Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

Class III antiarrhythmic drugs are a group of medications that can prolong action potentials in the heart. They achieve this by blocking potassium channels or enhancing inward currents from sodium channels. However, these drugs have a unique property of "reverse use-dependence," which is most pronounced at slower heart rates and can lead to torsades de pointes—a specific type of arrhythmia. However, it is essential to note that excessive QT interval prolongation—a measure of the heart's...

Hyperthyroidism II: Pathophysiology

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: Introduction

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...

Hypothyroidism II: Pathophysiology

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...

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

Class I antiarrhythmic drugs are used to treat various types of arrhythmias or irregular heart rhythms. These drugs block the sodium (Na+) channels in the cardiac cells, thereby affecting the movement of electrical impulses across the heart. Class I antiarrhythmic drugs are divided into three subgroups: Class IA, Class IB, and Class IC, each with distinct mechanisms of action and effects on the heart.
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...

Synthesis and Regulation of Thyroid Hormones

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

Cinacalcet Efficacy in Hyperparathyroidism-Chronic Kidney Disease-Non-Dialysis, Hemodialysis, Peritoneal Dialysis, Kidney Transplantation: Critical Review.

Biomedicines·2026

Same author

Hypercalcemia in Patients After Kidney Transplantation.

Cureus·2025

Same author

The Therapeutic Potential of Propranolol and Other Beta-Blockers in Hyperthyroidism.

International journal of molecular sciences·2025

Same author

Exon 11 Polymorphism (rs1126797) in the Thyroid Peroxidase (<i>TPO</i>) Gene Among Caucasian Polish Patients with Autoimmune Thyroiditis: A Short Communication.

International journal of molecular sciences·2025

Same author

Rationale for Testing TP53 Mutations in Thyroid Cancer-Original Data and Meta-Analysis.

International journal of molecular sciences·2025

Same author

Autoimmune Thyroid Disease in Patients with Down Syndrome-Review.

International journal of molecular sciences·2025

Search research articles

Related Experiment Video

Updated: May 8, 2026

Zebra II as A Novel System to Record Electrophysiological Signals in Zebrafish

Zebra II as A Novel System to Record Electrophysiological Signals in Zebrafish

Published on: August 16, 2024

[Amiodarone treatment and thyroid disorders].

Katarzyna Łacka¹, Magdalena Maria Fraczek

¹Uniwersytet Medyczny im. Katedra Endokrynologii, Przemiany Materii i Chorób Wewnetrznych. kktlacka@gmail.com

Polski Merkuriusz Lekarski : Organ Polskiego Towarzystwa Lekarskiego

|August 30, 2013

Summary

Amiodarone, an antiarrhythmic drug, can cause thyroid disorders, including thyrotoxicosis (types I and II) and hypothyroidism. Differentiating these types and appropriate treatment are crucial for patient management.

More Related Videos

A Versatile, Behavioral Method to Investigate Thyroid Hormone Effects on Cerebellar Function

A Versatile, Behavioral Method to Investigate Thyroid Hormone Effects on Cerebellar Function

Published on: October 6, 2023

Related Experiment Videos

Last Updated: May 8, 2026

Zebra II as A Novel System to Record Electrophysiological Signals in Zebrafish

Zebra II as A Novel System to Record Electrophysiological Signals in Zebrafish

Published on: August 16, 2024

A Versatile, Behavioral Method to Investigate Thyroid Hormone Effects on Cerebellar Function

A Versatile, Behavioral Method to Investigate Thyroid Hormone Effects on Cerebellar Function

Published on: October 6, 2023

Area of Science:

Endocrinology
Cardiology
Pharmacology

Background:

Amiodarone is an iodine-rich antiarrhythmic drug frequently used for severe tachyarrhythmias.
It causes thyroid dysfunction in 14-18% of patients, manifesting as amiodarone-induced thyrotoxicosis (AIT) types I and II, and amiodarone-induced hypothyroidism (AIH).
Geographical iodine intake influences AIT and AIH prevalence, with AIT more common in low-iodine areas and AIH in iodine-sufficient regions.

Discussion:

AIH diagnosis and treatment are generally straightforward, unlike AIT.
Diagnostic tools like ultrasound (USG), color Doppler flowmetry (CFDS), radioiodine uptake (RAIU), myocardial perfusion imaging (MIBI), and interleukin-6 (IL-6) levels aid in differentiating AIT types.
AIT I often shows increased vascularization (CFDS), MIBI uptake, and RAIU, while AIT II typically exhibits decreased values for these parameters.

Key Insights:

Amiodarone-induced thyrotoxicosis type I is often associated with Graves' disease or goiter.
Amiodarone-induced hypothyroidism can occur in patients with normal thyroid glands or Hashimoto's disease.
Serum IL-6 levels may be elevated in AIT II, though its diagnostic utility remains debated.

Outlook:

Discontinuation of amiodarone is a primary consideration upon diagnosis.
AIT I is typically managed with methimazole and potassium perchlorate; AIT II is treated with glucocorticoids.
Refractory cases or those with left ventricular systolic dysfunction may require thyroidectomy or radioiodine therapy (RIT).