Determinants of adrenal androgen hypofunction in premenopausal females with rheumatoid arthritis
Jazyk angličtina Země Česko Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
24564598
DOI
10.33549/physiolres.932663
PII: 932663
Knihovny.cz E-zdroje
- MeSH
- 11-beta-hydroxysteroiddehydrogenasa typ 1 metabolismus MeSH
- 17-alfa-hydroxyprogesteron krev MeSH
- adrenokortikotropní hormon MeSH
- androgeny metabolismus MeSH
- dospělí MeSH
- hormony kůry nadledvin krev MeSH
- kůra nadledvin patofyziologie MeSH
- lidé MeSH
- premenopauza krev MeSH
- revmatoidní artritida krev patofyziologie MeSH
- studie případů a kontrol MeSH
- stupeň závažnosti nemoci MeSH
- tuková tkáň metabolismus MeSH
- Check Tag
- dospělí MeSH
- lidé MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- 11-beta-hydroxysteroiddehydrogenasa typ 1 MeSH
- 17-alfa-hydroxyprogesteron MeSH
- adrenokortikotropní hormon MeSH
- androgeny MeSH
- hormony kůry nadledvin 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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