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

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Related Experiment Video

Updated: Jun 5, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Hypothyroxinemia and pregnancy.

Roberto Negro1, Offie P Soldin, Maria-Jesus Obregon

  • 1Division of Endocrinology, V. Fazzi Hospital, 73100, Lecce, Italy. dr.negro@libero.it

Endocrine Practice : Official Journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
|January 21, 2011
PubMed
Summary
This summary is machine-generated.

Adequate iodine intake before and during pregnancy is crucial for fetal brain development. Current data do not support levothyroxine therapy for isolated hypothyroxinemia in pregnancy.

Related Experiment Videos

Last Updated: Jun 5, 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
  • Obstetrics
  • Neuroscience

Background:

  • Maternal thyroxine (T4) is essential for fetal brain development.
  • Hypothyroxinemia during pregnancy can negatively impact offspring neurobehavioral outcomes.
  • Iodine deficiency is a significant factor affecting maternal thyroid hormone levels.

Purpose of the Study:

  • To review the literature on iodine deficiency and hypothyroxinemia in pregnancy.
  • To assess the impact of maternal hypothyroxinemia on fetal neurodevelopment.
  • To evaluate current diagnostic methods and therapeutic recommendations.

Main Methods:

  • Literature review of studies on isolated hypothyroxinemia in pregnancy.
  • Analysis of free thyroxine (T4) assay methodologies.
  • Examination of iodine deficiency's impact on free T4.
  • Review of ongoing randomized trials.

Main Results:

  • Hypothyroxinemia is common in pregnancy, with documented negative effects on fetal neurodevelopment.
  • Two studies showed improved neurodevelopment in infants of mothers supplemented with iodine.
  • Current free T4 assays have limitations, and optimal diagnostic tests are lacking.
  • Ongoing trials have yielded mixed preliminary results.

Conclusions:

  • Insufficient evidence exists to recommend levothyroxine therapy for pregnant women with isolated hypothyroxinemia.
  • Ensuring adequate iodine intake before conception and early in pregnancy is recommended.