Ali Asghar Ebrahimi; Hamid Noshad; Shahram Sadreddini; Mohammad Saeid Hejazi; Yashar Mohammadzadeh Sadigh; Yashar Eshraghi; Morteza Ghojazadeh
Volume 6, Issue 3 , Summer 2009, , Pages 147-153
Background: Rheumatoid arthritis (RA) is a chronic multisystem autoimmune disease common in all races and ethnics. Cytokines and cytokines receptors play an important role in RA pathogenesis and clinical presentation. Objective: To investigate the serum levels of TNF-α, TNF-α RI, TNF-α ...
Background: Rheumatoid arthritis (RA) is a chronic multisystem autoimmune disease common in all races and ethnics. Cytokines and cytokines receptors play an important role in RA pathogenesis and clinical presentation. Objective: To investigate the serum levels of TNF-α, TNF-α RI, TNF-α RII and IL-12 in RA patients and healthy control group. Methods: In this study 43 patients fulfilling the revised criteria of American College of Rheumatology (ACR) for RA and 13 healthy cases as a control group were selected for TNF-α, TNF-αRI, TNF-αRII and IL-12 serum level analysis. The patients' age was 42.2 ± 22 and the age of healthy group was 40.1 ± 19.2 years (p=0.1). The pa-tients had an active disease with at least six swollen and ten tender joints. Minimum ESR was 28 mm at first hours of the morning. Early morning stiffness in patients lasted longer than 45 minutes. Results: Our study showed that IL-12 serum level of the pa-tients (91.69 ± 43.07 ρg/ml) and control (61.79 ± 40.08 ρg/ml) group was significantly different (p<0.001). The serum level of TNF-αRI was 2.36 ± 0.77 ng/ml in the patient and 1.73 ± 0.37 ng/ml in the control group (p<0.01). TNF-αRII serum concentration in patients was 8.89 ± 2.3 ng/ml, while that of control group was 7.06±1.30 ng/ml (p=0.03). The serum level of TNF-α in patients was 32.90 ± 19.27 ρg/ml and that of the control group was 24.27± 8.28 ρg/ml (p=0.08) with no significant difference between the two. Conclusions: It is concluded that IL-12, TNF-αRI and TNF- αRII serum con-centrations are more important and better predictive factors than TNF-α in RA course and in the active forms of the disease.