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 (813 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
Hypersecretion of thyroid hormones from the thyroid gland. Elevated levels of thyroid hormones increase basal metabolic rate.
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: Hyperthyroid; Hyperthyroids; Primary Hyperthyroidism; Hyperthyroidism, Primary.
Where it fits in the MeSH classification
- Broader topics
- Thyroid Diseases
- Narrower topics
- Graves Disease; Thyrotoxicosis
- See also
- Long-Acting Thyroid Stimulator; Antithyroid Agents
Related concepts
- Thyroid Hormones
- Thyroid Gland
- Basal Metabolic Rate
Research landscape
PubMed indexes 48,496 records tagged with the MeSH heading “Hyperthyroidism” (counts retrieved 2026-11-04). 5,232 of them (10.8%) were published from 2020 onward, and the busiest period so far is through 1999 with 29,860 records.
Reviews account for 5,150 records (10.6%) and meta-analyses for 331. Randomized controlled trials number 461 (1.0%) 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 | 29,860 |
| 2000-2009 | 6,840 |
| 2010-2019 | 6,564 |
| 2020 onward | 5,232 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 5,150 | 10.6% |
| Meta-analyses | 331 | 0.7% |
| Randomized controlled trials | 461 | 1.0% |
Method: PubMed query "Hyperthyroidism"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.
Reading the evidence in metabolism and endocrine disease
Studies of diabetes, obesity and hormone disorders often follow blood tests such as glucose, HbA1c or hormone levels, which are stand-ins for outcomes that matter more, such as complications. Lifestyle and diet research is largely observational, and weight and diabetes trials can differ in how long people were followed. Nothing on this page is advice about medicines, insulin or diet; talk to a qualified clinician about your own situation. Check whether the outcome was a lab value or a clinical event, and the type and duration of the condition studied.
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 |
|---|---|---|---|---|
| GPX1-driven selenium nanoplatform reprograms MAMs-mediated organelle crosstalk to reverse inflammatory adipose expansion in thyroid eye disease | 2025 | Research article Design not recorded in structured metadata | 8 | cc by PMID 41041063 · DOI · PMC12486268 |
| The evolving therapeutic landscape of Graves' disease in adults: present and future | 2025 | Review article Design not recorded in structured metadata | 7 | cc by PMID 40622195 · DOI · PMC12284873 |
| PDGFRα+DPP4+ Fibroblasts-Macrophage Crosstalk Induces Orbital Fibrosis in Treatment-Resistant Thyroid Eye Disease via the GAS6-AXL Pathway | 2025 | Research article Design not recorded in structured metadata | 6 | cc by PMID 41017741 · DOI · PMC12677676 |
| Approach to the patient with thyroid storm | 2026 | Review article Design not recorded in structured metadata | 5 | cc by PMID 41655224 · DOI · PMC13099200 |
GPX1-driven selenium nanoplatform reprograms MAMs-mediated organelle crosstalk to reverse inflammatory adipose expansion in thyroid eye disease [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Background: Thyroid eye disease (TED) is a multifactorial autoimmune disorder with limited therapeutic options due to the complexity of its oxidative, metabolic, and inflammatory networks.
- Closing excerpt
- Conclusions: Se@LNT offers the first MAMs-targeted nanotherapy for TED by reprogramming organelle crosstalk, restoring metabolic-immune homeostasis, and modifying disease progression at the subcellular level.
- 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 (175 words)
Background: Thyroid eye disease (TED) is a multifactorial autoimmune disorder with limited therapeutic options due to the complexity of its oxidative, metabolic, and inflammatory networks. This study aims to develop a selenium-based nanoplatform that targets mitochondria-ER interactions to reverse inflammatory adipose expansion in TED. Methods: We designed a dual-responsive selenium nanoparticle (Se@LNT) modified with lentinan, capable of ROS/pH-triggered release. Human primary orbital fibroblasts, bioinformatic analysis of public datasets, and TED mouse models were used to investigate the therapeutic mechanism. Results: Se@LNT undergoes intracellular metabolic conversion into selenocysteine, which enhances GPX1 activity and promotes redox balance. It exerts triple regulatory effects by stabilizing mitochondrial membranes to reduce mtDNA leakage, downregulating GRP75 to normalize MAMs contact and calcium flux, and suppressing PERK-eIF2α-ATF4 signaling to relieve ER stress. Transcriptomic profiling reveals multi-target modulation of immune-stromal interactions. In vivo, Se@LNT achieves orbital targeting, rapid hepatic-renal clearance, and significant reduction of adipose expansion with immune remodeling. Conclusions: Se@LNT offers the first MAMs-targeted nanotherapy for TED by reprogramming organelle crosstalk, restoring metabolic-immune homeostasis, and modifying disease progression at the subcellular level.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41041063 · DOI · PMC12486268
The evolving therapeutic landscape of Graves' disease in adults: present and future [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The therapeutic landscape of Graves' hyperthyroidism has been rapidly evolving in the past few years.
- Closing excerpt
- Finally, new therapies will pose novel challenges in the management of patients that will necessitate adjustments to our clinical practices and development of guidelines suited for these new therapeutic options.
- 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 (193 words)
The therapeutic landscape of Graves' hyperthyroidism has been rapidly evolving in the past few years. There has been a shift worldwide toward antithyroid drugs as the preferred first-line therapy with significant interest in thyroid function preservation, even if it requires more than 2 years of antithyroid drug treatment. This approach, long term antithyroid drug therapy, has gained traction as a therapeutic option after it has been shown to be safe and associated with significantly higher rates of remission than the traditional 18-month course of medical treatment. In parallel, we see, after 80 years of antithyroid drugs as the only medical therapy available for Graves' disease, a strong interest in new drug development that follows more closely the pathophysiology of the disease. These approaches span the spectrum of targeting antigen presentation, B cell activation, TSHR antibody cycle and TSHR signaling. Separately, advances in wearable devices and artificial intelligence models present new opportunities for more timely diagnosis, monitoring, and treatment of patients with Graves' disease. Finally, new therapies will pose novel challenges in the management of patients that will necessitate adjustments to our clinical practices and development of guidelines suited for these new therapeutic options.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40622195 · DOI · PMC12284873
PDGFRα+DPP4+ Fibroblasts-Macrophage Crosstalk Induces Orbital Fibrosis in Treatment-Resistant Thyroid Eye Disease via the GAS6-AXL Pathway [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Thyroid eye disease (TED), the leading adult orbital disease, is an autoimmune disorder characterized by fibrosis.
- Closing excerpt
- By identifying pro-fibrotic intercellular networks in OAT, these findings establish a rapid and repeatable mouse model of TED fibrosis and propose the GAS6-AXL axis as a potential therapeutic target for 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 (211 words)
Thyroid eye disease (TED), the leading adult orbital disease, is an autoimmune disorder characterized by fibrosis. Effective anti-fibrotic treatments are scarce, except for orbital decompression surgery involving orbital adipose tissue (OAT) removal, due to high rates of drug resistance following hyperthyroidism treatment and the lack of suitable mouse models. Understanding the mechanisms behind fibrotic remodeling of OAT could aid mouse model development and identify novel therapies. In the present study, stromal vascular fraction cells of OAT from patients with inactive-stage TED, characterized by pronounced fibrosis, are analyzed at single-cell resolution. platelet-derived growth factor receptor (PDGFR)α+dipeptidyl peptidase (DPP)4+ fibroblasts exhibiting progenitor characteristics and fibrotic potential at the transcriptional level are identified. PDGFRα+DPP4+ fibroblasts showed the strongest interactions with macrophages, particularly M2 macrophages, which are enriched and topographically localized within the fibrotic area. Moreover, M2 macrophages promoted extracellular matrix production in PDGFRα+DPP4+ cells via the Growth arrest specific (GAS)6-AXL Receptor Tyrosine Kinase (AXL) signaling pathway. Using a specific AXL inhibitor or AXL knockdown, fibrosis is substantially reduced in PDGFRα+DPP4+ fibroblasts in vitro, and in patient cell-derived orthotopic xenograft models established via GAS6. By identifying pro-fibrotic intercellular networks in OAT, these findings establish a rapid and repeatable mouse model of TED fibrosis and propose the GAS6-AXL axis as a potential therapeutic target for TED.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41017741 · DOI · PMC12677676
Approach to the patient with thyroid storm [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Thyroid storm, or thyrotoxic crisis, is a rare but life-threatening hypermetabolic state arising from severe thyrotoxicosis with a high risk of multiorgan failure.
- Closing excerpt
- Early recognition and intensive management are crucial to prevent fatal outcomes, highlighting the need for vigilance in patients with severe thyrotoxicosis or decompensated hyperthyroidism.
- 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 (234 words)
Thyroid storm, or thyrotoxic crisis, is a rare but life-threatening hypermetabolic state arising from severe thyrotoxicosis with a high risk of multiorgan failure. It typically occurs in individuals with untreated or poorly controlled hyperthyroidism, most often Graves' disease, though various other disorders may also precipitate it. Common triggers include infection, surgery, trauma, abrupt discontinuation of antithyroid medication, severe emotional or physical stress, and iodine exposure. Clinical manifestations involve hyperthermia, tachyarrhythmia, cardiac and respiratory failure, and hepatic dysfunction. Neurological and gastrointestinal symptoms, such as agitation, confusion, delirium, vomiting, diarrhea, and profuse sweating, are frequent. Diagnosis is clinical rather than biochemical, and scoring systems are used to support the diagnosis. Thyroid storm is more common in females, with an incidence of approximately 0.2 to 1.1 per 100 000 in the general population and 4.8 to 6.3 per 100 000 among hospitalized patients. Without rapid intervention, mortality remains high (5 to 25%), primarily due to cardiovascular collapse or multiorgan dysfunction. Management requires immediate supportive therapy, including cardiovascular stabilization, respiratory support, and temperature control, along with identification and treatment of precipitating factors. Pharmacologic therapy involves antithyroid agents to block thyroid hormone synthesis, beta blockers to counteract adrenergic effects, corticosteroids to reduce peripheral conversion and support adrenal function, and, when appropriate, iodine administration after thionamides. Early recognition and intensive management are crucial to prevent fatal outcomes, highlighting the need for vigilance in patients with severe thyrotoxicosis or decompensated hyperthyroidism.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41655224 · DOI · PMC13099200
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 Hyperthyroidism, bone mineral, and fracture risk--a meta-analysis [5]
- Research article Comparative effectiveness of therapies for Graves' hyperthyroidism: a systematic review and network meta-analysis [6]
- Research article Prevalence of thyroid eye disease in Graves' disease: A meta-analysis and systematic review [7]
- Research article Meta-analysis of the association between vitamin D and autoimmune thyroid disease [8]
- Research article A critical review and meta-analysis of the association between overt hyperthyroidism and mortality [9]
- Research article Association between maternal thyroid function and risk of gestational hypertension and pre-eclampsia: a systematic review and individual-participant data meta-analysis [10]
Full-text reviews on EvidenceLib
Open-access review articles about this topic, reproduced in full with authors, licence and references.
Prevalence of hyperthyroidism, hypothyroidism, and euthyroidism in thyroid eye disease: a systematic review of the literature
Juliana Muñoz-Ortiz, Maria Camila Sierra-Cote, Estefanía Zapata-Bravo et al. · Systematic Reviews 2020 · CC BY 4.0
References
- Tan Y, Zhang F, Cao J, Feng L, Xie B, Gao L, et al.. GPX1-driven selenium nanoplatform reprograms MAMs-mediated organelle crosstalk to reverse inflammatory adipose expansion in thyroid eye disease. . 2025. PMID 41041063 · DOI · PMC12486268
- Stan MN, Dosiou C. The evolving therapeutic landscape of Graves' disease in adults: present and future. . 2025. PMID 40622195 · DOI · PMC12284873
- Cheng L, Cheng J, Liang G, Wang X, Ge Y, Liu J, et al.. PDGFRα+DPP4+ Fibroblasts-Macrophage Crosstalk Induces Orbital Fibrosis in Treatment-Resistant Thyroid Eye Disease via the GAS6-AXL Pathway. . 2025. PMID 41017741 · DOI · PMC12677676
- Kopp PA, Giordani I, Feldt-Rasmussen U, Forget-Renaud A. Approach to the patient with thyroid storm. . 2026. PMID 41655224 · DOI · PMC13099200
- Vestergaard P, Mosekilde L. Hyperthyroidism, bone mineral, and fracture risk--a meta-analysis. Thyroid. 2003. PMID 12930603 · DOI
- Sundaresh V, Brito JP, Wang Z, Prokop LJ, Stan MN, Murad MH, et al.. Comparative effectiveness of therapies for Graves' hyperthyroidism: a systematic review and network meta-analysis. J Clin Endocrinol Metab. 2013. PMID 23824415 · DOI · PMC3763977
- 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
- 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
- Brandt F, Green A, Hegedüs L, Brix TH. A critical review and meta-analysis of the association between overt hyperthyroidism and mortality. Eur J Endocrinol. 2011. PMID 21724839 · DOI
- Toloza FJK, Derakhshan A, Männistö T, Bliddal S, Popova PV, Carty DM, et al.. Association between maternal thyroid function and risk of gestational hypertension and pre-eclampsia: a systematic review and individual-participant data meta-analysis. Lancet Diabetes Endocrinol. 2022. PMID 35255260 · DOI · PMC10314731
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 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
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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.