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Administration of carbon tetrachloride to rats resulted in induction of hepatic fibrosis and a 60% reduction of hepatic S‐adenosylmethionine synthetase activity without producing any significant modification of hepatic levels of S‐adenosylmethionine synthetase messenger RNA. The reduction of S‐adenosylmethionine synthetase activity was corrected by treatment with S‐adenosylmethionine (3 mg/kg/day, intramuscularly). Administration of carbon tetrachloride also produced a 45% depletion of liver glutathione (reduced form) that was corrected by S‐adenosylmethionine treatment. After the rats received carbon tetrachloride, a 2.3‐fold increase in liver collagen was observed; prolyl hydroxylase activity was 2.5 times greater than that seen in controls. These increases were attenuated in animals treated with carbon tetrachloride and S‐adenosylmethionine. The attenuation by S‐adenosylmethionine treatment of the fibrogenic effect of carbon tetrachloride was associated with a decrease in the number of rats in which cirrhosis developed. (HEPATOLOGY 1992;16:1022–1027.)

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Caroli's disease is an uncommon congenital disorder of the intrahepatic biliary tree. It is characterized by multiple and segmental dilatations of the bile ducts. The clinical course of Caroli's disease is often complicated by recurrent episodes of bacterial cholangitis that seriously impair the patient's quality of life. Despite wide spectrum antimicrobial agents, medical treatment of cholangitis is frequently unsuccessful in patients with Caroli's disease due to the persistence of bacteria in dilatated bile ducts. Other therapies, including internal or external biliary drainages and various surgical or endoscopic procedures, have been used in the treatment of Caroli's disease, with poor results. There are no previous reports in the literature of liver transplantation for recurrent cholangitis in patients with Caroli's disease. We present two such cases, in which cholangitis is resolved.

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Four liver transplant recipients treated with cyclosporine developed a reversible neurologic syndrome characterized by a speech disorder leading to mutism. This complication, previously reported in a few liver transplant recipients treated with the immunosuppressive drug FK506, had not been described with cyclosporine. Recognition of this syndrome should prompt withdrawal of the drug and avoidance of unnecessary diagnostic procedures.

Response to antirejection treatment in ACR in liver transplantation can be predicted by several clinical and laboratory data. ACR episodes with factors predictive of therapeutic unresponsiveness could benefit from more aggressive antirejection treatment.