Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

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

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Thyroid eye disease (Graves' orbitopathy): clinical presentation, epidemiology, pathogenesis, and management.

The lancet. Diabetes & endocrinology·2025
Same author

Hyperthyroidism: aetiology, pathogenesis, diagnosis, management, complications, and prognosis.

The lancet. Diabetes & endocrinology·2023
Same author

Worldwide Consensus on Thyroid Eye Disease? What Is In a Name?

Thyroid : official journal of the American Thyroid Association·2022
Same author

Hypothyroid Symptoms Throughout Pregnancy Are Predominantly Associated with Thyroxine and Not with Thyrotropin Concentrations.

Thyroid : official journal of the American Thyroid Association·2022
Same author

<i>European Thyroid Journal:</i> Looking Backwards and Forwards.

European thyroid journal·2021
Same author

T4+T3 Combination Therapy: An Unsolved Problem of Increasing Magnitude and Complexity.

Endocrinology and metabolism (Seoul, Korea)·2021
Same journal

[Insulin intoxications caused by falsified semaglutide].

Nederlands tijdschrift voor geneeskunde·2026
Same journal

[Professional skepticism in medical research].

Nederlands tijdschrift voor geneeskunde·2026
Same journal

[Improving mobility in painful osteoarthritis].

Nederlands tijdschrift voor geneeskunde·2026
Same journal

[The effectiveness and costs of the Back At work After Surgery (BAAS) work-integrated care pathway on return to work for patients receiving knee arthroplasty].

Nederlands tijdschrift voor geneeskunde·2026
Same journal

[The rise of genetic therapies: urgent moral and societal questions].

Nederlands tijdschrift voor geneeskunde·2026
Same journal

[A man with a wound on his elbow].

Nederlands tijdschrift voor geneeskunde·2026
See all related articles

Related Experiment Videos

[Cardiovascular risks in patients with subclinical thyroid dysfunction].

Wilmar M Wiersinga1

  • 1Academisch Medisch Centrum, afd. Inwendige Geneeskunde - Endocrinologie en Metabolisme, Amsterdam, the Netherlands. w.m.wiersinga@amc.uva.nl

Nederlands Tijdschrift Voor Geneeskunde
|December 11, 2012
PubMed
Summary
This summary is machine-generated.

Subclinical thyroid dysfunction increases cardiovascular risks. Treatment is recommended for thyroid stimulating hormone (TSH) levels < 0.1 or > 10 mU/l, with individualized approaches for intermediate levels.

Related Experiment Videos

Area of Science:

  • Endocrinology
  • Cardiovascular Medicine
  • Internal Medicine

Background:

  • Subclinical thyroid dysfunction, characterized by abnormal thyroid stimulating hormone (TSH) levels with normal free thyroxine, is prevalent.
  • Recent meta-analyses have elucidated the cardiovascular implications of subclinical thyroid dysfunction.

Purpose of the Study:

  • To summarize the cardiovascular risks associated with subclinical hyperthyroidism and hypothyroidism.
  • To provide evidence-based recommendations for the management of subclinical thyroid dysfunction.

Main Methods:

  • Systematic review and meta-analysis of population-based studies with long-term follow-up.
  • Analysis of cardiovascular morbidity, mortality, and treatment outcomes based on TSH levels and patient demographics.

Main Results:

  • Subclinical hyperthyroidism (TSH < 0.1 mU/l) significantly increases atrial fibrillation and cardiovascular mortality risk.
  • Subclinical hypothyroidism (TSH > 10 mU/l) is linked to elevated cardiovascular morbidity and mortality.
  • Levothyroxine treatment reduced ischemic heart disease in patients ≤ 70 years but not in older individuals.

Conclusions:

  • Treatment is advised for TSH < 0.1 mU/l or TSH > 10 mU/l, irrespective of randomized trial evidence.
  • Management for TSH 0.1-0.4 mU/l or 4-10 mU/l requires consideration of patient age and cardiovascular risk factors.
  • Individuals over 65 with TSH 4-10 mU/l generally do not require treatment.