A level of tumor necrosis factor alpha (TNF-α) and morphological parameters of disease in seropositive and seronegative rheumatoid arthritis

One of the most current and still not sorted out clinical problems is the pathogenetic role the TNF-a factor plays in the development of RA. So far we have known that TNF-α factor is a key pro-inflammatory cytokine responsible for the destruction of cartilage and deletion of the bone in RA. Taking into account the existing knowledge on the pathogenetic role of TNF-α factor we have decided to determine the diagnostic usefulness of level of TNF-α in serum and correlation of TNF-α level with the degree of tissue damage in RA. The aim of the study is to determine how the level of TNF-α factor in serum of RA patients, positive and negative, correlates with the degree of bone damage measured by Steinbrocker and Larsen scale. In light of the above 60 RA patients were tested in the Outpatient Rheumatology Department CSK MSWiA. There were mainly women in the II-IV period according to Steinbrocker’s criteria. The control group consisted of 30 people with the osteoarthritis of the knee. The RA patients divided in two groups of 30 persons, the first was seropositive, the second was seronegative. The age of patients of I group during the tests ranged from 41 to 81 years, in the group II from 23 to 83 years, in the group III from 41 to 78 years. The disease duration during the tests in the group I ranged from 2 to 33 years, in the group II from 1 to 40 years, in the group III from 2 to 18 years. The results obtained were subject to statistical analysis. No correlation has been detected between the evaluation of the degree of the tissue damage and the TNF-a level. Whereas, there was detected a positive correlation between the degree of the tissue damage and CRP, seromucoid level in serum of mainly the seronegative individuals. The TNF concentration of patients with RA was higher, especially of certain seropositive individuals, what indicates the participation of the TNF-α factor in pathogenesis of the joints’ inflammation.