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Rheumatology (Oxford). 2009 Nov;48(11):1339-44. doi: 10.1093/rheumatology/kep221. Epub 2009 Jul 23.

Iron homoeostasis in rheumatic disease.

Author information

1
Division of Rheumatology, Department of Medicine, 5 Maloney Building, Suite 504, 3600 Spruce Street, Hospital of the University of Pennsylvania, Philadelphia, PA 19104, USA. bakerjo@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.

PMID:
19628641
DOI:
10.1093/rheumatology/kep221
[Indexed for MEDLINE]

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