Diagnosing juvenile idiopathic arthritis

McMahon, Anne-Marie; Tattersall, Rachel

doi:10.1016/j.paed.2011.07.005

Cited by 6 publications

(18 citation statements)

References 11 publications

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“…Juvenile idiopathic arthritis (JIA) is the most common form of arthropathy that begins before the age of 16 years. Its incidence is estimated at 2–20 cases per 100 000 children and its prevalence up to 150/100 000 1 , 2 , 3 , 4 . The term describes a heterogenous group of diseases associated with persistent joint inflammation lasting more than 6 weeks 3 , 4 , 5 , 6 .…”

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“…[1][2][3][4] The term describes a heterogenous group of diseases associated with persistent joint inflammation lasting more than 6 weeks. [3][4][5][6] JIA may be manifested as systemic arthritis, oligoarthritis (persistent or extended), polyarthritis (rheumatoid factor negative or positive), psoriatic arthritis, enthesitis-related arthritis or undifferentiated arthritis, 2,4,7 but oligoarthritis is by far the most prevalent. 2,4 JIA, especially when systemic, may lead to joint destruction, limitation of growth, osteoporosis and serious disability, as well as significant emotional and social consequences.…”

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“…[3][4][5][6] JIA may be manifested as systemic arthritis, oligoarthritis (persistent or extended), polyarthritis (rheumatoid factor negative or positive), psoriatic arthritis, enthesitis-related arthritis or undifferentiated arthritis, 2,4,7 but oligoarthritis is by far the most prevalent. 2,4 JIA, especially when systemic, may lead to joint destruction, limitation of growth, osteoporosis and serious disability, as well as significant emotional and social consequences. 2 Various etiological mechanisms have been proposed involving both genetic and environmental factors.…”

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“…2,4 JIA, especially when systemic, may lead to joint destruction, limitation of growth, osteoporosis and serious disability, as well as significant emotional and social consequences. 2 Various etiological mechanisms have been proposed involving both genetic and environmental factors. 4,5 Inflammatory processes in the synovial membrane of the articular cavity lead to elevation of the volume of the synovial fluid (SF) and changes to its composition.…”

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Lectin pathway factors in patients suffering from juvenile idiopathic arthritis

et al. 2017

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Both complement activation and certain infections (including those with Yersinia sp.) may contribute to the pathogenesis of juvenile idiopathic arthritis (JIA). We investigated factors specific for the lectin pathway of complement: mannose-binding lectin (MBL), ficolins and MBL-associated serine protease-2 (MASP-2), in 144 patients and 98 controls. One hundred and six patients had oligoarticular disease and 38 had polyarticular disease. In 51 patients (out of 133 tested), Yersinia-reactive antibodies were found (JIA Ye group). MBL deficiency was significantly more frequent in the JIA Ye group than in patients without Yersinia-reactive antibodies or in controls. Median serum ficolin-2 level was significantly lower (and proportion of values deemed ficolin-2 insufficient greater) in JIA patients irrespective of their Yersinia antibody status. The minority (C) allele at -64 of the FCN2 gene was less frequent among JIA patients than among control subjects. No differences were found in the frequency of FCN3 gene +1637delC or MASP2 +359 A>G mutations nor for median values of serum ficolin-1, ficolin-3 or MASP-2. However, high levels of serum ficolin-3 were under-represented in patients, in contrast to MBL. MBL, ficolin-1, ficolin-2, ficolin-3 and MASP-2 were also readily detectable in synovial fluid samples but at a considerably lower level than in serum. Our findings suggest a possible role for the lectin pathway in the pathogenesis of JIA, perhaps secondary to a role in host defence, and indicate that investigations on the specificity of lectin pathway recognition molecules towards specific infectious agents in JIA might be fruitful.

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Lectin pathway factors in patients suffering from juvenile idiopathic arthritis

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“…Histologically, there is hyperplasia of the lining of the synovium and infiltration of the sub-lining with various inflammatory cells. This chronic inflammatory process leads to the formation of pannus which causes cartilage and bone erosions and consequent joint damage [ 17 ]. These pathophysiological changes present clinically as a painful, red, swollen joint(s) with limited range of movement and, if the arthritis is prolonged, potential for joint deformities and growth disturbances [ 18 ].…”

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Juvenile Idiopathic Arthritis: A Review of Novel Diagnostic and Monitoring Technologies

et al. 2021

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Juvenile idiopathic arthritis (JIA) is the most common rheumatic disease of childhood and is characterized by an often insidious onset and a chronic relapsing–remitting course, once diagnosed. With successive flares of joint inflammation, joint damage accrues, often associated with pain and functional disability. The progressive nature and potential for chronic damage and disability caused by JIA emphasizes the critical need for a prompt and accurate diagnosis. This article provides a review of recent studies related to diagnosis, monitoring and management of JIA and outlines recent novel tools and techniques (infrared thermal imaging, three-dimensional imaging, accelerometry, artificial neural networks and fuzzy logic) which have demonstrated potential value in assessment and monitoring of JIA. The emergence of novel techniques to assist clinicians’ assessments for diagnosis and monitoring of JIA has demonstrated promise; however, further research is required to confirm their clinical utility.

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