Thyroid Eye Disease

What Is Thyroid Eye Disease

Thyroid Eye Disease (TED) — also called Graves’ ophthalmopathy or thyroid-associated orbitopathy — is an autoimmune inflammatory condition of the orbit that occurs when the immune system attacks the tissues behind the eyes. It is most commonly, though not exclusively, associated with Graves’ disease (autoimmune hyperthyroidism).

• TED affects up to 50% of patients with Graves’ disease to some degree; clinically significant disease occurs in 25–30%
• Severe, vision-threatening disease occurs in 3–5% of cases
• Female-to-male ratio is approximately 5:1; peak incidence between roughly ages 40 and 60
• Smoking is the single most important modifiable risk factor — it significantly worsens disease activity and reduces response to treatment
• TED can be present even when thyroid hormone levels are normal (“euthyroid Graves’ disease”)

Graves’ Disease & How It Affects the Eye

Graves’ disease is an autoimmune disorder in which the body produces antibodies against the thyroid-stimulating hormone receptor (TSH-R). These anti-TSH-R antibodies (also called TSHR-Ab, TRAb, or TSI) do two things simultaneously:

• In the thyroid: they stimulate the gland to overproduce thyroid hormone, causing hyperthyroidism (rapid heart rate, weight loss, tremor, heat intolerance)
• In the orbit: the same TSH-R is expressed on orbital fibroblasts — the antibodies activate these cells, triggering inflammation, fibrosis, and expansion of extraocular muscles and orbital fat

The result is a crowded, inflamed orbit that pushes the eye forward (proptosis), restricts eye movement, and exposes the cornea. Because the thyroid and orbital disease share the same autoimmune trigger, treatment of the thyroid does not always resolve the eye disease — and radioactive iodine treatment can sometimes worsen TED (in at-risk patients, such as smokers or those with active eye disease, a short course of oral steroids around treatment may be recommended to reduce this risk).

Thyroid Function Tests in TED

At your evaluation, thyroid function is assessed with:

• TSH — low in hyperthyroidism; elevated in primary hypothyroidism
• Free T4 and Free T3 — elevated in Graves’ hyperthyroidism
• TRAb / TSI — Thyroid receptor antibodies; typically elevated in active TED even when thyroid levels are controlled. These antibodies also correlate with disease activity and severity

Explore Thyroid Eye Disease

Thyroid eye disease has many facets — from how it is diagnosed to the medical and surgical treatments that rehabilitate the eye. Explore each in depth:

Symptoms of Thyroid Eye Disease

TED (also called Graves’ orbitopathy) is an autoimmune inflammation of the muscles and fat behind the eye. Because those tissues swell inside a fixed bony socket, the eye is pushed forward and the lids pull back. Common symptoms include:

• Bulging eyes (proptosis) and a startled or staring appearance
• Upper- or lower-eyelid retraction with visible white above or below the iris
• Grittiness, tearing, redness, and dryness from exposure
• Double vision (diplopia) when swollen muscles no longer move together
• Pain with eye movement, and pressure behind the eyes
• Rarely, blurred or dimmed vision from optic-nerve compression — a warning sign that needs urgent care

Active vs. Stable Disease

TED moves through two phases, and treatment depends on which you are in:

• Active (inflammatory) phase: months to a couple of years of swelling and change. Activity is scored with a Clinical Activity Score (CAS); active disease is generally a CAS of at least 3 of 7. This is the window for medical, anti-inflammatory treatment.
• Stable (fibrotic) phase: inflammation has burned out and measurements stop changing. This is when surgical rehabilitation is planned.

Medical Treatment

The first and most important step is controlling thyroid function and stopping smoking — smoking dramatically worsens TED and blunts treatment. For active disease, options include:

• Teprotumumab (Tepezza): an IGF-1-receptor antibody, FDA-approved in January 2020 and label-expanded in 2023 to treat TED regardless of activity or duration. Response is greatest in recent-onset disease (roughly the first 9–12 months) and in patients with significant proptosis (about 3 mm or more above normal).
• Corticosteroids (often IV) to calm acute inflammation.
• Selenium for mild disease (evidence is strongest in selenium-deficient populations), and orbital radiotherapy in selected cases.

Surgical Rehabilitation

Once disease is stable, reconstruction follows a deliberate order, because each step changes the next:

1. Orbital decompression first — making room in the socket to move the eye back and relieve optic-nerve pressure. See Orbital Decompression.
2. Strabismus (eye-muscle) surgery next, to correct double vision. See Eyelid & Strabismus Surgery.
3. Eyelid surgery last, to correct retraction and restore normal lid position.

Choosing Your Care Team

TED is best co-managed by an endocrinologist and an oculoplastic surgeon; ASOPRS fellowship-trained surgeons handle decompression, strabismus, and eyelid rehabilitation and coordinate the sequence above. Find one through our surgeon directory.

Disease Activity and Why Timing Matters

Thyroid eye disease is not one fixed state — it moves through an active (inflammatory) phase that lasts months to a couple of years, then settles into a stable (fibrotic) phase. Knowing which phase you are in decides what treatment helps.

• Active phase is scored with a Clinical Activity Score (CAS); a CAS of at least 3 of 7 signals active inflammation. This is the window for medical, anti-inflammatory treatment — and where teprotumumab (Tepezza) works best, with the greatest proptosis reduction in recent-onset disease (roughly the first 9–12 months) and in patients with about 3 mm or more of proptosis. A second IGF-1R–blocking antibody, veligrotug (Lumvoa) — FDA-approved in June 2026 — is approved for thyroid eye disease regardless of disease activity or duration, giving patients in both the active and chronic phases a medical option.
• Stable phase is when measurements stop changing — the point at which surgical rehabilitation is planned, in the deliberate order of decompression → strabismus surgery → eyelid surgery.

The practical implication: operating on a still-active orbit invites relapse and re-operation, while waiting for stability — unless the optic nerve is threatened — produces more durable results. Two things do not wait for the phase, though: controlling thyroid function and stopping smoking, the strongest modifiable driver of severity.

Continue Reading — Complete Thyroid Eye Disease Guide

• Diagnosis & Evaluation
• Treatment Overview
• Orbital Decompression
• Eyelid & Strabismus Surgery