Evidence map›Paper›PMID 20385333›Full record

ReviewSurvey of ophthalmology

Immunopathogenesis of thyroid eye disease: emerging paradigms.

Vibhavari M Naik, Milind N Naik, Robert A Goldberg, Terry J Smith, Raymond S Douglas

Open access · greenAbstract readReview
In one paragraph

Review in Survey of ophthalmology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

54 citing papers in PubMed, 120 citations in OpenAlex.

  1. Improvement of asymmetric thyroid eye disease with teprotumumab.The British journal of ophthalmology · 2022
    Trial
  2. Review
  3. Review
  4. Article
  5. Article
  6. Targeting the Aryl Hydrocarbon Receptor to Attenuate IGF1R Signaling in Thyroid Eye Disease.Thyroid : official journal of the American Thyroid Association · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Observational
  14. Teprotumumab and the Evolving Therapeutic Landscape in Thyroid Eye Disease.The Journal of clinical endocrinology and metabolism · 2022
    Review
  15. Article
  16. Review
  17. Observational
  18. Tocilizumab use in pediatric thyroid eye disease: First documented case.American journal of ophthalmology case reports · 2022
    Article
  19. Article
  20. 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

5 authors at 4 institutions in 2 countries.

Vibhavari M NaikJules Stein Eye Institute, Los Angeles, CA, USA.
Milind N Naik
Robert A Goldberg
Terry J Smith
Raymond S Douglas
University of California, Los Angeles · USL V Prasad Eye Institute · INUCLA Medical Center · USWest Los Angeles College · US

Funding

Immunoglobulin Activation of FibroblastsR01DK063121 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SMITH, TERRY J · 2004 to 2012
$3.2M
Immune Activation of FibroblastsK23EY016339 · NEI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DOUGLAS, RAYMOND S · 2004 to 2008
$986k
NEI NIH HHS K23 EY016339NIDDK NIH HHS R01 DK063121
6 · The paper itself

Abstract

Graves disease represents a systemic autoimmune process targeting the thyroid, orbit, and pretibial skin. The thyroid dysfunction is treatable, but no consistently effective medical therapy has yet been described for the orbital manifestations of Graves disease, also known as thyroid-associated ophthalmopathy or thyroid eye disease. Several autoantigens are potentially relevant to the pathogenesis of thyroid eye disease. Activating antibodies generated against the thyrotropin receptor can be detected in a majority of patients, and these drive hyperthyroidism. However, stimulating antibodies against the insulin-like growth factor-1 receptor (IGF-1R) may also play a role in the extra-thyroid manifestations of Graves disease. IGF-1R is overexpressed by orbital fibroblasts derived from patients with thyroid eye disease, whereas IGF-1R(+) T and IGF-1R(+) B cells are considerably more frequent in Graves disease. Actions of several cytokines and the molecular interplay peculiar to the orbit appear to provoke the inflammation, fat expansion, and deposition of excessive extracellular matrix molecules in thyroid eye disease. Based upon these new insights, several therapeutic strategies can now be proposed that, for the first time, might specifically interrupt its pathogenesis.

Indexed as

AutoantigensAutoimmune DiseasesB-LymphocytesFibroblastsGraves OphthalmopathyHumansOrbitReceptor, IGF Type 1T-LymphocytesAutoantigensReceptor, IGF Type 1

Identifiers

PMID20385333
PMCPMC2854657
OpenAlexW2000026315

What OpenQuestion holds

Textmetadata
LicenceTDM
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.