ECE2007 Poster Presentations (1) (659 abstracts)
1Institute of Experimental Endocrinology, Slovak Academy of Sciences, Bratislava, Slovakia; 2National Institute of Rheumatic Diseases, Piestany, Slovakia.
Objective: Changes of hypothalamic-pituitary-adrenal (HPA) axis activity, in particular decreased production of adrenal androgens, have been observed in patients with rheumatic diseases. However, data on adrenal steroid status in patients with psoriatic arthritis (PsA) are scarce. The present study was aimed at evaluation of HPA status in context of chronic inflammation in glucocorticoid-naïve premenopausal females with PsA.
Subjects and methods: Concentrations of ACTH, cortisol, androstenedione (ASD), 17OH-progesterone (17OHP), dehydroepiandrosterone (DHEA), and DHEA-sulphate (DHEAS) were analyzed before and during insulin-induced hypoglycaemia in 16 female premenopausal patients (age 40.1±1.4 y, BMI 23.5±1.1 kg/m2) with PsA and in 11 age and BMI matched healthy women. Basal levels of IL-1alpha, IL-1beta, IL-6, TNF alpha and CRP were measured in all studied subjects as well. The study was approved by local ethical committee.
Results: The disease activity of PsA patients was low. No significant differences in levels of IL-1alpha, IL-1beta, TNF alpha or CRP were found between patients and controls. IL-6 levels were higher in PsA compared to controls (P=0.045). Basal levels and response to stimulation of ACTH and cortisol did not differ between the study groups. PsA patients had lower basal levels of ASD (2.79±0.24 nmol/l vs. 4.89±0.87 nmol/l; P=0.013) and DHEAS (2.42±0.32 μmol/l vs. 3.79±0.63 μmol/l; P=0.044) and levels of DHEA tended to be lower (13.2±1.9 nmol/l vs. 20.4±3.5 nmol/l; P=0.065). During stimulation PsA patients had significantly lower response of 17OHP and ASD when compared to controls (P=0.046, P=0.004 respectively). We did not find any significant correlation between basal levels of steroid hormones and cytokines.
Conclusions: The results suggest a shift in production of adrenal steroids from adrenal androgens towards production of cortisol in patients with PsA. Whether or not the observed changes in production of adrenal androgens are secondary due to ongoing inflammatory process remains to be elucidated.