tacrolimus and Bile-Duct-Diseases

A safe and effective preservation solution is a precondition for liver transplantation, which is accepted as the radical treatment for patients with end-stage liver disease. The increasing use of marginal donors and non-heart beating donors as well as the establishment of a national organ allocation network call for better preservation. New preservation solutions like histidine-tryptophan-ketoglutarate (HTK) solution and Celsior solution have been introduced to liver preservation, and protective gene intervention and other modifications have also been investigated. In this article, we review recent advances in liver preservation solutions.. An English-language literature search was conducted using MEDLINE (1990-2005) on liver preservation solution, biliary complication, protective gene and other related subjects.. Although the high viscosity of the University of Wisconsin (UW) solution proved harmful to the hepatic microcirculation, three solutions showed equivalent preservation effects. When the cold ischemia time was short, there were no significant differences among the three solutions in the incidence of biliary complications. So far, modifications of preservation solutions have achieved great success. Several types of protective genes like A20, Bcl-2, Bcl-X(L) and HO-1 were reported to have definite liver protective effects. The addition of other substrates like TNF-alpha antibody, tacrolimus (FK506) and fructose-1,6-bisphosphate (FBP) can also improve the preservation effect. However, addition of insulin to UW solution is harmful to the graft.. In centers with highly-developed transplantation techniques, HTK and Celsior solutions are acceptable in liver preservation. Protective gene modification and addition of substrates like TNF-alpha antibody, FK506 and FBP are prominent approaches to improve liver preservation.

Topics: Adenosine; Allopurinol; Animals; Antibodies; Bile Duct Diseases; Disaccharides; Electrolytes; Fructosediphosphates; Glucose; Glutamates; Glutathione; Histidine; Humans; Insulin; Ischemia; Liver; Mannitol; Microcirculation; Organ Preservation Solutions; Potassium Chloride; Procaine; Raffinose; Tacrolimus; Transformation, Genetic; Tumor Necrosis Factor-alpha

Stevens-Johnson syndrome (SJS) is a serious and potentially life-threatening disease. Vanishing bile duct syndrome (VBDS) is a rare cause of progressive cholestasis. Both syndromes are mostly related with drugs. We report a case of a patient with ciprofloxacin-induced SJS and acute onset of VBDS, and reviewed the related literature. It is the first case of ciprofloxacin-induced VBDS successfully treated with tacrolimus. This case reminds physicians of the importance of drug reactions, their severity, techniques for diagnosis and methods of management.

Topics: Adult; Bile Duct Diseases; Ciprofloxacin; Deglutition Disorders; Dysuria; Female; Humans; Immunosuppressive Agents; Stevens-Johnson Syndrome; Tacrolimus; Treatment Outcome

Topics: Bile Duct Diseases; Bile Ducts, Intrahepatic; Carbamazepine; Child, Preschool; Cholestasis; Hepatitis B; Humans; Immunosuppression Therapy; Immunosuppressive Agents; Male; Methylprednisolone; Pancreatitis; Stevens-Johnson Syndrome; Tacrolimus

Acute vanishing bile duct syndrome is a rare but established cause of progressive cholestasis in adults, is most often drug or toxin related, and is of unknown pathogenesis. It has not been reported previously in children. Stevens-Johnson syndrome is a well-recognized immune complex-mediated hypersensitivity reaction that affects all age groups, is drug or infection induced, and has classic systemic, mucosal, and dermatologic manifestations. A previously healthy child who developed acute, severe, rapidly progressive vanishing bile duct syndrome shortly after Stevens-Johnson syndrome is described; this was temporally associated with ibuprofen use. Despite therapy with ursodeoxycholic acid, prednisone, and then tacrolimus, her cholestatic disease was unrelenting, with cirrhosis shown by biopsy 6 months after presentation. This case documents acute drug-related vanishing bile duct syndrome in the pediatric age group and suggests shared immune mechanisms in the pathogenesis of both Stevens-Johnson syndrome and vanishing bile duct syndrome.

Topics: Acute Disease; Adult; Bile Duct Diseases; Biopsy; Child; Cholestasis; Female; Humans; Ibuprofen; Liver; Liver Cirrhosis; Prednisone; Stevens-Johnson Syndrome; Tacrolimus; Time Factors; Ursodeoxycholic Acid