[Evaluation of 11beta-hydroxysteroid dehydrogenase type 1 activity in female patients with rheumatoid arthritis]
J Kerlik1, J Rovenský, M Vogeser
1Laboratórium endokrinológie cloveka Ustavu experimentálnej endokrinológie SAV Bratislava, Slovenska republika. jana.kerlik@savba.sk
Insights
Systemic 11beta-hydroxysteroid dehydrogenase type 1 (11BHSD1) activity is comparable between rheumatoid arthritis (RA) patients and healthy individuals, suggesting it does not cause relative adrenal deficiency in RA.
Area of Science:
- Endocrinology
- Rheumatology
- Molecular Biology
Introduction:
Cortisol levels in patients with rheumatoid arthritis (RA) are considered inadequate to ongoing inflammation. One possible mechanism ofthe relative cortisol deficit can be decreased 11beta-hydroxysteroid dehydrogenase type 1 (11BHSD1) activity, an enzyme that converts inactive cortisone to active cortisol. The aim of the study was to determine systemic and local activity of 11 BHSD1 in female patients with RA.
Methods:
Six female RA patients without glucocorticoid therapy (age 29 +/- 2 years, BMI 21 +/- 1 kg/m2) and six healthy women (age 30 +/- 2 years, BMI 21 +/- 1 kg/m2) were studied. Endogenous cortisol production was suppressed by dexamethasone. 11BHSD1 activity was evaluated by changes in concentrations of total plasma, free plasma, salivary and cortisol in subcutaneous adipose tissue after cortisone acetate administration (25 mg per os).
Results:
Concentrations of total plasma, free plasma, salivary, and tissue cortisol increased significantly, however there was no significant difference between RA patients and controls.
Conclusion:
The result suggests comparable systemic and adipose tissue conversion of cortisone to cortisol. Despite chronic inflammation, systemic activity of 11BHSD1 is not responsible for relative adrenal deficiency in RA. Changes in local activity of the enzyme in tissues affected by inflammatory process cannot be excluded.
