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

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...
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...

You might also read

Related Articles

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

Sort by
Same author

Efficacy of 15 mg Edoxaban on Long-Term Outcome after Percutaneous Coronary Intervention in Patients with Atrial Fibrillation and High Bleeding Risk.

International heart journal·2026
Same author

Trajectory of Heart Failure Severity After Acute Myocardial Infarction.

JACC. Asia·2026
Same author

Switching from Conventional Fibrates to Pemafibrate Improves Lipid Profiles, Liver Enzymes, Renal Function, and Fibrosis Markers in Dyslipidemic Patients with MASLD: A Multicenter Real-World Study.

Journal of atherosclerosis and thrombosis·2026
Same author

Health-related quality of life with encorafenib plus binimetinib for BRAF V600E thyroid cancer.

European thyroid journal·2026
Same author

A study to learn how well the combination of encorafenib and binimetinib works and how safe it is in adults with thyroid cancer: a plain language summary.

Future oncology (London, England)·2026
Same author

Medullary Thyroid Carcinoma That Progressed From Low- to High-Grade During Treatment: A Case Report.

Pathology international·2026

Related Experiment Video

Updated: Jun 10, 2026

Transoral Robotic Total Thyroidectomy and Bilateral Central Regional Lymph Node Dissection for Papillary Thyroid Carcinoma
04:01

Transoral Robotic Total Thyroidectomy and Bilateral Central Regional Lymph Node Dissection for Papillary Thyroid Carcinoma

Published on: September 15, 2023

Does postoperative thyrotropin suppression therapy truly decrease recurrence in papillary thyroid carcinoma? A

Iwao Sugitani1, Yoshihide Fujimoto

  • 1Division of Head and Neck, Cancer Institute Hospital, Koto-ku, Tokyo, Japan. isugitani@jfcr.or.jp

The Journal of Clinical Endocrinology and Metabolism
|July 28, 2010
PubMed
Summary

TSH suppression therapy is not superior to no suppression for papillary thyroid cancer recurrence. Thyroid-conserving surgery without TSH suppression may be considered for low-risk patients.

More Related Videos

Identification and Protection of the Recurrent Laryngeal Nerve during Transoral Robotic Thyroidectomy
05:25

Identification and Protection of the Recurrent Laryngeal Nerve during Transoral Robotic Thyroidectomy

Published on: October 24, 2025

Related Experiment Videos

Last Updated: Jun 10, 2026

Transoral Robotic Total Thyroidectomy and Bilateral Central Regional Lymph Node Dissection for Papillary Thyroid Carcinoma
04:01

Transoral Robotic Total Thyroidectomy and Bilateral Central Regional Lymph Node Dissection for Papillary Thyroid Carcinoma

Published on: September 15, 2023

Identification and Protection of the Recurrent Laryngeal Nerve during Transoral Robotic Thyroidectomy
05:25

Identification and Protection of the Recurrent Laryngeal Nerve during Transoral Robotic Thyroidectomy

Published on: October 24, 2025

Area of Science:

  • Endocrinology
  • Oncology
  • Surgical Oncology

Background:

  • Thyroid-stimulating hormone (TSH) suppression therapy is a common strategy to reduce thyroid cancer recurrence.
  • High-quality evidence validating its effectiveness has been limited.

Purpose of the Study:

  • To test if disease-free survival (DFS) in papillary thyroid carcinoma (PTC) patients without TSH suppression is non-inferior to those with TSH suppression.

Main Methods:

  • A single-center, open-label, randomized controlled trial.
  • Patients were stratified by AMES risk (low/high) and randomized to TSH suppression (Group A) or no suppression (Group B).
  • TSH levels were maintained <0.01 μU/ml in Group A and within normal ranges in Group B. Recurrence assessed via ultrasonography and CT.

Main Results:

  • 218 patients in Group A and 215 in Group B were analyzed on an intention-to-treat basis.
  • No significant difference in DFS between the groups.
  • The 95% confidence interval for recurrence hazard ratio (0.85-1.27) was within the non-inferiority margin (2.12).

Conclusions:

  • Disease-free survival without TSH suppression was not inferior by more than 10% compared to TSH suppression.
  • Thyroid-conserving surgery without TSH suppression is a viable option for low-risk PTC patients, potentially avoiding adverse effects.