Ferroportin-1 in the recurrence of hepatic iron overload after liver transplantation.
Hepatic siderosis is frequent in patients with Hepatitis C virus (HCV) chronic hepatitis and considered secondary to advanced liver disease when detected in the explanted liver of cirrhotic patients submitted to transplantation. Here, we document the early recurrence of hepatic iron overload starting from host Kupffer cells and later involving hepatocytes in an Italian male submitted to liver transplantation for HCV-related cirrhosis, whose hemosiderosis was interpreted as related to a primary defect of iron handling by monocytic cells due to decreased Ferroportin-1 expression. He was negative for HFE mutations, had normal liver function, did not drink alcohol and had no erythropoietic defect. He was positive for the (CGG)(8/9) and the IVS1 -24 G>C Ferroportin-1 polymorphisms, associated with non-parenchymal iron overload, and had decreased Ferroportin-1 expression in monocytes. In conclusion, this case report documents the recurrence of progressive liver siderosis, which recalls Ferroportin disease, associated with decreased Ferroportin-1 expression in host monocytes repopulating the donor liver.
Valenti
L
L
Department of Internal Medicine, University of Milan, Milan, Italy.
Guido
M
M
Dongiovanni
P
P
Cremonesi
L
L
Fracanzani
A L
AL
Fargion
S
S
D027682:Cation Transport Proteins / Q000235:genetics* / Q000378:metabolism; D006486:Hemosiderosis / Q000235:genetics*; D019698:Hepatitis C, Chronic / Q000503:physiopathology* / Q000601:surgery; D006801:Humans; D016031:Liver Transplantation; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism; D020641:Polymorphism, Single Nucleotide; D012008:Recurrence; D000098742:Ferroportin
D027682:Cation Transport Proteins; D000098742:Ferroportin