Graves Orbitopathy

Graves orbitopathy (also called thyroid eye disease) is an autoimmune eye condition that happens most often in people who have an overactive thyroid due to Graves disease. “Autoimmune” means the immune system mistakenly attacks the body’s own tissues. In Graves orbitopathy, the immune system targets the tissues in the eye socket (the orbit), especially the fat behind the eye and the muscles that move the eye. When these tissues are attacked, they become swollen and inflamed. The swelling draws in water and salt, and the tissues fill with gel-like molecules called glycosaminoglycans. The eye muscles get thicker, the fat behind the eye increases in volume, and pressure inside the bony eye socket goes up. This pressure can push the eye forward, which is called “proptosis,” so the eyes may look prominent or “bulging.” The swollen muscles can become stiff and do not move smoothly, so the eyes may not move together, and this can cause double vision. If the swelling and pressure become very high at the back of the eye where the optic nerve enters, the nerve can be squeezed, and vision can become blurred or dim. Because the eyelids can be pulled back and the eye can protrude, the front surface of the eye can dry out and get irritated, which causes pain, redness, and light sensitivity. Graves orbitopathy can be mild and mostly a cosmetic problem, or it can be severe and threaten sight. It has an “active” phase where inflammation and swelling are ongoing and symptoms change from week to week, and a later “inactive” phase where inflammation settles, but some changes, like eye bulging or restricted movement, may remain.

Graves orbitopathy is an autoimmune eye condition that often happens in people with Graves disease (an overactive thyroid caused by the immune system). In this condition, the body’s defense system mistakenly targets tissues around the eyes. The eye muscles and the soft tissues behind the eyes swell and hold water. Over time, these tissues can also build extra scar-like material. Because the space in the bony eye socket is fixed, the swollen tissues push the eyes forward (proptosis), make the eyelids retract (look wider open), and can restrict eye movements, causing double vision. In the most serious cases, the swelling presses on the optic nerve and threatens sight. Doctors classify the disease by activity (whether it is inflamed and changing) and severity (how much it affects vision, alignment, eyelids, and appearance). In clinic, a simple 7-item score called the Clinical Activity Score (CAS) helps decide if the disease is “active.” A CAS of ≥3 on the 7-point checklist usually means active inflammation, and a CAS of ≥4 on the 10-point follow-up scale means the disease is still active. NCBIWebEye

Types

There are two main ways doctors describe types: by phase and by severity. Understanding both helps set realistic expectations and guides testing.

By phase

1. Active (inflammatory) phase: This is the early, “hot” phase. The immune system is actively inflaming the tissues. The eyes may change rapidly. Redness, swelling, and pain can be pronounced. Symptoms often get worse over several months and then stabilize. This phase usually lasts 6–18 months. Treatment in this phase focuses on calming inflammation and protecting the eye surface.

2. Inactive (fibrotic) phase: This is the later, “quiet” phase. Inflammation has settled, but the tissues may have healed with scarring and stiffening. Eye muscles can remain thick and tight, and the eye may still protrude. Symptoms change slowly. In this phase, surgery to adjust muscles, eyelids, or the orbit may be considered if function or appearance is still affected.

By severity (simple language overview of common clinical groupings)

1. Mild: Symptoms are bothersome but do not threaten sight. Typical features include mild redness, irritation, tearing, a gritty feeling, and slight eyelid retraction or very small proptosis. Daily activities are mostly unaffected.

2. Moderate-to-severe: There is clear eye prominence, eyelid retraction, and more than mild involvement of eye muscles. Double vision may interfere with reading, driving, or work. Eye surface exposure can be significant, and discomfort is frequent.

3. Sight-threatening: There is corneal breakdown from severe exposure or there is compressive optic neuropathy, which means the swollen tissues press on the optic nerve. Vision can drop, colors can look washed-out, and the visual field can shrink. This is an emergency because permanent vision loss can occur without prompt treatment.

Doctors may also mention older or more detailed systems, such as the NOSPECS classification, or they may score inflammation with a “Clinical Activity Score.” These systems help track change over time, but the plain-language groupings above usually make sense to most people.

Causes

Graves orbitopathy is driven by autoimmunity, but many things can trigger it, worsen it, or increase the chance of developing it. Below are 20 well-recognized contributors explained in simple terms.

1. Underlying Graves disease: Most patients have an overactive thyroid caused by Graves disease. The same antibodies that stimulate the thyroid can also react with tissues in the orbit.

2. TSH-receptor antibodies and related immune signals: The immune system makes antibodies that stimulate the thyroid and also interact with receptors in orbital fat and muscle cells, setting off inflammation and swelling.

3. Smoking: Smoking is the strongest lifestyle risk factor. Smokers are more likely to develop eye disease, and their disease tends to be more severe and less responsive to treatment.

4. Second-hand smoke: Even if a person does not smoke, regular exposure to smoke can worsen the risk and severity, likely by amplifying inflammation.

5. Radioactive iodine therapy in active smokers or uncontrolled disease: Radioactive iodine is a common and effective treatment for thyroid overactivity, but in some people—especially smokers or those with poorly controlled thyroid levels—it can trigger or worsen eye disease unless preventive measures are used.

6. Rapid changes in thyroid hormone levels: Big swings from high to low or low to high thyroid levels can “wake up” immune activity in the orbit.

7. Poorly controlled hyperthyroidism: When the thyroid stays overactive, inflammatory signals remain high, which can aggravate the eye condition.

8. Hypothyroidism after treatment: If treatment overshoots and thyroid levels become too low, this imbalance can also worsen orbital inflammation until levels are corrected.

9. Genetic tendency: Family history of autoimmune thyroid disease raises risk. Certain HLA types and other immune-related genes can make the immune system more likely to attack orbital tissues.

10. Female sex: Women are affected more often than men, probably because autoimmune conditions in general are more common in women.

11. Middle age: On average, Graves orbitopathy appears in mid-life, but it can occur at younger or older ages.

12. Stressful life events: Severe stress can modulate immunity and may act as a trigger in people who are already at risk.

13. Iodine excess: Very high iodine intake can change thyroid activity and may contribute to immune instability in susceptible individuals.

14. Selenium deficiency: Low selenium status may be linked to more active or persistent disease because selenium is important in antioxidant and thyroid enzyme systems.

15. Other autoimmune diseases: People with one autoimmune disease are at higher risk of developing another, including autoimmune thyroid conditions that can involve the eyes.

16. Orbital fibroblast sensitivity: Cells behind the eye (fibroblasts) in some people are unusually responsive to thyroid-related antibodies and growth factors, so they produce more swelling molecules and fat.

17. Environmental pollutants: Chronic exposure to certain pollutants or irritants can enhance inflammation and oxidative stress, which may worsen the eye condition.

18. Immune-modulating medicines: Rarely, drugs that alter the immune system (for example, some checkpoint inhibitors used in cancer therapy) can trigger thyroid autoimmunity and eye inflammation.

19. Upper respiratory infections: Infections can shift immune balance and, in predisposed people, may precipitate a flare by increasing inflammatory mediators.

20. Delay in thyroid stabilization: Waiting a long time before bringing thyroid hormone levels into a normal range allows the autoimmune process to keep stimulating the orbit.

Symptoms

Each symptom below is explained in plain language so it is easy to understand how it feels and why it happens.

1. Eye redness: The white of the eye looks red because small blood vessels are dilated by inflammation.

2. Grittiness or a sandy feeling: The front of the eye dries out because the eyelids do not close fully or blink smoothly, so the surface becomes rough.

3. Excess tearing: The eye waters more because it is irritated; paradoxically, watery eyes are a common sign of dryness.

4. Light sensitivity (photophobia): Bright light bothers the eye because the surface is inflamed and the tear film is unstable.

5. Eye pain or aching: Aching comes from swollen tissues and tight muscles in the orbit; the eye can hurt more with movement.

6. Pressure or fullness behind the eye: The orbit is a bony box. When tissues swell, people feel pressure because there is no room to expand.

7. Eyelid swelling (periorbital edema): The tissues of the eyelids hold extra fluid due to inflammation, so lids look puffy, especially in the morning.

8. Eyelid retraction: The upper eyelid rides higher and the lower lid sits lower because muscles are overactive or fibrotic, making more of the eye visible and causing a staring look.

9. Proptosis (eye prominence): The eye looks more forward because fat and muscles behind the eye have expanded.

10. Double vision (diplopia): The eyes do not move in perfect sync because some muscles are stiff and enlarged, so the brain receives two different images.

11. Difficulty looking in certain directions: Thick, tight muscles limit movement; for example, looking up may be hard if the inferior rectus is tight.

12. Blurred vision: Blurring can come from a dry corneal surface, unstable tears, or compressed optic nerve function.

13. Color desaturation: Colors, especially red, may look less vivid if the optic nerve is under pressure.

14. Headache around the eyes: Strain from eye misalignment and pressure in the orbit can cause a dull headache.

15. Decreased peripheral vision or dimming episodes: If the optic nerve is compromised, parts of the visual field may be reduced, or vision may seem dim at times. These are warning signs that need urgent evaluation.

Diagnostic tests

Below are 20 specific tests, grouped into five categories. Each entry describes what the test is, why it is done, and what it can show in Graves orbitopathy. The language is kept simple so it is easy to follow.

A) Physical exam

1. Overall ocular inspection and activity grading
   What it is: The clinician looks carefully at the eyes, eyelids, and surrounding tissues and may score inflammation with a standard scale.
   Why it is done: To see if the disease is “active” (red, swollen, tender) and to measure visible changes.
   What it shows: Redness, swelling, eyelid retraction, and chemosis (swollen conjunctiva). It helps decide whether anti-inflammatory treatment is needed now.

2. Ocular motility assessment in nine gaze positions
   What it is: The clinician asks the patient to look up, down, and to the sides while watching how each eye moves.
   Why it is done: To check for restricted muscles that could cause double vision.
   What it shows: Limited movement in the directions controlled by stiff, enlarged muscles, such as poor upgaze with an enlarged inferior rectus.

3. Visual acuity and color vision check
   What it is: Reading letters on a chart for sharpness and using color plates (like Ishihara) for color perception.
   Why it is done: To screen for optic nerve involvement and surface problems.
   What it shows: Any drop in clarity or color discrimination that might signal compressive optic neuropathy or severe dry eye effects.

4. Eyelid position and lagophthalmos evaluation
   What it is: Measuring how wide the eyelid opening is and seeing if the eyelids close completely when blinking or sleeping.
   Why it is done: Incomplete closure causes exposure of the cornea and raises the risk of damage.
   What it shows: Eyelid retraction and any gap on closure that needs urgent tear protection measures.

B) Manual tests

5. Hertel exophthalmometry
   What it is: A simple device with mirrors measures how far each eye protrudes relative to the bony rim.
   Why it is done: To quantify proptosis and compare sides over time.
   What it shows: An exact number in millimeters for eye prominence, helping track change and plan care.

6. Intraocular pressure (IOP) in primary gaze and upgaze
   What it is: Measuring eye pressure with a tonometer while looking straight and then looking up.
   Why it is done: Tight eye muscles can raise pressure in certain gaze positions.
   What it shows: A rise in IOP on upgaze suggests restrictive myopathy and helps explain discomfort and risk.

7. Fluorescein staining and tear breakup time
   What it is: A safe orange dye is placed in the eye to show dry spots, and the time until the tear film breaks up is measured.
   Why it is done: To assess dry eye and surface damage from exposure.
   What it shows: Areas of damaged surface and unstable tears, guiding lubrication and protection strategies.

8. Diplopia field (Hess chart or red-glass test)
   What it is: Simple charts or colored lenses map where double vision appears and how images are displaced.
   Why it is done: To document which muscles are tight and how double vision affects daily life.
   What it shows: A pattern of restriction that helps choose prisms or plan muscle surgery.

C) Lab and pathological tests

9. TSH (thyroid-stimulating hormone)
   What it is: A blood test that reflects how the brain is signaling the thyroid.
   Why it is done: To see if the thyroid is overactive, normal, or underactive.
   What it shows: Low TSH usually means hyperthyroidism; high TSH means hypothyroidism; both states can influence the eye disease.

10. Free T4
    What it is: A blood test measuring the free, active thyroxine hormone.
    Why it is done: To define how high or low the thyroid activity is.
    What it shows: Elevated free T4 supports hyperthyroidism; low levels suggest under-replacement or hypothyroidism.

11. Free T3
    What it is: A blood test for the active triiodothyronine hormone.
    Why it is done: Some people have T3-predominant hyperthyroidism.
    What it shows: High free T3 with low TSH reinforces the diagnosis and guides thyroid control.

12. TSH-receptor antibodies (TRAb) or thyroid-stimulating immunoglobulins (TSI)
    What it is: Blood tests for antibodies that drive Graves disease and interact with orbital tissues.
    Why it is done: Higher levels are linked to eye disease activity and risk of worsening.
    What it shows: Presence and level of these antibodies support the autoimmune cause and help with risk assessment.

13. Thyroid peroxidase antibodies (TPOAb)
    What it is: A blood test for another thyroid autoantibody.
    Why it is done: To profile autoimmunity because multiple antibodies may be present.
    What it shows: Confirms autoimmune thyroid involvement, which aligns with Graves orbitopathy.

14. Thyroglobulin antibodies (TgAb)
    What it is: A blood test for antibodies against thyroglobulin.
    Why it is done: To complete the autoimmune profile.
    What it shows: Adds evidence for autoimmune thyroid disease in complex cases.

D) Electrodiagnostic tests

15. Visual Evoked Potential (VEP)
    What it is: A test that measures the electrical response of the brain to a patterned visual stimulus.
    Why it is done: To objectively assess the function of the optic nerve when compression is suspected.
    What it shows: Delayed or reduced signals suggest impaired conduction in the optic nerve from pressure or inflammation.

16. Pattern Electroretinography (pERG)
    What it is: A test recording electrical signals from retinal ganglion cells in response to patterned light.
    Why it is done: To distinguish retinal issues from optic nerve problems and to assess early ganglion cell stress.
    What it shows: Abnormal pERG with a relatively preserved full-field ERG supports optic nerve involvement rather than primary retinal disease.

E) Imaging tests

17. Orbital CT scan
    What it is: A quick X-ray–based scan that shows detailed images of the bones and soft tissues of the orbit.
    Why it is done: To see muscle enlargement, fat expansion, and the tightness of the bony orbit.
    What it shows: Classic “muscle belly” enlargement with tendon sparing, crowding at the apex, and degree of proptosis. This helps confirm the diagnosis and assess optic nerve risk.

18. Orbital MRI with fat suppression and contrast
    What it is: A magnetic scan that shows soft tissues clearly and can highlight active inflammation.
    Why it is done: To judge how “active” the inflammation is and to differentiate muscle swelling from scarring.
    What it shows: Bright signal in inflamed muscles and fat, patterns of tissue edema, and any compression at the orbital apex.

19. Orbital ultrasonography (B-scan)
    What it is: An ultrasound test using sound waves to image the orbit.
    Why it is done: It is fast, safe, and useful to measure muscle thickness and detect fluid.
    What it shows: Enlarged extraocular muscles and characteristic reflectivity changes that track with disease state.

20. Optical Coherence Tomography (OCT) of the retinal nerve fiber layer and macula
    What it is: A light-based scan that measures the thickness of the layers in the back of the eye.
    Why it is done: To look for early damage to the optic nerve fibers and to assess macular health when vision is reduced.
    What it shows: Thinning of the nerve fiber layer over time suggests optic nerve stress or damage, guiding urgency and follow-up.

Non-pharmacological treatments (therapies & others)

1. Stop smoking completely: the single most effective lifestyle step; lowers risk of flares and improves treatment response. Mechanism: reduces oxidative stress and toxic effects on orbital tissues; reduces antibodies over time. FrontiersBOPSS :

2. Achieve and maintain euthyroidism (normal thyroid levels): stabilizes the immune drive; prevents swings that aggravate eyes. Mechanism: reduces TRAb stimulation at the orbit. PMC

3. Artificial tears (preservative-free) by day: soothes surface inflammation; protects the cornea by restoring moisture. Mechanism: replaces unstable tear film and dilutes inflammatory mediators. PMC

4. Lubricating gel/ointment at night: helps if lids don’t fully close; prevents painful morning dryness. Mechanism: thick barrier to reduce evaporation. PMC

5. Moisture chamber glasses or nighttime moisture shields: traps humidity around eyes; decreases tear evaporation.

6. Sunglasses and wind protection: lowers light sensitivity and environmental irritation; reduces reflex tearing/dryness.

7. Cool compresses during active flares: reduces surface redness and eyelid swelling by vasoconstriction.

8. Head-of-bed elevation (10–15 cm): improves venous outflow from the orbit overnight; less morning puffiness.

9. Temporary prism glasses: corrects double vision in a straight-ahead gaze without surgery; mechanism: optical fusion aid by bending light. PMC

10. Patching one eye when needed: simple way to stop double vision during flares or when tired.

11. Blink training & screen hygiene: scheduled breaks, full blinks, humidifier use; reduces evaporative dry eye.

12. Omega-3-rich diet (see diet section): improves tear film quality; anti-inflammatory effect on lids/tear glands.

13. Selenium (for mild, active TED) – see supplements: short course can improve quality of life and slow progression. PubMed

14. Treat lid margin disease (warm compresses/lid hygiene): helps meibomian oil flow; stabilizes tear film.

15. Protective taping at night if lash exposure occurs: prevents corneal drying and erosions.

16. Rigorous diabetes and lipid control: lowers microvascular stress in the orbit; may improve healing and lower risk of radiation retinopathy if radiotherapy is used. PMC

17. Counseling & support: appearance changes can affect mood and social function; mental health care improves adherence and outcomes.

18. Avoid irritants (smoke, dust, fans to the face): reduces reflex dryness and redness.

19. Careful RAI planning (when RAI is chosen for thyroid): use preventive steroids if you’re high-risk; correct hypothyroidism quickly afterward. BOPSS :PMC

20. Specialist multidisciplinary care (endocrinology + oculoplastics + orthoptics): coordinated plans reduce delays and overtreatment. PMC

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Drug treatments

Important: Doses below are typical study/guideline frameworks. Exact choice, timing, and safety checks must be individualized by your specialist.

1. Intravenous methylprednisolone (IVMP) — glucocorticoid

• Dose/Time: Common regimen is 0.5 g weekly × 6 weeks, then 0.25 g weekly × 6 weeks (total 4.5 g over 12 weeks). Higher single weekly doses or a second course can be used in selected cases.

• Purpose: First-line anti-inflammatory for active moderate-to-severe TED; rapidly lowers redness, swelling, and pain.

• Mechanism: Broad cytokine suppression; reduces immune-driven tissue edema.

• Side effects: Transient liver enzyme rises, blood sugar elevation, infection risk, mood/sleep changes; very high cumulative doses carry rare liver/cardiac risks—hence guideline caps and monitoring. PMCPubMed

2. Mycophenolate (sodium 0.72 g/day or mofetil 1 g/day) — add-on immunomodulator

• Dose/Time: Given daily for ~24 weeks with IVMP in many protocols.

• Purpose: First-line combination with IVMP (better response than IVMP alone).

• Mechanism: Inhibits lymphocyte purine synthesis; steroid-sparing.

• Side effects: GI upset, leukopenia, infection risk; contraception needed in childbearing potential. BOPSS :ScienceDirect

3. Teprotumumab (TEPEZZA, anti-IGF-1R mAb)

• Dose/Time: IV infusion q3 weeks, 8 doses (trial dosing: 10 mg/kg then 20 mg/kg).

• Purpose: Reduces proptosis, diplopia, and inflammation in active moderate-to-severe TED, especially with big eye bulge.

• Mechanism: Blocks IGF-1 receptor on orbital fibroblasts; interrupts autoantibody signaling.

• Side effects: Muscle cramps, hyperglycemia, hearing changes (tinnitus, hearing loss), dysgeusia, alopecia, fatigue—hearing effects require counseling and monitoring. AAOJwatchTepezza HCP

4. Tocilizumab (IL-6 receptor blocker)

• Dose/Time: IV 8 mg/kg monthly (varied), used second-line for steroid-resistant active TED.

• Purpose: Inactivates inflammation when steroids fail.

• Mechanism: Blocks IL-6 signaling that fuels orbital inflammation.

• Side effects: Infection risk, liver enzyme rise, lipid changes; TB/hepatitis screening needed. PubMedPMC

5. Rituximab (anti-CD20 B-cell depletion)

• Dose/Time: Protocols vary (e.g., 500 mg once, or 1000 mg ×2); mixed RCT results; considered second-line in selected patients.

• Purpose: Reduce relapses/inflammation in recent-onset active disease when steroids fail; not for DON risk situations.

• Mechanism: Depletes B cells that produce autoantibodies.

• Side effects: Infusion reactions, infections; rare delayed neutropenia. PMCSvedyn

6. Oral prednisone/prednisolone

• Dose/Time: Sometimes used with cyclosporine/azathioprine as second-line, or as prophylaxis around RAI in high-risk patients (e.g., 0.3–0.5 mg/kg/day tapered over ~3 months; lower-dose options exist).

• Purpose: Anti-inflammatory; RAI-flare prevention in at-risk patients.

• Mechanism: Broad immunosuppression.

• Side effects: Weight gain, hyperglycemia, mood, blood pressure, bone loss—minimize duration and use add-ons when possible. BOPSS :PMC

7. Cyclosporine

• Dose/Time: Second-line (often combined with oral steroids).

• Purpose: Steroid-sparing immunosuppression to reduce activity.

• Mechanism: T-cell calcineurin inhibition.

• Side effects: Kidney effects, tremor, hypertension, gum hyperplasia—requires drug-level monitoring. BOPSS :

8. Azathioprine

• Dose/Time: Second-line (usually with oral steroids).

• Purpose: Steroid-sparing effect during active disease.

• Mechanism: Purine analog that suppresses lymphocytes.

• Side effects: Bone-marrow suppression (TPMT testing helps), liver injury, infection risk. BOPSS :

9. IV “pulse” methylprednisolone for sight-threatening DON (urgent)

• Dose/Time: 500–1000 mg IV for 3 doses in the first week (often alternate days), with urgent decompression if no clear response.

• Purpose: Save vision by rapidly shrinking apical congestion.

• Mechanism: Powerful anti-edema effect around the optic nerve.

• Side effects: As above; hospital-level monitoring. BOPSS :

10. Orbital radiotherapy (adjunct)

• Dose/Time: Common schedules 20 Gy in 10 fractions over 2 weeks; usually combined with steroids in active, motility-dominant disease.

• Purpose: Improves double vision and motility in active inflammation; not a cosmetic therapy.

• Mechanism: Dampens radiosensitive lymphocytes/fibroblasts in extraocular muscles.

• Side effects: Rare retinopathy (care in diabetics), mild skin/tear effects; avoid in very young patients. Evidence is mixed historically, but modern series and guidelines support it in the right patients. PMCPubMed

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Dietary “molecular” supplements

(Always discuss with your physician; supplements can interact with medicines.)

1. Selenium: 100 mcg twice daily for 6 months in mild, active TED improved symptoms and slowed progression in an RCT; acts as an antioxidant (glutathione peroxidases) reducing oxidative stress in the orbit. PubMed

2. Omega-3 fatty acids (e.g., fish oil 1–2 g/day EPA+DHA): anti-inflammatory lipid mediators; supports meibomian oil quality and tear film.

3. Vitamin D (target sufficiency per labs): immune modulation and bone protection if using steroids.

4. Vitamin C (250–500 mg/day): antioxidant that supports collagen and surface healing.

5. Vitamin E (100–200 IU/day): antioxidant; avoid very high doses if on anticoagulants.

6. Zinc (as part of a balanced multinutrient): supports epithelial repair and immune balance.

7. Curcumin (turmeric extract) (standardized, with piperine unless contraindicated): NF-κB modulation; adjunct anti-inflammatory.

8. L-carnitine or acetyl-L-carnitine: mitochondrial support; small thyroid studies suggest symptom benefits in hyperthyroidism fatigue.

9. N-acetylcysteine (NAC) (600 mg/day): antioxidant precursor to glutathione; theoretical benefit for oxidative stress.

10. Mixed carotenoids (diet-first): surface antioxidant support.

Evidence strength varies; only selenium has RCT-level support in mild active TED. Use other supplements as supportive care, not as treatment replacements. PubMed

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Regenerative / stem-cell drugs

There are no approved “stem-cell drugs” for Graves orbitopathy. Some biologic agents modulate immunity and can be very effective (e.g., teprotumumab, tocilizumab, rituximab), but they are not “boosters”—they suppress or redirect the immune response and require specialist oversight. Below are research-or-specialist options; dosing strictly follows clinical protocols.

1. Teprotumumab (anti-IGF-1R) — effective for proptosis/diplopia in active TED; monitor for hearing changes and hyperglycemia. AAOTepezza HCP

2. Tocilizumab (anti-IL-6R) — useful in steroid-resistant active TED; monitor labs/infection risk. PubMed

3. Rituximab (anti-CD20) — mixed trials; selective second-line where expertise exists. PMC

4. Emerging anti-TSHR approaches / other biologics — experimental; clinical trials only. Nature

5. Low-dose radiotherapy as an immune modulator — not “regenerative,” but can calm motility-dominant active disease with steroids. PMC

6. Mesenchymal stem cell or “regenerative” therapies — experimental; not recommended outside trials for TED due to insufficient efficacy and safety data. (If interested, ask your team to check for registered clinical trials.)

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Surgeries

Most surgeries wait until disease is inactive for ~6 months; urgent exceptions exist for sight-threatening cases.

1. Orbital decompression: removes bone and/or fat to make more space in the socket, reducing eye bulge and pressure. Done early if optic nerve is threatened or later for appearance/comfort. Techniques include medial/lateral wall, floor, balanced, and endoscopic approaches. PMCNature

2. Strabismus (eye muscle) surgery: recesses tight muscles to re-align eyes and reduce double vision, after decompression when TED is inactive. PMC

3. Eyelid retraction repair: lengthens/relaxes retracted lids (levator or Müller’s muscle procedures) to protect the cornea and improve appearance—after the first two steps. PMC

4. Tarsorrhaphy (partial eyelid closure): temporary or permanent stitch to protect the cornea in severe exposure or neurotrophic risk; sometimes used during active disease to save the surface.

5. Urgent decompression for DON: when high-dose IV steroids do not quickly improve optic nerve function, decompression is done promptly to protect vision. BOPSS :

The usual sequence for rehabilitative surgery is decompression → strabismus → eyelids, because each step can change the next. PMCAmerican Thyroid Association

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Preventions

1. Don’t smoke; avoid secondhand smoke. Frontiers

2. Keep thyroid levels normal and stable (close follow-up when starting or changing therapy). PMC

3. If choosing radioiodine and you’re high-risk, use steroid prophylaxis and correct post-RAI hypothyroidism promptly. BOPSS :

4. Control diabetes, blood pressure, and lipids to support healing and lower radiation risks. PMC

5. Follow eye lubrication routines early to prevent corneal injury. PMC

6. Use sunglasses and moisture strategies in wind/sun/AC.

7. Sleep with head elevated to reduce morning swelling.

8. Manage stress and sleep (immune balance).

9. Vaccination and infection prevention if you’re on immunosuppressants (per doctor’s advice).

10. Regular multidisciplinary reviews to catch changes early. PMC

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When to see a doctor urgently

• Vision dims, colors look washed-out, or you have a new visual field “shadow.”

• New double vision that worsens quickly.

• Severe eye pain, corneal “scratchy” feeling that won’t settle, or inability to close the eye.

• Fast breathing/heart beats, mood changes, very high blood sugars when on steroids/biologics.

• Any hearing change (muffled hearing, tinnitus) or rising blood sugars if receiving teprotumumab—report promptly. Tepezza HCP

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Diet: what to eat” and what to avoid”

Eat (supportive, anti-inflammatory, eye-surface-friendly):

1. Fatty fish (salmon/sardine/mackerel) 2–3×/week for omega-3s.

2. Colorful vegetables & berries (antioxidants).

3. Nuts & seeds (walnut, flax, chia) for plant omega-3s.

4. Whole grains & legumes (steady energy; fiber to tame steroid-related appetite swings).

5. Lean proteins (eggs, poultry, tofu) for healing.

6. Hydration (plain water; helps tear film).

7. Olive-oil–based cooking (Mediterranean pattern).

8. Selenium-rich foods (Brazil nuts—use sparingly; seafood, eggs).

9. Yogurt/fermented foods (gut support during immunotherapy if approved by your doctor).

10. Vitamin D and calcium sources (bone health if on steroids).

Avoid/limit (practical):

1. Smoking and secondhand smoke (top harm). Frontiers

2. Very high-iodine spikes (e.g., kelp tablets) that can upset thyroid balance.

3. Excess sugar/refined carbs (worsens dry-eye inflammation and steroid hyperglycemia).

4. Excess alcohol (drying, blood pressure, liver stress with meds).

5. Ultra-processed, high-salt foods (fluid retention—puffier lids).

6. Energy drinks (sleep disturbance → eye irritation).

7. Large caffeine late-day (sleep quality).

8. High vitamin A supplements (dry the surface in excess).

9. Mega-doses of selenium (risk of toxicity; stick to evidence-based amounts). PubMed

10. Herbal stimulants without disclosure (interactions with steroids/biologics).

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FAQs

1) Can Graves eye disease get better on its own?
Yes. Many patients improve as inflammation settles over 6–24 months, but some changes persist as scarring. Early care lowers risks.

2) What’s the single best lifestyle step?
Quit smoking completely; it meaningfully lowers severity and improves treatment response. Frontiers

3) Why do my eyes look wider open?
Upper lid muscles are stimulated and shortened by inflammation and scarring, so lids retract.

4) Is double vision permanent?
Often it improves as activity cools or after muscle surgery/prisms. Some diplopia persists and is treated with surgery once disease is stable. PMC

5) What is “active” vs “inactive” disease?
Active means inflamed and changing (higher CAS); inactive means quiet and stable for months. Treatment choices depend on this. NCBI

6) Do I need teprotumumab?
It’s an effective option for active, moderate-to-severe TED with big proptosis/diplopia. Discuss benefits and risks, especially hearing and glucose monitoring. AAOTepezza HCP

7) Are steroids always IV?
IV pulse regimens are preferred in guidelines for efficacy and fewer side effects than long oral courses; exact plan is individualized. PMC

8) What about orbital radiotherapy?
It’s an adjunct—best when motility problems dominate in active disease, usually combined with steroids. Modern series typically use 20 Gy/10 fx. PMC

9) Will radioiodine make my eyes worse?
It can in at-risk patients. Steroid prophylaxis around RAI prevents most flares; quickly fixing post-RAI hypothyroidism helps too. BOPSS :

10) Can selenium help?
In mild, active TED, a 6-month selenium course improved quality of life and slowed progression in an RCT. It’s not a substitute for medical therapy in moderate-to-severe cases. PubMed

11) How are surgeries sequenced?
Decompression → strabismus → eyelids (to avoid one step undoing another). PMC

12) When is vision in danger?
With dysthyroid optic neuropathy (DON) or severe corneal exposure; this needs urgent high-dose IV steroids and often decompression. BOPSS :

13) Can rituximab or tocilizumab replace steroids?
They’re second-line for selected steroid-resistant cases and require specialist centers. PMC

14) How long does active disease last?
Commonly 6–24 months. Treatments aim to shorten the active period and reduce long-term changes.

15) Who should manage my care?
A combined team—endocrinologist, oculoplastic/orbital surgeon, orthoptist—gives the best results. PMCY

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: August 28, 2025.