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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...
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...
Hypersensitivity Reactions: Delayed Hypersensitivity Reactions01:29

Hypersensitivity Reactions: Delayed Hypersensitivity Reactions

Delayed-Type Hypersensitivity (DTH), or Type IV hypersensitivity, is a cell-mediated immune response. It occurs when T cells, rather than antibodies, mediate a reaction to specific antigens. It is characterized by a delayed onset (1-2 days) and involves the recruitment of macrophages to the inflammation site.The initiation of a DTH response begins with the sensitization of T cells. During this phase, which lasts at least 1-2 weeks, antigen-specific T cells are activated, clonally expanded, and...

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Related Experiment Video

Updated: Jun 29, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Acute-phase reactans in Hashimoto thyroiditis.

Sacide Erden1, Suna Buyukozturk, Pervin Vural

  • 1Istanbul University, Faculty of Medicine, Department of Internal Medicine, Turkey.

International Immunopharmacology
|October 7, 2008
PubMed
Summary
This summary is machine-generated.

Hashimoto thyroiditis (HT) may involve low-grade systemic inflammation. This study found elevated acute-phase proteins, including C-reactive protein (CRP), serum amyloid A (SAA), and fibrinogen, in euthyroid HT patients compared to controls.

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Last Updated: Jun 29, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Synchronous Triplanar Reconstruction Integrated with Color Doppler Mapping for Precise and Rapid Localization of Thyroid Lesions
05:41

Synchronous Triplanar Reconstruction Integrated with Color Doppler Mapping for Precise and Rapid Localization of Thyroid Lesions

Published on: February 9, 2024

Area of Science:

  • Endocrinology
  • Immunology
  • Internal Medicine

Background:

  • Hashimoto thyroiditis (HT) is an autoimmune thyroid disease.
  • HT involves lymphocytic infiltration and anti-thyroid antibodies.
  • Emerging evidence suggests HT may be a systemic disorder.

Purpose of the Study:

  • To investigate systemic inflammation in euthyroid Hashimoto thyroiditis patients.
  • To measure blood concentrations of acute-phase proteins: C-reactive protein (CRP), serum amyloid A (SAA), and fibrinogen.

Main Methods:

  • Cross-sectional study comparing 30 euthyroid HT patients with 30 healthy controls.
  • Blood samples analyzed for CRP, SAA, fibrinogen, and erythrocyte sedimentation rate (ESR).

Main Results:

  • Mean ESR was significantly higher in HT patients (p=0.024).
  • Mean fibrinogen (p=0.03) and SAA (p=0.002) levels were significantly elevated in HT patients.
  • No significant difference in CRP levels was mentioned in the abstract.

Conclusions:

  • Euthyroid patients with Hashimoto thyroiditis exhibit elevated levels of certain acute-phase proteins.
  • These findings suggest a potential low-grade systemic inflammation in HT, even in the absence of overt hypothyroidism.