A comprehensive overview of juvenile idiopathic arthritis: From pathophysiology to management

Bansal, Nancy; Pasricha, Chirag; Kumari, Pratima; Jangra, Sarita; Kuar, Rupinder; Singh, Ravinder J.

doi:10.1016/j.autrev.2023.103337

Cited by 12 publications

(6 citation statements)

References 130 publications

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“…However, it has been observed that there is a deficiency in IL-10 production in both JIA mouse models and patients, which may not be sufficient to counteract the effects of pro-inflammatory cytokines ( 31 ). Additionally, the disease activity of JIA is correlated with reduced IL-10 expression ( 32 ). This suggests that the deficiency of IL-10 could potentially contribute to the development of JIA.…”

Section: Discussionmentioning

confidence: 99%

Juvenile idiopathic arthritis and primary ovarian failure: a two-sample Mendelian randomization analysis in a mixed-gender cohort

Mo,

Shang,

Wei

et al. 2024

Front. Endocrinol.

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BackgroundThe causal relationship between juvenile idiopathic arthritis (JIA) and primary ovarian failure (POF) remains uncertain. To elucidate this relationship, we employed a two-sample Mendelian randomization analysis.MethodsThe single nucleotide polymorphisms (SNPs) associated with JIA were obtained from a previously published genome-wide association study (GWAS), while the pooled data for POF originated from the FinnGen consortium. The study populations consisted exclusively of individuals of European descent. In our Mendelian randomization analysis, we performed inverse-variance weighted analysis, weighted-median analysis, weighted-mode analysis and Mendelian randomization-Egger regression analysis, supplemented by sensitivity analyses to validate the accuracy and robustness of the findings.ResultsThe IVW (OR = 1.23, 95% CI 1.06-1.43; P = 0.007) and weighted median (OR = 1.25, 95% CI 1.06-1.47; P = 0.009), along with sensitivity analysis validation, provide compelling evidence of a significant causal association between JIA and POF.ConclusionThe study revealed a significant causal association between genetically predicted JIA and POF, indicating that JIA significantly elevates the risk of developing POF. Therefore, it is recommended to implement screening for premature ovarian failure in women diagnosed with JIA.

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Section: Discussionmentioning

confidence: 99%

Juvenile idiopathic arthritis and primary ovarian failure: a two-sample Mendelian randomization analysis in a mixed-gender cohort

Mo,

Shang,

Wei

et al. 2024

Front. Endocrinol.

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“…RA is a chronic inflammatory condition that not only affects the musculoskeletal system but also has negative impacts on multiple systems and organs in the body, as highlighted in several studies [1,[14][15][16]. Therefore, early intervention and treatment for RA in AYAs is of utmost importance.…”

Section: Discussionmentioning

confidence: 99%

Global burden of rheumatoid arthritis among adolescents and young adults aged 10–24 years: A trend analysis study from 1990 to 2019

Li,

Yuan,

2024

PLoS ONE

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Background In recent decades, there has been a global increase in the burden of rheumatoid arthritis (RA) among adolescents and young adults (AYAs), making it a significant public health issue. However, our understanding of the disease burden, harm, and influencing factors of RA in this population remains insufficient. This study aimed to assess the trends in RA burden among AYAs aged 10–24 years from 1990 to 2019 at the global, regional, and national levels. Methods Incidence, prevalence, and disability-adjusted life years (DALYs) rate per 100,000 population, as well as average annual percentage changes (AAPCs), of RA among individuals aged 10–24 years were reported globally, regionally, and nationally based on the Global Burden of Diseases, Injuries, and Risk Factors Study 2019 (GBD 2019). These global trends were further analyzed by age, sex, and Sociodemographic index (SDI). Joinpoint regression analysis was used to determine the year in which the most significant changes in global trends occurred. Results Globally, the incidence of RA among AYAs increased from 4.98 per 100,000 population in 1990 to 5.41 per 100,000 population in 2019, with an AAPCs of 0.29 (95%CI: 0.26, 0.32, p < 0.001). The most significant increase occurred in 2000, while the most significant decrease occurred in 2014. The prevalence increased from 34.11 per 100,000 population in 1990 to 36.34 per 100,000 population in 2019, with an AAPCs of 0.22 (95%CI: 0.19, 0.24, p<0.001); The most significant increase was observed in 2000, and the most significant decrease occurred in 2014. DALYs rate with RA were 5.96 per 100,000 population in 1990 and 5.79 per 100,000 population in 2019 for AYAs, with an average decrease of 0.1 years per year (AAPCs = -0.1, 95%CI: -0.2, -0.01, p = 0.04). In terms of gender, the incidence, prevalence, and DALYs rate were higher for females compared to males during the same period. Regarding age, the incidence, prevalence, and DALYs rate increased with increasing age. Based on the SDI quintile, the incidence, prevalence, and DALYs rate of RA were highest in countries with high SDI and lowest in countries with low SDI from 1990 to 2019. However, the relationship between incidence and SDI is non-linear. In terms of regions, Tropical Latin America exhibited the highest incidence, prevalence, and DALYs rate, while Andean Latin America experienced the most rapid increase in incidence and prevalence. Southern Latin America saw the fastest growth in DALYs rate, whereas Southern Sub-Saharan Africa witnessed the most significant decline. Conclusion In conclusion, the study revealed an overall increase in the incidence and prevalence of RA among adolescents and young adults (AYAs) over the past three decades, while DALYs rate remained relatively stable. Furthermore, the incidence, prevalence, and DALYs rate of RA were found to increase with age. Fortunately, recent proactive preventive measures and treatment methods have shown promising results. Moving forward, it is crucial to prioritize the female population and AYAs patients in order to further alleviate the global burden of RA.

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“…The cause of JIA is not well known but involves the inflammation of the synovium and the destruction of tissues in joints, which can cause the early onset of oligo articular JIA. It is challenging to diagnose in some children who initially complain of pain and joint swelling, as there is no single blood test that can confirm its diagnosis [4]. Some monogenic forms of JIA have been described, linked to variants in the genes encoding perforin (PRF1), Munc13-14 (UNC13D), syntaxin 11 (STX11), tumor necrosis factor-α-induced protein 3 (TNFAIP3) [5], laccase (multicopper reductase) domain-containing protein 1 (LACC1), and nuclear factor interleukin 3-regulated (NFIL3) [1], besides syndromic JIA conditions such as Blau syndrome (NOD2), Camptodactyly-arthropathy-coxa vara-pericarditis (CACP) syndrome (PRG4 and TRHR), multicentric carpotarsal osteolysis (MCTO) syndrome (MAFB) [2], and Majeed syndrome (LPIN2) [6].…”

Section: Introductionmentioning

confidence: 99%

Genome Sequencing in an Individual Presenting with 22q11.2 Deletion Syndrome and Juvenile Idiopathic Arthritis

de Oliveira-Sobrinho,

Appenzeller,

Holanda

et al. 2024

Genes

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Juvenile idiopathic arthritis is a heterogeneous group of diseases characterized by arthritis with poorly known causes, including monogenic disorders and multifactorial etiology. 22q11.2 proximal deletion syndrome is a multisystemic disease with over 180 manifestations already described. In this report, the authors describe a patient presenting with a short stature, neurodevelopmental delay, and dysmorphisms, who had an episode of polyarticular arthritis at the age of three years and eight months, resulting in severe joint limitations, and was later diagnosed with 22q11.2 deletion syndrome. Investigation through Whole Genome Sequencing revealed that he had no pathogenic or likely-pathogenic variants in both alleles of the MIF gene or in genes associated with monogenic arthritis (LACC1, LPIN2, MAFB, NFIL3, NOD2, PRG4, PRF1, STX11, TNFAIP3, TRHR, UNC13DI). However, the patient presented 41 risk polymorphisms for juvenile idiopathic arthritis. Thus, in the present case, arthritis seems coincidental to 22q11.2 deletion syndrome, probably caused by a multifactorial etiology. The association of the MIF gene in individuals previously described with juvenile idiopathic arthritis and 22q11.2 deletion seems unlikely since it is located in the distal and less-frequently deleted region of 22q11.2 deletion syndrome.

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A comprehensive overview of juvenile idiopathic arthritis: From pathophysiology to management

Cited by 12 publications

References 130 publications

Juvenile idiopathic arthritis and primary ovarian failure: a two-sample Mendelian randomization analysis in a mixed-gender cohort

Juvenile idiopathic arthritis and primary ovarian failure: a two-sample Mendelian randomization analysis in a mixed-gender cohort

Global burden of rheumatoid arthritis among adolescents and young adults aged 10–24 years: A trend analysis study from 1990 to 2019

Genome Sequencing in an Individual Presenting with 22q11.2 Deletion Syndrome and Juvenile Idiopathic Arthritis

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