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Related Concept Videos

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 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...
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...
Functions of Thyroid Hormones01:18

Functions of Thyroid Hormones

The thyroid hormone (TH) plays a pivotal role in the intricate orchestration of physiological processes, exerting profound effects on development, metabolism, and homeostasis throughout different life stages.
TH is indispensable for the normal development and maturation of the skeletal, muscular, and nervous systems during fetal and childhood growth. It facilitates bone mineral turnover and regulates protein synthesis in developing tissues, contributing significantly to overall growth and...
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...

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Related Experiment Video

Updated: Jun 12, 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 does not decrease thyroid peroxidase antibody concentration in children and adolescents with

W Bonfig1, R Gärtner, H Schmidt

  • 11Pediatric Endocrinology, Dr. von Haunersches Children's Hospital and 2Endocrinology, Internal Medicine, Medical Department-Innenstadt, Ludwig Maximilians University, Munich. Walter.Bonfig@med.uni-muenchen.de

Thescientificworldjournal
|June 8, 2010
PubMed
Summary

Selenium supplementation did not reduce thyroid peroxidase antibody (TPO Ab) levels in children with autoimmune thyroiditis (AIT). This study found no significant decrease in TPO Ab in pediatric patients receiving selenium with levothyroxine.

Related Experiment Videos

Last Updated: Jun 12, 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:

  • Pediatric Endocrinology
  • Immunology
  • Nutritional Science

Background:

  • Autoimmune thyroiditis (AIT) is common in children.
  • Selenium supplementation has shown promise in reducing thyroid peroxidase antibody (TPO Ab) concentrations in adults with AIT.
  • The efficacy of selenium in pediatric AIT requires further investigation.

Purpose of the Study:

  • To evaluate the effect of oral sodium selenite supplementation on TPO Ab and thyroglobulin antibody (Tg Ab) concentrations in children and adolescents with newly diagnosed autoimmune thyroiditis (AIT).
  • To compare the effects of two different doses of sodium selenite (100 µg and 200 µg daily) in conjunction with levothyroxine therapy.

Main Methods:

  • A randomized controlled trial involving 49 children (mean age 12.2 years) diagnosed with AIT and hypothyroidism.
  • Participants were assigned to receive levothyroxine alone, levothyroxine plus 100 µg sodium selenite, or levothyroxine plus 200 µg sodium selenite daily for 12 months.
  • Thyroid peroxidase antibody (TPO Ab) and thyroglobulin antibody (Tg Ab) concentrations were measured at baseline and after 12 months.

Main Results:

  • Selenium supplementation did not significantly decrease TPO Ab concentrations in any of the treatment groups compared to levothyroxine alone.
  • Thyroglobulin antibody (Tg Ab) concentrations decreased significantly in the levothyroxine-only group and the 200 µg selenium group, but not in the 100 µg selenium group.
  • Levothyroxine dosage requirements were similar across all groups to achieve target TSH levels.

Conclusions:

  • Oral selenium supplementation with sodium selenite at daily doses of 100 µg or 200 µg does not reduce TPO Ab concentrations in children and adolescents with autoimmune thyroiditis.
  • Further research may be needed to explore the role of selenium in pediatric AIT, potentially with different formulations or in different patient subgroups.
  • Tg Ab levels showed some reduction, but the lack of TPO Ab reduction suggests selenium's efficacy in this pediatric population is limited.