This site is intended for healthcare professionals

Go to /sign-in page

You can view 5 more pages before signing in

Graves' disease

Authoring team

Graves' disease is an autoimmune disease mediated by thyroid-stimulating IgG immunoglobulins directed against the TSH receptor, resulting in hyperthyroidism.

The autoimmune process involved in Graves' disease also typically is directed to soft tissues within the orbit - this results in inflammation and swelling, with periorbital oedema, proptosis, and ophthalmoplegia (Graves' ophthalmology).

The presence of pre-tibial myxoedema in association with hyperthyroidism is diagnostic but is uncommon, occurring in about 6% of cases.

Estimated prevalences of different aspects of Graves' disease:

  • hyperthyroidism and diffuse goitre - 95%
  • thyroid eye disease - 50%
  • pretibial myxoedema - 6%
  • acropachy - 1%
  • thyroid eye disease without hyperthyroidism ['Euthyroid Graves' disease'] - 5%

The natural history is one of alternating relapse and remission; less than 40% of patients have a single episode during their lifetime.

Reference:

  • Girgis CM, Champion BL, Wall JR. Current concepts in graves' disease. Ther Adv Endocrinol Metab. 2011 Jun;2(3):135-44.

Create an account to add page annotations

Annotations allow you to add information to this page that would be handy to have on hand during a consultation. E.g. a website or number. This information will always show when you visit this page.

The content herein is provided for informational purposes and does not replace the need to apply professional clinical judgement when diagnosing or treating any medical condition. A licensed medical practitioner should be consulted for diagnosis and treatment of any and all medical conditions.

Connect

Copyright 2024 Oxbridge Solutions Limited, a subsidiary of OmniaMed Communications Limited. All rights reserved. Any distribution or duplication of the information contained herein is strictly prohibited. Oxbridge Solutions receives funding from advertising but maintains editorial independence.