Ferroportin-1 in the recurrence of hepatic iron overload after liver transplantation

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2 Citations (Scopus)

Abstract

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.

Original languageEnglish
JournalDigestive and Liver Disease
Volume41
Issue number7
DOIs
Publication statusPublished - Jul 2009

Fingerprint

Iron Overload
Liver Transplantation
Recurrence
Liver
Siderosis
Hepacivirus
Monocytes
Hemosiderosis
Kupffer Cells
Chronic Hepatitis
metal transporting protein 1
Liver Diseases
Hepatocytes
Fibrosis
Iron
Transplantation
Alcohols
Tissue Donors
Mutation

Keywords

  • Cirrhosis
  • Ferroportin-1
  • Hepatitis C virus
  • Iron overload
  • Liver transplantation

ASJC Scopus subject areas

  • Gastroenterology
  • Hepatology

Cite this

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title = "Ferroportin-1 in the recurrence of hepatic iron overload after liver transplantation",
abstract = "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.",
keywords = "Cirrhosis, Ferroportin-1, Hepatitis C virus, Iron overload, Liver transplantation",
author = "L. Valenti and M. Guido and P. Dongiovanni and L. Cremonesi and Fracanzani, {A. L.} and S. Fargion",
year = "2009",
month = "7",
doi = "10.1016/j.dld.2008.01.020",
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T1 - Ferroportin-1 in the recurrence of hepatic iron overload after liver transplantation

AU - Valenti, L.

AU - Guido, M.

AU - Dongiovanni, P.

AU - Cremonesi, L.

AU - Fracanzani, A. L.

AU - Fargion, S.

PY - 2009/7

Y1 - 2009/7

N2 - 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.

AB - 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.

KW - Cirrhosis

KW - Ferroportin-1

KW - Hepatitis C virus

KW - Iron overload

KW - Liver transplantation

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