Abstract:
Rheumatoid arthritis (RA) is an autoimmune, systemic disease that affects the joints. In RA, the
body‟s immune system destroy body‟s tissue for a foreign invader. This leads immune system to attack the
protective cushion of tissue and fluid between the joints. The result is swelling, stiffness, and pain in the joint. The
body‟s misfiring immune system also may go after the body‟s soft tissues, like cartilage, and organs such as the
heart, eyes, and veins. According to the literature, the number of publications on the study of endogenous
pathological factors as the reason of systematic inflammatory reaction in patients with RA is
limited. Methods: Retrospective analysis representing in this article was performed through 68 patients with RA
who was received inpatient treatment in the Department of Rheumatology 3-clinic Tashkent Medical Academy
(TMA) in period from 2013 to 2015. The activity of rheumatoid arthritis was estimated on DAS-28 indicators, the
erythrocyte sedimentation rate (ESR) levels and quantity of leukocytes. The research included 16 patients suffering
from RA without anemia (Hb>120g/l) – the first group of patients, 20 patients (second group) of RA with anemia
(Hb<110g/l) and without helicobacter pylori infection and 32 patients (the third group) of RA with an anemia a
positive helicobacter pylori infection. For control group, 14 almost healthy people of both sexes were
chosen. Results: Cytokine attack to endotheliocytes cause "oxygen explosion" of a cell which is also associated
with the increase pool middle molecular weight (MMW) on average by 1.6 times in plasma of blood and by 1.8
times in erythrocytes in patients with RA without anemia. An increase of malondialdehyde in blood erythrocytes
for 25% was noted. The hepatocellular answer is shown by production and release of proteins of a sharp phase, i.e.
the increase of C-reactive protein by 1.7 times and fibrinogen by 1.4 times [PL 0.05] in RA patients without
anemia. Tumor necrosis factor level in patients of the III group exceeded the initial level of healthy people by 2.9
times [PL 0.05]. The cascade of anti-inflammatory cytokine at this group of patients starts the main mechanism of
development of disease where IL-6 stimulates development of proteins of inflammation's sharp phase in liver, in
particular C-reactive protein and fibrinogen whose contents exceeded reference values respectively by 2.9 times
and by 1.9 times [PL 0.05]. Conclusion: Several endogenous pathological factors such as TNF-α, C-reactive
protein, fibrinogen, malondialdehyde were determined as the reason of system inflammatory reaction in
rheumatoid arthritis.