A defect in cortisol production in rheumatoid arthritis: why are we still looking?
Abstract
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)-α. ‘In other words’, we concluded, ‘the HPA axis response in RA is defective precisely because it is normal’.
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In untreated chronic inflammatory diseases, serum levels of cortisol are usually normal or somewhat higher.
“Similarly, in untreated CIDs, serum levels of cortisol are usually normal or somewhat higher [113], but they are inadequately low to suppress the ongoing inflammatory process.”
From Interaction of the endocrine system with inflammation: a function of energy and volume regulation (2014) · cites this paper as [113]
In aging and in chronic inflammatory diseases, both the SNS and the HPA axis are chronically activated.
“Indeed, in aging and in chronic inflammatory diseases, both the SNS and the HPA axis are chronically activated [41, 46–48].”
From Evolutionary medicine and chronic inflammatory state—known and new concepts in pathophysiology (2012) · cites this paper as [47]
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- Authors
- Jessop, D. S., & Harbuz, M. S.
- Affiliations
- University of Bristol (GB)
- Corresponding author
- Jessop, D. S.
- Venue
- Rheumatology
- Publisher
- Oxford University Press (OUP)
- Published
- 2005-04-12
- Volume
- 44
- Issue
- 9
- Pages
- 1097-1100
- ISSN
- 1462-0324 (ISSN-L)
- 1462-0332
- OpenAlex
- W2122751765
- Cited by
- 49
- References
- 42
- Citations by year
- 2021: 1 · 2020: 2 · 2019: 1 · 2017: 2 · 2016: 2 · 2015: 4 · 2014: 4 · 2013: 3 · 2012: 6
- FWCI
- 0.38
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Lara D. Veeken (publishedVersion)
- PubMed (publishedVersion)
- Bristol Research (University of Bristol) (publishedVersion)
- Explore Bristol Research (submittedVersion)
- Funders
- Wellcome Trust
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
- Keywords
- rheumatoid arthritis, hypothalamic-pituitary-adrenal axis, cortisol production, glucocorticoid response, inflammatory cytokines, interleukin-1, interleukin-6, TNF-α, glucocorticoid therapy, stress response
- MeSH terms
- Arthritis, Rheumatoid, Humans, Hydrocortisone, Hypothalamo-Hypophyseal System, Pituitary-Adrenal System
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