ArticleInternal medicine (Tokyo, Japan)2017
Graves' Disease in Pediatric and Elderly Patients with 22q11.2 Deletion Syndrome.
Article in Internal medicine (Tokyo, Japan), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- A Systematic Review of Autoimmunity in 22q11.2 Deletion Syndrome.Expert reviews in molecular medicine · 2026Pooled it
- [Van Wyk-Grombach syndrome as a result of late diagnosis of autoimmune thyroiditis (ait) in a patient with chromosome 22 deletion syndrome. Description of the clinical case and a brief review of the literature].Problemy endokrinologii · 2025Review
- Chronic inflammatory arthritis in 22q11.2 deletion (DiGeorge) syndrome: a multicentric study.Orphanet journal of rare diseases · 2025Article
- Chromosome 22q11.2 Deletion Syndrome: A Comprehensive Review of Molecular Genetics in the Context of Multidisciplinary Clinical Approach.International journal of molecular sciences · 2023Review
- Endocrine and Growth Disorders in Taiwanese Children With 22q11.2 Deletion Syndrome.Frontiers in endocrinology · 2022Article
- Review
- Autoimmune Thyroid Disease in Specific Genetic Syndromes in Childhood and Adolescence.Frontiers in endocrinology · 2020Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
22q11.2 Deletion Syndrome (22qDS) is often complicated by autoimmune diseases. To clarify the causal relationship, we examined the lymphocyte subset distribution and the human leucocyte antigen (HLA) in two female patients (one child and an elderly) with Graves' disease (GD) and 22qDS. Thymus dysgenesis might have contributed to the T-cell imbalance and the lack of negative selection in both cases. Notably, HLA-DR14, a known risk factor for GD in Japanese individuals and the decreased regulatory T-cell numbers that were seen in the pediatric case, may affect the early onset of GD. Central and peripheral tolerance and Th1 cells appeared to be associated with the pathogenesis of GD in 22qDS.
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Registered trials
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