding to conservative management. ABO incompatible livers transplanted in emergency circumstances may prove lifesaving either by functioning successfully or by providing time during which ABO compatible grafts become available. Despite the availability of liver transplantation, many patients with fulminant hepatic failure in Australia still die, some before hepatic transplantation can be undertaken. Early referral of patients with fulminant hepatic failure to established centres with liver transplantation programmes is required.