ICEECE2012 Poster Presentations Steroid metabolism + action (19 abstracts)
1Clinic for Endocrinology, Diabetes and Metabolic Diseases, Clinical Centre of Serbia, Belgrade, Serbia; 2Medical Faculty, University of Belgrade, Belgrade, Serbia; 3Institute for Rheumatology, Belgrade, Serbia.
Introduction: Rheumatoid arthritis (RA) is a chronic inflammatory disease which is characterized with dysregulation of the immune system. Recent studies suggest that dysregulation of the HPA axis may as well play a contributory role in the pathogenesis of RA. Glucocorticoid hormones (GC) accomplish their effects through binding to glucocorticoid receptor (GR). Presence of GR gene polymorphisms can modulate GC effects. The A3669G polymorphism in human GR gene has been connected to decreased and BclI polymorphism to increased sensitivity to GC.
Study population/methods: The aim of this study was to detect frequency of BclI and A3669G polymorphisms and find possible association between these polymorphisms in 40 patients with RA (34 women, mean age 50.85±9.31; 6 men, mean age 49.33±15.72) and 160 healthy volunteers (92 women, mean age 46.29±9.28; 68 men, mean age 45.47±7.28) with presence of RA.
Healthy volunteers were recruited from the National Institute for Blood Transfusion. All subjects underwent medical, hormonal, genetic and biochemical testing. DNA was obtained from peripheral blood leucocytes. The BclI and A3669G polymorphisms were detected by using PCR, RFLP and DNA sequencing.
Results: The BclI polymorphism was detected in 26 (65%) patients and 47 (28.13%) healthy subjects, P<0.001. A3669G polymorphism was found in 15 (37.5%) patients and 14 (8.75%) healty volunteers, P<0.001.
Conclusion: The presented results show an increased frequency of BclI and A3669G polymorphisms carriers between RA patients, comparing to healthy volunteers. This may point to a contributory role of GC sensitivity in the predisposition to develop RA.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.