REVIEW - Iron homeostasis in rheumatic disease

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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

Reviews

Iron homoeostasis in rheumatic disease

F. Baker1 and J. Ghio2

1Division of Rheumatology, Department of Medicine, University of

Pennsylvania, Philadelphia, PA and 2Human Studies Division, US EPA,

Chapel Hill, NC, USA.

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.

http://rheumatology.oxfordjournals.org/cgi/content/abstract/48/11/1339?etoc

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