Evidence map›Paper›PMID 33193078›Full record

ArticleFrontiers in endocrinology2020

Analysis of Polymorphisms rs7093069-IL-2RA, rs7138803-FAIM2, and rs1748033-PADI4 in the Group of Adolescents With Autoimmune Thyroid Diseases.

Beata Sawicka, Hanna Borysewicz-Sańczyk, Natalia Wawrusiewicz-Kurylonek, Tommaso Aversa, Domenico Corica, Joanna Gościk, Adam Krętowski, Małgorzata Waśniewska, Artur Bossowski

Open access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 2 pooled it
0.9field-weighted citation impact, top 26% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 2 syntheses or guidelines pooled it, 20 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Beata SawickaDepartment of Pediatrics, Endocrinology, Diabetology, with Cardiology Division, Medical University of Bialystok, Białystok, Poland.
Hanna Borysewicz-SańczykDepartment of Pediatrics, Endocrinology, Diabetology, with Cardiology Division, Medical University of Bialystok, Białystok, Poland.
Natalia Wawrusiewicz-KurylonekDepartment of Endocrinology, Diabetes with Internal Medicine, Medical University of Bialystok, Białystok, Poland.
Tommaso AversaDepartment of Human Pathology of Adulthood and Childhood, University of Messina, Messina, Italy.
Domenico CoricaDepartment of Human Pathology of Adulthood and Childhood, University of Messina, Messina, Italy.
Joanna GościkSoftware Department, Faculty of Computer Science, Białystok University of Technology, Bialystok, Poland.
Adam KrętowskiDepartment of Endocrinology, Diabetes with Internal Medicine, Medical University of Bialystok, Białystok, Poland.
Małgorzata WaśniewskaDepartment of Human Pathology of Adulthood and Childhood, University of Messina, Messina, Italy.
Artur BossowskiDepartment of Pediatrics, Endocrinology, Diabetology, with Cardiology Division, Medical University of Bialystok, Białystok, Poland.
Medical University of Białystok · PLUniversity of Messina · ITBialystok University of Technology · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: The pathogenesis of autoimmune thyroid diseases is complicated and not completely known. Among the causes of thyroid autoimmunity, we distinguish genetic predisposition and environmental factors. Graves' disease and Hashimoto's thyroiditis are associated with a disturbance of immune tolerance of thyroid antigen molecules. The IL2RA gene is located on chromosome 10 and encodes the interleukin 2 receptor (IL2RA), which is expressed by the regulatory T-cells (Tregs) responsible for suppression. It has been shown that this gene and its polymorphism occur in people with various autoimmune diseases ( Aim: The aim of the study was to analyze the polymorphisms of the IL-2RA (rs7093069), FAIM2 (rs7138803) and PADI4 (rs1748033) genes and their correlation to thyroid hormones and anti-thyroid antibodies in pediatric patients with Graves' disease and Hashimoto's thyroiditis compared to the control group. Material and Methods: The study was performed in 180 patients with GD (mean age 16.5 ± 2), 80 with HT (mean age, 15.2 ± 2.2), and 114 children without any autoimmune diseases (mean age 16.3 ± 3) recruited from the endocrinology outpatient clinic. Three single nucleotide polymorphisms (SNPs): rs7138803-FAIM2, rs7093069-IL-2RA, and rs1748033 PADI4 were determined by TaqMan SNP QuanStudio 12K Flex-OpenArray genotyping with PCR and correlated to thyroid hormones and anti-thyroid antibodies. Results: Rs7090369-IL-2RA allele T was more frequent in patients with AITDs (33.7% in GD Conclusions: 1). Polymorphisms rs7138803-FAIM2 and rs1748033-PADI4 are more frequent in patients with autoimmune thyroid diseases, more frequent in patients with Hashimoto' thyroiditis, but the occurrence of GG rs7138803-FAIM2 genotype could reduce the risk of thyrocyte apoptosis inhibition. 2). The TT rs7093069-IL2RA genotype may increase the risk of autoimmune thyroid diseases. 3). Analysis of polymorphisms of given genes in clinical practice will allow to determine predisposition to autoimmune thyroid disease development, to find symptoms of thyroid gland dysfunction earlier and to use appropriate treatment.

Indexed as

Polymorphism, Single NucleotideAdolescentApoptosis Regulatory ProteinsAutoimmune DiseasesFemaleGene FrequencyGenetic Predisposition to DiseaseHumansInterleukin-2 Receptor alpha SubunitMaleMembrane ProteinsProtein-Arginine Deiminase Type 4Thyroid DiseasesApoptosis Regulatory ProteinsFAIM2 protein, humanIL2RA protein, humanInterleukin-2 Receptor alpha SubunitMembrane ProteinsPADI4 protein, humanProtein-Arginine Deiminase Type 4FAIM2gene polymorphismGraves’ diseaseHashimoto’s thyroiditisIl-2RAPADI4

Identifiers

PMID33193078
PMCPMC7645032
OpenAlexW3094374514

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Registered trials

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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 OpenQuestion graph.