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Hepcidin response to acute iron intake and chronic iron loading in dysmetabolic iron overload syndrome
Author(s) -
Trombini Paola,
Paolini Valentina,
Pelucchi Sara,
Mariani Raffaella,
Nemeth Elizabeta,
Ganz Tomas,
Piperno Alberto
Publication year - 2011
Publication title -
liver international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.873
H-Index - 110
eISSN - 1478-3231
pISSN - 1478-3223
DOI - 10.1111/j.1478-3231.2011.02520.x
Subject(s) - hepcidin , medicine , endocrinology , basal (medicine) , hemochromatosis , iron deficiency , homeostasis , anemia , insulin
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.