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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...
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...
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...

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Related Experiment Video

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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

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Published on: March 17, 2023

Primary antiphospholipid syndrome and thyroid involvement.

Jozélio Freire de Carvalho1, Maria Teresa Correia Caleiro

  • 1Rheumatology Division, Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo e Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil. jotafc@gmail.com

Journal of Clinical Rheumatology : Practical Reports on Rheumatic & Musculoskeletal Diseases
|April 22, 2010
PubMed
Summary
This summary is machine-generated.

Twenty-two percent of patients with primary antiphospholipid syndrome (PAPS) have hypothyroidism, and 18% have thyroid autoantibodies, suggesting a shared cause between PAPS and autoimmune thyroid disease.

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Area of Science:

  • Endocrinology
  • Rheumatology
  • Immunology

Background:

  • Limited data exist on thyroid dysfunction in primary antiphospholipid syndrome (PAPS).
  • Existing studies on thyroid involvement in PAPS are scarce and inconclusive.

Purpose of the Study:

  • To determine the frequency of thyroid dysfunction and antibodies in PAPS patients.
  • To investigate the association between thyroid alterations and clinical/immunologic features in PAPS.

Main Methods:

  • 50 PAPS patients (mean age 39.7 years) were studied.
  • Chart review, interviews, and clinical exams collected data on thyroid dysfunction and PAPS.
  • Serum levels of TSH, free T4, TgAb, TPOAb, TRAb, and antiphospholipid autoantibodies were analyzed.

Main Results:

  • No hyperthyroidism was observed; 22% of patients had hypothyroidism.
  • 18% of patients had at least one thyroid autoantibody (TgAb, TPOAb, or both).
  • No significant differences were found in demographic, disease, or antiphospholipid antibody features between hypothyroid and euthyroid groups.

Conclusions:

  • Hypothyroidism affects 22% of PAPS patients, and 18% exhibit thyroid autoantibodies.
  • These findings suggest a potential common pathophysiologic mechanism linking antiphospholipid syndrome and autoimmune thyroid diseases.