Article Text

AB0476 Superoxide dismutase is associated to large vessels involvement in behcet syndrome
  1. O. Harzallah1,
  2. R. Klii1,
  3. D. Brahem1,
  4. M. Kechida1,
  5. S. Mahjoub1
  1. 1Internal Medicine Department, Fattouma Bourguiba Hospital, Monastir, Tunisia


Background In Behçet’s Syndrome (BS), all polymorphonuclear cells (PMN) capacities are enhanced: chemoattraction, phagocytosis and free radicals (FR) production (1, 2). The excess of FR, responsible for an oxidative stress (OS) state, could present an endothelial toxicity (3) and could be implicated in tissue lesions genesis in BS.

Objectives The aim of our work was to analyze the correlation between oxidative stress biological markers and main vessels involvement in BS.

Methods 40 BD patients (27 males, 13 females; mean age: 38.8 years) were prospectively enrolled in the study. Plasma malondialdehyde (MDA), erythrocyte superoxide dismutase (SOD), catalase and glutathione peroxidase (GSH-PX) were analyzed. Levels of these parameters were compared between patients having or not neurological (NI), ocular (OI) and large vascular involvement (LVI).

Results There were 16 patients with large vessels involvement (LVI), 10 with neurological involvement and 13 having Behçet’s eye disease. Patients with LVI were: 14 with deep venous thromboses and 2 with arterial aneurysms. Only SOD was significantly decreased (p = 0.01) in patients having LVI when compared to patients without LVI (table 1). There were any differences in MDA, SOD, catalase and GSH-PX levels when comparing patients with and without ocular; with and without neurological involvement.

Conclusions SOD is decreased in patients with LVI in BS. This preliminary result deserves further investigation by other studies with larger samples. However, it probably indicates that SOD, the first line anti-oxidant enzymatic defense, has a probable role in the endothelial membrane protection against free radicals aggression in BS.

  1. Takeno M, Kariyone AI, Yamashita N et al. Excessive functions of peripheral blood neutrophils frompatients with Behçet’s disease and from HLA B51 transgenic mice. Arthritis Rheum 1995; 3:426 –33

  2. Harzallah O, Kerkeni A, Baati T. Oxidative stress: Correlation with Behçet’s activity and severity European Journal of Internal Medicine 2008; 19: 541– 7

  3. Niwa Y, Miyake S, Sakane T. Autooxidative damage in Behçet’s disease-endothelial cell damage following the elevated oxygen radicals generated by stimulated neutrophils. Clin Exp Immunol 1982; 49: 247–55

Disclosure of Interest None Declared

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