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Rheumatology Advance Access originally published online on July 23, 2009
Rheumatology 2009 48(11):1339-1344; doi:10.1093/rheumatology/kep221
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© The Author 2009. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Reviews

Iron homoeostasis in rheumatic disease

Joshua F. Baker1 and Andrew J. Ghio2

1Division of Rheumatology, Department of Medicine, University of Pennsylvania, Philadelphia, PA and 2Human Studies Division, US EPA, Chapel Hill, NC, USA.

Correspondence to: Joshua F. Baker, Division of Rheumatology, Department of Medicine, 5 Maloney Building, Suite 504, 3600 Spruce Street, Hospital of the University of Pennsylvania, Philadelphia, PA 19104, USA. E-mail: bakerjo{at}uphs.upenn.edu


  Abstract

Iron is critical in nearly all cell functions and the ability of a cell, tissue and organism to procure this metal is obligatory for survival. Iron is necessary for normal immune function, and relative iron deficiency is associated with mild immunosuppression. Concentrations of this metal in excess of those required for function can present both an oxidative stress and elevate risks for infection. As a result, the human has evolved to have a complex mechanism of regulating iron and limiting its availability. This homoeostasis can be disrupted. Autoimmune diseases and gout often present with abnormal iron homoeostasis, thus supporting a participation of the metal in these injuries. We review the role of iron in normal immune function and discuss both clinical evidence of altered iron homoeostasis in autoimmune diseases and gout as well as possible implications of both depletion and supplementation of this metal in this patient population. We conclude that altered iron homoeostasis may represent a purposeful response to inflammation that could have theoretical anti-inflammatory benefits. We encourage physicians to avoid routine iron supplementation in those without depleted iron stores.

KEY WORDS: Iron, Inflammation, Rheumatoid arthritis, Systemic lupus erythematosus, Gout

Submitted 19 February 2009; revised version accepted 25 June 2009.
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