Evidence map›Paper›PMID 25127106›Full record

ArticlePloS one2014

Polymorphisms in the TNFA and IL6 genes represent risk factors for autoimmune thyroid disease.

Cecília Durães, Carla S Moreira, Inês Alvelos, Adélia Mendes, Liliana R Santos, José Carlos Machado, Miguel Melo, César Esteves, Celestino Neves, Manuel Sobrinho-Simões and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 3 pooled it
2.8field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 3 syntheses or guidelines pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Association ofBioscience reports · 2018
    Pooled it
  3. Promoter Polymorphism (-174, G/C) of Interleukin-6 and Arterial Thromboembolic Events: A Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Pooled it
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Interaction of Genetic Variations inThyroid : official journal of the American Thyroid Association · 2019
    Article
  10. Article
  11. Article
  12. The Association BetweenFrontiers in genetics · 2018
    Article
  13. Article
  14. Article
  15. Article
  16. Observational
  17. Observational
  18. Review
  19. Article
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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

11 authors at 3 institutions in 1 country.

Cecília DurãesInstitute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), Porto, Portugal.
Carla S MoreiraInstitute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), Porto, Portugal; Faculty of Medicine of the University of Porto, Porto, Portugal.
Inês AlvelosInstitute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), Porto, Portugal.
Adélia MendesInstitute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), Porto, Portugal.
Liliana R SantosFaculty of Medicine of the University of Porto, Porto, Portugal; Faculty of Medicine of the University of Coimbra, Coimbra, Portugal.
José Carlos MachadoInstitute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), Porto, Portugal; Faculty of Medicine of the University of Porto, Porto, Portugal.
Miguel MeloInstitute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), Porto, Portugal; Department of Endocrinology, Diabetes and Metabolism, University and Hospital Center of Coimbra, Coimbra, Portugal; Unit of Endocrinology, Faculty of Medicine, University of Coimbra, Coimbra, Portugal.
César EstevesDepartment of Endocrinology, Hospital of S. João, Porto, Portugal.
Celestino NevesFaculty of Medicine of the University of Porto, Porto, Portugal; Department of Endocrinology, Hospital of S. João, Porto, Portugal.
Manuel Sobrinho-SimõesInstitute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), Porto, Portugal; Faculty of Medicine of the University of Porto, Porto, Portugal; Department of Pathology and Oncology, Faculty of Medicine of the University of Porto, Porto, Portugal.
Paula SoaresInstitute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), Porto, Portugal; Faculty of Medicine of the University of Porto, Porto, Portugal; Department of Pathology and Oncology, Faculty of Medicine of the University of Porto, Porto, Portugal.
Universidade do Porto · PTHospital de São João · PTUniversity of Coimbra · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAutoimmune thyroid disease (AITD) comprises diseases including Hashimoto's thyroiditis and Graves' disease, both characterized by reactivity to autoantigens causing, respectively, inflammatory destruction and autoimmune stimulation of the thyroid-stimulating hormone receptor. AITD is the most common thyroid disease and the leading form of autoimmune disease in women. Cytokines are key regulators of the immune and inflammatory responses; therefore, genetic variants at cytokine-encoding genes are potential risk factors for AITD.

methodsPolymorphisms in the IL6-174 G/C (rs1800795), TNFA-308 G/A (rs1800629), IL1B-511 C/T (rs16944), and IFNGR1-56 T/C (rs2234711) genes were assessed in a case-control study comprising 420 Hashimoto's thyroiditis patients, 111 Graves' disease patients and 735 unrelated controls from Portugal. Genetic variants were discriminated by real-time PCR using TaqMan SNP genotyping assays.

resultsA significant association was found between the allele A in TNFA-308 G/A and Hashimoto's thyroiditis, both in the dominant (OR = 1.82, CI = 1.37-2.43, p-value = 4.4×10(-5)) and log-additive (OR = 1.64, CI = 1.28-2.10, p-value = 8.2×10(-5)) models. The allele C in IL6-174 G/C is also associated with Hashimoto's thyroiditis, however, only retained significance after multiple testing correction in the log-additive model (OR = 1.28, CI = 1.06-1.54, p-value = 8.9×10(-3)). The group with Graves' disease also registered a higher frequency of the allele A in TNFA-308 G/A compared with controls both in the dominant (OR = 1.85, CI = 1.19-2.87, p-value = 7.0×10(-3)) and log-additive (OR = 1.69, CI = 1.17-2.44, p-value = 6.6×10(-3)) models. The risk for Hashimoto's thyroiditis and Graves' disease increases with the number of risk alleles (OR for two risk alleles is, respectively, 2.27 and 2.59).

conclusionsThis study reports significant associations of genetic variants in TNFA and IL6 with the risk for AITD, highlighting the relevance of polymorphisms in inflammation-related genes in the etiopathogenesis of AITD.

Indexed as

AdultCase-Control StudiesFemaleGene FrequencyGenetic Association StudiesGenetic Predisposition to DiseaseGraves DiseaseHashimoto DiseaseHumansInterleukin-6MaleMiddle AgedPolymorphism, Single NucleotideRisk FactorsTumor Necrosis Factor-alphaIL6 protein, humanInterleukin-6TNF protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID25127106
PMCPMC4134306
OpenAlexW2017845233

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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.