Related Experiment Video
Updated: Jul 11, 2026

07:02
In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
[Recombinant human TSH use in differentiated thyroid cancer]
Hans Graf1, Gilberto Paz-Filho
1Serviço de Endocrinologia e Metabologia, Universidade Federal do Paraná, Curitiba, PR, Brazil. hansgraf@bighost.com.br
Arquivos Brasileiros De Endocrinologia E Metabologia
|September 25, 2007
Summary
Recombinant human TSH (rhTSH) aids differentiated thyroid carcinoma (DTC) treatment, improving quality of life without compromising efficacy. This approach helps identify cured patients and offers benefits in metastatic DTC.
Area of Science:
- Endocrinology
- Oncology
- Nuclear Medicine
Context:
- Differentiated thyroid carcinoma (DTC) management traditionally involves 131I thyroid remnant ablation (TRA) during hypothyroidism post-total thyroidectomy (TT).
- Late DTC follow-up includes T4 suppression, thyroglobulin (Tg) monitoring, 131I whole body scans (WBS), and cervical ultrasound (US).
Purpose:
- To evaluate the efficacy and impact of recombinant human TSH (rhTSH)-aided TRA in DTC patients.
- To assess the role of stimulated Tg and cervical US in identifying low-risk DTC patients for adjusted TSH suppression.
- To explore the clinical benefit of rhTSH in metastatic DTC.
Summary:
- TRA with rhTSH avoids hypothyroidism symptoms and maintains quality of life, demonstrating equal efficacy to TRA during endogenous TSH elevation.
- Stimulated Tg levels (9-12 months post-treatment) combined with cervical US identify patients with high cure probability, allowing less strict TSH suppression and mitigating side effects.
- While randomized data for metastatic DTC is limited, rhTSH combined with 131I shows clinical benefits in most treated patients.
Impact:
- rhTSH offers an improved quality of life for DTC patients undergoing TRA.
- Optimized TSH suppression strategies based on stimulated Tg and US can reduce long-term complications.
- rhTSH represents a promising therapeutic option for DTC, including metastatic disease.
Related Concept Videos
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...
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: 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 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: 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: 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...
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...

