A Preliminary Study On The Relationship Between Inflammatory Cytokines And The Activity In Behcet's Disease

Aims: Behcet's disease(BD)is a systemic chronic inflammatory and autoimmune disease.It is mainly characterized by vasculitis,oral ulcer,genital ulcer,ophthalmitis and skin damage.Severe people can involve gastrointestinal,nervous and cardiovascular systems,with self-limited and recurrent characteristics,mainly prevalent in Asian countries.Onset age and clinical manifestations are related to mortality.There is no specific diagnostic tools at present.No specific serological markers were found to predict the severity of the disease.The pathogenesis of BD is not clear.It is believed that it is mainly related to heredity,environment and immune response.Cytokines play an important role in the pathophysiological process of BD,and the specific mechanism has not been clarified.The main treatment is colchicine,Non-steroidal anti-inflammatory drugs,interferon-a and empirical use of non-specific immunosuppressive drugs,with the further study of the pathogenesis of BD.Biological therapy has became a hot spot.The levels of 40 kinds of inflammatory cytokines were measured in the patient of Behcet's disease and healthy controls.We analyze the correlation between cytokines with the scores of activity,inflammatory indexes(erythrocyte sedimentation rate,c-reactive protein)and humoral immunity(Ig G,Ig M,Ig A)in this paper.Results:(1)T test showed there was no significant difference in 40 serum inflammatory factors between BD patients and healthy controls(p > 0.05).(2)Pearson correlation analysis show that IL-18?OPN?CD163?PF4?Resistin were correlated with BD disease activity,ESR and CRP.(P<0.05)Conclusion: IL-18,Resistin,PF4,CD163 may be involved with the activity of diease in Behcet's Disease.It is speculated that IL-18 is through Th1,Th17 cells,OPN through Th1 cells,CD163 through activation of monocytes-macrophages,and PF4,resistin through activation of neutral cells,which leads to immune disorders and participates in the pathogenesis of BD.