ArticleClinical and experimental pediatrics2026
Thyroid peroxidase gene variants and susceptibility to congenital hypothyroidism and autoimmune thyroid disease among Egyptian pediatric cohort.
Article in Clinical and experimental pediatrics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Pediatric thyroid disorders arise from complex interactions among genetic susceptibility, immune dysregulation, and metabolic factors that influence their onset and severity. Purpose: This study aimed to evaluate the clinical, biochemical, micronutrient, and genetic determinants of thyroid dysfunction in children with particular emphasis on the thyroid peroxidase (TPO) Arg386His and Thr725Pro polymorphisms. Methods: This case-control study enrolled 150 Egyptian children aged 2-15 years, including 50 with congenital hypothyroidism (CH), 50 with autoimmune thyroiditis (AIT), and 50 controls. The participants underwent clinical assessments, routine laboratory investigations, thyroid function tests, and tests for selenium, copper, and thyroid autoantibodies (Tg Abs and TPO Abs). Following genomic DNA extraction from peripheral blood, the TPO gene polymorphisms (Arg386His and Thr725Pro) were analyzed using polymerase chain reaction-restriction fragment length polymorphism. Results: Children with thyroid disorders exhibit a higher prevalence of anemia and significantly lower ferritin levels. Profound micronutrient disturbances were evident and characterized by severe selenium deficiency and elevated copper concentrations. The genetic analysis demonstrated a strong association between the TPO exon-8 Arg386His polymorphism and pediatric thyroid disorders. The His allele and His-containing genotypes were significantly more frequent among cases, particularly in children with CH. A genotype-phenotype correlation revealed that the histidine/histidine (His/His) genotype was consistently associated with the highest serumthyroid-stimulating hormone levels in both CH and AIT, suggesting greater functional impairment of thyroid hormone synthesis. Distinct genetic patterns were observed between disease subtypes, with a predominance of the His allele in CH and the Arg allele in AIT. No variation was detected in the Thr725Pro polymorphism, and all participants exhibited the Thr/Thr genotype. Conclusion: These findings support a multifactorial model of pediatric thyroid disease, with the TPO Arg386His variant, particularly the His/His genotype, emerging as a key genetic contributor to disease susceptibility and severity.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.