Evidence map›Paper›PMID 28942732›Full record

ReviewBMC medicine2017

Is Graves' disease a primary immunodeficiency? New immunological perspectives on an endocrine disease.

Tristan Struja, Alexander Kutz, Stefan Fischli, Christian Meier, Beat Mueller, Mike Recher, Philipp Schuetz

Open access · goldAbstract readReview
In one paragraph

Review in BMC medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Regulatory T Cells in the Pathogenesis of Graves' Disease.International journal of molecular sciences · 2023
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Endocrinopathies in Inborn Errors of Immunity.Frontiers in immunology · 2021
    Review
  12. Article
  13. Review
  14. Decreased expression of FcγRII in active Graves' disease patients.Journal of clinical laboratory analysis · 2019
    Article
  15. Article
  16. 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

7 authors at 3 institutions in 1 country.

Tristan StrujaMedical University Department, Clinic for Endocrinology, Diabetes & Metabolism, Kantonsspital Aarau, Aarau, Switzerland. tristan.struja@gmail.com.ORCID 0000-0003-0199-0184
Alexander KutzMedical University Department, Clinic for Endocrinology, Diabetes & Metabolism, Kantonsspital Aarau, Aarau, Switzerland.
Stefan FischliMedical Clinic, Department for Endocrinology, Diabetes & Metabolism, Kantonsspital Luzern, Luzern, Switzerland.
Christian MeierMedical Faculty of the University of Basel, Basel, Switzerland.
Beat MuellerMedical University Department, Clinic for Endocrinology, Diabetes & Metabolism, Kantonsspital Aarau, Aarau, Switzerland.
Mike RecherMedical Faculty of the University of Basel, Basel, Switzerland.
Philipp SchuetzMedical University Department, Clinic for Endocrinology, Diabetes & Metabolism, Kantonsspital Aarau, Aarau, Switzerland.
University of Basel · CHKantonsspital Aarau · CHLuzerner Kantonsspital · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundUncertainty about factors influencing the susceptibility and triggers for Graves' disease persists, along with a wide variation in the response to anti-thyroid drugs, currently at approximately 50% of non-responders. The aim of this narrative review is to summarize immunological concepts, with a combined endocrine and immunological perspective, to highlight potential new areas of research. MAIN TEXT: Relevant studies were identified through a systematic literature search using the PubMed and EMBASE databases in March 2016. No cut-offs regarding dates were imposed. We used the terms "Graves' Disease" or "Basedow" or "thyrotoxicosis" together with the terms "etiology", "pathophysiology", "immunodeficiency", "causality", and "autoimmunity". The terms "orbitopathy", "ophthalmopathy", and "amiodarone" were excluded. Articles in English, French, German, Croatian, Spanish, and Italian were eligible for inclusion.

conclusionsWhile concepts such as the impact of iodine, smoking, human leucocyte antigen, infections, and ethnicity are established, new ideas have emerged. Pertaining evidence suggests the involvement of autoimmunity and immunodeficiency in the pathophysiology of Graves' disease. Recent studies point to specific immunological mechanisms triggering the onset of disease, which may also serve as targets for more specific therapies.

Indexed as

Immunologic Deficiency SyndromesAnimalsAutoimmunityGraves DiseaseHumansEtiologyGraves’ diseasePathophysiologyPrimary immunodeficiencyReview

Identifiers

PMID28942732
PMCPMC5611589
OpenAlexW2757806407

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.