Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (732 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A common form of hyperthyroidism with a diffuse hyperplastic goiter. It is an autoimmune disorder that produces antibodies against the thyroid stimulating hormone receptor. These autoantibodies activate the TSH receptor, thereby stimulating the thyroid gland and hypersecretion of thyroid hormones. These autoantibodies can also affect the eyes (graves ophthalmopathy) and the skin (Graves dermopathy).
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Disease, Graves; Basedow Disease; Disease, Basedow; Hyperthyroidism, Autoimmune; Exophthalmic Goiter; Exophthalmic Goiters; Goiters, Exophthalmic; Goiter, Exophthalmic.
Where it fits in the MeSH classification
- Broader topics
- Exophthalmos; Goiter; Hyperthyroidism; Autoimmune Diseases
- Narrower topics
- Graves Ophthalmopathy
Related concepts
- Goiter
- Thyroid Stimulating Hormone Receptor
- Thyroid Gland
- Thyroid Hormones
- Graves Ophthalmopathy
Research landscape
PubMed indexes 20,483 records tagged with the MeSH heading “Graves Disease” (counts retrieved 2026-10-29). 3,540 of them (17.3%) were published from 2020 onward, and the busiest period so far is through 1999 with 9,498 records.
Reviews account for 2,539 records (12.4%) and meta-analyses for 184. Randomized controlled trials number 305 (1.5%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 9,498 |
| 2000-2009 | 3,651 |
| 2010-2019 | 3,794 |
| 2020 onward | 3,540 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 2,539 | 12.4% |
| Meta-analyses | 184 | 0.9% |
| Randomized controlled trials | 305 | 1.5% |
Method: PubMed query "Graves Disease"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in immunology
Immune responses are studied in model organisms, in cells from donors and in patients, and the same pathway can behave differently across these settings. Mouse immune systems differ from human ones in important ways, and blood measurements may not reflect what happens in tissues. Clinical conclusions about immune-mediated disease or immunotherapy come mainly from controlled trials and long-term cohorts. Check the species and tissue studied, whether markers were linked to outcomes patients notice, and the follow-up time.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Targeted immunotherapies for Graves' thyroidal & orbital diseases | 2025 | Review article Design not recorded in structured metadata | 15 | cc by PMID 40145088 · DOI · PMC11936961 |
| Graves' Disease: Is It Time for Targeted Therapy? A Narrative Review | 2025 | Review article Design not recorded in structured metadata | 12 | cc by PMID 40142311 · DOI · PMC11943693 |
| Transcriptomic profiling of thyroid eye disease orbital fat demonstrates differences in adipogenicity and IGF-1R pathway | 2024 | Research article Design not recorded in structured metadata | 11 | cc by PMID 39704170 · DOI · PMC11665563 |
| Exploring tear fluid biomarkers and the ocular surface in thyroid eye disease | 2026 | Research article Design not recorded in structured metadata | 5 | cc by PMID 40622704 · DOI · PMC12803598 |
Targeted immunotherapies for Graves' thyroidal & orbital diseases [1]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundGraves' hyperthyroidism and its associated Graves' orbitopathy are common autoimmune disorders associated with significant adverse health impact.
- Closing excerpt
- ConclusionTherapeutic advances will continue to optimize our management of Graves' hyperthyroidism and its associated orbitopathy in an effective and safe manner.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (285 words)
BackgroundGraves' hyperthyroidism and its associated Graves' orbitopathy are common autoimmune disorders associated with significant adverse health impact. Current standard treatments have limitations regarding efficacy and safety, and most do not specifically target the pathogenic mechanisms. We aim to review the latest development of targeted immunotherapies in these two closely related disorders.SummaryTargeted immunotherapies of Graves' hyperthyroidism have recently demonstrated clinical efficacy in early phase clinical studies. They include rituximab, an anti-CD20 monoclonal antibody which causes rapid B cell depletion; ATX-GD-59, an antigen specific immunotherapy which restores immune tolerance to thyrotropin receptor; iscalimab, an anti-CD40 monoclonal antibody which blocks the CD40-CD154 co-stimulatory pathway in B-T cell interaction; and K1-70, a thyrotropin receptor blocking monoclonal antibody. Furthermore, there have been major therapeutic advances in the management of Graves' orbitopathy. Mycophenolate has a dual mechanism of action both inhibiting the proliferation of activated B & T cells as well as the mammalian target of rapamycin growth intracellular pathway. Rituximab appears to be effective in active disease of recent onset without impending dysthyroid optic neuropathy. Both tocilizumab (anti-interleukin 6 receptor monoclonal antibody) and sirolimus (mammalian target of rapamycin inhibitor) showed promise in glucocorticoid resistant active disease. Teprotumumab, an anti-insulin-like growth factor-1 receptor monoclonal antibody, demonstrated remarkable all-round efficacy across a wide disease spectrum. Linsitinib, a dual small molecule inhibitor of insulin-like growth factor-1 receptor and insulin receptor, displayed significant proptosis reduction in its phase 2b/3 study. Finally, Batoclimab, an anti-neonatal fragment crystallizable receptor monoclonal antibody, which blocks recycling of pathogenic thyrotropin receptor antibody, showed promising signals for significant proptosis reduction, disease inactivation, overall response, and improvement of quality of life.ConclusionTherapeutic advances will continue to optimize our management of Graves' hyperthyroidism and its associated orbitopathy in an effective and safe manner.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40145088 · DOI · PMC11936961
Graves' Disease: Is It Time for Targeted Therapy? A Narrative Review [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Current therapies for Graves' disease (GD) primarily aim to manage hyperthyroidism through synthetic antithyroid drugs, radioiodine, or surgery.
- Closing excerpt
- Here, we present a narrative review of the literature on emerging therapeutic approaches for GD that are currently under investigation.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (135 words)
Current therapies for Graves' disease (GD) primarily aim to manage hyperthyroidism through synthetic antithyroid drugs, radioiodine, or surgery. However, these approaches are often limited by their incomplete efficacy and the risk of inducing hypothyroidism. The latest advances in understanding the autoimmune mechanisms driving GD have paved the way for novel therapies targeting the thyrotropin receptor (TSH-R) or immune pathways. Overall, key targets include cluster of differentiation 20 (CD20), cluster of differentiation 40 (CD40), protein tyrosine phosphatase non-receptor type 22 (PTPN22), cytotoxic T lymphocyte antigen-4 (CTLA-4), B cell-activating factor (BAFF), and the Fc receptor-like protein 3 (FcRL3). Recent preclinical studies and clinical trials testing targeted therapies have shown promising results in terms of efficacy and safety. Here, we present a narrative review of the literature on emerging therapeutic approaches for GD that are currently under investigation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40142311 · DOI · PMC11943693
Transcriptomic profiling of thyroid eye disease orbital fat demonstrates differences in adipogenicity and IGF-1R pathway [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Despite recent advances in the treatment of thyroid eye disease thyroid-related eye disease (TED), marked gaps remain in our understanding of the underlying molecular mechanisms, particularly concerning the insulin-like growth factor-1 receptor (IGF-1R) pathway.
- Closing excerpt
- Our findings reveal that, beyond immune dysfunction, abnormal IGF-1R signaling leading to enhanced adipogenesis is a crucial pathogenic mechanism in TED.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (174 words)
Despite recent advances in the treatment of thyroid eye disease thyroid-related eye disease (TED), marked gaps remain in our understanding of the underlying molecular mechanisms, particularly concerning the insulin-like growth factor-1 receptor (IGF-1R) pathway. To dissect the pathophysiology of TED, we used single-nucleus RNA-Seq to analyze orbital fat specimens from both patients with TED and matched individuals acting as controls. The analysis demonstrated a marked increase in the proportion of fibroblasts transitioning to adipogenesis in the orbital fat of patients with TED compared with that in control patients. This was associated with diverse alterations in immune cell composition. Significant alterations in the IGF-1R signaling pathway were noted between TED specimens and those from control patients, indicating a potential pathological mechanism driven by IGF-1R signaling abnormalities. Additionally, our data showed that linsitinib, a small-molecule inhibitor of IGF-1R, effectively reduced adipogenesis in TED orbital fibroblasts in vitro, suggesting its potential utility as a therapeutic agent. Our findings reveal that, beyond immune dysfunction, abnormal IGF-1R signaling leading to enhanced adipogenesis is a crucial pathogenic mechanism in TED.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39704170 · DOI · PMC11665563
Exploring tear fluid biomarkers and the ocular surface in thyroid eye disease [4]
Abstract reading summary — source excerpts
- Opening excerpt
- PurposeTo examine ocular surface changes and inflammatory tear fluid biomarkers in patients with thyroid eye disease (TED).
- Closing excerpt
- Increased ocular discomfort in patients with TED could be related to impaired meibum quality.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (138 words)
PurposeTo examine ocular surface changes and inflammatory tear fluid biomarkers in patients with thyroid eye disease (TED).MethodsWe included 106 Graves' disease (GD) patients (36 without TED, 32 with active and 38 with inactive TED) and 106 age- and sex-matched healthy subjects for ophthalmological evaluation, including ocular surface status and Meibomian gland function. Tear fluid was analysed for 40 inflammatory biomarkers by a Luminex multiplex bead assay. The parameters were compared across subgroups.ResultsGD patients with TED had significantly higher median (min-max) Ocular Surface Disease Index (OSDI) score than GD patients without TED, with a median score of 31.4 (0-86.4) compared to 7.3 (0-45.8) (p ConclusionsOur findings demonstrate increased tear fluid levels of CD40L and CCL2 in patients with TED, indicating their potential as diagnostic biomarkers. Increased ocular discomfort in patients with TED could be related to impaired meibum quality.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40622704 · DOI · PMC12803598
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Management of Thyroid Eye Disease: A Consensus Statement by the American Thyroid Association and the European Thyroid Association [5]
- Research article Hyperthyroidism: aetiology, pathogenesis, diagnosis, management, complications, and prognosis [6]
- Research article Molecular Mechanisms in Autoimmune Thyroid Disease [7]
- Research article Prevalence of thyroid eye disease in Graves' disease: A meta-analysis and systematic review [8]
- Research article Current concepts regarding Graves' orbitopathy [9]
- Research article Meta-analysis of the association between vitamin D and autoimmune thyroid disease [10]
References
- Lee ACH, Kahaly GJ. Targeted immunotherapies for Graves' thyroidal & orbital diseases. . 2025. PMID 40145088 · DOI · PMC11936961
- Viola N, Colleo A, Casula M, Mura C, Boi F, Lanzolla G. Graves' Disease: Is It Time for Targeted Therapy? A Narrative Review. . 2025. PMID 40142311 · DOI · PMC11943693
- Kim DW, Kim S, Han J, Belday K, Li E, Mahoney N, et al.. Transcriptomic profiling of thyroid eye disease orbital fat demonstrates differences in adipogenicity and IGF-1R pathway. . 2024. PMID 39704170 · DOI · PMC11665563
- Neset MT, Nilsen RM, Løvås K, Halsøy K, Reikvam H, Stokland AM, et al.. Exploring tear fluid biomarkers and the ocular surface in thyroid eye disease. . 2026. PMID 40622704 · DOI · PMC12803598
- Burch HB, Perros P, Bednarczuk T, Cooper DS, Dolman PJ, Leung AM, et al.. Management of Thyroid Eye Disease: A Consensus Statement by the American Thyroid Association and the European Thyroid Association. Thyroid. 2022. PMID 36480280 · DOI · PMC9807259
- Wiersinga WM, Poppe KG, Effraimidis G. Hyperthyroidism: aetiology, pathogenesis, diagnosis, management, complications, and prognosis. Lancet Diabetes Endocrinol. 2023. PMID 36848916 · DOI
- Vargas-Uricoechea H. Molecular Mechanisms in Autoimmune Thyroid Disease. Cells. 2023. PMID 36980259 · DOI · PMC10047067
- Chin YH, Ng CH, Lee MH, Koh JWH, Kiew J, Yang SP, et al.. Prevalence of thyroid eye disease in Graves' disease: A meta-analysis and systematic review. Clin Endocrinol (Oxf). 2020. PMID 32691849 · DOI
- Bartalena L, Tanda ML. Current concepts regarding Graves' orbitopathy. J Intern Med. 2022. PMID 35604323 · DOI · PMC9796560
- Wang J, Lv S, Chen G, Gao C, He J, Zhong H, et al.. Meta-analysis of the association between vitamin D and autoimmune thyroid disease. Nutrients. 2015. PMID 25854833 · DOI · PMC4425156
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.