title: Hepcidin response to acute iron intake and chronic iron loading in dysmetabolic iron overload syndrome.
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.
  
  
  OBJECTIVE
  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.
authors: Department of Clinical Medicine and Prevention, Centre for Diagnosis and Therapy of Hemochromatosis, S. Gerardo Hospital, University of Milano-Bicocca, Monza, Italy.
authors: Paola
authors: P
authors: Trombini
authors: Valentina
authors: V
authors: Paolini
authors: Sara
authors: S
authors: Pelucchi
authors: Raffaella
authors: R
authors: Mariani
authors: Elizabeta
authors: E
authors: Nemeth
authors: Tomas
authors: T
authors: Ganz
authors: Alberto
authors: A
authors: Piperno
mesh_terms: D000284:Administration, Oral; D000410:Alanine Transaminase / Q000097:blood; D023181:Antimicrobial Cationic Peptides / Q000378:metabolism* / Q000652:urine; D001786:Blood Glucose / Q000032:analysis; D002097:C-Reactive Protein / Q000032:analysis; D002784:Cholesterol / Q000097:blood; D004252:DNA Mutational Analysis; D005260:Female; D000071020:Hemochromatosis Protein; D006454:Hemoglobins / Q000032:analysis; D064451:Hepcidins; D015395:Histocompatibility Antigens Class I / Q000235:genetics; D006801:Humans; D007328:Insulin / Q000097:blood; D007501:Iron / Q000008:administration & dosage / Q000378:metabolism*; D019190:Iron Overload / Q000378:metabolism* / Q000503:physiopathology*; D007558:Italy; D008099:Liver / Q000378:metabolism / Q000473:pathology*; D008297:Male; D008565:Membrane Proteins / Q000235:genetics; D018709:Statistics, Nonparametric; D014280:Triglycerides / Q000097:blood; D005723:gamma-Glutamyltransferase / Q000097:blood
chemical_list: D023181:Antimicrobial Cationic Peptides; D001786:Blood Glucose; C578702:HAMP protein, human; C103673:HFE protein, human; D000071020:Hemochromatosis Protein; D006454:Hemoglobins; D064451:Hepcidins; D015395:Histocompatibility Antigens Class I; D007328:Insulin; D008565:Membrane Proteins; D014280:Triglycerides; D002097:C-Reactive Protein; D002784:Cholesterol; D007501:Iron; D005723:gamma-Glutamyltransferase; D000410:Alanine Transaminase