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Related Concept Videos

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...
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 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...
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...
The Thyroid Gland01:23

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...

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Related Experiment Video

Updated: Jun 17, 2026

Minimal Invasive Resection of Large Retrosternal Thyroid Goiter
04:09

Minimal Invasive Resection of Large Retrosternal Thyroid Goiter

Published on: September 20, 2024

Painless thyroiditis complicated by acromegaly.

Takatoshi Saito1, Katsuyoshi Tojo, Naoko Tajima

  • 1Division of Diabetes, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo. tsaito@jikei.ac.jp

Internal Medicine (Tokyo, Japan)
|January 16, 2010
PubMed
Summary
This summary is machine-generated.

Acromegaly can lower thyroid stimulating hormone (TSH) levels, mimicking central hypothyroidism. Distinguishing this from painless thyroiditis requires measuring thyroglobulin and radioactive iodine uptake (RAIU).

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Area of Science:

  • Endocrinology
  • Thyroidology

Background:

  • Serum thyroid stimulating hormone (TSH) levels are often decreased in acromegaly.
  • This reduction is hypothesized to result from somatostatin's enhanced secretion, suppressing TSH production, though unproven.

Observation:

  • A 60-year-old woman with acromegaly presented with low TSH levels.
  • She was diagnosed with painless thyroiditis, characterized by elevated thyroglobulin, low radioactive iodine uptake (RAIU), normal thyroid vascularity and size, and normal thyroid hormone levels (T3, T4, free T3, free T4).

Findings:

  • This case represents the second report of acromegaly complicated by painless thyroiditis.
  • The differential diagnosis between central hypothyroidism and painless thyroiditis is critical in such cases.

Implications:

  • Diagnosing painless thyroiditis in acromegalic patients can be challenging with only low TSH and normal thyroid hormones.
  • Measuring thyroglobulin and RAIU is recommended for accurate diagnosis when painless thyroiditis is suspected in acromegaly.