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Graves’ Ophthalmopathy

Also Known As: Thyroid Eye Disease (TED), Thyroid-Associated Ophthalmopathy (TAO), Graves’ Orbitopathy
System: Immune System, Endocrine System, and Eyes
Autoantibodies:

  • Thyroid-Stimulating Immunoglobulins (TSI)

  • TSH Receptor Antibodies (TRAb)

Primary Organ or Body Part Affected: Eyes and surrounding orbital tissues
Acceptance as Autoimmune: Confirmed
Graves' Ophthalmopathy

What is Graves’ Ophthalmopathy?

Graves’ ophthalmopathy is an autoimmune inflammatory disorder that affects the muscles and other tissues around the eyes. It is most commonly associated with Graves’ disease, an overactive thyroid condition (hyperthyroidism), but it can also occur in people with normal or underactive thyroid levels. The immune system mistakenly targets tissues in the eye socket (orbit), causing inflammation, swelling, and tissue remodeling.

What are the signs and symptoms of Graves’ Ophthalmopathy?

  • Bulging eyes (proptosis or exophthalmos)

  • Gritty or dry sensation in the eyes

  • Redness and swelling around the eyes

  • Double vision (diplopia)

  • Eyelid retraction (staring appearance)

  • Eye pain or pressure

  • Difficulty moving the eyes

  • Vision loss in severe cases (due to optic nerve compression)

What are the causes of Graves’ Ophthalmopathy?

Graves’ ophthalmopathy is caused by an autoimmune attack on tissues in the orbit, especially the eye muscles and connective tissue. It is often associated with autoantibodies that also stimulate the thyroid gland in Graves’ disease. Risk factors include:

  • Graves’ disease

  • Smoking (which worsens the condition)

  • Radioactive iodine therapy (can temporarily worsen eye symptoms)

  • Genetic predisposition

  • Female sex (more commonly affected, although severe cases are more common in men)

Diagnosis

  • Clinical examination of eye symptoms

  • Thyroid function tests (TSH, Free T4, Free T3)

  • Antibody tests: TSH receptor antibodies (TRAb), TSI

  • Orbital imaging: MRI or CT to assess muscle swelling, inflammation, or optic nerve compression

  • Visual field testing and color vision tests (if optic nerve involvement is suspected)

Treatment

Treatment depends on the severity and phase of the disease (active vs. inactive).

General management:

  • Stop smoking

  • Manage thyroid function (antithyroid drugs, radioactive iodine, or surgery)

For eye symptoms:

  • Lubricating eye drops

  • Selenium supplements (in mild, active disease)

  • Corticosteroids (oral or IV) to reduce inflammation

  • Orbital radiation (in select cases)

  • Immunosuppressive therapy (e.g., teprotumumab, rituximab, or methotrexate)

  • Surgery (for severe or inactive cases):

    • Orbital decompression

    • Eye muscle surgery

    • Eyelid surgery

Prognosis

Most patients experience mild to moderate symptoms that stabilize over time. About 5–10% develop severe eye complications, including vision-threatening optic nerve compression. Early detection and smoking cessation improve outcomes. The active inflammatory phase typically lasts 6 months to 2 years, followed by an inactive (burned-out) phase where surgery may be considered for lasting changes.

Prevalence

  • Occurs in up to 50% of patients with Graves’ disease

  • Severe forms affect approximately 3–5 per 100,000 people per year

  • More common in women, but men are more likely to develop severe symptoms

Citations

  • Bahn RS. Graves’ ophthalmopathy. N Engl J Med. 2010;362(8):726-738.

  • Smith TJ, Hegedüs L. Graves’ Disease. N Engl J Med. 2016;375(16):1552-1565.

  • Bartalena L, et al. The 2021 European Group on Graves’ Orbitopathy (EUGOGO) Clinical Practice Guidelines. Eur J Endocrinol. 2021;185(4):G43–G67.

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