Ocular Amyloidosis

Types of ocular amyloidosis
Causes
Common symptoms and signs
Diagnostic tests
Non-pharmacological treatments
Drug treatments
Dietary molecular supplements
Advanced / “regenerative or immune-related” therapies
Surgeries
Practical preventions
When to see a doctor urgently
What to eat & what to avoid
FAQs

Ocular amyloidosis means “amyloid” protein builds up in parts of the eye. Amyloid is a mis-folded protein that the body cannot clear well. Over time, the extra protein settles in tissues and forms firm deposits. These deposits are not normal. They can change how the eye looks and works. Where the deposits sit determines the symptoms. For example, deposits on the eyelid or conjunctiva may cause a visible lump or easy bruising. Deposits in the cornea can make the window of the eye cloudy. Deposits in the vitreous gel can create floaters and blur. Deposits in the drainage angle can raise eye pressure and lead to glaucoma. These patterns are well described in medical reviews of ocular amyloidosis. NCBI

Proteins are long chains that must fold into the right shape to work. In amyloidosis, some proteins fold the wrong way and stick together as rigid fibers. These fibers collect between cells. The body has trouble breaking them down, so they stay and grow. Under the microscope, doctors can stain these fibers with a dye called Congo red. When viewed with special polarized light, the amyloid shows a classic “apple-green” glow. This glow helps confirm the diagnosis. PMCNature

Types of ocular amyloidosis

Primary localized ocular amyloidosis.
The amyloid sits only in eye tissues (often the conjunctiva, eyelids, or orbit). There is no disease in the rest of the body. It can look like a yellow-pink lump, cause repeated small bleeds on the white of the eye, or make the eyelid heavy.
Ocular involvement from systemic AL amyloidosis (light-chain type).
Here, an abnormal group of bone-marrow cells makes too many light chains (parts of antibodies). These light chains form amyloid that can deposit in the eye and in many organs (heart, kidneys, nerves). Eye signs can be bruising around the lids, conjunctival lumps, or angle deposits that raise pressure.
Ocular involvement from systemic AA amyloidosis (inflammation-related).
Long-standing inflammatory diseases (for example, rheumatoid arthritis or chronic infections) can lead to amyloid made from a protein called serum amyloid A. The eye can be involved but less often than with AL.
Hereditary transthyretin amyloidosis (ATTR, inherited).
A change (mutation) in the TTR gene makes the transthyretin protein unstable. Abnormal transthyretin can form amyloid that settles in many organs and in the eye. A very important eye clue in hereditary amyloidosis is vitreous amyloidosis—dense floaters and “clouds” in the gel of the eye that slowly worsen. This finding is strongly linked to hereditary forms and should trigger genetic testing. PMC
Wild-type transthyretin amyloidosis (ATTRwt, age-related).
In older adults, normal transthyretin can slowly form amyloid. Systemic disease is more common than eye disease, but ocular signs can occur.
Gelsolin amyloidosis (AGel, “Finnish type”).
A change in the gelsolin gene leads to amyloid that often affects the cornea, causing a lattice-like haze that blurs vision over time. People may also have loose skin and nerve problems. PMCBioMed Central
Corneal stromal amyloid dystrophies (for example, lattice corneal dystrophy).
In these inherited corneal conditions, amyloid collects in the cornea and gradually makes it cloudy. Vision declines slowly and may need corneal surgery in advanced stages. NCBI
Other rare hereditary or localized amyloid forms.
Less common genes (for example, lysozyme or apolipoprotein variants) and long-standing local irritation can rarely lead to amyloid in eye tissues. Doctors confirm the exact protein type with special tests on biopsy tissue (see “Lab and Pathological tests”).

Causes

Think of “cause” here as the underlying reason the abnormal protein forms or deposits in the eye. Some causes are diseases of the whole body (systemic). Some are inherited. Some are local to the eye.

Primary localized conjunctival amyloid—unknown trigger, limited to the eye surface tissue.
Primary localized eyelid amyloid—deposits inside the lid or lid margin.
Primary localized orbital amyloid—deposits inside the eye socket tissues.
Systemic AL amyloidosis from a plasma-cell disorder (too many light chains made in bone marrow).
Systemic AA amyloidosis from long-term inflammation (for example, rheumatoid arthritis, chronic infections).
Hereditary transthyretin (ATTRv) amyloidosis—a TTR gene mutation passed in families. PMC
Wild-type transthyretin (ATTRwt) amyloidosis—age-related misfolding of normal TTR.
Gelsolin amyloidosis (AGel)—inherited gelsolin gene variant causing corneal lattice changes and other signs. PMCBioMed Central
Lattice corneal dystrophy type I (TGFBI-related)—inherited corneal amyloid disorder. NCBI
Lattice corneal dystrophy type II (gelsolin-related)—inherited corneal amyloid with systemic features. IOVS
Chronic eye surface irritation (for example, trichiasis, long-standing inflammation) that triggers local amyloid in the conjunctiva. canadianjournalofophthalmology.ca
Long-standing glaucoma or angle disease with secondary amyloid in the drainage tissues (less common). NCBI
Old vitreous hemorrhage or inflammation that promotes vitreous protein clumping and secondary amyloid changes (rare).
Long-standing eyelid or conjunctival tumors that undergo localized amyloid change (rare).
Previous eye surgery or trauma with chronic tissue damage and secondary local amyloid (rare).
Chronic systemic infections (for example, tuberculosis, osteomyelitis) driving AA amyloid that can involve the eye.
Autoimmune diseases (for example, rheumatoid arthritis, inflammatory bowel disease) causing AA amyloid with possible ocular deposits.
Chronic kidney failure on long-term dialysis (β2-microglobulin amyloid) with very rare ocular involvement.
Lysozyme or apolipoprotein AI hereditary amyloidosis with occasional eye signs.
Mixed or untyped amyloidosis where the protein type is unknown until specialized testing is done (see below). In modern care, mass-spectrometry typing on biopsy is used to identify the exact amyloid protein. PMC

Common symptoms and signs

A painless, rubbery, or yellow-pink lump on the white of the eye (conjunctiva). The lump can slowly grow and sometimes bleeds.
Red eye that comes and goes. Small blood vessels may break easily over the deposit.
Eyelid heaviness or droopy lid (ptosis). Amyloid makes the lid heavier or affects the muscles.
Easy bruising around the eye. The skin can bruise with small touches because vessels are fragile.
Foreign-body sensation. It can feel like a grain of sand is in the eye, especially if the cornea is involved.
Tearing or dry-eye feeling. Surface deposits can change the tear film.
Light sensitivity (photophobia). A cloudy cornea or irritated surface scatters light.
Blurry vision that changes through the day. Corneal or vitreous deposits scatter light and reduce clarity.
Floaters (spots, clouds, “cobwebs”). Vitreous amyloid causes dense floaters that may slowly worsen; this is a red flag for hereditary amyloidosis. PMCRetina Specialist
Glare and halos at night. Cloudy media (cornea or vitreous) cause scatter.
Eye pain or pressure with headaches. This can happen if eye pressure rises from angle deposits (glaucoma). Rare Disease Advisor
Double vision (diplopia) or restricted eye movements. Deposits in eye muscles or the orbit can limit motion. NCBI
Bulging eye (proptosis). An orbital mass of amyloid can push the eye forward. NCBI
Color-vision changes or dimmer vision. If the retina or optic nerve is stressed, colors may fade.
Slow, painless loss of vision over months to years. This happens when deposits grow and the cornea or vitreous becomes more opaque.

Diagnostic tests

Doctors choose tests based on where they think the amyloid sits (lid, surface, cornea, angle, vitreous, retina, or orbit) and whether the disease might be only in the eye or part of a whole-body condition. Below are grouped tests with clear purposes.

A) Physical examination

External eye and eyelid inspection.
The doctor looks closely at the eyelids, skin, and white of the eye. They check for lumps, color changes, easy bruising, and swelling. They note the size, shape, and location of any mass. They also see if both eyes are involved. This first look guides all other testing. Findings like conjunctival masses, lid malposition, or proptosis are classic in ocular amyloidosis. NCBI
Palpation of lids and orbit.
The doctor gently feels the eyelids and the bony eye socket. A firm, rubbery, non-tender mass raises concern for amyloid. They feel for tenderness, softness, or hard areas that suggest other diagnoses.
Visual acuity and color vision.
A simple eye-chart test measures sharpness of sight. Color plates check for color loss. These numbers help track change over time and show how much the deposits are affecting vision.
Pupil and visual-field screening.
Pupil reactions show if the optic nerve is stressed. Quick confrontation field testing screens for missing areas of vision. If fields are abnormal, more detailed testing follows.

B) Manual/office ophthalmic tests

Slit-lamp biomicroscopy.
This is a microscope with a light beam. The doctor inspects the cornea, conjunctiva, and anterior chamber in detail. In amyloidosis, they may see yellow-pink deposits on the conjunctiva, glassy lines or lattice in the cornea, or tiny flakes in the front chamber. The slit lamp is the core tool to map where deposits sit.
Fluorescein staining of the cornea.
A safe orange dye highlights dry spots and surface damage. In amyloidosis, irregular corneal surfaces may pick up dye, explaining pain or light sensitivity.
Intraocular pressure measurement (tonometry).
A small puff or a blue-light tip measures eye pressure. If amyloid blocks the drainage angle, pressure can rise, which risks glaucoma. This test is repeated over time to protect the nerve. Rare Disease Advisor
Gonioscopy (angle exam).
A mirrored contact lens lets the doctor see the drainage angle. They look for abnormal material, scarring, or narrow angles. In amyloidosis, tiny deposits may sit in the trabecular meshwork and slow fluid outflow.
Schirmer test and tear film assessment.
Small paper strips in the lower eyelid measure tear production. If surface deposits or lid changes disturb normal blinking or tear spread, this helps explain irritation and dryness.
Exophthalmometry and motility testing.
A small ruler (Hertel exophthalmometer) measures how far the eye protrudes. Eye movement tests check for muscle restrictions. In orbital amyloid, the eye may bulge and movements may be limited. NCBI

C) Lab and pathological tests

Conjunctival or eyelid biopsy with Congo red staining.
A tiny piece of the lesion is removed under local anesthesia. In the lab, tissue is stained with Congo red and viewed under polarized light. The classic “apple-green” glow confirms amyloid. This is the key diagnostic step when a mass is present. PMCNature
Amyloid protein typing by mass spectrometry.
After confirming amyloid, the lab can use laser microdissection and mass spectrometry to identify the exact protein (for example, AL, AA, TTR, gelsolin). Correct typing guides treatment and genetic counseling. PMC
Immunohistochemistry (IHC) panel.
Antibody stains can suggest the amyloid type (for example, light-chain markers or TTR), but IHC can be misleading; mass spectrometry is often more accurate for final typing. PMC
Serum and urine protein electrophoresis with immunofixation (SPEP/UPEP) and free light chains.
These blood and urine tests look for abnormal monoclonal proteins that cause AL amyloidosis. If positive, a hematology evaluation is needed.
Genetic testing for TTR and other amyloid genes (for example, gelsolin).
If vitreous amyloid or corneal lattice is present—especially with a family history—genetic testing confirms a hereditary form and directs family screening. Verywell HealthBioMed Central
Systemic screening labs (kidney, liver, inflammation markers).
Basic blood and urine tests check for organ involvement (for example, protein in urine, abnormal creatinine, elevated inflammatory markers) when systemic disease is suspected.

D) Electrodiagnostic tests

Electroretinography (ERG).
Small contact lenses and lights measure how the retina responds. If dense vitreous amyloid blocks light or if the retina is affected, ERG can show reduced responses.
Visual evoked potentials (VEP).
Electrodes on the scalp measure how fast and how strong visual signals reach the brain. If high pressure or optic-nerve stress exists, the signal may slow or weaken.
Electro-oculography (EOG).
This test measures the eye’s standing potential during light and dark changes. It helps evaluate the retinal pigment epithelium if deposits or chronic stress affect it.

E) Imaging tests

Anterior-segment optical coherence tomography (AS-OCT).
This painless scan uses light waves to make detailed cross-sections of the cornea and angle. It shows where amyloid sits in the cornea and whether it changes the drainage angle.
Macular and optic-nerve OCT.
These scans check the retina and nerve for swelling or thinning, which may occur if pressure is high or if deposits disturb retinal layers.
Ultrasound biomicroscopy (UBM) and B-scan ultrasound.
UBM gives high-detail images of the front of the eye; B-scan looks through cloudy media to map vitreous opacities and any mass in the back of the eye. In vitreous amyloidosis, B-scan can show dense clumps and strands. Retina Specialist
Orbit CT or MRI.
These scans map a deep mass behind the eye, show if muscles or fat are involved, and help plan surgery or biopsy. They also separate amyloid from tumors or vascular lesions.
Fluorescein angiography (FA) or indocyanine green angiography (ICGA).
If the retina or choroid is involved, dye studies can show leakage, blocked vessels, or abnormal staining. Photos document the pattern and help follow change.

Non-pharmacological treatments

These options do not dissolve amyloid, but they reduce symptoms, protect the eye, or delay complications. Your ophthalmologist will tailor them to you.

Watchful waiting with scheduled reviews – Small, quiet deposits that are not causing problems can be observed; this avoids overtreatment and lets the doctor act if growth, bleeding, pressure rise, or symptoms appear. Purpose: safety first. Mechanism: none—monitoring. Wiley Online Library
Eye protection & “no-rub” rule – Use protective glasses and avoid rubbing to cut down micro-trauma and bleeding from fragile amyloid-laden vessels in the conjunctiva. Mechanism: reduces mechanical trigger of hemorrhage. EyeWiki
Cold compresses during bleeds – Short periods of cool compresses can shrink superficial vessels and slow subconjunctival bleeding. Mechanism: vasoconstriction; edema control. (Supportive measure; clinical common sense in hemorrhagic conditions.)
Humidification and blink hygiene – A room humidifier, deliberate blinking, and screen breaks stabilize the tear film, easing irritation when deposits roughen the surface. Mechanism: reduces tear evaporation and shear stress.
Scleral or large-diameter contact lenses (when cornea is involved) – These vault the cornea with a liquid reservoir, masking surface irregularities and improving comfort/vision. Mechanism: creates a smooth optical surface. (Specialist fitting.)
Low-vision rehabilitation – Magnifiers, contrast tools, task lighting, and training maximize remaining vision if vitreous haze or glaucoma has limited acuity/fields. Mechanism: improves function despite disease.
Head elevation for eyelid edema – Sleeping with the head slightly elevated can reduce morning lid swelling that sometimes worsens ptosis. Mechanism: gravity-aided fluid shift.
Manage blood thinners with your medical team – If you’re on anticoagulants/antiplatelets, your doctors may optimize dosing around procedures to reduce conjunctival bleeding risk (never stop on your own). Mechanism: lowers bleed tendency in fragile tissues. PMC
Eyelid hygiene & warm compresses (if meibomian gland dysfunction) – Keeps the ocular surface healthier and reduces irritation around deposits. Mechanism: thins oil; stabilizes tear film.
Treat systemic amyloidosis aggressively (team care) – Timely systemic therapy (e.g., for AL or ATTR) can reduce ongoing seeding of amyloid; note that ocular TTR can persist because the eye makes its own TTR. Mechanism: reduces circulating precursors; eye may need independent care. PMC+1
Genetic counseling (for hereditary ATTR) – Helps families understand inheritance, testing, and early eye checks. Mechanism: earlier detection → earlier care. PMC
Blood pressure, glucose, and lipid control – Stable vascular health reduces hemorrhage and ischemic risks in fragile ocular tissues. Mechanism: protects micro-vasculature.
Smoking cessation – Improves vascular and ocular surface health; reduces surgical risks. Mechanism: better perfusion, less oxidative stress.
Protective shields after surgery – Night shields help avoid friction or trauma to healing conjunctiva/eyelids. Mechanism: mechanical protection.
Moisture chamber goggles at night – For exposure or severe dryness (e.g., from ptosis), keeps cornea bathed, easing irritation. Mechanism: reduces evaporation.
Nutritional adequacy (not megadoses) – Balanced diet with leafy greens, fish, nuts, and citrus supports ocular surface and general health; does not remove amyloid. Mechanism: antioxidant/anti-inflammatory support.
Activity modification – For people with frequent bleeds, avoid high-impact activities that jar the head/face until stabilized. Mechanism: less shear on conjunctival vessels.
Plan surgeries with experienced oculoplastic/retina/glaucoma teams – Tissue with amyloid is friable; specialists reduce complications (e.g., conjunctival buttonholes during glaucoma surgery). Mechanism: technique expertise. AAO Journal
Written action plan – Know who to call for sudden vision loss, severe pain, or big bleeds. Mechanism: faster care → better outcomes.
Regular pressure checks – Amyloid can raise IOP and cause difficult glaucoma; scheduled checks catch pressure spikes early. Mechanism: early glaucoma control. PMC

Drug treatments

Important safety note: Doses below are typical references—your clinician will individualize based on diagnosis (localized vs systemic, AL vs ATTR), other diseases, and your eye exam. Some drugs treat the body-wide disease, not the eye directly; ocular disease may still need local procedures.

Tafamidis (TTR stabilizer; oral) – 61 mg once daily (Vyndamax) or tafamidis meglumine 80 mg/day (Vyndaqel). Purpose: slows ATTR cardiomyopathy; may help overall amyloid burden. Mechanism: stabilizes TTR tetramers, reducing misfolding. Side effects: generally mild (GI symptoms), expensive; doesn’t reliably stop ocular TTR because the eye makes its own TTR. FDA Access Data+1PMC
Patisiran (siRNA; IV) – 0.3 mg/kg every 3 weeks (30 mg fixed if ≥100 kg). Purpose: treats hATTR polyneuropathy (and has cardiomyopathy data); lowers circulating TTR. Mechanism: gene-silencing in the liver. Side effects: infusion reactions; vitamin A monitoring. Caveat: limited effect on ocular TTR synthesis. FDA Access DataDrugs.comPMC
Inotersen (antisense oligonucleotide; SC) – 284 mg weekly. Purpose: hATTR polyneuropathy. Mechanism: TTR mRNA knock-down (liver). Side effects: thrombocytopenia and glomerulonephritis risks—requires regular labs. FDA Access DataNCBI
Vutrisiran (siRNA; SC) – 25 mg every 3 months. Purpose: hATTR polyneuropathy (and expanding cardiomyopathy label). Mechanism: hepatic TTR reduction ~80% at steady state. Side effects: low vitamin A—RDA-level vitamin A supplementation and eye checks for night blindness are recommended. FDA Access Data+1
IOP-lowering eye drops (for amyloid-related secondary glaucoma):
- Timolol 0.25–0.5% BID; latanoprost 0.005% at night; dorzolamide 2% TID; brimonidine 0.2% TID (used singly or in combo). Purpose: lower pressure. Mechanism: reduce aqueous production / increase outflow. Side effects: vary (e.g., asthma worsening with β-blockers; redness with PGAs). Note: glaucoma may be refractory; surgery often needed. PubMedEyeWiki
Short courses of topical corticosteroid (e.g., loteprednol/prednisolone—dose per clinician) for inflamed surface around deposits. Purpose: reduce irritation/chemosis. Mechanism: anti-inflammatory. Side effects: IOP rise, cataract with overuse—doctor monitoring essential. (Supportive ophthalmic practice.)
Lubricating eye drops/gels (non-prescription; dose to comfort). Purpose: soothe roughened ocular surface. Mechanism: tear supplementation/barrier. Side effects: minimal (choose preservative-free if frequent). Note: symptom control, not amyloid removal. PMC
Chemotherapy for AL amyloidosis (systemic; hematology-led) – Common first-line: daratumumab + cyclophosphamide + bortezomib + dexamethasone (Dara-CyBorD); alternatives include bortezomib-based regimens and high-dose melphalan with autologous stem cell transplant for selected patients. Purpose: stop light-chain production, reducing new amyloid. Mechanism: targets plasma cells. Side effects: infusion reactions, neuropathy, cytopenias; transplant-specific risks. Wikipedia
Doxycycline ± tauroursodeoxycholic acid (TUDCA) (off-label, systemic) – Studied as amyloid fibril disruptors; mixed clinical results (signal in small studies; negative in more recent ATTRwt trial). Typical research doses: doxycycline 100 mg BID; TUDCA 250–500 mg TID (trial protocols vary). Purpose/mechanism: potential fibril destabilization/proteostasis support. Side effects: GI upset, photosensitivity (doxy); diarrhea (TUDCA). Not standard of care. PubMedCirculation ResearchVJHemOnc
Peri-operative antibiotics / hemostatic support (as needed) – Around eye surgery, your team may choose antibiotics or adjust anticoagulation to reduce infection/bleeding risk. Purpose: safer surgery. Mechanism: prophylaxis and hemostasis. (Standard surgical care.)

Dietary molecular supplements

Supplements do not dissolve amyloid. They may support ocular surface comfort, antioxidant balance, or nerve health. Always clear supplements with your doctors, especially if you’re on chemo or anticoagulants.

AREDS2-style antioxidant mix (per day: lutein 10 mg + zeaxanthin 2 mg, vitamin C 500 mg, vitamin E 400 IU, zinc 80 mg as zinc oxide + copper 2 mg) – Function: antioxidant network; Mechanism: quenches free radicals in ocular tissues.
Omega-3 (EPA+DHA 1–2 g/day) – Function: tear film and anti-inflammatory support; Mechanism: resolvin pathways, meibum quality.
Vitamin A at RDA (700–900 µg RAE/day) unless your doctor advises otherwise – Function: photoreceptor and ocular surface health. Mechanism: retinoid cycle. Caution: If you’re on liver-targeted TTR gene silencing (e.g., vutrisiran), vitamin A levels fall—supplement at RDA only and report night blindness. FDA Access Data
Curcumin (turmeric extract 500–1000 mg/day standardized) – Function: general anti-inflammatory/antioxidant. Mechanism: NF-κB modulation; Caution: interacts with anticoagulants.
Coenzyme Q10 (100–200 mg/day) – Function: mitochondrial support; Mechanism: electron transport antioxidant.
Alpha-lipoic acid (300–600 mg/day) – Function: antioxidant; Mechanism: redox cycling; note glucose-lowering effect (monitor diabetes meds).
Vitamin B-complex (B1/B6/B12 at RDA) – Function: nerve health; Mechanism: cofactor support.
Magnesium (200–400 mg/day, citrate/glycinate) – Function: neuromuscular comfort; Mechanism: enzymatic cofactor.
Taurine (500–1000 mg/day) – Function: retinal support; Mechanism: osmolyte/antioxidant; caution if on certain cardiac meds.
TUDCA (if approved by your physician, 250–500 mg TID used in studies) – Function: chemical chaperone; Mechanism: helps protein folding/ER stress. Evidence is mixed; not a standard amyloidosis therapy. PubMed

Advanced / “regenerative or immune-related” therapies

There are no proven “immunity booster drugs” for ocular amyloidosis. Below are advanced, systemic or procedural strategies used in selected amyloidosis patients; they are not eye-specific cures but can reduce disease drivers.

Autologous hematopoietic stem cell transplant (ASCT) – What it is: collect your stem cells, give high-dose melphalan, then re-infuse your stem cells. Function: deep, durable control of AL amyloidosis by wiping out faulty plasma cells. Mechanism: myeloablation + rescue. Notes: selection is strict (cardiac status, organ function); transplant has risks; coordinate with an experienced center. ASC PublicationsASH Publications
High-dose melphalan (conditioning for ASCT; or as therapy) – Typical dose: 200 mg/m² in fit patients (lower in frail). Function/Mechanism: alkylates rapidly dividing plasma cells → halts light-chain production. Cautions: cytopenias, mucositis, infection risk. (Hematology-led.) ScienceDirect
G-CSF (filgrastim) ± plerixafor for stem-cell mobilization – Dose: per transplant protocol. Function: move stem cells into blood for collection. Mechanism: CXCR4/SDF-1 axis modulation. (Supportive to ASCT.)
CRISPR-based TTR gene editing (NTLA-2001; investigational) – What it is: one-time IV gene editing targeting liver TTR to dramatically lower serum TTR. Function/Mechanism: cuts TTR gene in hepatocytes → reduces TTR output; early trials show large TTR reductions and acceptable safety. Status: Phase 1/2 data positive; ongoing development. Caveat: ocular TTR is locally produced, so eye disease may still progress and require eye-focused care. PMC+1
Daratumumab (anti-CD38 monoclonal antibody) as part of AL regimens – Dose: per protocol (e.g., SC 1,800 mg on schedule). Function: depletes plasma cells; deep hematologic responses. Mechanism: antibody-dependent cellular cytotoxicity. Note: infection prophylaxis may be needed. Wikipedia
Vitamin A supplementation (RDA only) during liver-targeted siRNA therapy – Function: prevents deficiency (night blindness) when TTR falls. Mechanism: replaces reduced retinol transport bound to TTR. Dose: RDA, not megadoses. Eye tip: report night vision problems promptly. FDA Access Data

Surgeries

Excisional biopsy / surgical debulking of conjunctival or eyelid deposits (often with cryotherapy to the bed)
Why: relieve foreign-body sensation, reduce mass effect/bleeding, and confirm diagnosis. Procedure: remove circumscribed lesions; diffuse disease may need partial debulking; some teams add liquid nitrogen cryotherapy to reduce recurrence. Notes: recurrence can occur, so long-term follow-up is normal. PMC+1
Ptosis surgery (levator advancement/Müller’s resection)
Why: amyloid in the levator complex can weigh down the lid; surgery restores the opening. Procedure: tighten or reattach the lifting muscles/tendons. Outcome: improved field and comfort. PMC
Dacryocystorhinostomy (DCR) if the nasolacrimal duct is blocked by amyloid
Why: treat constant tearing/infections when amyloid narrows the tear duct. Procedure: make a new bypass channel from lacrimal sac into the nose (external or endoscopic). Evidence: rare but reported cases of lacrimal sac amyloidosis managed surgically. PMCPubMed
Glaucoma surgery (trabeculectomy or tube shunt) for amyloid-related secondary glaucoma
Why: pressure often resists drops; surgery protects the optic nerve. Notes: conjunctiva can be fragile; buttonholes/leaks may complicate filtration; multiple or staged procedures may be required. AAO JournalPubMed
Pars plana vitrectomy (PPV) for vitreous amyloidosis
Why: when cloudy vitreous severely blurs vision. Procedure: remove the cloudy gel; visual recovery is often excellent; recurrence/re-opacification can occur and glaucoma risk needs long-term follow-up. NaturePubMed

Practical preventions

Keep regular eye appointments (pressure checks, dilated exam).
Avoid eye rubbing/trauma; use protective eyewear for activities.
Follow glaucoma treatment closely—this is a key vision saver. PMC
Control BP, blood sugar, and lipids to protect fragile ocular vessels.
If on blood thinners, coordinate timing around procedures to limit bleeding (never adjust on your own).
Treat systemic amyloidosis early—reducing the production of amyloid precursors matters, even if ocular TTR can persist. PMC
Don’t smoke; keep weight and sleep healthy.
Use humidifiers and frequent blinking to protect the surface.
Carry a care plan for sudden vision changes or big bleeds.
Family screening/genetic counseling when ATTR is suspected. PMC

When to see a doctor urgently

Sudden vision loss, big new floaters, or flashes of light (retina risk).
Eye pain with redness and blurred vision (possible high IOP or inflammation).
New or worsening ptosis, double vision, or a growing mass on the eye surface.
Recurrent or severe subconjunctival hemorrhages.
Night blindness or very dry eye symptoms if you’re on TTR gene-silencing therapy (vitamin A review needed). FDA Access Data

What to eat & what to avoid

Diet won’t remove amyloid, but it supports eye surface and vascular health. Use RDA-level vitamins unless your clinician says otherwise.

Eat more of:

Leafy greens (lutein/zeaxanthin).
Oily fish (EPA/DHA) 2–3×/week.
Citrus/berries (vitamin C).
Nuts/seeds (vitamin E, healthy fats).
Orange/yellow veg (vitamin A precursors).

Limit/avoid:

Excess salt (edema/BP).
Ultra-processed foods and trans fats (vascular inflammation).
Smoking & heavy alcohol (vascular and nerve harm).
Megadoses of vitamin A (especially if on siRNA/ASO therapy—use RDA only and report night-vision issues). FDA Access Data
Supplements that interact with your chemo/anticoagulants (always cross-check with your clinicians).

FAQs

Is ocular amyloidosis cancer or infection?
No. It’s abnormal protein deposits, not cancer and not infection. Biopsy confirms it. PMC
Can it be only in the eye?
Yes. Some people have localized conjunctival/eyelid/orbital amyloidosis with no systemic disease—but a systemic work-up is still important. PMC
What symptoms should I expect?
Droopy lids, “salmon” patches, recurrent red eye, tearing from blocked ducts, floaters/blur, or high eye pressure are common patterns. EyeWiki
Will eye drops cure it?
No drop dissolves amyloid. Drops help comfort and pressure, but deposits usually need observation, procedures, or surgery if bothersome. EyeWiki
Does vitrectomy fix cloudy vitreous?
Often yes—vision usually improves a lot, though recurrence can happen and glaucoma demands long follow-up. PubMed
Why is glaucoma harder to treat in this condition?
Amyloid can clog or stiffen the drainage angle; pressure may stay high despite drops, so surgery (trabeculectomy or tube) is frequently needed. PubMed
Will tafamidis or patisiran fix my eye?
They help the body by lowering/stabilizing liver-made TTR, but the eye makes its own TTR, so ocular disease can continue; local eye care is still needed. PMC
What about doxycycline/TUDCA?
Research is mixed: early small studies suggested benefit; newer data in ATTRwt were negative. These are not standard of care for eye disease. PubMedVJHemOnc
Is there gene editing for this?
Yes, under study. A CRISPR-Cas9 therapy (NTLA-2001) lowered blood TTR in early trials. It’s not routine, and eye disease may still need local treatment. PMC
Do lesions come back after removal?
They can. Recurrence after excision/debulking or after PPV for vitreous amyloid has been reported; hence long-term follow-up. Lippincott JournalsScienceDirect
Could my tear duct be blocked by amyloid?
Rarely yes; surgeons may do a DCR to bypass the blockage. PMC
Is radiotherapy used?
Occasionally in diffuse orbital disease when surgery is not feasible, but debulking is the mainstay; decisions are case-by-case. ScienceDirect
If I have AL amyloidosis, will treating the plasma cells help my eyes?
Treating AL (Dara-CyBorD, ASCT in selected patients) reduces new amyloid production and may help stabilize disease, but local eye issues still need eye-specific care. Wikipedia
Can diet or vitamins clear amyloid?
No. Diet supports general and ocular surface health only. Stick to RDA-level vitamins unless your doctor says otherwise (and mind vitamin A with TTR-silencing). FDA Access Data
What’s the outlook?
For localized eye disease, outlook is often good with proper care, though recurrence is possible. For systemic disease, outcome depends on the underlying type and organ involvement, plus how well modern therapies work for you. Regular eye and medical follow-up are key. PMC

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