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 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...
Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The iodine is then...
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...
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

Levothyroxine therapy and serum free thyroxine and free triiodothyronine concentrations.

Journal of endocrinological investigation·2002
Same author

Update on the management of hyperthyroidism and hypothyroidism.

Archives of family medicine·2000
Same author

Update on the management of hyperthyroidism and hypothyroidism.

Archives of internal medicine·2000
Same author

The year in review: the thyroid.

Annals of internal medicine·1999
Same author

Potentiation of warfarin sodium by amiodarone-induced thyrotoxicosis.

The Western journal of medicine·1999
Same author

Subclinical thyroid dysfunction.

Archives of internal medicine·1997

Related Experiment Video

Updated: Jun 8, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Relationship between thyroid stimulating hormone and thyroid stimulating immunoglobulin in Graves' hyperthyroidism.

K A Woeber1

  • 1University of California San Francisco, Campus Box 1640, San Francisco, CA 94143-1640, USA. ken.woeber@ucsf.edu

Journal of Endocrinological Investigation
|September 22, 2010
PubMed
Summary

Thyroid stimulating immunoglobulin (TSI) does not directly suppress TSH in Graves' hyperthyroidism. While TSI levels were lower in patients whose TSI disappeared, no correlation was found between TSH and TSI levels.

Related Experiment Videos

Last Updated: Jun 8, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Area of Science:

  • Endocrinology
  • Immunology

Background:

  • Graves' hyperthyroidism involves TSH-receptor antibodies impacting TSH suppression.
  • The role of thyroid stimulating immunoglobulin (TSI) in pituitary TSH suppression is debated.

Purpose of the Study:

  • To investigate the relationship between TSH and TSI during the follow-up of Graves' hyperthyroidism patients.

Main Methods:

  • 23 Graves' hyperthyroidism patients with over 24 months of follow-up on methimazole were studied.
  • Concurrent serum TSH and TSI levels were measured throughout the study period.

Main Results:

  • TSI disappeared in 12 patients and persisted in 11.
  • Patients with disappearing TSI had significantly lower initial TSI levels.
  • No correlation was observed between serum TSH and TSI levels in either group.

Conclusions:

  • The study findings do not support the hypothesis that TSI directly suppresses TSH secretion.
  • Further research may be needed to fully elucidate the mechanisms of TSH suppression in Graves' disease.