Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Video

Updated: May 16, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Current concepts in graves' disease.

Christian M Girgis1, Bernard L Champion, Jack R Wall

  • 1Department of Medicine, University of Sydney, Sydney, Australia.

Therapeutic Advances in Endocrinology and Metabolism
|November 14, 2012
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence in...
Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...
Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...
Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
Hypothyroidism II: Pathophysiology01:23

Hypothyroidism II: Pathophysiology

Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...
Goiter01:27

Goiter

Goiter refers to an abnormal enlargement of the thyroid gland that may appear as a diffuse goiter (uniform enlargement) or nodular (single or multiple nodules). Functionally, it is classified as nontoxic (normal/low hormone levels) or toxic (excess hormone production).PathophysiologyDiffuse thyroid enlargement typically results from prolonged stimulation by thyroid-stimulating hormone (TSH) or TSH-like agents, commonly seen in hypothyroidism or iodine deficiency. In contrast, in hyperthyroid...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Denosumab discontinuation and fracture risk: getting the balance right.

Internal medicine journal·2026
Same author

Central Giant Cell Granuloma: A Decade of Institutional Experience and Curative Potential of Neoadjuvant Denosumab.

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research·2026
Same author

Risk stratification improves outcomes in an osteoporosis fracture liaison service.

Archives of osteoporosis·2026
Same author

Asian ethnicity is associated with shorter anti-resorptive exposure prior to atypical femur fracture (AFF): a Transcontinental Atypical Femoral Fracture Consortium (TrAFFiC) cohort study.

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research·2026
Same author

A new age of osteoanabolic therapy? A real-world, two-centre study comparing effects of romosozumab, teriparatide, and antiresorptive therapies for osteoporosis.

Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA·2026
Same author

Personalised Pathways (PP) in the Medical Curriculum: How Does It Influence Students?

The clinical teacher·2026
Same journal

Comparative 24-month cardiovascular outcomes and biomarker trajectories with semaglutide, empagliflozin, and sitagliptin in people with obesity and type 2 diabetes: a multicenter real-world study.

Therapeutic advances in endocrinology and metabolism·2026
Same journal

Association between dietary intake of fatty acids, central obesity, and OAB: insights from a prospective cohort for weight management and dietary prevention.

Therapeutic advances in endocrinology and metabolism·2026
Same journal

Diabetes-type-specific thyroid safety of GLP-1 receptor agonists: evidence from a large real-world cohort.

Therapeutic advances in endocrinology and metabolism·2026
Same journal

Response to the Letter by Zhang "The hidden variable in a 'neutral' upgrade: why parameter re-tuning and perceived reliability matter after G6 → G7 in Control-IQ".

Therapeutic advances in endocrinology and metabolism·2026
Same journal

Association of prediabetes phenotypes with metabolic dysfunction-associated fatty liver disease and liver fibrosis: a population-based study.

Therapeutic advances in endocrinology and metabolism·2026
Same journal

Exploring the link between atherosclerosis indicators and QT interval in type 2 diabetes: a retrospective cross-sectional analysis.

Therapeutic advances in endocrinology and metabolism·2026
See all related articles

Graves' disease, an autoimmune disorder causing hyperthyroidism, requires prompt recognition to prevent severe health risks. This review covers its investigation, management, and emerging therapeutic targets for better patient outcomes.

Area of Science:

  • Endocrinology
  • Immunology
  • Autoimmune Diseases

Background:

  • Graves' disease is the leading cause of hyperthyroidism globally.
  • It stems from an immune defect leading to excess thyroid hormone production and thyroid enlargement.
  • Unmanaged Graves' disease can lead to psychosis, heart rhythm disorders, and heart failure.

Purpose of the Study:

  • To review the investigation and management of Graves' disease.
  • To discuss the safety concerns of propylthiouracil, including liver toxicity.
  • To explore novel therapeutic strategies targeting the TSH receptor.

Main Methods:

  • Literature review of Graves' disease.
  • Analysis of recent findings on propylthiouracil hepatotoxicity.
  • Examination of emerging small-molecule TSH receptor ligands.
Keywords:
Graves' diseaseautoimmune thyroid diseasehyperthyroidismneomercazolepropylthiouracilradioactive iodinethionamidesthyroid eye diseasethyroidectomy

More Related Videos

Synchronous Triplanar Reconstruction Integrated with Color Doppler Mapping for Precise and Rapid Localization of Thyroid Lesions
05:41

Synchronous Triplanar Reconstruction Integrated with Color Doppler Mapping for Precise and Rapid Localization of Thyroid Lesions

Published on: February 9, 2024

An In Vitro Model for the Study of Cellular Pathophysiology in Globoid Cell Leukodystrophy
07:45

An In Vitro Model for the Study of Cellular Pathophysiology in Globoid Cell Leukodystrophy

Published on: October 21, 2014

Related Experiment Videos

Last Updated: May 16, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Synchronous Triplanar Reconstruction Integrated with Color Doppler Mapping for Precise and Rapid Localization of Thyroid Lesions
05:41

Synchronous Triplanar Reconstruction Integrated with Color Doppler Mapping for Precise and Rapid Localization of Thyroid Lesions

Published on: February 9, 2024

An In Vitro Model for the Study of Cellular Pathophysiology in Globoid Cell Leukodystrophy
07:45

An In Vitro Model for the Study of Cellular Pathophysiology in Globoid Cell Leukodystrophy

Published on: October 21, 2014

Main Results:

  • Graves' disease presents with thyroid dysfunction and systemic autoimmune effects, notably thyroid eye disease.
  • Propylthiouracil's use is debated due to potential liver toxicity.
  • Novel TSH receptor ligands show promise for targeted treatment.

Conclusions:

  • Early diagnosis and management of Graves' disease are crucial for preventing serious complications.
  • Careful consideration of medication risks, such as propylthiouracil's hepatotoxicity, is necessary.
  • Targeting the TSH receptor offers a potential new avenue for Graves' disease therapy.