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Growing evidence supports the hypothesis that alterations of the stress response and interactions between the neuroendocrine and immune systems contribute to the pathogenesis of rheumatoid arthritis (RA).1,–,4 Central to the maintenance of homeostasis is an appropriate response of the hypothalamic–pituitary–adrenal (HPA) axis as well as the sympathetic nervous system.3 5 Corticotropin-releasing hormone (CRH) is the strongest known activator of the HPA axis, which has been functionally implicated in the regulation of many endocrine functions such as glucocorticoid release from the adrenal gland and associated endocrine-immune responses.6 Recently, we described several polymorphisms, named A1B1, A2B1 and A2B2, in the highly conserved regulatory region of the CRH gene, which modulated gene transcription in vitro.7 To further evaluate the impact of CRH promoter polymorphisms in vivo, the activity of the HPA axis in patients with early RA was studied by measuring hormone levels during an insulin hypoglycaemia test (IHT), a standardised form …
Competing interests None.
Funding This work was supported by a grant from Deutsche Forschungsgemeinschaft (DFG), grant BA 1770/2±1.
Ethics approval All subjects signed informed consent and the study was approved by the ethical committee of the authors' university, University Leipzig, Germany.
Provenance and peer review Not commissioned; externally peer reviewed.