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SAT0351 Adipokines as New Laboratory Markers in Osteoarthritis
  1. Y. R. Akhverdyan1,
  2. B. V. Zavodovsky1,
  3. L. E. Seewordova1,
  4. Y. V. Polyakova1,
  5. E. S. Simakova1,
  6. I. A. Zborovskaya1,
  7. V. E. Kononov1
  1. 1The laboratory of treatment and prevention of joints diseases, FEDERAL STATE BUDGETARY INSTITUTION “RESEARCH INSTITUTE OF CLINICAL AND EXPERIMENTAL RHEUMATOLOGY” UNDER THE RUSSION ACADEMY OF MEDICAL SCIENCES, Volgograd, Russian Federation

Abstract

Background There is some data that osteoarthritis (OA) may be part of systemic lipid metabolism disorder. Some authors suppose that fat tissue may be origin of biologically active substances such as adiponectin, resistin, leptin and visfatin that may influence on chondrogenesis. Now there is a question about a level adipokines in degenerative diseases of joints. In this connection the researches related to studying of those markers in OA are relevant.

Objectives The aim of the study was to improve diagnostic, to clarify OA pathogenesis by examining the levels of adiponectin, resistin, leptin and visfatin in OA sera.

Methods We examined 80 patients with OA and 50 healthy donors (HD). Adipokines level were determined by indirect immunoenzyme method using a commercial test systems (Bio Vendor, cat № RD195023100 for adiponectin; Bio Vendor, cat № RD191016100 for resistin; DBC Inc cat № CAN-L-4260 for leptin and RaiBiotech, cat № EIA-VIS-1 for visfatin measuring).

Results We revealed decrease of adiponectin levels in 28 (35%) OA patients (2 - in HD group (4%), chi-square=16,66, p<0,001), increase of resistin levels – in 31 (38,75%) (1 - in HD (2%), chi-square=22,39, p<0,001), leptin - in 26 (32,5%) (2 - in HD (4%), chi-square=14,79, p<0,001), and visfatin - in 23 (28,75%) OA patients (3 - in HD (6%), chi-square=9,95, p<0,001). These results indicate that lipid metabolism in OA may be disturbed. There was no significant difference in adipokines levels depending on the sex of OA patients. Resistin and leptin levels in patients with metabolic syndrome (mean BMI = 36,8 ± 3,3, corresponds to the degree of obesity II) were significantly higher than in those without metabolic syndrome. Low levels of adiponectin, high levels of resistin, leptin and visfatin were noted in patients with OA with reactive synovitis, radiographic stage III-IV, functional impairment of the joints III. We observed an inverse correlation between adiponectin level and CRP, ESR, and WOMAC index, Lequesne indeces for gonarthrosis and coxarthrosis, direct correlation between resistin, leptin, and visfatin levels and CRP, ESR and algofunctional indices. Follow weight reduction (5 kg in 3 months) resulted in significant decrease leptin and resistin levels, the severity of articular symptoms and manifestations of insulin resistance.

Conclusions Thus adipokines may have important significance in pathogenesis of OA. We suppose adiponectin may be a protective factor in OA. Patients with increased levels of resistin, leptin and visfatin have more aggressive manifestations of OA. Osteoarthritis patients with low adiponectin level and a high level of resistin, leptin and visfatinhave more severe form of disease.

Disclosure of Interest None Declared

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