Evidence map›Paper›PMID 29931474›Full record

ArticleJournal of endocrinological investigation2018

How much of the predisposition to Hashimoto's thyroiditis can be explained based on previously reported associations?

A Jabrocka-Hybel, A Skalniak, J Piątkowski, R Turek-Jabrocka, P Vyhouskaya, A Ludwig-Słomczyńska, J Machlowska, P Kapusta, M Małecki, D Pach and 3 more

Abstract read
In one paragraph

Article in Journal of endocrinological investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Review
  2. Exon 11 Polymorphism (rs1126797) in the Thyroid Peroxidase (International journal of molecular sciences · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. An update on the pathogenesis of Hashimoto's thyroiditis.Journal of endocrinological investigation · 2021
    Review
  9. Review
  10. Review
  11. Observational
  12. Article
  13. Article
  14. Autosomal dominant Hashimoto's thyroiditis with a mutation inClinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology · 2019
    Article
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

13 authors.

A Jabrocka-HybelDepartment of Endocrinology, Medical Faculty, Jagiellonian University Medical College, Krakow, Poland.
A SkalniakDepartment of Endocrinology, University Hospital in Krakow, ul. Kopernika 17, 31-501, Krakow, Poland. anna.skalniak@uj.edu.pl.
J PiątkowskiDepartment of Endocrinology, University Hospital in Krakow, ul. Kopernika 17, 31-501, Krakow, Poland.
R Turek-JabrockaDepartment of Endocrinology, Medical Faculty, Jagiellonian University Medical College, Krakow, Poland.
P VyhouskayaDepartment of Medical Diagnostics, Pharmacy Faculty, Jagiellonian University Medical College, Krakow, Poland.
A Ludwig-SłomczyńskaCenter for Medical Genomics OMICRON, Jagiellonian University Medical College, Krakow, Poland.
J MachlowskaCenter for Medical Genomics OMICRON, Jagiellonian University Medical College, Krakow, Poland.
P KapustaCenter for Medical Genomics OMICRON, Jagiellonian University Medical College, Krakow, Poland.
M MałeckiDepartment of Metabolic Diseases, Medical Faculty, Jagiellonian University Medical College, Krakow, Poland.
D PachDepartment of Endocrinology, Medical Faculty, Jagiellonian University Medical College, Krakow, Poland.
M Trofimiuk-MüldnerDepartment of Endocrinology, Medical Faculty, Jagiellonian University Medical College, Krakow, Poland.
K Lizis-KolusEndocrinology Department-Oncology Center, Kielce, Poland.
A Hubalewska-DydejczykDepartment of Endocrinology, Medical Faculty, Jagiellonian University Medical College, Krakow, Poland.

Funding

Narodowe Centrum Nauki 2011/01/B/NZ5/00337
6 · The paper itself

Abstract

purposeOur insight in the genetics of Hashimoto's thyroiditis (HT) has become clearer through information provided by genome-wide association studies and candidate gene studies, but remains still not fully understood. Our aim was to assess how many different genetic risk variants contribute to the development of HT.

methods147 HT cases (10.2% men) and 147 controls (13.6% men) were qualified for the analysis. Intrinsic and environmental factors were controlled for. Polymorphisms (SNP) were chosen based on the literature and included markers of the genes PTPN22, CTLA4, TG, TPO among others, and of genomic regions pointed by GWAS studies. SNP were typed on a microarray. Variants in the HLA-DRB1 gene were identified by Sanger sequencing.

resultsMultivariate predisposition to HT was modeled. Based on the investigated group, a model of seven variables was obtained. The variability explained by this model was assessed at only 5.4821% (p = 2 × 10

conclusionsWe analyzed genetic regions commonly and most significantly associated with autoimmune thyroid disorders in the literature, on a carefully selected cohort. Our results indicated a lack of possibility to predict the risk of HT development, even with a multivariate model. We therefore conclude that strong associations of single genetic regions with HT should be interpreted with great caution. We believe that a change in the attitude towards genetic association analyses of HT predisposition is necessary. Studies including multiple factors simultaneously are needed to unravel the intricacies of genetic associations with HT.

Indexed as

Case-Control StudiesCohort StudiesFemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyHashimoto DiseaseHLA-DRB1 ChainsHumansHypothyroidismMalePolymorphism, Single NucleotideHLA-DRB1 ChainsAutoimmuneGeneticsHashimoto thyroiditisHLAPolymorphism

Identifiers

PMID29931474
PMCPMC6244553

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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.