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Hyperthyroidism II: Pathophysiology

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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...

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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 II: Pathophysiology

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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,...

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Hypothyroidism II: Pathophysiology

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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...

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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...

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Updated: Apr 20, 2026

Spontaneous Murine Model of Anaplastic Thyroid Cancer

Spontaneous Murine Model of Anaplastic Thyroid Cancer

Published on: February 3, 2023

Papillary thyroid cancer case masked by subacute thyroiditis.

Bekir Ucan¹, Tuncay Delibasi¹, Erman Cakal¹

¹Department of Endocrinology and Metabolism, Diskapi Yildirim Beyazit Training and Research Hospital, Ankara, Turkey.

Arquivos Brasileiros De Endocrinologia E Metabologia

|December 4, 2014

Summary

Subacute thyroiditis (SAT) can rarely be associated with thyroid cancer. Follow-up ultrasounds after SAT treatment are crucial for detecting potential papillary thyroid cancer, especially new hypoechogenic lesions.

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Area of Science:

Endocrinology
Oncology
Radiology

Background:

Subacute thyroiditis (SAT) is an inflammatory thyroid condition.
The association between SAT and thyroid carcinoma is infrequently documented.
Early diagnosis and management of thyroid nodules are critical.

Observation:

A case of a 54-year-old female presenting with symptoms of SAT.
Initial diagnosis of SAT confirmed by clinical, laboratory, and ultrasonographic findings.
Post-treatment thyroid ultrasound revealed a new hypoechogenic lesion with suspicious features (irregular borders, microcalcification).

Findings:

The suspicious nodule, initially obscured by SAT-related changes, was biopsied.
Fine needle aspiration biopsy and subsequent pathology confirmed papillary microcarcinoma.
This case highlights how SAT can mask underlying thyroid cancer on ultrasound.

Implications:

Subacute thyroiditis may alter thyroid ultrasound appearance, potentially obscuring concurrent thyroid malignancies.
Post-treatment ultrasonography in SAT patients is recommended for detecting residual or new suspicious nodules.
Hypoechogenic lesions >1 cm on follow-up ultrasound post-SAT require biopsy for accurate diagnosis.