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Rheumatoid arthritis (RA) is a chronic systemic disease of connective tissue with preferential lesion of peripheral joints by type of erosive-destructive arthritis [Astapenko, 1989). It occupies one of the leading places in a number of rheumatic diseases, and on the “severity of the clinical picture and its consequences (Ankilozirovanie) is unparalleled among other types of arthritis”
According to strict criteria, the prevalence of “certain” i.e. undeniable RA is close to 1%, and with the “probable” it reaches 2.5% in males and 5.2% in women [Barnes, 1990]. In general, women are ill in 3 – 5, and according to some data – 9 times more often. Maximum morbidity falls on the fifth decade.
At present, the significant importance in the development of RA is given to the hereditary factor. As it is known, the nearest relatives of patients have higher frequency of RA and more significant annual increase of new cases in comparison with the general population. [Benevolenskaja L.I., 1983; Hollander, Lee, 1965; Benn, Wood, 1972]. In the same vein, more frequent detections of HLA antigens – DR4 and Dh4 [Treves, 1986; Gran, 1987]. The question of the involvement of the infection, presumably viral, has not been definitively removed, although only circumstantial evidence is available. Special attention is drawn to the virus Ebstein-Barra, which is able to persistirovat for a long time in lymphocytes, breaking the synthesis of Immunoglobulins [Astapenko, 1989]. According to Barnes , to Ra, apparently, people with inborn inferiority immunoregulation, the reflection of which can be elevated detection antigens of loci DR and D. It is not excluded that the direct trigger factor The disease is an infectious agent that has not yet been identified.
According to modern representations, at the basis of the pathogenesis of Ra lie immunopatologicheskie, more precisely autoimmune, reactions, the main bridgehead of which are joint formation: synovial membrane, synovial fluid and articular cartilage. This is indicated (slide № 1)
1. Similarity of histological changes of the affected tissues with manifestations of immune (sterile) inflammation;
2. Failure of antimicrobial therapy, and vice versa, rheumatoid arthritis convincing effect of means and methods influencing the immune system;
3. Presence in the blood of most patients of the so-called factor (RF). As a matter of fact, due to his discovery of RA he was included in immunological problems [Woaler, Rose, 1940].
Briefly the chain of pathological disorders under RA can be presented as follows:
Pathogenesis of RA. EF RA (?) Þ Transformation of IgG (more precisely its Fe-fragment) in Autoag Þ production ß-lymphocytes and plasma cells of the synovial membrane IgH; A; G-so-called rheumatoid factors Þ rf + Autoag = CEC Þ synovial tissue Þ increased activity mediators inflammation, Insight microvascular, phagocytosis cec Þ damage lysosomes leukocytes and macrophages Þ release lysosomal Enzymes Þ damage to cellular structures Þ formation of new Autoag Þ chain reaction.
It should be noted that IR can be fixed and circulating. Fixed ir long time stored in the synovial membrane, supporting inflammatory and destructive tendencies. Circulating IR increase the risk and form the basis of vnesustavnyh (systemic) manifestations of the disease rheumatoid arthritis.