title: Increased hepatic iron and cirrhosis: no evidence for an adverse effect on patient outcome following liver transplantation.
abstract: It has been suggested that preexisting severe hepatic iron overload may adversely affect outcome after liver transplantation. The pathogenesis of iron overload in cirrhosis in the absence of hemochromatosis gene (HFE) mutations is poorly understood. The relationships between liver disease severity and etiology, degree of hepatic iron overload, and post-liver transplantation outcome were studied in 282 consecutive adult patients with cirrhosis. Thirty-seven percent of patients had stainable hepatic iron. Increased hepatic iron concentration was significantly associated with more severe liver disease (P<.001), male sex (P = .05), the presence of spur cell anemia (P<.0001), and hepatocellular liver disease (P<.0001). The HFE mutations were uncommon in patients with increased hepatic iron stores. Increased hepatic iron concentration was not associated with greater utilization of resources or a lower survival after liver transplantation. Child-Pugh score at the time of liver transplantation was the only independent variable affecting patient survival (P = .0008). In summary, our data suggest that the severity of the liver disease rather than hepatic iron concentration is the most important determinant of outcome after liver transplantation and that, in general, increasing hepatic iron concentration in cirrhosis is a surrogate marker of the severity of the underlying liver disease.
authors.affiliation: Department of Gastroenterology and Hepatology, Princess Alexandra Hospital, Brisbane, Australia.
authors.forename: K A
authors.initials: KA
authors.lastname: Stuart
authors.forename: L M
authors.initials: LM
authors.lastname: Fletcher
authors.forename: A D
authors.initials: AD
authors.lastname: Clouston
authors.forename: S V
authors.initials: SV
authors.lastname: Lynch
authors.forename: D M
authors.initials: DM
authors.lastname: Purdie
authors.forename: P
authors.initials: P
authors.lastname: Kerlin
authors.forename: D H
authors.initials: DH
authors.lastname: Crawford
mesh_terms: D000328:Adult; D000740:Anemia / Q000150:complications; D015331:Cohort Studies; D005260:Female; D006680:HLA Antigens / Q000235:genetics; D000071020:Hemochromatosis Protein; D015395:Histocompatibility Antigens Class I / Q000235:genetics; D006801:Humans; D019190:Iron Overload / Q000150:complications / Q000235:genetics / Q000378:metabolism*; D008099:Liver / Q000378:metabolism*; D008103:Liver Cirrhosis / Q000150:complications / Q000378:metabolism*; D016031:Liver Transplantation; D008297:Male; D008565:Membrane Proteins; D008875:Middle Aged; D009154:Mutation; D012720:Severity of Illness Index; D012727:Sex Characteristics; D016019:Survival Analysis; D016896:Treatment Outcome
chemical_list: C103673:HFE protein, human; D006680:HLA Antigens; D000071020:Hemochromatosis Protein; D015395:Histocompatibility Antigens Class I; D008565:Membrane Proteins