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Rheumatology Advance Access originally published online on July 27, 2004
Rheumatology 2004 43(11):1323-1325; doi:10.1093/rheumatology/keh345
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Rheumatology Vol. 43 No. 11 © British Society for Rheumatology 2004; all rights reserved


EDITORIAL

Hepcidin: inflammation's iron curtain

H. McGrath, Jr and P. G. Rigby1

Louisiana State Health Sciences Center, Department of Medicine, Section of Rheumatology, 1542 Tulane Avenue, New Orleans, LA 70112 and 1 Department of Medicine, Section of Hematology, Chancellors Office, Resource Center, 433 Bolivar Street, New Orleans, LA 70112, USA

Correspondence to: H. McGrath. E-mail: hmcgra@lsuhsc.edu

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Rheumatologists and their patients are the beneficiaries of a recently identified peptide, hepcidin (Table 1). Isolated from human urine and plasma in the year 2000 [1, 2], hepcidin appears to be the long-sought iron-regulatory hormone responsible for the anaemia of chronic disease [3, 4]. It is more than that: it is an acute-phase reactant, responding to infection and inflammation [5]; it is an antimicrobial peptide that disrupts microbial membranes [1, 6]; and it provides an iron-restricted internal milieu inhospitable to microbes [7, 8].


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TABLE 1. Dynamics of iron and hepcidin regulation

 
Hepcidin is a 25 amino acid, 2–3 kDa, cationic peptide that has broad antibacterial and antifungal actions [1]. In concert with other antimicrobial peptides, . . . [Full Text of this Article]


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