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Related Concept Videos

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

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Related Experiment Video

Updated: May 10, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Selenium supplementation for Hashimoto's thyroiditis.

Esther J van Zuuren1, Amira Y Albusta, Zbys Fedorowicz

  • 1Department of Dermatology, Leiden University Medical Center, Leiden, Netherlands. E.J.van_Zuuren@lumc.nl.

The Cochrane Database of Systematic Reviews
|June 8, 2013
PubMed
Summary
This summary is machine-generated.

Selenium supplementation may reduce thyroid antibodies in Hashimoto's thyroiditis but evidence is limited. More high-quality trials are needed to confirm benefits and guide clinical decisions for this common autoimmune disorder.

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Preparation of Mouse Pituitary Immunogen for the Induction of Experimental Autoimmune Hypophysitis
10:52

Preparation of Mouse Pituitary Immunogen for the Induction of Experimental Autoimmune Hypophysitis

Published on: December 17, 2010

Related Experiment Videos

Last Updated: May 10, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Preparation of Mouse Pituitary Immunogen for the Induction of Experimental Autoimmune Hypophysitis
10:52

Preparation of Mouse Pituitary Immunogen for the Induction of Experimental Autoimmune Hypophysitis

Published on: December 17, 2010

Area of Science:

  • Endocrinology and Autoimmune Diseases
  • Nutritional Biochemistry and Supplementation

Background:

  • Hashimoto's thyroiditis is a prevalent autoimmune condition characterized by thyroid hormone deficiency.
  • Current treatment involves levothyroxine (LT4) hormone replacement therapy.
  • Selenium supplementation is explored for its potential to reduce antibody levels and improve quality of life.

Purpose of the Study:

  • To systematically assess the effects of selenium supplementation in individuals diagnosed with Hashimoto's thyroiditis.

Main Methods:

  • Searched multiple databases (CENTRAL, MEDLINE, EMBASE, Web of Science) and trial registries up to October/November 2012.
  • Included randomized controlled trials evaluating selenium supplementation in adults with Hashimoto's thyroiditis.
  • Data extraction, risk of bias assessment (GRADE), and analysis were performed by two independent reviewers; meta-analysis was not feasible due to heterogeneity.

Main Results:

  • Four studies (463 participants) with unclear to high risk of bias were included; mean study duration was 7.5 months.
  • Selenomethionine supplementation significantly reduced anti-thyroid peroxidase (TPO) antibodies in three studies, though clinical relevance is unclear.
  • Sodium selenite did not significantly affect antibody levels in one study; selenium did not appear to increase adverse events.

Conclusions:

  • Current evidence on selenium supplementation efficacy for Hashimoto's thyroiditis is insufficient due to study limitations and heterogeneity.
  • The existing randomized controlled trials are of insufficient quality for confident clinical decision-making.
  • There is a clear need for well-designed, placebo-controlled trials to establish reliable evidence on selenium's role in managing Hashimoto's thyroiditis.