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 24h after a 65mg 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. © 2011 John Wiley & Sons A/S.

Trombini, P., Paolini, V., Pelucchi, S., Mariani, R., Nemeth, E., Ganz, T., et al. (2011). Hepcidin response to acute iron intake and chronic iron loading in dysmetabolic iron overload syndrome. LIVER INTERNATIONAL, 31(7), 994-1000 [10.1111/j.1478-3231.2011.02520.x].

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

PAOLINI, VALENTINA;PELUCCHI, SARA;PIPERNO, ALBERTO
2011

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 24h after a 65mg 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. © 2011 John Wiley & Sons A/S.
Articolo in rivista - Articolo scientifico
hepcidin, iron, metabolic syndrome, iron overload
English
994
1000
Trombini, P., Paolini, V., Pelucchi, S., Mariani, R., Nemeth, E., Ganz, T., et al. (2011). Hepcidin response to acute iron intake and chronic iron loading in dysmetabolic iron overload syndrome. LIVER INTERNATIONAL, 31(7), 994-1000 [10.1111/j.1478-3231.2011.02520.x].
Trombini, P; Paolini, V; Pelucchi, S; Mariani, R; Nemeth, E; Ganz, T; Piperno, A
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10281/26089
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