What is the etiology of hyperthyroidism?

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Etiology of Hyperthyroidism

The most common causes of hyperthyroidism are Graves' disease (accounting for approximately 70% of cases), toxic adenoma, toxic multinodular goiter, and subacute thyroiditis, with rarer causes including trophoblastic disease, thyroid hormone resistance, amiodarone-induced thyroiditis, iatrogenic thyrotoxicosis, factitious ingestion of thyroid hormone, and struma ovarii. 1

Primary Causes of Hyperthyroidism

1. Graves' Disease

  • Most common cause in iodine-sufficient areas (70% of hyperthyroidism cases) 2
  • Autoimmune disorder characterized by TSH receptor antibodies that bind and activate the thyrotropin receptor (TSHR) 3
  • More common in women, with global prevalence of 2% in women and 0.5% in men 4
  • May present with diffusely enlarged thyroid gland, exophthalmos, and other extrathyroidal manifestations 4

2. Toxic Nodular Disease

  • Accounts for approximately 16% of hyperthyroidism cases 2
  • Includes:
    • Toxic multinodular goiter: Multiple autonomously functioning nodules
    • Toxic adenoma: Single hyperfunctioning nodule
  • More common in older adults and in areas with iodine deficiency
  • May cause local compression symptoms (dysphagia, orthopnea, voice changes) 4

3. Thyroiditis

  • Accounts for approximately 3-9% of hyperthyroidism cases 2
  • Types include:
    • Subacute (granulomatous) thyroiditis: Often follows viral infection
    • Painless (silent) thyroiditis: Often postpartum or autoimmune
    • Radiation-induced thyroiditis
  • Characterized by destruction of thyroid follicles causing release of preformed thyroid hormone
  • Typically self-limiting with transient hyperthyroidism followed by euthyroidism or hypothyroidism

Secondary Causes of Hyperthyroidism

1. Medication/Drug-Induced (9% of cases) 2

  • Amiodarone (contains iodine and can cause both hyper- and hypothyroidism)
  • Tyrosine kinase inhibitors
  • Immune checkpoint inhibitors
  • Excessive thyroid hormone replacement
  • Iodine-containing contrast media or supplements

2. Other Rare Causes

  • TSH-secreting pituitary adenoma
  • Human chorionic gonadotropin (hCG)-mediated hyperthyroidism:
    • Gestational hyperthyroidism
    • Trophoblastic disease (choriocarcinoma, hydatidiform mole)
  • Struma ovarii (ectopic thyroid tissue in ovarian teratoma)
  • Factitious thyrotoxicosis (intentional ingestion of excess thyroid hormone)
  • Thyroid hormone resistance syndrome (rare genetic disorder)

Pathophysiological Mechanisms

Hyperthyroidism occurs through three main mechanisms:

  1. Increased synthesis and secretion of thyroid hormones (Graves' disease, toxic nodular disease)
  2. Excessive release of preformed thyroid hormones (thyroiditis)
  3. Exogenous sources of thyroid hormones (medication-induced, factitious)

Risk Factors for Developing Hyperthyroidism

  • Female sex (5-10 times more common in women)
  • Advancing age
  • Family history of thyroid disorders
  • Personal history of autoimmune disorders
  • Smoking (particularly for Graves' disease and ophthalmopathy)
  • Recent pregnancy (postpartum thyroiditis)
  • Iodine excess or deficiency
  • Radiation exposure to the neck
  • Certain medications (amiodarone, lithium, interferon-alpha)

Clinical Implications

Understanding the etiology of hyperthyroidism is crucial for appropriate management, as treatment approaches differ based on the underlying cause:

  • Graves' disease typically requires antithyroid drugs, radioactive iodine, or surgery
  • Toxic nodular goiter is usually treated with radioactive iodine or surgery
  • Thyroiditis often requires only symptomatic treatment as it is typically self-limiting

Early identification and appropriate management are essential to prevent complications such as atrial fibrillation, heart failure, osteoporosis, and thyroid storm, which can significantly impact morbidity and mortality.

References

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Research

Hyperthyroidism: A Review.

JAMA, 2023

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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