Evidence map›Paper›PMID 28382505›Full record

ArticleJournal of endocrinological investigation2017

Association of established hypothyroidism-associated genetic variants with Hashimoto's thyroiditis.

A Barić, L Brčić, S Gračan, V Torlak Lovrić, I Gunjača, M Šimunac, M Brekalo, M Boban, O Polašek, M Barbalić and 3 more

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Article in Journal of endocrinological investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.1field-weighted citation impact, top 22% 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, 18 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

13 authors at 1 institution in 1 country.

A BarićDepartment of Nuclear Medicine, University Hospital Split, Split, Croatia.
L BrčićDepartment of Medical Biology, School of Medicine, University of Split, Split, Croatia.
S GračanDepartment of Nuclear Medicine, University Hospital Split, Split, Croatia.
V Torlak LovrićDepartment of Nuclear Medicine, University Hospital Split, Split, Croatia.
I GunjačaDepartment of Medical Biology, School of Medicine, University of Split, Split, Croatia.
M ŠimunacDepartment of Nuclear Medicine, University Hospital Split, Split, Croatia.
M BrekaloDepartment of Nuclear Medicine, University Hospital Split, Split, Croatia.
M BobanDepartment of Pharmacology, School of Medicine, University of Split, Split, Croatia.
O PolašekDepartment of Public Health, School of Medicine, University of Split, Split, Croatia.
M BarbalićDepartment of Medical Biology, School of Medicine, University of Split, Split, Croatia.
T ZemunikDepartment of Medical Biology, School of Medicine, University of Split, Split, Croatia.
A PundaDepartment of Nuclear Medicine, University Hospital Split, Split, Croatia.
V Boraska PericaDepartment of Medical Biology, School of Medicine, University of Split, Split, Croatia. vboraska@mefst.hr.
University of Split · HR

Funding

Hrvatska Zaklada za Znanost 4950
6 · The paper itself

Abstract

purposeHashimoto's thyroiditis (HT) as a chronic autoimmune disease of the thyroid gland is the most common cause of hypothyroidism. Since HT and hypothyroidism are closely related, the main aim of this study was to explore the association of established hypothyroidism single-nucleotide polymorphisms (SNPs) with HT.

methodsThe case-control dataset included 200 HT cases and 304 controls. Diagnosis of HT cases was based on clinical examination, measurement of thyroid antibodies (TgAb, TPOAb), hormones (TSH and FT4) and ultrasound examination. We genotyped and analysed 11 known hypothyroidism-associated genetic variants. Case-control association analysis was performed in order to test each SNP for the association with HT using logistic regression model. Additionally, each SNP was tested for the association with thyroid-related quantitative traits (TPOAb levels, TgAb levels and thyroid volume) in HT cases only using linear regression.

resultsWe identified two genetic variants nominally associated with HT rs3184504 in SH2B3 gene (P = 0.0135, OR = 0.74, 95% CI = 0.57-0.95) and rs4704397 in PDE8B gene (P = 0.0383, OR = 1.32, 95% CI = 1.01-1.74). The SH2B3 genetic variant also showed nominal association with TPOAb levels (P = 0.0163, β = -0.46) and rs4979402 inside DFNB31 gene was nominally associated with TgAb levels (P = 0.0443, β = 0.41).

conclusionsSH2B3 gene has previously been associated with susceptibility to several autoimmune diseases, whereas PDE8B has been associated with TSH levels and suggested to modulate thyroid physiology that may influence the manifestation of thyroid disease. Identified loci are novel and biologically plausible candidates for HT development and represent good basis for further exploration of HT susceptibility.

Indexed as

Polymorphism, Single Nucleotide3',5'-Cyclic-AMP PhosphodiesterasesAdaptor Proteins, Signal TransducingAutoantibodiesBiomarkersCase-Control StudiesFollow-Up StudiesHashimoto DiseaseHumansHypothyroidismIntracellular Signaling Peptides and ProteinsPhenotypePrognosisProteins3',5'-Cyclic-AMP PhosphodiesterasesAdaptor Proteins, Signal TransducingAutoantibodiesBiomarkersIntracellular Signaling Peptides and ProteinsPDE8B protein, humanProteinsSH2B3 protein, humanCandidate gene studyGenetic epidemiologyHashimoto’s thyroiditisHypothyroidismSingle-nucleotide polymorphism

Identifiers

PMID28382505
OpenAlexW2604544233

What OpenQuestion holds

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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.