The aim of this study was to assess relations among depression, anxiety and pain in children with juvenile idiopathic arthritis (JIA). Pain was measured with the visual analogue scale (VAS), and depression and anxiety with depression and anxiety subscales from the Trauma Symptom Checklist for Children (TSC-C). Pain perception was significantly correlated with depression scores.
Association of juvenile spondyloarthritis (jSpA) with the HLA-B27 genotype is well established, but there is little knowledge of other genetic factors with a role in the development of the disease. To date, only a few studies have tried to find those associated genes by obtaining expression profiles, but with inconsistent results due to various patient selection criteria and methodology. The aim of the present study was to identify and confirm gene signatures and novel biomarkers in highly homogeneous cohorts of untreated and treated patients diagnosed with jSpA and other forms of juvenile idiopathic arthritis (JIA) according to ILAR criteria. For the purposes of the research, total RNA was isolated from whole blood of 45 children with jSpA and known HLA genotype, 11 children with oligo- and polyarticular forms of JIA, as well as 12 age and sex matched control participants without diagnosis of inflammatory disease. DNA microarray gene expression was performed in 11 patients with jSpA and in four healthy controls, along with bioinformatical analysis of retrieved data. Carefully selected differentially expressed genes where analyzed by qRT-PCR in all participants of the study. Microarray results and bioinformatical analysis revealed 745 differentially expressed genes involved in various inflammatory processes, while qRT-PCR analysis of selected genes confirmed data universality and specificity of expression profiles in jSpA patients. The present study indicates that jSpA could be a polygenic disease with a possible malfunction in antigen recognition and activation of immunological response, migration of inflammatory cells and regulation of the immune system. Among genes involved in these processes TLR4, NLRP3, CXCR4 and PTPN12 showed almost consistent expression in study patients diagnosed with jSpA. Those genes and their products could therefore potentially be used as novel biomarkers, possibly predictive of disease prognosis and response to therapy, or even as a target for new therapeutic approaches.
Single nucleotide polymorphisms (SNP) of toll-like and NOD-like receptors have been associated with altered receptor activity and modified production of proinflammatory cytokines leading to a number of diseases. Our aim was to determine whether SNP of TLR2 (Arg753Gln), TLR4 (Asp299Gly, Thr399Ile), and NLRP3 (Q705K) influence susceptibility to juvenile spondyloarthrtis (jSpA) and juvenile idiopathic arthritis (JIA). After the DNA extraction, 26 patients with jSpA, 11 with oligoarticular, polyarticular, or systemic JIA, and 40 healthy controls were genotyped for Arg753Gln, Asp299Gly, Thr399Ile, and Q705K SNP using real-time PCR-SNP analysis. Statistically significant difference in genotype frequency for Thr399Ile SNP of TLR4 was observed in the jSpA (χ2 = 6.705, p = 0.035) and not in the JIA group (χ2 = 3005, p = 0.223). Regarding Asp299Gly SNP, no significant difference in genotype frequency was found; however, allele frequency was significant in both jSpA and JIA patients. No significant difference in genotype or allele frequency was observed for Arg735Gln and Q705K SNP. The399Ile polymorphism of TLR4 may be responsible for altered immune response to microbial infection in variant carriers and represent a mechanism of triggering overproduction of proinflammatory cytokines and long-term inflammation in jSpA. SNP of TLR2, NLRP3, and TLR4 (Asp299Gly) were not associated with jSpA or JIA.
78.8%); Erythema marginatum in 7 (21.2%); Sydenham chorea, 4 (12.1%); Subcutaneous nodules, 2 (6.1%), respectively. And minor criteria were; fever, 27 (81.8%); first degree heart block, 7 (21.2%); elevated inflammatory markers (ESR, CRP), 30 (90.9%). ARF patients were treated with antimicrobial agent therapy 33 (100%); NSAIDs 24 (72.7%); and glucocorticoids therapy 15 (45.4%). All ARF patients were prescribed with antimicrobial agent prophylaxis. On the other hand, the mean age of PSRA was 8.0 years (3-14 years), and female/male ratio was 17/14. Three patients (9.4%) had monoarthritis, 15 patients (46.9%) had oligoarthritis, and 14 patients (43.6%) had polyarthritis. Two patients had arthritis and enthesitis. And fever in 24 (75.0%) and Elevated inflammatory markers in 29 (90.6%). PSRA patients were treated with antimicrobial agent therapy 25 (78.1%); NSAIDs 27 (84.4%); and glucocorticoids therapy 3 (9.4%). During the follow up, there was no patient with carditis. 18 (56.3%) patients with PSRA were prescribed with antimicrobial agent prophylaxis. Conclusion: In this study, ARF is rare in the Japanese pediatric population, but ARF has not yet disappeared. We observed high incidence of arthritis, carditis and erythema marginatum. No PSRA case was complicated with carditis. General pediatrician need to have updated information about ARF and PSRA even in industrialized countries.
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