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Rheumatology Advance Access originally published online on April 12, 2005
Rheumatology 2005 44(9):1097-1100; doi:10.1093/rheumatology/keh644
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Published by Oxford University Press on behalf of the British Society for Rheumatology 2005.

REVIEW

A defect in cortisol production in rheumatoid arthritis: why are we still looking?

D. S. Jessop and M. S. Harbuz

Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology (LINE), University of Bristol, Bristol, UK.

Correspondence to: D. S. Jessop, Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology (LINE), University of Bristol, Dorothy Hodgkin Building, Whitson Street, Bristol BS1 3NY, UK. E-mail: David.Jessop@bris.ac.uk

The first 150 words of the full text of this article appear below.

The question of whether patients with rheumatoid arthritis (RA) might have a defective hypothalamo–pituitary–adrenal (HPA) axis was first raised when RA patients who were treated with glucocorticoids in the 1950s showed dramatic improvement in their symptoms. It was initially hypothesized that this was due to an impaired ability of RA patients to synthesize sufficient amounts of endogenous glucocorticoids, but intensive investigations over the next few decades failed to reveal any significant defects in HPA axis activity in RA patients. In our review of the literature [1] we found no compelling evidence for significant differences in either basal or stress-stimulated HPA axis activity in RA compared with normal healthy individuals. However, we did highlight an inherent defect, which resided in the inability of RA patients to mount an appropriately enhanced glucocorticoid response to increased secretion of proinflammatory cytokines such as interleukin (IL)-1, IL-6 and tumour necrosis factor (TNF)-{alpha}. . . . [Full Text of this Article]


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