AB0249 Serum Visfatin Determination in Rheumatoid Arthritis

Abstract

Background There are now some data about role of adipose tissue in the pathogenesis of chronic inflammatory processes. Adipokines can influence on inflammation in rheumatoid arthritis (RA) and other rheumatic diseases. The literature contains some data on relieving of collagen-induced arthritis in mouse model with pharmacological visfatin inhibition injection. We suppose that visfatin is involved in the processes of degradation of cartilage and development of inflammation in joint disease by stimulating of interleukin-6 and 8, tumor necrosis factor, metalloproteinase-1 and 3 production. Objectives The aim of this study was to investigate clinical and pathogenic significance of visfatin determination in sera of RA patients. Methods We observed 170 people: 120 patients with diagnosed RA and 50 healthy controls (HC). Serum visfatin levels were measured by ELISA- test (RaiBiotech, cat No. EIA-VIS-1). Results We revealed that visfatin level in HC was 2,30+1,72 ng/ml, (mean and standard error accordingly), in RA patients - 6,27+0,59 ng/ml (p<0,001). We noted increased visfatin level in 46 RA patients (38,3%). We divided 120 RA patients into 2 subgroups – 1st (n=46) with high visfatin level in sera, and 2nd (n=74) - with normal visfatin concentration. We revealed that patients in 1st group had a higher level of activity index DAS28 (II-III degree of activity), high levels of autoantibodies to cyclic citrullinated peptide, higher levels of C-reactive protein and erythrocyte sedimentation rate. Conclusions The present study shows visfatin may have important significance in RA pathogenesis. RA patients with high visfatin level in sera have more aggressive form of disease. In this study serum visfatin strongly correlated with systemic inflammation markers and functional impairment in RA. Thus serum visfatin could be used as marker of RA activity and progression. We suppose visfatins inhibition may be used as a new pharmacological target in RA treatment. References Busso N., Karababa M., Nobile M. et al. Pharmacological inhibition of nicotinamide phosphoribosyltransferase/visfatin enzymatic activity identifies a new inflammatory pathway linked to NAD. PLoS ONE 2008; 3: e2267. Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.2011

The Role of Nampt / Pbef1 in the Pathogenesis of Rheumatoid Arthritis

“…Nampt/PBEF1 может регулировать активацию лейкоцитов и синовиоцитов человека как за счет увеличения количества костимуляторных молекул, стимуляции синтеза интерлейкина-1β (IL), IL-6 и TNFα, так и воздействуя на предполагаемые рецепторы мембран клеток. Положительная корреляция между Nampt/PBEF1 и СРБ подтверждает его роль, как медиатора воспаления [4]. Считается, что повышенные концентрации Nampt/PBEF1 могут стимулировать системное воспаление.…”

Association of serum fetuin-a levels and rheumatoid arthritis clinical and immunological features

“…In order to improve the understanding of RA pathogenesis and diagnostic and therapeutic approaches numerous studies are performed [1]. In recent years the role of tissue cytokines, such as fetuin-A (FA), is thoroughly investigated [2]. This study aimed to determine the association between serum FA levels and RA clinical and immunological features.…”

Neointimal phosphoribosiltransftrase is a proinflammatori molecule characterizing severiti of rheumatoid arthritis

“…В хондроцитах, обработанных Nampt, отмечается повышенное содержание металлопротеиназ и металлопептидаз, в то время как синтез аггрекана снижен [2], что может свидетельствовать о деструктивной и катаболической роли Nampt в суставном хряще. Положительная корреляция между Nampt и СРБ подтверждает его роль, как медиатора воспаления [10]. Считается, что повышенные концентрации Nampt могут стимулировать системное воспаление.…”

“…Данные большого количества исследований подтверждают, что Nampt играет важную роль в патологии воспалительных и онкологических заболеваний [7,10,13]. Дальнейшее изучение молекулярных механизмов активации адипокинов может привести к разработке новых терапевтических средств для лечения различных заболеваний.…”