The controlled data accumulated so far support only subtle alterations in HPA axis function in RA, mainly at the adrenal level, and particularly in a subset of premenopausal-onset women. Such interpretation is supported by consistent findings of lower levels of adrenal androgens, particularly DHEAS, in premenopausal-onset RA patients. Consequences of the subtle HPA alterations in RA for the disease development remain unclear. From a broader perspective, the unresponsiveness of the HPA axis to chronic inflammation in RA simply can be seen as an ongoing adaptation to the disease state with higher priority to proper regulation of core body functions over the immune homeostasis.
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