What causes Graves' disease?

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Last updated: April 1, 2025View editorial policy

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From the Guidelines

Graves' disease is an autoimmune disorder that occurs when the immune system produces antibodies called thyroid-stimulating immunoglobulins (TSIs) that attach to thyroid cells and stimulate overproduction of thyroid hormones. The exact cause of this autoimmune response is not fully understood, but several factors contribute to its development, including genetics, female sex, advancing age, and personal or family history of thyroid disease 1. Some common causes of hyperthyroidism include Graves disease, Hashimoto thyroiditis, and functional thyroid nodules, with risk factors for a low TSH level including female sex, advancing age, black race, low iodine intake, and ingestion of iodine-containing drugs, such as amiodarone 1. Key points to consider in the development of Graves' disease include:

  • Genetics play a significant role, as having family members with Graves' disease increases one's risk
  • Women are more likely to develop the condition than men, particularly between ages 30 and 50
  • Stress, pregnancy, and smoking can trigger or worsen the disease in genetically susceptible individuals
  • Other autoimmune conditions like rheumatoid arthritis or type 1 diabetes also increase the risk
  • There is no way to prevent Graves' disease, but early diagnosis and treatment can help manage symptoms and prevent complications
  • Common treatments include anti-thyroid medications (methimazole or propylthiouracil), radioactive iodine therapy, or thyroid surgery depending on the severity and individual factors 1. It is essential to note that the optimal screening interval for thyroid dysfunction is unknown, and the USPSTF found no direct evidence that treatment of thyroid dysfunction based on risk level alters final health outcomes 1. However, early diagnosis and treatment can help manage symptoms and prevent complications, and treatment is generally recommended for patients with a TSH level that is undetectable or less than 0.1 mIU/L, particularly those with overt Graves disease or nodular thyroid disease 1.

From the Research

Causes of Graves' Disease

  • Graves' disease is an autoimmune disorder with a genetic component 2, 3
  • It is characterized by the presence of circulating autoantibodies that bind to and stimulate the thyroid hormone receptor (TSHR), resulting in hyperthyroidism and goiter 3
  • The exact etiology of Graves' disease remains to be completely understood, but it is believed to result from a complex interaction between genetic susceptibility and environmental factors 3

Risk Factors for Developing Graves' Disease

  • Genetic predisposition 2, 3
  • Autoimmune disorders 3
  • Environmental factors, although the exact factors are not well understood 3
  • Hyperthyroidism affects 2% of women but only one-tenth as many men 2

Diagnosis of Graves' Disease

  • Diagnosed by patient history, physical examination, and laboratory tests 2
  • Characterized by the manifestations of thyrotoxicosis as well as by its extrathyroidal features when present 3
  • Serum anti-TSHR autoantibodies (TRAbs) are used to confirm the diagnosis 3

Treatment of Graves' Disease

  • Antithyroid drugs, radioactive iodine, and/or surgery, plus supportive therapy 2
  • Radioactive iodine (RAI) therapy is a common treatment option 4, 5, 6
  • The success rate of RAI therapy can be influenced by factors such as the course of disease and 2-hour radioactive iodine uptake (RAIU) 6

References

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Research

Diagnosis and classification of Graves' disease.

Autoimmunity reviews, 2014

Research

Increased Risk of Radioiodine Treatment Failure Associated with Graves Disease Refractory to Methimazole.

Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists, 2020

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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