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Liver Int. 2011 Aug;31(7):994-1000. doi: 10.1111/j.1478-3231.2011.02520.x. Epub 2011 Apr 18.

Hepcidin response to acute iron intake and chronic iron loading in dysmetabolic iron overload syndrome.

Author information

1
Department of Clinical Medicine and Prevention, Centre for Diagnosis and Therapy of Hemochromatosis, S. Gerardo Hospital, University of Milano-Bicocca, Monza, Italy.

Abstract

BACKGROUND:

The pathogenesis of dysmetabolic iron overload syndrome (DIOS) is still unclear. Hepcidin is the key regulator of iron homeostasis controlling iron absorption and macrophage release.

AIM:

To investigate hepcidin regulation by iron in DIOS.

METHODS:

We analysed urinary hepcidin at baseline and 24 h after a 65 mg oral iron dose in 24 patients at diagnosis and after iron depletion (n = 13) and compared data with those previously observed in 23 healthy controls. Serum iron indices, liver histology and metabolic data were available for all patients.

RESULTS:

At diagnosis, hepcidin values were significantly higher than in controls (P < 0.001). After iron depletion, hepcidin levels decreased to normal values in all patients. At baseline, a significant response of hepcidin to iron challenge was observed only in the subgroup with lower basal hepcidin concentration (P = 0.007). In iron-depleted patients, urinary hepcidin significantly increased after oral iron test (P = 0 .006).

CONCLUSIONS:

Ours findings suggest that in DIOS, the progression of iron accumulation is counteracted by the increase in hepcidin production and progressive reduction of iron absorption, explaining why these patients develop a mild-moderate iron overload that tends to a plateau.

PMID:
21733088
PMCID:
PMC4048852
DOI:
10.1111/j.1478-3231.2011.02520.x
[Indexed for MEDLINE]
Free PMC Article

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