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Related Concept Videos

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...
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...
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...
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...

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Related Experiment Video

Updated: Jun 7, 2026

An Ex vivo Culture System to Study Thyroid Development
08:33

An Ex vivo Culture System to Study Thyroid Development

Published on: June 6, 2014

SLC26A4 variations among Graves' hyper-functioning thyroid gland.

Hassen Hadj-Kacem1, Rihab Kallel, Salima Belguith-Maalej

  • 1Unité Cibles pour le Diagnostic et la Thérapie, Centre de Biotechnologie de Sfax, Tunisie. hassen.hadjkacem@cbs.rnrt.tn

Disease Markers
|November 4, 2010
PubMed
Summary

Mutations in the SLC26A4 gene are linked to hearing loss and thyroid disorders. This study identified new SLC26A4 variants in Graves' disease patients, suggesting a broader role for this gene beyond deafness.

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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
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Last Updated: Jun 7, 2026

An Ex vivo Culture System to Study Thyroid Development
08:33

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Published on: June 6, 2014

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:

  • Genetics
  • Endocrinology
  • Otolaryngology

Background:

  • Deleterious SLC26A4 mutations cause Pendred syndrome (PS) and nonsyndromic hearing loss (NSHL).
  • SLC26A4 hyperactivity has been linked to autoimmune thyroid diseases (AITD) and asthma.
  • The role of SLC26A4 in thyroid disorders beyond PS requires further investigation.

Purpose of the Study:

  • To investigate SLC26A4 gene sequences in patients with Graves' disease (GD) hyperthyroidism.
  • To identify novel variants and assess the presence of known variants in a GD cohort.
  • To explore the potential association of SLC26A4 variants with thyroid diseases.

Main Methods:

  • Direct sequencing of SLC26A4 coding exons (2-21) and intron-exon junctions.
  • Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) for variant detection.
  • Analysis of variants in GD patients, Hashimoto thyroiditis (HT) patients, healthy subjects, and families with NSHL.

Main Results:

  • Ten mono-allelic SLC26A4 variants were identified in GD patients, including seven novel intronic variants.
  • Two non-synonymous exonic variants, p.I300L and p.F354S, were found.
  • The p.F354S variant was present in GD, HT, and healthy subjects, while p.I300L was exclusively found in GD patients.

Conclusions:

  • Systematic analysis of SLC26A4 is crucial for understanding its role beyond deafness.
  • The study identified new SLC26A4 variants and suggests a potential link between mono-allelic variants and Graves' disease.
  • Further research is warranted to elucidate the pathogenic effects of SLC26A4 variants in thyroid disorders.