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Article

Hepcidin mutation in a beta-thalassemia major patient with persistent severe iron overload despite chelation therapy.

Internal and emergency medicine - 1 Feb 2010

Duca Lorena, Delbini Paola, Nava Isabella, Cappellini Maria Domenica, Meo Anna

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Share to Antimicrobial Cationic Peptides
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 19756955
DOI: 10.1007/s11739-009-0306-8

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

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Hepcidin mutation in a beta-thalassemia major patient with persistent severe iron overload despite chelation therapy.PMID 19756955Read ↗

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Anemia, Ineffective Erythropoiesis, and Hepcidin: Interacting Factors in Abnormal Iron Metabolism Leading to Iron Overload in β-ThalassemiaSemantic proximity Read ↗

Understanding the Intricacies of Iron Overload Associated With β-Thalassemia: A Comprehensive ReviewSemantic proximity Read ↗

Association of hepcidin promoter c.-582 A>G variant and iron overload in thalassemia major.Semantic proximity Read ↗

Iron disorders of genetic origin: a changing world.Semantic proximity Read ↗

Iron Metabolism in Thalassemia and Sickle Cell Anemia: The influence of Genetic ModifiersSemantic proximity Read ↗

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Twenty Years of Ferroportin Disease: A Review or An Update of Published Clinical, Biochemical, Molecular, and Functional FeaturesSemantic proximity Read ↗

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