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Behcet's disease (BD) is accepted as a systemic vasculitis. Vasculitis is observed predominantly on the venous system. Vessel involvement is frequently seen in males. This study was planned retrospectively evaluate demographic features, clinical features, vessel involvements in BD. Furthermore, we aimed to prospectively compare consecutively chosen patients with and without thrombosis and healthy volunteers in terms of their biochemical, immunological, coagulation parameters. One hundred fifty-two Behcet's patients were retrospectively evaluated. Blood samples were collected from 52 consecutively chosen patients and 41 healthy subjects. Papulopustular skin lesions, eye involvement and venous lesions were detected frequent in males. In terms of evaluated parameters (biochemical parameters, coagulation parameters, C-reactive protein, erythrocyte sedimentation rate, anticardiolipin antibodies, antinuclear antibody positivity) was not found a significant difference among groups (patients without thrombosis, healthy control subjects, patients with thrombosis). We detected statistically significant difference in terms of factor V levels between patient and control group. The tendency to thrombosis in patients with BD is well known. The endothelial lesion, increased procoagulant activity, hypofibrinolysis were found to be responsible from these events. In our study, there was no significant difference in terms of coagulation parameters between the patients without and with thrombosis. [ABSTRACT FROM AUTHOR]

Background All aspects of aetiopathogenesis of recurrent aphthous stomatitis (RAS) have not been elucidated. RAS and Behçet's disease (BD) have clinical and immunological characteristics in common. Although T17 cytokines and alpha-enolase have been shown to play effective roles in BD and many other autoinflammatory diseases recently, their roles in RAS have not been studied extensively. In the present study, we investigated levels of several Th1, Th2 and Th17 pathways related cytokines and alpha-enolase to elucidate pathogenesis of RAS and to obtain data about possible treatment alternatives for the condition. Methods Serum interleukin-1, interleukin-13, interleukin-17, interleukin-18, interferon gamma and alpha-enolase levels in 24 patients with RAS, 30 patients with BD and 20 healthy controls were measured. Results Serum interleukin-1, interleukin-13, interleukin-17, interleukin-18, interferon gamma and alpha-enolase levels were higher in patients with RAS and patients with BD than in healthy controls ( P < 0.005). Conclusion Like Th1 and Th2 cells, Th17 cells were found to be effective in pathogenesis of RAS. In addition, alpha-enolase, the levels of which were high, may play an important role in etio-pathogenesis of RAS. Further studies to be designed in the light of these findings are required to shed light on pathogenesis and treatment of the condition. [ABSTRACT FROM AUTHOR]

Systemic sclerosis (SSc) is a disease characterized by inflammation, vascular abnormalities and fibrosis. The role of Rho/Rho-kinase pathway was demonstrated in the pathogenesis of fibrosis, inflammation and vascular abnormalities. This study was aimed to investigate the relation between SSc and Rho/Rho-kinase gene polymorphisms. The study included 339 patients with SSc and 302 healthy subjects who were apparently healthy and at similar age and gender. Genotype distributions and allele frequencies were detected by using Chi-square test or Fisher's exact Chi-square test between groups, and the haplotype analysis was applied using online program (SHEsis). Significant association was found in a polymorphism in the ROCK1 gene (rs35996865), a polymorphism in ROCK2 gene (rs10178332), a polymorphism in RhoA gene (rs2177268) and two polymorphisms in RhoC gene (rs11102522 and rs11538960) with SSc disease ( p < 0.0022). In this study, association between SSc disease and Rho/Rho-kinase gene polymorphisms was investigated for the first time; significant associations between ROCK1, ROCK2, RhoA and RhoC gene polymorphisms and SSc disease were demonstrated. The results strongly suggest that this SNP may be an important risk factor for development of SSc. However, further validation of these findings in an independent cohort is necessary. [ABSTRACT FROM AUTHOR]