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Children
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Diagnosis, Treatment and Care of Pediatric Rheumatology
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Diagnosis, Treatment and Care of Pediatric Rheumatology

A special issue of Children (ISSN 2227-9067). This special issue belongs to the section "Pediatric Allergy and Immunology".

Deadline for manuscript submissions: 20 October 2024 | Viewed by 2173

Special Issue Editors

Dr. Olcay Y. Jones

E-Mail Website
Guest Editor
1. Division of Pediatric Rheumatology, Walter Reed National Military Medical Center, Bethesda, MD, USA
2. Division of Rheumatology, Department of Medicine, George Washington University School of Medicine and Health Sciences, Washington, DC, USA
Interests: autoimmunity and inflammation; immunopathogenesis; stem cells and cell based treatment
Prof. Dr. Deborah K. McCurdy

E-Mail Website
Guest Editor
1. Division of Allergy, Immunology and Rheumatology, David Geffen School of Medicine, 10833 Le Conte Ave, Los Angeles, CA 90095, USA
2. Program Director of Pediatric Rheumatology, Mattel Children's Hospital UCLA, 757 Westwood Plaza, Los Angeles, CA 90095, USA
Interests: juvenile idiopathic arthritis (JIA); systemic lupus erythematosus (SLE); DNA repair in autoimmune disease

Special Issue Information

Dear Colleagues, 

It is a pleasure to invite you to take part in an upcoming Special Issue entitled “Diagnosis, Treatment and Care of Pediatric Rheumatology” in “Children” (ISSN 2227-9067). This is an international, peer-reviewed, open access journal published by MDPI and listed under PubMed as clinical and preclinical research with an impact factor of 2.835.  

This issue offers authors with the opportunity to publish their latest studies on practice-based learning in the care of children with rheumatic diseases for primary care providers and supportive literature advocating for medications that may need authorization from insurance companies.  We welcome original research papers and reviews on autoimmune, autoinflammatory, and immune dysregulatory conditions in children.  

Feel free to contact us directly with any questions. We look forward to receiving your papers.  

Dr. Olcay Y. Jones
Prof. Dr. Deborah K. McCurdy
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Children is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2400 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • pediatric rheumatology
  • autoimmune
  • inflammation
  • referral
  • multispecialty care
  • diagnosis
  • treatment
  • outcomes
  • advocacy
  • access to medicine

Published Papers (3 papers)

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Research

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11 pages, 1551 KiB  
Article
Application of Interferon-γ Release Assay in the Assessment of T-Cell Immunity to SARS-CoV-2 Antigens in the Cohort of Pediatric Patients with Juvenile Idiopathic Arthritis
by Katarzyna Kapten, Krzysztof Orczyk and Elzbieta Smolewska
Children 2024, 11(6), 736; https://doi.org/10.3390/children11060736 - 16 Jun 2024
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Abstract
Background: an accurate assessment of the immunity against SARS-CoV-2 can facilitate a better understanding and management of not only the recent coronavirus but similar pathogens as well. Objective: the aim of this study was to evaluate T-cell immunity with reference to antibody titers [...] Read more.
Background: an accurate assessment of the immunity against SARS-CoV-2 can facilitate a better understanding and management of not only the recent coronavirus but similar pathogens as well. Objective: the aim of this study was to evaluate T-cell immunity with reference to antibody titers in a group of pediatric patients with autoimmune arthritides utilizing the widely known Interferon-γ Release Assay (IGRA). Materials and Methods: This study was conducted in the cohort of 55 children suffering from Juvenile Idiopathic Arthritis (JIA). This research analyzed the SARS-CoV-2 T-cell response measured by a specific quantitative IGRA, followed by a serological ELISA test measuring the presence and quantity of IgG, IgM, and IgA antibodies in serum. Results: The cellular response to SARS-CoV-2 measured by the IGRA test significantly correlated with the antibody titers, IgA (p < 0.00003, R = 0.537), IgG (p < 0.0001, R = 0.668), and IgG nucleocapsid protein (NCP) (p < 0.003, R = 0.0399), with no correlation with IgM levels. The antibody levels in patients receiving biological agents were significantly lower compared to the rest of the cohort (p = 0.0369), while traditional disease-modifying antirheumatic drugs had no such effect. Limitations: the main limitation of the research is the small sample size, mostly due to the specific cohort of patients and the lack of a healthy control. Conclusions: IGRA appears to be a viable tool in the accurate evaluation of T-cell responses to SARS-CoV-2, and serodiagnostics alone is not always sufficient in the assessment of immune responses. Full article
(This article belongs to the Special Issue Diagnosis, Treatment and Care of Pediatric Rheumatology)
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Review

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15 pages, 983 KiB  
Review
Macrophage Activation Syndrome in Children: Update on Diagnosis and Treatment
by Jin Lee, Kil Seong Bae, Jung Woo Rhim, Soo-Young Lee, Dae Chul Jeong and Jin Han Kang
Children 2024, 11(7), 755; https://doi.org/10.3390/children11070755 - 21 Jun 2024
Viewed by 449
Abstract
Macrophage activation syndrome (MAS) is potentially fatal; so, early diagnosis and timely treatment are essential. However, detecting MAS is sometimes challenging because its principal features can be observed in other pediatric diseases that cause severe inflammation. Cytokine storm due to immune dysregulation represents [...] Read more.
Macrophage activation syndrome (MAS) is potentially fatal; so, early diagnosis and timely treatment are essential. However, detecting MAS is sometimes challenging because its principal features can be observed in other pediatric diseases that cause severe inflammation. Cytokine storm due to immune dysregulation represents the clinical and laboratory features of MAS that are included in the diagnostic criteria. Most cases of MAS occur as an underlying condition worsens and progresses. Therefore, a patient with autoimmune or autoinflammatory disease who shows unexplained clinical deterioration despite appropriate management should be considered at high risk for MAS (i.e., occult MAS). The basic principles of treatment are control of triggering factors, supportive care, and relief of hyperinflammation. Systemic steroids and cyclosporine A are frequently used as a first-line treatment. For the treatment of refractory MAS, cytokine-specific biologic agents such as anakinra have recently become preferred over traditional immunosuppressive agents such as etoposide. MAS might be underrecognized in pediatric patients with infectious and inflammatory diseases due to its diverse clinical presentations. Clinical suspicion of MAS is of the utmost importance for early recognition of the disease. Full article
(This article belongs to the Special Issue Diagnosis, Treatment and Care of Pediatric Rheumatology)
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Other

Jump to: Research, Review

9 pages, 747 KiB  
Brief Report
Does the esv3587290 Copy Number Variation in the VANGL1 Gene Differ as a Genetic Factor for Developing Nephritis in Mexican Childhood-Onset Systemic Lupus Erythematosus Patients?
by Miguel Angel Alcántara-Ortigoza, Ana Luisa Rodríguez-Lozano, Bernardette Estandía-Ortega, Ariadna González-del Angel, Luisa Díaz-García, Francisco Eduardo Rivas-Larrauri and Ruth Guadalupe Nájera-Velázquez
Children 2024, 11(6), 712; https://doi.org/10.3390/children11060712 - 10 Jun 2024
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Abstract
A ~3-kb deletion-type DNA copy number variation (CNV, esv3587290) located at intron 7 of the VANGL1 gene (1p13.1, MIM*610132) has been proposed as a genetic factor in lupus nephritis (LN) development in adult systemic lupus erythematosus (SLE) patients across European-descent populations, but its [...] Read more.
A ~3-kb deletion-type DNA copy number variation (CNV, esv3587290) located at intron 7 of the VANGL1 gene (1p13.1, MIM*610132) has been proposed as a genetic factor in lupus nephritis (LN) development in adult systemic lupus erythematosus (SLE) patients across European-descent populations, but its replication in other ethnicities has been inconsistent and its association with LN in childhood-onset SLE (cSLE) remains unknown. Here, we performed an exploratory association study in a sample of 66 unrelated cSLE Mexican patients (11 males, 55 females; ages 7.8 to 18.6 years). Two stratified groups were compared: cSLE patients with (N = 39) or without (N = 27) LN, as diagnosed by renal biopsy (N = 17), proteinuria (N = 33), urinary protein–creatinine ratio > 0.2 (N = 34), and erythrocyturia and/or granular casts in urinary sediment (N = 16). For esv3587290 CNV genotyping, we performed an end-point PCR assay with breakpoint confirmation using Sanger sequencing. We also determined the allelic frequencies of the esv3587290 CNV in 181 deidentified ethnically matched individuals (reference group). The obtained genotypes were tested for Hardy–Weinberg equilibrium using the χ2 test. Associations between LN and esv3587290 CNV were tested by calculating the odds ratio (OR) and using Pearson’s χ2 tests, with a 95% confidence interval and p ≤ 0.05. The esv3587290 CNV allele (OR 0.108, 95% CI 0.034–0.33, p = 0.0003) and the heterozygous genotype (OR 0.04, 95% CI 0.119–0.9811, p = 0.002) showed a significant protective effect against LN development. Finally, we characterized the precise breakpoint of the esv3587290 CNV to be NG_016548.1(NM_138959.3):c.1314+1339_1315-897del in our population. This report supports the notion that a broad genetic heterogeneity underlies the susceptibility for developing LN. Full article
(This article belongs to the Special Issue Diagnosis, Treatment and Care of Pediatric Rheumatology)
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