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

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...

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...

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...

Graves Disease II: Pathophysiology

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,...

Graves' Disease I: Introduction

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...

Goiter

Goiter

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...

You might also read

Related Articles

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

Sort by

Same author

New Paradigm in Ocular Surface Squamous Neoplasia-Insights from a Case Report on the Use of Interferon in Treatment.

Oncology research·2026

Same author

Sodium-glucose cotransporter 2 inhibitors in breast cancer patients on endocrine therapy: a targeted strategy to mitigate long-term cardiometabolic risk.

Journal of translational medicine·2026

Same author

Environmental endocrine disruptors in cardio-oncology: emerging modifiers of cardiovascular vulnerability in patients with cancer.

Cardio-oncology (London, England)·2026

Same author

Heart-Type Fatty Acid-Binding Protein (H-FABP) as a Candidate Adjunctive Biomarker for Immune Checkpoint Inhibitor-Related Cardiotoxicity: Linking Early Immune-Metabolic Myocardial Injury with Translational Cardio-Oncology.

International journal of molecular sciences·2026

Same author

Cytopathology Terminology Systems: European Federation of Cytological Societies Survey on Practice in Europe.

Cytopathology : official journal of the British Society for Clinical Cytology·2026

Same author

Role of ancillary techniques in the WHO classification of lymph node fine-needle cytology.

Journal of the American Society of Cytopathology·2026

Search research articles

Related Experiment Video

Updated: Apr 21, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Thyroid dysfunction following a kelp-containing marketed diet.

Tiziana Di Matola¹, Pio Zeppa², Maurizio Gasperi³

¹A.O.R.N. dei Colli Hospital, Naples, Italy.

BMJ Case Reports

|October 31, 2014

Summary

This summary is machine-generated.

Kelp-containing weight loss diets can cause thyroid dysfunction. Excessive iodine from kelp led to hyperthyroidism, then hypothyroidism, reversible with treatment.

More Related Videos

Author Spotlight: Accurately Assessing Thyroid Hormone-Driven Motor Alterations in Mouse

Author Spotlight: Accurately Assessing Thyroid Hormone-Driven Motor Alterations in Mouse

Published on: October 6, 2023

Related Experiment Videos

Last Updated: Apr 21, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Author Spotlight: Accurately Assessing Thyroid Hormone-Driven Motor Alterations in Mouse

Author Spotlight: Accurately Assessing Thyroid Hormone-Driven Motor Alterations in Mouse

Published on: October 6, 2023

Area of Science:

Endocrinology
Nutritional Science
Toxicology

Background:

Dietary supplements, particularly herbal and complementary medicines for weight loss, are increasingly popular.
Kelp is a common ingredient in such supplements due to its purported weight loss benefits.

Observation:

A 45-year-old woman with no prior thyroid disease developed hyperthyroidism after consuming a kelp-containing diet.
Her hyperthyroidism resolved over two months, followed by overt hypothyroidism.
Thyroid scintiscan showed extremely low uptake, and Doppler ultrasonography revealed pulsatile flow.

Findings:

The patient's condition is consistent with iodine-induced thyrotoxicosis.
Excessive iodine intake from kelp likely inhibited the sodium-iodide symporter.
Thyroid function normalized after three months of levothyroxine therapy and discontinuation.

Implications:

Consumers using kelp-rich diets should be aware of potential thyroid dysfunction risks.
Even individuals without pre-existing thyroid conditions can be affected by high iodine intake.
This case highlights the importance of monitoring thyroid function when using iodine-rich supplements.