Abstract
Following the model of hereditary hemochromatosis, the possible role of iron overload as a cofactor for disease progression in acquired liver diseases has been investigated with controversial results. In recent years, progress has been made in understanding the regulation of iron metabolism, thereby allowing the evaluation of the mechanisms linking liver diseases to excessive iron accumulation. Indeed, deregulation of the transcription of hepcidin, emerging as the master regulator of systemic iron metabolism, has been implicated in the pathogenesis of hepatic iron overload in chronic liver diseases. Whatever the cause, hepatocellular iron deposition promotes liver fibrogenesis, while an emerging possible aggravating factor is represented by the strong link between iron stores and insulin resistance, a recently recognized risk factor for the progression of liver diseases. Overall, these pathogenic mechanisms, together with the known proliferative and mutagenic effect of excess iron, converge in determining an increased susceptibility to hepatocellular carcinoma. Finally, an association between serum ferritin levels and mortality in patients with end-stage liver disease has recently been reported.Prospective, randomized studies are required to evaluate whether iron depletion may reduce fibrosis progression, hepatocellular carcinoma development, and eventually mortality in patients with chronic liver diseases.
| Original language | English |
|---|---|
| Pages (from-to) | 89-95 |
| Number of pages | 7 |
| Journal | Digestive and Liver Disease |
| Volume | 43 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - Feb 2011 |
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Keywords
- Chronic hepatitis C
- Hepatocarcinoma
- Hepcidin
- Nonalcoholic steatohepatitis
ASJC Scopus subject areas
- Gastroenterology
- Hepatology
Cite this
Beyond hereditary hemochromatosis : New insights into the relationship between iron overload and chronic liver diseases. / Fargion, Silvia; Valenti, Luca; Fracanzani, Anna Ludovica.
In: Digestive and Liver Disease, Vol. 43, No. 2, 02.2011, p. 89-95.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Beyond hereditary hemochromatosis
T2 - New insights into the relationship between iron overload and chronic liver diseases
AU - Fargion, Silvia
AU - Valenti, Luca
AU - Fracanzani, Anna Ludovica
PY - 2011/2
Y1 - 2011/2
N2 - Following the model of hereditary hemochromatosis, the possible role of iron overload as a cofactor for disease progression in acquired liver diseases has been investigated with controversial results. In recent years, progress has been made in understanding the regulation of iron metabolism, thereby allowing the evaluation of the mechanisms linking liver diseases to excessive iron accumulation. Indeed, deregulation of the transcription of hepcidin, emerging as the master regulator of systemic iron metabolism, has been implicated in the pathogenesis of hepatic iron overload in chronic liver diseases. Whatever the cause, hepatocellular iron deposition promotes liver fibrogenesis, while an emerging possible aggravating factor is represented by the strong link between iron stores and insulin resistance, a recently recognized risk factor for the progression of liver diseases. Overall, these pathogenic mechanisms, together with the known proliferative and mutagenic effect of excess iron, converge in determining an increased susceptibility to hepatocellular carcinoma. Finally, an association between serum ferritin levels and mortality in patients with end-stage liver disease has recently been reported.Prospective, randomized studies are required to evaluate whether iron depletion may reduce fibrosis progression, hepatocellular carcinoma development, and eventually mortality in patients with chronic liver diseases.
AB - Following the model of hereditary hemochromatosis, the possible role of iron overload as a cofactor for disease progression in acquired liver diseases has been investigated with controversial results. In recent years, progress has been made in understanding the regulation of iron metabolism, thereby allowing the evaluation of the mechanisms linking liver diseases to excessive iron accumulation. Indeed, deregulation of the transcription of hepcidin, emerging as the master regulator of systemic iron metabolism, has been implicated in the pathogenesis of hepatic iron overload in chronic liver diseases. Whatever the cause, hepatocellular iron deposition promotes liver fibrogenesis, while an emerging possible aggravating factor is represented by the strong link between iron stores and insulin resistance, a recently recognized risk factor for the progression of liver diseases. Overall, these pathogenic mechanisms, together with the known proliferative and mutagenic effect of excess iron, converge in determining an increased susceptibility to hepatocellular carcinoma. Finally, an association between serum ferritin levels and mortality in patients with end-stage liver disease has recently been reported.Prospective, randomized studies are required to evaluate whether iron depletion may reduce fibrosis progression, hepatocellular carcinoma development, and eventually mortality in patients with chronic liver diseases.
KW - Chronic hepatitis C
KW - Hepatocarcinoma
KW - Hepcidin
KW - Nonalcoholic steatohepatitis
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U2 - 10.1016/j.dld.2010.07.006
DO - 10.1016/j.dld.2010.07.006
M3 - Article
VL - 43
SP - 89
EP - 95
JO - Digestive and Liver Disease
JF - Digestive and Liver Disease
SN - 1590-8658
IS - 2
ER -