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Related Concept Videos

Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

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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...
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Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

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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,...
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Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

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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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Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

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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...
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Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

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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...
28
Goiter01:27

Goiter

32
Goiter refers to an abnormal enlargement of the thyroid gland that may appear as a diffuse goiter (uniform enlargement) or nodular (single or multiple nodules). Functionally, it is classified as nontoxic (normal/low hormone levels) or toxic (excess hormone production).PathophysiologyDiffuse thyroid enlargement typically results from prolonged stimulation by thyroid-stimulating hormone (TSH) or TSH-like agents, commonly seen in hypothyroidism or iodine deficiency. In contrast, in hyperthyroid...
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Related Experiment Video

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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
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Is Recombinant Human TSH a Trigger for Graves' Orbitopathy?

C Daumerie1, A Boschi2, P Perros3

  • 1Department of Endocrinology, Université catholique de Louvain, University Hospital St-Luc, Brussels, Belgium, UK.

European Thyroid Journal
|May 1, 2014
PubMed
Summary

Recombinant human TSH (rhTSH) may reactivate Graves' orbitopathy (GO) in patients with coexisting thyroid cancer. This suggests TSHR binding, not just thyroid status, impacts GO progression, warranting clinical caution.

Keywords:
Graves' diseaseGraves' orbitopathyRadioiodineRecombinant human TSHThyroid cancer

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Area of Science:

  • Endocrinology
  • Ophthalmology
  • Oncology

Background:

  • The exact cause of Graves' orbitopathy (GO) is unknown.
  • Autoimmunity against the TSH receptor (TSHR) is hypothesized to cause GO.
  • Radioiodine treatment can worsen or trigger GO, potentially due to antigen release.

Purpose of the Study:

  • To investigate the potential link between recombinant human TSH (rhTSH) administration and GO reactivation.
  • To report cases of GO reactivation following rhTSH treatment in patients with incidental thyroid cancer.

Main Methods:

  • Retrospective analysis of 3 patients with Graves' disease (GD) and GO.
  • Treatment involved thyroidectomy for GD, incidental thyroid cancer discovery, and subsequent rhTSH administration for remnant ablation.
  • Monitoring of GO activity, thyroid status, and TSHR antibodies post-rhTSH.

Main Results:

  • All 3 patients experienced GO reactivation 3-6 weeks after rhTSH administration.
  • GO reactivation occurred despite euthyroidism and no rise in TSHR antibodies post-radioiodine.
  • One patient received steroids without preventing GO reactivation.

Conclusions:

  • rhTSH administration may trigger GO reactivation, independent of thyroid status.
  • TSHR binding by TSH or TSHR antibodies might directly influence GO severity.
  • Clinicians should consider GO risk before prescribing rhTSH and consider prophylactic steroids for high-risk patients.