Increased serum hepcidin levels during treatment with deferasirox in iron-overloaded patients with myelodysplastic syndrome

Br J Haematol. 2011 Apr;153(1):118-20. doi: 10.1111/j.1365-2141.2011.08587.x. Epub 2011 Feb 20.

Abstract

Hepcidin is a major regulator of iron metabolism. We evaluated changes in serum hepcidin during 3 months of therapy with the iron-chelator deferasirox in patients with low-risk myelodysplastic syndrome and iron overload. Serum hepcidin was found to be high in these patients, correlated with their iron and oxidative status, and further increased by treatment with deferasirox. These findings support the concept that the hepcidin level represents a balance between the stimulating effect of iron overload and the inhibitory effects of erythropoietic activity and oxidative stress. These preliminary findings favour the rationale for iron chelation therapy in such patients.

Publication types

  • Clinical Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Antimicrobial Cationic Peptides / blood*
  • Benzoates / pharmacology
  • Benzoates / therapeutic use*
  • Blood Transfusion
  • Deferasirox
  • Erythropoiesis / drug effects
  • Erythropoiesis / physiology
  • Female
  • Hepcidins
  • Humans
  • Iron Chelating Agents / pharmacology
  • Iron Chelating Agents / therapeutic use*
  • Iron Overload / blood
  • Iron Overload / drug therapy*
  • Iron Overload / etiology
  • Male
  • Middle Aged
  • Myelodysplastic Syndromes / blood
  • Myelodysplastic Syndromes / complications*
  • Oxidative Stress / drug effects
  • Oxidative Stress / physiology
  • Transferrin / metabolism
  • Triazoles / pharmacology
  • Triazoles / therapeutic use*

Substances

  • Antimicrobial Cationic Peptides
  • Benzoates
  • HAMP protein, human
  • Hepcidins
  • Iron Chelating Agents
  • Transferrin
  • Triazoles
  • Deferasirox