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Related Concept Videos

The Thyroid Gland01:23

The Thyroid Gland

The thyroid gland is a small, butterfly-shaped gland located in the neck and covers the anterior surface of the trachea. The gland has two lateral lobes connected by a thin tissue mass called the isthmus. Internally, each lobe comprises many small spherical structures known as thyroid follicles, surrounded by a network of blood vessels.
The follicles have a central cavity lined by simple cuboidal to squamous epithelial cells called follicular cells. These cells produce the glycoprotein...
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...
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...

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Basophil Activation Test for Allergy Diagnosis
07:22

Basophil Activation Test for Allergy Diagnosis

Published on: May 31, 2021

The thyroid and urticaria.

Stephen C Dreskin1, Karen Y Andrews

  • 1University of Colorado Health Sciences, Denver, Colorado 80262, USA. stephen.dreskin@uchsc.edu

Current Opinion in Allergy and Clinical Immunology
|September 1, 2005
PubMed
Summary
This summary is machine-generated.

Thyroid autoimmunity is common in chronic urticaria patients, but its role in disease development remains unclear. New research suggests complement activation may be involved in chronic urticaria pathogenesis.

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Area of Science:

  • Immunology
  • Dermatology
  • Endocrinology

Background:

  • Thyroid autoimmunity is more frequent in chronic urticaria patients than the general population.
  • The clinical significance of this association and the impact of thyroid autoimmunity on chronic urticaria treatment outcomes are not well understood.
  • Some patients with chronic urticaria and thyroid autoimmunity experience remission with l-thyroxine treatment, while others do not.

Purpose of the Study:

  • To review the historical context and current understanding of the relationship between thyroid autoimmunity and chronic urticaria.
  • To explore the potential role of thyroid autoimmunity in the pathophysiology of chronic urticaria.
  • To discuss recent findings regarding autoantibodies and complement activation in chronic urticaria.

Main Methods:

  • Literature review of studies investigating thyroid autoimmunity in chronic urticaria.
  • Analysis of recent findings on autoantibodies targeting the IgE receptor (FcepsilonRI) and thyroid.
  • Examination of the role of complement activation in urticarial pathogenesis.

Main Results:

  • Subsets of chronic urticaria patients exhibit autoantibodies against FcepsilonRI, anti-IgE, and thyroid antigens.
  • Patients with chronic urticaria and thyroid autoimmunity may present with active thyroid disease or be clinically euthyroid.
  • These patients often show poor response to standard urticaria therapies and may have a more persistent disease course.
  • New evidence highlights the pathogenic role of anti-FcepsilonRI and antithyroid antibodies, particularly through complement activation.

Conclusions:

  • There is currently insufficient evidence to definitively establish a significant role for thyroid autoimmunity in chronic urticaria pathogenesis.
  • Emerging research on complement activation in chronic urticaria may provide future insights into this complex relationship.