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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...

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 receptors...

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...

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 in...

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, and heat...

Synthesis and Regulation of Thyroid Hormones

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...

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Updated: Jul 10, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

High serum bile acids cause hyperthyroidism and goiter.

Ken-Ichi Mukaisho¹, Yoshio Araki, Hiroyuki Sugihara

¹Department of Pathology, Shiga University of Medical Science, Ohtsu, Shiga, Japan.

Digestive Diseases and Sciences

|October 13, 2007

Summary

Elevated serum bile acids (BAs) in rats led to thyroid gland enlargement and reduced thyroid-stimulating hormone (TSH). This suggests BAs may induce hyperthyroidism, highlighting the need for TSH monitoring when using BAs for obesity treatment.

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Substernal Thyroid Biopsy Using Endobronchial Ultrasound-guided Transbronchial Needle Aspiration

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Last Updated: Jul 10, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

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Published on: March 17, 2023

Substernal Thyroid Biopsy Using Endobronchial Ultrasound-guided Transbronchial Needle Aspiration

Substernal Thyroid Biopsy Using Endobronchial Ultrasound-guided Transbronchial Needle Aspiration

Published on: November 10, 2014

Area of Science:

Endocrinology
Gastroenterology
Thyroid Research

Background:

Duodenal content reflux in rats is associated with elevated serum bile acids (BAs) and thyroid gland swelling.
The potential impact of bile acids on thyroid function remains largely unexplored.

Purpose of the Study:

To investigate whether elevated bile acids enhance thyroid function.
To determine the relationship between bile acids and thyroid hormone levels in a rat model.

Main Methods:

A duodenal content reflux model was established in rats via esophago-jejunostomy.
Serum samples were analyzed for bile acids, triiodothyronine (T3), thyroxine (T4), free T3 (fT3), free T4 (fT4), and thyroid-stimulating hormone (TSH).
Thyroid gland weight and histology were assessed at 10 and 30 weeks post-operation.

Main Results:

Rats with duodenal reflux exhibited thyroid gland enlargement due to follicular epithelial hypertrophy.
While T3, T4, fT3, and fT4 levels remained unchanged, serum TSH levels were significantly lower in the reflux group at 10 weeks.
An inverse correlation was observed between serum bile acids and TSH levels in the reflux model.
Microscopic examination revealed increased thyroid follicle size and number with paler colloids in the reflux group.

Conclusions:

Elevated serum bile acids appear to induce thyroid follicular hyperplasia and suppress TSH levels.
These findings suggest that bile acids may contribute to hyperthyroidism.
Close monitoring of TSH is crucial when considering bile acid-based therapies for obesity.