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Development of nonalcoholic fatty liver disease after orthotopic liver transplantation for cryptogenic cirrhosis
Author(s) -
Contos Melissa J.,
Cales Wendy,
Sterling Richard K.,
Luketic Velimir A.,
Shiffman Mitchell L.,
Mills A. Scott,
Fisher Robert A.,
Ham John,
Sanyal Arun J.
Publication year - 2001
Publication title -
liver transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.814
H-Index - 150
eISSN - 1527-6473
pISSN - 1527-6465
DOI - 10.1053/jlts.2001.23011
Subject(s) - medicine , cirrhosis , gastroenterology , liver transplantation , steatosis , nonalcoholic fatty liver disease , steatohepatitis , liver biopsy , alcoholic liver disease , primary sclerosing cholangitis , fatty liver , transplantation , biopsy , disease
Many subjects with cryptogenic cirrhosis have underlying nonalcoholic steatohepatitis (NASH). The natural history of NASH‐related cryptogenic cirrhosis after orthotopic liver transplantation (OLT) is not well defined. A primarily retrospective study of patients with the clinical histological phenotype of NASH‐related cirrhosis undergoing OLT was performed. Data were compared with 2 sets of age‐ and weight‐matched controls with (1) primary biliary cirrhosis or primary sclerosing cholangitis or (2) alcoholic liver disease. After OLT, all patients were managed by a standard immunosuppressive protocol. Liver biopsies were performed at 6 and 12 months after OLT and at 1‐ to 2‐year intervals thereafter, as well as when liver enzyme levels were elevated enough to warrant diagnostic biopsy. Twenty‐seven subjects with cryptogenic cirrhosis and a clinical histological phenotype of NASH and 3 patients with a long‐standing diagnosis of NASH before OLT were included. The 30‐day perioperative mortality was 1 in 30 patients. During a median follow‐up of 3.5 ± 2.7 years, 2 additional patients died of sepsis. There was a time‐dependent increase in the risk for allograft steatosis that approached 100% by 5 years compared with only an approximately 25% incidence of steatosis in the control groups ( P < .009, log‐rank test). On multivariate analysis, only the cumulative steroid dose correlated with time to development of allograft steatosis. Three patients developed histological progression from hepatic steatosis to steatohepatitis. Of these, 1 patient developed progressive fibrosis. Four patients experienced at least 1 episode of acute cellular rejection; however, no patient developed chronic rejection or graft failure. In conclusion, nonalcoholic fatty liver disease occurs frequently after OLT in patients with the phenotype of NASH‐related cirrhosis. Despite the frequent histological recurrence of disease, clinical outcomes are similar to those of other groups of patients undergoing OLT. ( Liver Transpl 2001;7:363‐373. )