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Hydroxychloroquine does not decrease serum methotrexate concentrations in children with juvenile idiopathic arthritis.

Jarkko Haapasaari·Hannu Kautiainen·Heikki Isomäki·Markku Hakala
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Arthritis, JuvenileChildFemaleHumansHydroxychloroquineMaleMethotrexateLetter

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Jarkko Haapasaari, Hannu Kautiainen, Heikki Isomäki, Markku Hakala. 2005. Hydroxychloroquine does not decrease serum methotrexate concentrations in children with juvenile idiopathic arthritis.. https://doi.org/10.1002/art.21037

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PubMed2026

Rare variant analysis of whole genome sequenced juvenile idiopathic arthritis multiplex pedigrees identifies rare variants in NOD2 and ACVR1.

Juvenile idiopathic arthritis is a complex rheumatic disease that is influenced by environmental and genetic factors. Linkage and genome-wide association studies have identified genes that contribute to the risk of developing juvenile idiopathic arthritis but are limited in their ability to identify disease-risk variants of large effect. Penetrant, heritable risk variants can be detected in high-risk families, but such cases are uncommon due to the low prevalence of juvenile idiopathic arthritis. This study utilizes whole-genome sequencing of 23 multiplex families, the largest such cohort to date, to discover variants and genes relevant to JIA pathogenesis. Pathogenic variants in NOD2 associated with Blau syndrome, an ultra-rare Mendelian inflammatory disorder, are the most recurrent variants in the cohort, consistent with previous reports that milder presentations of Blau syndrome are oftentimes misdiagnosed as juvenile idiopathic arthritis. For the first time, however, rare variants in ACVR1 and SMAD6, integral components of the Bone Morphogenic Protein pathway, are found to be associated with juvenile idiopathic arthritis. Identified ACVR1 variants map to critical protein domains. AlphaFold modeling predicts that the ACVR1 interaction with its inhibitor OGT is disrupted by these variants, indicating that the patient-mutated protein has a gain-of-function phenotype. Drosophila melanogaster expressing either a wild-type or patient-mutated version of ACVR1 exhibit embryonic lethality, with the mutant exhibiting 1.4-fold greater lethality than wild-type. The combination of family-based cohorts for gene discovery, AI-based computational tools, and animal model studies for tests of variant function underscores shared disease pathogenesis between JIA and monogenic disorders of immunity and connective tissue.

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PubMed2005

Does systemic-onset juvenile idiopathic arthritis belong under juvenile idiopathic arthritis?

'Science is the systematic classification of experience' George Henry Lewes (1817-78), English philosopher, critic, dramatist, scientist. Juvenile idiopathic arthritis (JIA) is prevalent in about 1 in 1000 children. The earliest formal description of this disease was by Sir George Frederick Still in 1897. This work was done when he was a registrar at the Hospital for Sick Children, Great Ormond Street, London. In this initial description of 19 patients he identified three patterns of arthritis, one of which came to be known later as Still's disease [now known as systemic-onset juvenile idiopathic arthritis (SoJIA)]. Over the next few decades it came to be appreciated that one form of arthritis in children is very different and dominated by the presence of systemic manifestations. Over the last two decades several paediatric rheumatologists have come together to classify juvenile arthritis for purposes of better disease identification and research. All along, the systemic form of juvenile arthritis was always recognized as belonging to a distinct group; in fact for several decades (and even now in some countries) the systemic form of juvenile arthritis was referred to as Still's disease. In this article we will attempt to highlight the reasons why we feel that SoJIA is perhaps not best retained in the company of JIA.

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