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

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...
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...
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 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...
Goiter01:27

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

In Memoriam: Lawrence Crane Wood (1935-2026).

Thyroid : official journal of the American Thyroid Association·2026
Same author

In Memoriam: Lawrence Crane Wood (1935-2026).

Thyroid : official journal of the American Thyroid Association·2026
Same author

<i>Letter to the Editor:</i> A Patient-Centered Survey-Based Assessment of Prenatal Management of Hypothyroidism for Women of Reproductive Age.

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

Commentary on "Long Work Hours Are Associated with Hypothyroidism: A Cross-Sectional Study with Population-Representative Data" by Lee <i>et al</i>.

Thyroid : official journal of the American Thyroid Association·2020
Same author

An Online Survey of Hypothyroid Patients Demonstrates Prominent Dissatisfaction.

Thyroid : official journal of the American Thyroid Association·2018
Same author

OPEN ACCESS TO DIABETES CENTER FROM THE EMERGENCY DEPARTMENT REDUCES HOSPITALIZATIONS IN THE SUSEQUENT YEAR.

Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists·2016
Same journal

EDITORIAL INTRODUCTION.

Current opinion in endocrinology, diabetes, and obesity·2026
Same journal

Exploring the role of parathyroid hormone in sarcopenia: A review.

Current opinion in endocrinology, diabetes, and obesity·2026
Same journal

Normocalcemic primary hyperparathyroidism: an update on diagnostic and management challenges.

Current opinion in endocrinology, diabetes, and obesity·2026
Same journal

Prediabetes before pregnancy: implications for risk stratification and research.

Current opinion in endocrinology, diabetes, and obesity·2026
Same journal

Secondary hyperparathyroidism in chronic kidney disease: update on pathophysiology and new treatment targets.

Current opinion in endocrinology, diabetes, and obesity·2026
Same journal

Revisiting the relationship between weight loss and bone health in people living with obesity: insights from the latest evidence.

Current opinion in endocrinology, diabetes, and obesity·2026
See all related articles

Related Experiment Video

Updated: May 8, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Nonthyroidal illness syndrome.

Alan P Farwell1

  • 1Section of Endocrinology, Diabetes and Nutrition, Boston University School of Medicine, Boston Medical Center, Boston, Massachusetts 01583, USA. alan.farwell@bmc.org

Current Opinion in Endocrinology, Diabetes, and Obesity
|August 27, 2013
PubMed
Summary
This summary is machine-generated.

Nonthyroidal illness syndrome involves complex thyroid hormone metabolism changes. While therapy is generally not indicated, new research suggests potential benefits for a small patient subset.

More Related Videos

Gasless Endoscopic Thyroidectomy via the Trans-Axillary Approach
05:10

Gasless Endoscopic Thyroidectomy via the Trans-Axillary Approach

Published on: September 15, 2023

Related Experiment Videos

Last Updated: May 8, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Gasless Endoscopic Thyroidectomy via the Trans-Axillary Approach
05:10

Gasless Endoscopic Thyroidectomy via the Trans-Axillary Approach

Published on: September 15, 2023

Area of Science:

  • Endocrinology
  • Thyroidology
  • Metabolic Research

Background:

  • Nonthyroidal illness syndrome (NTIS) is characterized by altered thyroid hormone levels during critical illness.
  • Historically, NTIS pathophysiology was linked to deiodinase activity, TSH secretion, and protein binding.

Purpose of the Study:

  • To review the current understanding of NTIS pathophysiology, diagnosis, and therapeutic implications.
  • To synthesize recent findings on the multifactorial nature of NTIS.

Main Methods:

  • Literature review of studies on thyroid hormone metabolism in illness.
  • Analysis of data on NTIS development and potential therapeutic interventions.

Main Results:

  • NTIS involves complex alterations in thyroid hormone metabolism, including deiodinase activity, TSH secretion, and plasma protein binding.
  • Emerging evidence implicates thyroid hormone transport and nuclear receptor function in NTIS.
  • Therapeutic strategies for NTIS remain controversial, with limited evidence supporting widespread hormone replacement.

Conclusions:

  • NTIS affects all aspects of thyroid hormone metabolism and action due to acute and chronic illness.
  • Mediators underlying these metabolic alterations are not fully elucidated.
  • Thyroid hormone therapy is not recommended for most NTIS patients, though specific subgroups may benefit.