Background The pathogenesis of Behçet’s disease (BD) remains unsolved. Endothelial damage and/or defects in coagulation or fibrinolysis are thought to take a part.

Objectives Our aim was to determine d-dimers levels, tissue type plasminogen activator (t-PA), and plasminogen activator inhibitor 1 (PAI-1) in Tunisian patients with BD and to compare them with matched healthy controls. We also investigated the relation of these findings to patients’ clinical features, activity and severity.

Methods The patient group included 57 BD (International Study Group criteria). According to the Yosipovitch severity scale, patients were divided into three subgroups: mild, moderate and severe disease. The activity index has been elaborated according to the Yazici scale. We excluded all patients with other physiological and pathological situations that may increase d-dimer. The control group consisted of Tunisian healthy individuals matched for age and sex. Levels of d-dimers were determined by a quantitative assay test and Plasma concentrations of t-PA and PAI-1 were determined by enzyme linked immunoabsorbent assay (ELISA).

Results We included 57 BD patients (sex ratio M/F: 42/15, mean age: 40 years). One patient was excluded from statistical analysis due to a high rate of d-dimers (10µg/ml). The frequency of positive d-dimer was significantly higher in BD ptients than in healthy controls (17 (30%) vs 8 (13.8%) p=0.03). Table 1 summarizes the variation of d-dimer’s positivity according to demographic characteristics, clinical features, activity scale, and severity in BD patients.

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Financial limitations allowed us to realize t-Pa determination only in 42 patients and 44 healthy controls. The average rate of t-PA patients (4.85 ± 7.36 ng / ml) was lower than that of controls (5.62 ± 8.49 ng/ml). No significant correlation was found between the average t-PA, clinical manifestations and disease activity. The comparison of the frequencies of the different clinical manifestations depending on the average of PAI-1 showed a significantly lower level during ocular involvement (p=0.03). Average rates of PAI-1 were elevated in active forms of the disease.

Conclusions The scarcity of publications on fibrinolytic abnormalities in BD does not help us to an easy interpretation of these results and their implication in the pathogenesis of the disease as a causative agent or a consequence, even if this seems to be most likely.

Disclosure of Interest None Declared