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Arthritis Care & Research Oct 2023
Topics: Humans; Arthritis, Juvenile; Lung Diseases
PubMed: 37038966
DOI: 10.1002/acr.25126 -
International Journal of Rheumatic... Oct 2023
Topics: Humans; Arthritis, Juvenile; Rheumatology
PubMed: 37807617
DOI: 10.1111/1756-185X.14813 -
Rheumatic Diseases Clinics of North... May 2020This article provides an overview of juvenile spondyloarthritis and important differences in the classification criteria, clinical presentation, outcomes, and pathology... (Comparative Study)
Comparative Study Review
This article provides an overview of juvenile spondyloarthritis and important differences in the classification criteria, clinical presentation, outcomes, and pathology in juvenile versus adult-onset disease. Key differences in classification criteria between children and adults with spondyloarthritis are important to understand, as they can make transition from pediatric to adult care challenging. MRI and ultrasonography are increasingly relied on for the assessment of adult-onset disease activity and change over time in the pediatric population. The unique features of the maturing axial and peripheral skeleton are described for each modality, as they are key to understand for accurate interpretation of pathology in the pediatric population.
Topics: Adolescent; Adult; Arthritis, Juvenile; Child; Humans; Spondylarthritis; Transition to Adult Care
PubMed: 32340699
DOI: 10.1016/j.rdc.2020.01.003 -
Zeitschrift Fur Rheumatologie Feb 2022Axial spondylarthritis in adulthood (SpAA) is frequently initially manifested as a sacroiliitis, whereas this not true for enthesitis-related arthritis (EAA), which... (Review)
Review
Axial spondylarthritis in adulthood (SpAA) is frequently initially manifested as a sacroiliitis, whereas this not true for enthesitis-related arthritis (EAA), which begins in childhood and adolescence. Classically, EAA begins with peripheral arthritis and only a part transitions into a juvenile SpA (jSpA) or SpAA. The criteria used for classification of SpAA and EAA are currently being validated and revised. For the first time imaging is included for EAA. For both diseases nonsteroidal anti-inflammatory drugs (NSAID) are initially used therapeutically, followed by biologicals or synthetic targeted disease-modifying drugs in refractory courses. Steroids should be avoided in long-term treatment. For optimal transition and further care in adulthood, a close cooperation between internistic and pediatric rheumatologists is necessary.
Topics: Adolescent; Adult; Anti-Inflammatory Agents, Non-Steroidal; Arthritis, Juvenile; Biological Products; Child; Humans; Sacroiliitis; Spondylarthritis
PubMed: 34985566
DOI: 10.1007/s00393-021-01135-8 -
The Journal of Rheumatology Jul 2022
Topics: Arthritis, Juvenile; Arthritis, Psoriatic; Humans; Psoriasis; Uveitis
PubMed: 35428714
DOI: 10.3899/jrheum.220163 -
World Journal of Pediatrics : WJP Dec 2020
Review
Topics: Arthritis, Juvenile; Child; Diagnosis, Differential; Female; Humans; Male; Sex Factors; Uveitis
PubMed: 31965444
DOI: 10.1007/s12519-019-00331-6 -
Current Opinion in Rheumatology Sep 2019IL-18 is a pleiotropic cytokine involved in the regulation of innate and adaptive immune responses. IL-18 pro-inflammatory activities are finely regulated in vivo by the... (Review)
Review
PURPOSE OF REVIEW
IL-18 is a pleiotropic cytokine involved in the regulation of innate and adaptive immune responses. IL-18 pro-inflammatory activities are finely regulated in vivo by the inhibitory effects of the soluble IL-18-binding protein (IL-18BP). The elevation of circulating levels of IL-18 has been described in children with systemic juvenile idiopathic arthritis (sJIA). In the recent years, the role of IL-18 in the pathogenesis of secondary haemophagocytic lymphohistiocytosis (sHLH), also referred to as macrophage activation syndrome (MAS), in the context of autoinflammatory diseases, including sJIA, is emerging.
RECENT FINDINGS
A large number of studies in patients and animal models pointed to the imbalance in IL-18/IL-18BP levels, causing increased systemic levels of free bioactive IL-18, as a predisposing factor in the development of MAS. Although the exact mechanisms involved in the development of MAS are not clearly understood, increasing evidence demonstrate the role of IL-18 in upregulating the production of interferon (IFN)-γ.
SUMMARY
On the basis of the first emerging data on the possibility of blocking IL-18, we here discuss the scientific rationale for neutralizing the IL-18/IFNγ axis in the prevention and treatment of sHLH and MAS.
Topics: Arthritis, Juvenile; Biomarkers; Child; Humans; Immunity, Innate; Interleukin-18
PubMed: 31192813
DOI: 10.1097/BOR.0000000000000634 -
Deutsches Arzteblatt International Aug 2020
Topics: Arthralgia; Arthritis, Juvenile; Child; Humans; Pain
PubMed: 33161946
DOI: 10.3238/arztebl.2020.0599b -
Pediatric Rheumatology Online Journal Mar 2021Juvenile Idiopathic Arthritis is one of the most prevalent chronic diseases in children, with an annual incidence of 2-20 cases per 100,000 and a prevalence of 16-150... (Review)
Review
Juvenile Idiopathic Arthritis is one of the most prevalent chronic diseases in children, with an annual incidence of 2-20 cases per 100,000 and a prevalence of 16-150 per 100,000. It is associated with several complications that can cause short-term or long-term disability and reduce the quality of life. Among these, growth and pubertal disorders play an important role. Chronic inflammatory conditions are often associated with growth failure ranging from slight decrease in height velocity to severe forms of short stature. The prevalence of short stature in JIA varies from 10.4% in children with polyarticular disease to 41% of patients with the systemic form, while oligoarthritis is mostly associated with localized excessive bone growth of the affected limb, leading to limb dissymmetry. The pathogenesis of growth disorders is multifactorial and includes the role of chronic inflammation, long-term use of corticosteroids, undernutrition, altered body composition, delay of pubertal onset or slow pubertal progression. These factors can exert a systemic effect on the GH/IGF-1 axis and on the GnRH-gonadotropin-gonadic axis, or a local influence on the growth plate homeostasis and function. Although new therapeutic options are available to control inflammation, there are still 10-20% of patients with severe forms of the disease who show continuous growth impairment, ending in a short final stature. Moreover, delayed puberty is associated with a reduction in the peak bone mass with the possibility of concomitant or future bone fragility. Monitoring of puberty and bone health is essential for a complete health assessment of adolescents with JIA. In these patients, an assessment of the pubertal stage every 6 months from the age of 9 years is recommended. Also, linear growth should be always evaluated considering the patient's bone age. The impact of rhGH therapy in children with JIA is still unclear, but it has been shown that if rhGH is added at high dose in a low-inflammatory condition, post steroids and on biologic therapy, it is able to favor a prepubertal growth acceleration, comparable with the catch-up growth response in GH-deficient patients. Here we provide a comprehensive review of the pathogenesis of puberty and growth disorders in children with JIA, which can help the pediatrician to properly and timely assess the presence of growth and pubertal disorders in JIA patients.
Topics: Adolescent; Arthritis, Juvenile; Child; Growth Disorders; Humans; Puberty
PubMed: 33712046
DOI: 10.1186/s12969-021-00521-5 -
Cells Oct 2020Juvenile idiopathic arthritis (JIA) is highly heterogeneous in terms of etiology and clinical presentation with ambiguity in JIA classification. The advance of... (Review)
Review
Juvenile idiopathic arthritis (JIA) is highly heterogeneous in terms of etiology and clinical presentation with ambiguity in JIA classification. The advance of high-throughput omics technologies in recent years has gained us significant knowledge about the molecular mechanisms of JIA. Besides a minor proportion of JIA cases as monogenic, most JIA cases are polygenic disease caused by autoimmune mechanisms. A number of alleles (including both class I and class II genes), and 23 non- genetic loci have been identified of association with different JIA subtypes. Omics technologies, i.e., transcriptome profiling and epigenomic analysis, contributed significant knowledge on the molecular mechanisms of JIA in addition to the genetic approach. New molecular knowledge on different JIA subtypes enables us to reconsider the JIA classification, but also highlights novel therapeutic targets to develop a cure for the devastating JIA.
Topics: Arthritis, Juvenile; Autoimmune Diseases; Epigenome; Genetic Predisposition to Disease; Genome-Wide Association Study; HLA Antigens; Humans; Multifactorial Inheritance; Transcriptome
PubMed: 33076506
DOI: 10.3390/cells9102301