Abstract:
Abstract. Despite significant progress in establishing the causes, mechanisms of occurrence, approaches to diagnosis and treatment, rheumatoid arthritis remains one of the most widespread and prognostically unfavorable diseases.
In recent years, scientists have discovered dozens of new areas in the human genome associated with rheumatoid arthritis and found out that certain candidate genes play an important role in the development and progression of rheumatoid arthritis, which requires the search for new approaches to the prevention and treatment of this disease.
Purpose: to study changes in the state of the proteolysis and fibrinolysis system in patients with rheumatoid arthritis after personalized treatment depending on the T-786C genotypes of the eNOS gene. Materials and methods: To study the T-786C polymorphism of the eNOS gene promoter, 2 groups of patients were selected: a control group – 20 practically healthy individuals and an experimental group – 60 patients with rheumatoid arthritis. The state of the proteolysis system was assessed by lysis of azoalbumin, azocasein, and azocol. The fibrinolytic activity of the blood plasma was evaluated by the lysis of azofibrin with subsequent determination of the total, non-enzymatic and enzymatic fibrinolytic activity of the blood plasma. Results: Positive dynamics of changes in fibrinolytic activity of blood plasma were noted in all studied groups of patients, regardless of polymorphic variants of the eNOS gene (rs 2070744): increase in enzymatic fibrinolytic activity among carriers of the TT genotype – by 18.06% (p<0.05), carriers TС-genotype – by 11.39% and СС-genotype carriers – by 13.24% (p<0.05). When evaluating the proteolytic system of the blood after treatment, a decrease in azoalbumin lysis and azocasein lysis was found in carriers of the TT genotype – by 16.6% (p<0.05) and 15% (p<0.05), in carriers of the TС genotype – by 23.57% (p<0.05) and 13.26% (p<0.05), and in СС genotype carriers – by 17.36% (p<0.05) and 10.77%, respectively. Azocol lysis decreased only in СС-genotype carriers – by 15.38% (p<0.05), with no significant difference in T-allele carriers.
