Determinants of adrenal androgen hypofunction in premenopausal females with rheumatoid arthritis
Language English Country Czech Republic Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
24564598
DOI
10.33549/physiolres.932663
PII: 932663
Knihovny.cz E-resources
- MeSH
- 11-beta-Hydroxysteroid Dehydrogenase Type 1 metabolism MeSH
- 17-alpha-Hydroxyprogesterone blood MeSH
- Adrenocorticotropic Hormone MeSH
- Androgens metabolism MeSH
- Adult MeSH
- Adrenal Cortex Hormones blood MeSH
- Adrenal Cortex physiopathology MeSH
- Humans MeSH
- Premenopause blood MeSH
- Arthritis, Rheumatoid blood physiopathology MeSH
- Case-Control Studies MeSH
- Severity of Illness Index MeSH
- Adipose Tissue metabolism MeSH
- Check Tag
- Adult MeSH
- Humans MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- 11-beta-Hydroxysteroid Dehydrogenase Type 1 MeSH
- 17-alpha-Hydroxyprogesterone MeSH
- Adrenocorticotropic Hormone MeSH
- Androgens MeSH
- Adrenal Cortex Hormones MeSH
The aim of our study was to investigate adrenocortical function in the context of disease activity and inflammatory status in premenopausal RA females. Adrenal glucocorticoid and androgen responses to the 1 microg ACTH 1-24 test were investigated in 23 premenopausal RA and in 15 age- and BMI-matched healthy females. Twelve RA patients were on low-dose prednisone (<8.5 mg/day). Patients with DAS28>3.2 had lower (p<0.05) total plasma cortisol, 17-hydroxyprogesterone, dehydroepiandrosterone and androstenedione responses in the ACTH test compared to healthy controls. Patients with DAS28>3.2 had lower (p<0.05) dehydroepiandrosterone response in the ACTH test compared to patients with DAS28=3.2. C-reactive protein (CRP), DAS28, and interleukin (IL)-6 negatively correlated with androstenedione response to ACTH 1-24. Responses of all measured adrenal steroids were lower (p<0.05) in patients on low-dose glucocorticoids compared to healthy controls. RA patients not treated with glucocorticoids had lower total cortisol response (p=0.038) but did not differ in free plasma cortisol in the ACTH test. The results indicate an association of increased disease activity with a decrease in adrenal androgen production in RA and normal cortisol bioavailability in patients not treated with glucocorticoids.
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