Related Experiment Video
Updated: Jun 21, 2026

05:12
Transoral Endoscopic Thyroidectomy Vestibular Approach for Thyroid Lobectomy
Published on: May 12, 2023
Levothyroxine therapy in preventing nodular recurrence after hemithyroidectomy: a retrospective study
M Alba1, D Fintini, R M Lovicu
1Endocrinology Unit, Catholic University of Sacred Heart, Via Federico Cesi, 72, 00193 Rome, Italy.
Journal of Endocrinological Investigation
|July 29, 2009
Summary
Levothyroxine (L-T4) therapy after surgery for benign nodular goiter significantly reduced disease recurrence. TSH suppression was not necessary for this preventative effect in remnant thyroid tissue.
Area of Science:
- Endocrinology
- Thyroid Surgery
- Pharmacology
Background:
- Benign nodular goiter is a common thyroid condition.
- Lobectomy is a surgical option for managing benign nodular goiter.
- Recurrence of nodular disease after surgery is a clinical concern.
Purpose of the Study:
- To evaluate the impact of levothyroxine (L-T4) therapy on the recurrence rate of nodular disease.
- To compare recurrence rates in patients treated with and without L-T4 post-lobectomy.
- To investigate whether TSH suppression is required for recurrence prevention.
Main Methods:
- A cohort of 233 patients who underwent lobectomy for benign nodular goiter were followed annually.
- Patients were monitored using serum TSH levels and ultrasound (US) for nodular recurrence (lesion ≥ 5 mm).
- Patients were divided into a control group (no L-T4) and an L-T4 treated group (substitutive or suppressive doses).
Main Results:
- The overall recurrence rate was 30.5% (71/233 patients).
- Patients receiving L-T4 therapy (Group 2) had a significantly lower recurrence rate (19.5%-27.7%) compared to those without L-T4 (Group 1, 64.4%; p<0.001).
- No significant difference in recurrence rates was found between L-T4 substitutive and TSH-suppressive doses.
Conclusions:
- Levothyroxine (L-T4) therapy following hemithyroidectomy for benign monolobar nodular disease may prevent recurrence.
- TSH suppression is not essential for preventing nodular disease recurrence in the remaining thyroid tissue.
Related Concept Videos
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...
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...
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...
The Thyroid Gland
The thyroid gland is a small, butterfly-shaped gland located in the neck and covers the anterior surface of the trachea. The gland has two lateral lobes connected by a thin tissue mass called the isthmus. Internally, each lobe comprises many small spherical structures known as thyroid follicles, surrounded by a network of blood vessels.
The follicles have a central cavity lined by simple cuboidal to squamous epithelial cells called follicular cells. These cells produce the glycoprotein...
The follicles have a central cavity lined by simple cuboidal to squamous epithelial cells called follicular cells. These cells produce the glycoprotein...
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...