Evidence map›Paper›PMID 38108994›Full record

ReviewReviews in endocrine & metabolic disorders2024

The genetics of Graves' disease.

Lydia Grixti, Laura C Lane, Simon H Pearce

Open access · hybridAbstract readReview
In one paragraph

Review in Reviews in endocrine & metabolic disorders, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 2 pooled it
15.3field-weighted citation impact, top 1% 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

30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 50 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Article
  7. Abnormal Elevation of the Expression of Costimulatory Molecule CD226 in Graves' DiseaseEndocrine, metabolic & immune disorders drug targets · 2026
    Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Thyroid-Targeted Nano-Bombs Empower HIFU for Graves' Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review
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

3 authors at 2 institutions in 1 country.

Lydia GrixtiTranslational and Clinical Research Institute, Newcastle University, BioMedicine West, Central Parkway, Newcastle-upon-Tyne, NE1 3BZ, UK.ORCID 0009-0001-6250-4808
Laura C LaneTranslational and Clinical Research Institute, Newcastle University, BioMedicine West, Central Parkway, Newcastle-upon-Tyne, NE1 3BZ, UK.ORCID 0000-0002-6630-2701
Simon H PearceTranslational and Clinical Research Institute, Newcastle University, BioMedicine West, Central Parkway, Newcastle-upon-Tyne, NE1 3BZ, UK. simon.pearce@ncl.ac.uk.ORCID 0000-0001-8384-8063
Royal Victoria Infirmary · GBGreat North Children's Hospital · GB

Funding

Medical Research Council MR/S001611/1Medical Research Council MR/V005898/1
6 · The paper itself

Abstract

Graves' disease (GD) is the commonest cause of hyperthyroidism and has a strong female preponderance. Everyday clinical practice suggests strong aggregation within families and twin studies demonstrate that genetic factors account for 60-80% of risk of developing GD. In this review, we collate numerous genetic studies and outline the discoveries over the years, starting with historic candidate gene studies and then exploring more recent genome-wide linkage and association studies, which have involved substantial cohorts of East Asian patients as well as those of European descent. Variants in genes including HLA, CTLA4, and PTPN22 have been shown to have substantial individual effects on disease susceptibility. In addition, we examine emerging evidence concerning the possibility that genetic variants may correlate with relevant clinical phenotypes including age of onset of GD, severity of thyrotoxicosis, goitre size and relapse of hyperthyroidism following antithyroid drug therapy, as well as thyroid eye disease. This review supports the inheritance of GD as a complex genetic trait, with a growing number of more than 80 susceptibility loci identified so far. Future implementation of more targeted clinical therapies requires larger studies investigating the influence of these genetic variants on the various phenotypes and different outcomes of conventional treatments.

Indexed as

Graves DiseaseGraves OphthalmopathyFemaleGenetic Predisposition to DiseaseGenotypeHumansPolymorphism, Single NucleotideProtein Tyrosine Phosphatase, Non-Receptor Type 22Protein Tyrosine Phosphatase, Non-Receptor Type 22PTPN22 protein, humanAutoimmune thyroid diseaseGenome-wide associationGenotype-phenotype correlationGraves’ diseaseImmunogeneticsThyroid eye disease

Identifiers

PMID38108994
PMCPMC10808215
OpenAlexW4389868417

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.