Interrelations of impaired biochemical and immunological homeostasis in patients with juvenile rheumatoid arthritis taking into account the disease duration
Background. Juvenile rheumatoid arthritis (JRA) is a life-long pathological condition. Therefore, the study of the mechanisms of its development, the metabolic systems functioning, the formation of dystrophic changes on the background of the inflammatory process is relevant. The purpose of the work was to study the features of metabolism of connective tissue structures depending on the state of immune homeostasis at the stages of evolution of the JRA in pediatric patients. Material and methods. The peculiarities of the structural composition of the connective tissue components, the content of trace elements, and immunological homeostasis in children with JRA were studied. Three hundred fifty-five clinical observations of JRA taking into account retro- and advanced studies for 2012–2016 were analyzed. The clinical group consisted of 117 arthritis patients aged 2 to 18 years (average 6.0 ± 0.5 years). Results. Investigation of immune status determined the decreased T-common lymphocytes (p < 0.001), T-lymphocytes-helper (p < 0.001), T-suppressors/cytotoxic (p < 0.001) immuno-regulatory index (p < 0.05), reduction of bactericidal neutrophil activity (p < 0.001), increase in NST test and decrease in the index of stimulation of neutrophils (p < 0.001), elevated circulating immune complexes (p < 0.001). Analysis of proinflammatory cytokines content showed an increased IL-1 (p < 0.05) and IL-6 level. The study demonstrated the dependence of immunological parameters on disease duration and increased chondroitin-4- and -6-sulfates and blood keratin and dermatan sulfates. The largest deviations were noted at the early stages of the disease, which is undoubtedly related to the activity of the pathological process prior to the anti-inflammatory treatment initiation or at its early stages. The long-term periods of the disease are associated with decrease in the total glycosaminoglycanase, chondroitin-4- and chondroitin-6-sulfates, and the decreased excretion of uronic acid (pt < 0.05). The analysis of changes in the content of inorganic components, depending on the disease duration, revealed a slight decrease in phosphorus loss in the JRA period within 3–5 years. The analysis of deviations in immuno-biochemical correlations at different stages of the pathological process evolution revealed changes in the number and nature of the relationship between the parameters of connective tissue metabolism and immunological homeostasis. Conclusions. High activity of the disease is the main predictor of the dystrophic changes development, which is confirmed by numerous correlation interactions of the parameters of connective tissue metabolism and immunological parameters. The most unfavorable periods are the first 1.5 years and 3–5 years from the disease onset. The revealed changes requires medical correction of the biochemical composition of the connective tissue structures in order to prevent the development of secondary dystrophic changes in the affected joints in children with JRA, and may also reflect the inadequate effect of treatment and maintaining of subclinical activity of inflammation.
Full Text:PDF (Українська)
Aguiara F, Brito I. Structural damage to the hip in systemic juvenile idiopathic arthritis: A case of regression with Anakinra. Reumatol Clin. 2017 Mar - Apr;13(2):118-119. doi: 10.1016/j.reuma.2015.12.007.
Lin YT, Wang CT, Gershwin ME, Chiang BL. The pathogenesis of oligoarticular/polyarticular vs systemic juvenile idiopathic arthritis. Autoimmun Rev. 2011 Jun;10(8):482-9. doi: 10.1016/j.autrev.2011.02.001.
Winsz-Szczotka K, Kuźnik-Trocha K, Komosińska-Vassev K, Jura-Półtorak A, Olczyk K. Laboratory Indicators of Aggrecan Turnover in Juvenile Idiopathic Arthritis. Dis Markers. 2016;2016:7157169. doi: 10.1155/2016/7157169.
- There are currently no refbacks.
Copyright (c) 2018 CHILD`S HEALTH
This work is licensed under a Creative Commons Attribution 4.0 International License.
© Publishing House Zaslavsky, 1997-2018