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Juvenile idiopathic arthritis is a chronic inflammatory joint disease in children under 16 years of age associated with pathological immune response to various antigens. Probable factors are infectious and immunogenetic. The process begins with the activation of humoral immunity. One of the key components of juvenile idiopathic arthritis pathogenesis is damage to the vascular endothelium. Immune complex vasculitis develops with hemostasis and microcirculation disorders in synovial membrane. Proinflammatory cytokines are produced, causing the destruction of the synovial membrane of the joint, cartilage, bone, contributing to the chronicity of the inflammatory process. In patients with rheumatic diseases, hemostatic changes occur in 4.5–63 % of cases, especially with high activity of the inflammatory process. In juvenile idiopathic arthritis, hemostasis disorders include thrombinemia, decreased antithrombin III, increased D-dimer level, and decreased fibrinolysis activity. Thrombodynamics test in adults with rheumatoid arthritis has shown the presence of a chronic hypercoagulable state. Rheumatoid arthritis is a risk factor for thrombotic complications in adults. There are no data on the study of thrombodynamic parameters in juvenile idiopathic arthritis. Currently, the pathogenetic commonality between autoimmune diseases such as systemic lupus erythematosus, rheumatoid arthritis, and immune-mediated antiphospholipid syndrome is known. The mechanisms of development of antiphospholipid syndrome are associated with an imbalance in the hemostasis system under the influence of autoantibodies to phospholipids of cell membranes, which can interact with endothelial cells, various components of the coagulation system, causing thrombotic complications. The importance of studying immune-mediated antiphospholipid syndrome in juvenile idiopathic arthritis is beyond doubt, but data on this issue in the pediatric population are extremely limited, including the relationship of antiphospholipid syndrome with immune hemostasis parameters. Single studies of immune-mediated antiphospholipid syndrome in children with juvenile idiopathic arthritis indicate that antiphospholipid syndrome markers are found in all variants of juvenile idiopathic arthritis, although thrombotic complications are rare.
Juvenile idiopathic arthritis is a chronic inflammatory joint disease in children under 16 years of age associated with pathological immune response to various antigens. Probable factors are infectious and immunogenetic. The process begins with the activation of humoral immunity. One of the key components of juvenile idiopathic arthritis pathogenesis is damage to the vascular endothelium. Immune complex vasculitis develops with hemostasis and microcirculation disorders in synovial membrane. Proinflammatory cytokines are produced, causing the destruction of the synovial membrane of the joint, cartilage, bone, contributing to the chronicity of the inflammatory process. In patients with rheumatic diseases, hemostatic changes occur in 4.5–63 % of cases, especially with high activity of the inflammatory process. In juvenile idiopathic arthritis, hemostasis disorders include thrombinemia, decreased antithrombin III, increased D-dimer level, and decreased fibrinolysis activity. Thrombodynamics test in adults with rheumatoid arthritis has shown the presence of a chronic hypercoagulable state. Rheumatoid arthritis is a risk factor for thrombotic complications in adults. There are no data on the study of thrombodynamic parameters in juvenile idiopathic arthritis. Currently, the pathogenetic commonality between autoimmune diseases such as systemic lupus erythematosus, rheumatoid arthritis, and immune-mediated antiphospholipid syndrome is known. The mechanisms of development of antiphospholipid syndrome are associated with an imbalance in the hemostasis system under the influence of autoantibodies to phospholipids of cell membranes, which can interact with endothelial cells, various components of the coagulation system, causing thrombotic complications. The importance of studying immune-mediated antiphospholipid syndrome in juvenile idiopathic arthritis is beyond doubt, but data on this issue in the pediatric population are extremely limited, including the relationship of antiphospholipid syndrome with immune hemostasis parameters. Single studies of immune-mediated antiphospholipid syndrome in children with juvenile idiopathic arthritis indicate that antiphospholipid syndrome markers are found in all variants of juvenile idiopathic arthritis, although thrombotic complications are rare.
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