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AB0669 The Importance of Serum Visfatin Levels in Behcet's Disease Patients
  1. M.E. Enecik1,
  2. Z. Ozbalkan1,
  3. G. Keskin2,
  4. Y. Karaaslan1
  1. 1Rheumatology Department, Ankara Numune Education and Research Hospital
  2. 2Immunology Department, Ankara University School of Medicine, Ankara, Turkey

Abstract

Background It's a known fact that serum levels of the tumor necrosis factor Alfa (TNF-α) interleucin-6 (IL-6) and other proinflammatory cytokines which are released from the adipose tissue are increased in Behcet's disease (BD). In BD adipose tissue is not a passive energy depot, it is an active endocrine organ and releases adipositokines. Visfatine is one of them. Visfatin is related to TNF-α and IL-6, IL-1 beta, co-stimulators like CD40, CD54, CD 80 and endothelial ICAM-1 and ICAM-2. We aimed to search the relation among levels of serum visfatin in BD activity.

Methods 60BD patients (30 in active state and 30 in remission) who were diagnosed according to The Criteria of Working Group on International BD and 20 healthy subjects as controls were involeved in to the study. Serum visfatin levels were compared in between three groups.

Results Visfatin levels were significantly higher in both group of patients compared to the healthy control group (both p<0,001). Serum visfatin levels in active state patients were higher than those in inactive state (p<0.001). The same way in all cases statistically significant correlation between visfatin and CRP (p<0.001) and visfatin and ESR (p<0.01). According to the symptoms of the patients in the active state, patients with genital aphtous ulcers had higher serum visfatin levels than the active patients without genital aphthous ulcers (p<0,001).

Conclusions Serum visfatin levels in BD patients with active and inactive states are higher than the healthy control group. That could be concluded as visfatin as a proinflammatory cytokines have a role in chronic inflammatory reactions and sustains the cellular expression of the inflammatory cytokines in BD.

References

  1. Samara A, Clin Endocrinol (Oxf). 2008;29.

  2. Moschen AR, J Immunol. 2007;178:1748-1758.

  3. Yazici H, Curr Opin Rheumatol. 2001; 13:18-22.

  4. Sahin M, Ann Clin Lab Sci. 2006; 36:449-454.

  5. Moschen AR, J Immunol. 2007;178:1748-1758. 6- Samara AClin Endocrinol (Oxf). 2008;29.

Disclosure of Interest None declared

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