Primary Localized Conjunctival Amyloidosis (PLCA)

Primary localized conjunctival amyloidosis means abnormal protein material called amyloid slowly builds up only in the thin pink tissue that lines the eyelids and covers the white of the eye (the conjunctiva). “Primary” means the amyloid forms without a different disease driving it. “Localized” means the problem is limited to one place—in this case, the eye’s surface—rather than spreading through the whole body. The deposits can look yellow, pink, or “salmon-colored,” sometimes with a waxy, firm feel. Many people notice a lump on the inner side of the eyelid or in the upper fold, and some people get repeated bright-red subconjunctival bleeds because fragile tiny vessels in the conjunctiva break more easily when amyloid sits in the vessel wall. The condition is rare and often appears in adults, but it has been reported at many ages. Doctors can suspect it from the look and feel of the lesion, but the only sure way to diagnose it is a biopsy of the conjunctiva that shows amyloid on special stains. EyeWiki+1NCBI

In medical terms, amyloid is made of misfolded proteins that stack into rigid fibrils. These fibrils settle outside cells, disturb normal tissue structure, and can make blood vessels fragile. Under the microscope, the classic test is Congo red staining with apple-green birefringence when the pathologist looks through polarized light. These are the hallmark features that confirm amyloid. EyeWiki

In the conjunctiva, local immune cells can produce bits of antibody “light chains.” In a tiny fraction of people, these light chains misfold and stick together in the conjunctival tissue. Over time, the sticky fibers build up like grout between the normal tissue “bricks.” The deposit can press on tiny vessels, seep into vessel walls, and weaken them, which is why recurrent surface bleeding is a frequent clue. Because this process starts locally, most patients do not have a body-wide amyloidosis, but doctors still check for systemic disease to be safe. BioMed CentralPubMed

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Types

1. By extent
   • Nodular (focal): one or a few firm bumps.
   • Diffuse (sheet-like): a smoother, broader, waxy “salmon-pink” plaque.
   Diffuse deposits are common on the upper tarsal conjunctiva and superior fornix. EyeWiki

2. By location
   • Palpebral (tarsal) conjunctiva under the eyelids—often upper lids and folds.
   • Bulbar conjunctiva on the white of the eye.
   • Less commonly, caruncle/plica, and nearby adnexal tissues. EyeWiki+1

3. By clinical behavior
   • Hemorrhagic-predominant (repeated subconjunctival bleeds).
   • Mass-predominant (lump, thickening, “waxy” look).
   • Ptosis-dominant (droopy lid from weight and infiltration). EyeWikiNCBI

4. By protein type (pathology)
   Most localized conjunctival cases are AL (light-chain) amyloid produced locally; AA is far less likely in this setting. BioMed Central

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Causes and contributors

For PLCA the exact cause is often unknown. Many patients have no body-wide disease and no single trigger. Research and case reports suggest several possible mechanisms and associations. Below are 20 items explained in clear terms. Items 1–6 have the strongest support; items 7–20 are associations or plausible contributors reported in the literature or used in clinical reasoning.

1. Local plasma-cell light-chain production (AL type). A small group of immune cells in the conjunctiva may make excess light chains that deposit nearby as amyloid. This is the leading explanation for truly localized eye disease. PubMed

2. Localized disease without systemic involvement. Even with sensitive mass spectrometry and full work-ups, many conjunctival cases remain purely local. PubMed

3. Fragile conjunctival vessels from amyloid itself. The deposit infiltrates vessel walls and makes them prone to bleeding; this explains repeated subconjunctival hemorrhage as an early sign. PubMed Central

4. Middle-age tissue vulnerability. Many patients present in mid-life, suggesting age-related tissue changes may make local deposition more likely. EyeWiki

5. Infrequent link to systemic AL amyloidosis. Most PLCA is local, but doctors still check because systemic disease can rarely coexist. EyeWiki

6. Rarity (stochastic chance). The condition is so rare that chance and individual factors likely play a role; large series confirm the low frequency. ScienceDirect

Associations or plausible contributors (variable evidence):

7. Prior or chronic conjunctival inflammation. Some reports describe PLCA after inflammatory eye conditions. Chronic inflammation could attract immune cells that release light chains locally. Nature

8. History of trachoma or chronic conjunctivitis. These infections can cause long-term conjunctival changes; case reports have linked them to amyloid. Nature

9. Autoimmune disease nearby the eye. Rare links include rheumatoid arthritis or vasculitis (eosinophilic granulomatosis with polyangiitis/Churg–Strauss) in reports; the mechanism would again be chronic inflammation and plasma cells. Nature

10. Allergy and eye rubbing. Persistent rubbing and allergic swelling may irritate tissue and small vessels, possibly encouraging local deposition. (Clinical reasoning consistent with inflammatory associations.) ScienceDirect

11. Local micro-bleeds as a cycle. Small bleeds change tissue proteins and may set a loop of further irritation and deposition. (Mechanistic inference alongside hemorrhage findings.) PubMed Central

12. Contact lens wear (long-term). Long-term mechanical friction and solution preservatives may add low-grade irritation in susceptible people. (Occasional mention in case narratives; evidence limited.) ResearchGate

13. Prior ocular surgery or trauma. Tissue injury changes the conjunctival matrix and vessels; a few cases follow procedures or injuries. (Case-based reasoning.) ResearchGate

14. Local lymphoproliferation confined to the conjunctiva. A tiny, localized B-cell clone can make light chains without systemic disease—this fits the “primary localized AL” pattern confirmed on mass spectrometry. PubMed

15. Coexisting ocular adnexal amyloidosis (lids/orbit). Some patients have nearby deposits in eyelids or orbit, suggesting regional biology rather than a body-wide problem. canadianjournalofophthalmology.ca

16. Misdiagnosed “other lesions” that behave like PLCA. Salmon-patch or pyogenic-granuloma-like appearances can in fact be amyloid; awareness helps early diagnosis. Oxford Academic

17. Atopy or meibomian gland disease (chronic irritation). These common surface problems can keep the conjunctiva inflamed over years, a plausible contributor in susceptible eyes. (Clinical inference consistent with inflammatory links.) ScienceDirect

18. Idiopathic (no identifiable trigger). In many patients, no clear factor is found despite full evaluation—this is common in rare diseases. PubMed Central

19. Younger age outliers exist. Although mid-life is typical, even patients in their 20s have been reported, reminding us that biology varies. PubMed

20. Systemic disease is usually not the driver here. Even in myeloma and systemic AL, conjunctival involvement is uncommon; PLCA usually stands alone. Nature

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Common symptoms

1. Visible lump or thickening on the inner eyelid or eye surface that looks yellow-pink or “salmon-colored.” People often spot it while looking sideways in a mirror. EyeWiki

2. Foreign-body sensation like grit under the lid, especially when blinking over a firm deposit.

3. Recurrent bright-red patches on the white of the eye (subconjunctival hemorrhage) that come back again and again without clear trauma. PubMed

4. Recurrent red patches (subconjunctival hemorrhage). A sudden red area on the white of the eye that comes back again and again. PubMed

5. A flat “salmon-colored” patch or a small lump. It may look like a pale pink area or a small, firm bump on the eye surface. Lippincott Journals

6. Foreign-body sensation. Feels like sand in the eye because the surface is uneven. EyeWiki

7. Irritation or mild pain. The tissue can be tender, especially if it rubs with blinking. EyeWiki

8. Droopy eyelid (ptosis). Heavier tissue can weigh the lid down. EyeWiki

9. Tearing (watering). Surface irregularity can trigger reflex tearing.

10. Redness that comes and goes. Vessels are fragile and reactive. PubMed

11. Cosmetic concern. The patch or lump may be visible. Lippincott Journals

12. Mild light sensitivity. Irritated surfaces can be light-sensitive.

13. Blurred vision (usually mild or intermittent). Vision is usually okay, but can blur if the lesion touches the cornea or if tearing is heavy.

14. Feeling of pressure or fullness in the lid. Thicker tissue can feel heavy.

15. Itching. Especially if allergy coexists. ScienceDirect

16. Frequent small “blood spots” after rubbing. Vessels can break more easily. PubMed Central

17. Occasional discharge or stickiness. From surface inflammation.

18. Very rarely, double vision or limited eye movement (usually when deposits extend to the orbit or extraocular muscles—not typical for pure conjunctival disease). NCBI

19. Double vision or movement restriction only when disease extends beyond the conjunctiva into deeper tissues, which is uncommon in purely localized cases. EyeWiki

Diagnostic tests

Doctors start with history and slit-lamp examination. The appearance—firm, waxy, yellow-pink deposits in typical locations, sometimes with repeated bleeds—raises suspicion. But biopsy is essential because many eye surface lesions (for example, lymphoma) can look very similar. In the lab, the pathologist sees eosinophilic, amorphous material on H&E, Congo red positivity with apple-green birefringence on polarized light, and may use immunohistochemistry or mass spectrometry to define the protein type. Even if the eye disease looks localized, doctors commonly do a systemic screen (blood and urine protein tests, heart and kidney checks) to be careful, because very rarely the eye can be the first sign of a body-wide amyloidosis. EyeWiki+1NCBI

A) Physical examination tests

1. Visual acuity test
   You read letters on a chart. It tells the doctor how sharp your vision is and whether the surface problem is disturbing the tear film enough to blur vision. This is basic but important for baseline and follow-up.

2. External inspection and palpation
   The doctor looks closely at the eyelids and eye surface and gently feels the lids. Amyloid often looks smooth, waxy, and yellow-pink. Palpation helps judge firmness and whether the mass seems attached to deeper tissues. EyeWiki

3. Slit-lamp biomicroscopy
   A bright microscope lets the doctor study the color, surface, and edges of the deposit, look for tiny vessels inside it, and check for old or new bleeding under the conjunctiva. The superior fornix and tarsal conjunctiva are frequent sites, so the doctor sweeps the beam there. EyeWiki

4. Complete lid eversion and fornix examination
   The upper lid is flipped to expose the tarsal plate and deep fold where deposits often hide. This simple maneuver is key because many lesions sit deep in the upper fold and are missed if lids are not everted. EyeWiki

B) Manual or bedside tests

5. Schirmer tear test
   A small paper strip in the lower lid measures tear production. It helps explain irritation and blurring and guides comfort care, even though it does not diagnose amyloid by itself.

6. Tear film break-up time (TBUT)
   A drop of fluorescein dye shows how fast the tear film breaks into dry spots. Amyloid bumps can destabilize the tear film and make the surface dry out faster.

7. Digital intraocular pressure check (gentle palpation)
   With eyes closed, gentle fingertip pressure gives a rough idea of pressure. It is not a substitute for real tonometry, but it is a quick bedside sense of whether pressure seems normal while you wait for formal measurements if the surface is too irritated.

8. Cotton-swab corneal sensitivity test
   A wisp of cotton touches the cornea to be sure surface sensation is normal. Long-standing irritation or scarring can alter sensitivity, which can change comfort and healing.

C) Laboratory and pathological tests

9. Conjunctival biopsy with hematoxylin–eosin (H&E) stain
   A tiny piece of the lesion is removed. On H&E, amyloid looks like homogeneous, amorphous, eosinophilic material in the conjunctival stroma. This is the cornerstone first look under the microscope. EyeWiki

10. Congo red stain with polarized light
    This is the definitive hallmark: Congo red binds the amyloid, and under polarized light the pathologist sees apple-green birefringence. This feature clinches the diagnosis. EyeWiki

11. Crystal violet (metachromasia) or thioflavin-T fluorescence
    These special stains also support the diagnosis by highlighting amyloid in different ways. They are helpful if the Congo red signal is subtle or if the lab performs a full panel. NCBI

12. Immunohistochemistry (IHC) for typing
    Antibodies against kappa and lambda light chains can suggest an AL-type deposit if one light chain predominates, which is typical for localized conjunctival disease. BioMed Central

13. Mass-spectrometry–based proteomic typing
    When available, this test identifies the exact amyloid protein reliably by analyzing peptide fingerprints. It is the modern gold standard for amyloid typing in specialized centers. EyeWiki

14. Serum and urine protein studies
    Protein electrophoresis and immunofixation, plus serum free light chains, look for signs of a monoclonal light-chain disorder in the body. In primary localized conjunctival cases, these tests are usually negative, but they are recommended to rule out a body-wide process. EyeWikiNCBI

D) Electrodiagnostic tests

15. Electrocardiogram (ECG)
    A simple heart tracing can screen for silent heart involvement if the clinician has any concern about possible systemic amyloidosis. In a localized eye-only case this is often normal, but it is part of a cautious screen mentioned in ophthalmology references. NCBI

16. Nerve conduction studies (when symptoms suggest)
    If there are numbness, tingling, or weakness outside the eye, doctors may test nerve function to rule out a body-wide amyloid neuropathy. This is only for selected patients and not routine in clearly localized disease. NCBI

E) Imaging tests

17. Anterior-segment optical coherence tomography (AS-OCT)
    AS-OCT is a painless light-based scan. In conjunctival amyloidosis, it can show wavy, hyper-reflective subepithelial deposits and can help with presumptive diagnosis and follow-up, especially when the clinical picture overlaps with other lesions like lymphoma. It does not replace biopsy, but it is very useful. Lippincott Journals

18. Ultrasound biomicroscopy (UBM)
    UBM uses high-frequency ultrasound to map how deep the deposit goes in the conjunctiva and the lid margin. It helps surgical planning and is useful when AS-OCT penetration is limited in the lids or deep fornix. Lippincott Journals

19. Computed tomography (CT) of the orbits
    CT can show calcifications and extent if there is concern the process reaches beyond the conjunctiva into the orbit. It is more sensitive than MRI for calcification; radiology is used only when deeper spread is suspected. NCBI

20. Magnetic resonance imaging (MRI) of the orbits
    MRI gives excellent soft-tissue detail and helps define the anatomic boundaries of any deeper involvement. Most purely conjunctival cases do not need MRI, but it is helpful if the exam suggests extension. NCBI

Non-pharmacological treatments

1. Watchful waiting (active observation).
   What: Regular check-ups and photos without immediate surgery.
   Purpose: Avoids risks of surgery when the lesion is small and quiet.
   How it helps: Many deposits grow very slowly. Monitoring catches change early and prevents overtreatment. EyeWiki

2. Lubricating artificial tears (preservative-free preferred).
   What: Moisturizing drops or gels used several times daily.
   Purpose: Reduces friction, grit, and redness from a roughened surface.
   How it helps: Smooths the tear film so the eyelid glides over the deposit more comfortably. EyeWiki

3. Cold compress during flare or fresh bleed.
   What: Clean, cool compress for 5–10 minutes.
   Purpose: Calms irritation and slows minor bleeding.
   How it helps: Cold makes small blood vessels constrict.

4. Eyelid hygiene (warm compress + gentle lid cleaning).
   What: Warm compress then clean the lash line daily.
   Purpose: Controls blepharitis that can worsen redness and rubbing.
   How it helps: Removes oils and debris that inflame the surface.

5. Allergy control (non-drug measures).
   What: Keep windows closed on high-pollen days, rinse eyes with sterile saline, use wraparound glasses.
   Purpose: Cuts itching that leads to eye rubbing.
   How it helps: Avoiding triggers reduces mast-cell activation and micro-trauma.

6. Protective eyewear (safety glasses, sunglasses).
   What: Physical barrier outdoors or in dusty settings.
   Purpose: Prevents mechanical irritation and new micro-injuries.
   How it helps: Less irritation → fewer flares and bleeds.

7. Humidified air and blink breaks (screen hygiene).
   What: Use room humidifier; 20-20-20 rule for screens.
   Purpose: Keeps the eye surface moist.
   How it helps: More frequent blinking refreshes tears over the deposit.

8. Avoid eye rubbing.
   What: Hands off; tap the brow or use chilled tears instead if itchy.
   Purpose: Prevents capillary rupture and growth of the deposit.
   How it helps: Less mechanical stress means fewer subconjunctival hemorrhages.

9. Medication review with your doctor.
   What: Discuss blood thinners and antiplatelets. Do not stop on your own.
   Purpose: Some patients bleed easily; your physicians may adjust therapy if safe.
   How it helps: Balances eye bleeding risk with heart/stroke protection.

10. Nutritional pattern for ocular surface comfort.
    What: Omega-3-rich foods, leafy greens, adequate hydration.
    Purpose: Supports tear film quality and general eye surface health.
    How it helps: Omega-3s can modulate tear oil layer; hydration stabilizes tears (adjunctive only).

11. Smoking cessation.
    What: Quit plans or counseling.
    Purpose: Smoking worsens ocular surface inflammation and healing.
    How it helps: Less oxidative stress aids comfort and recovery.

12. Manage systemic dryness triggers.
    What: Treat meibomian gland dysfunction, thyroid eye disease, or autoimmune dry eye if present.
    Purpose: Healthier surface tolerates deposits better.
    How it helps: Reduces baseline inflammation.

13. Photodocumentation at visits.
    What: Standardized photos each visit.
    Purpose: Tracks subtle change over months/years.
    How it helps: Side-by-side comparison guides timely treatment.

14. Pressure patch briefly for active bleed (clinic-directed).
    What: Short, supervised patching.
    Purpose: Stops oozing from fragile vessels.
    How it helps: Gentle pressure promotes clotting.

15. Education on warning signs.
    What: Seek care for fast growth, new bleeding, pain, or droopy lid.
    Purpose: Early attention prevents complications.
    How it helps: You’ll know when to act.

16. Cryotherapy (as a non-drug office procedure).
    What: After debulking or for small lesions, targeted liquid-nitrogen freezing.
    Purpose: Shrinks remaining amyloid and feeder vessels.
    How it helps: Freezing damages small blood vessels that nourish the deposit; fewer nutrients → slower regrowth. EyeWiki

17. Bandage contact lens (short term, selected cases).
    What: Soft lens under close follow-up.
    Purpose: Reduces friction if surface is rough after biopsy.
    How it helps: Lens acts like a cushion while tissues heal.

18. Amniotic membrane (biologic dressing; procedure).
    What: Surgeon places a biologic membrane over a defect post-excision.
    Purpose: Speeds healing and reduces scarring.
    How it helps: Provides growth factors and a smooth scaffold (adjunct to surgery).

19. Low-dose external radiotherapy (select refractory cases).
    What: Targeted radiation delivered by a radiation oncologist.
    Purpose: Considered when disease repeatedly recurs and surgery is not enough.
    How it helps: Radiation can suppress local plasma-cell activity that makes amyloid; used rarely, not standard. EyeWiki

20. Regular systemic screening (rule-out only).
    What: Blood/urine tests, sometimes fat-pad biopsy, guided by a hematologist if suspicious signs appear.
    Purpose: Ensures deposits are truly localized.
    How it helps: Catches the uncommon patient with body-wide disease needing different therapy. PubMed

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Medication options

There is no proven eye drop or pill that dissolves conjunctival amyloid. Medicines support comfort, quiet inflammation, and protect the surface. Surgery addresses the deposit itself. EyeWiki

1. Artificial tears / gels (lubricants).
   Class: Ocular lubricants.
   Typical use: 1 drop 4–6×/day; gel at bedtime.
   Purpose: Ease grittiness and redness.
   How it works: Replaces and stabilizes the tear film.
   Possible side effects: Temporary blur, rare irritation. EyeWiki

2. Topical antihistamine/mast-cell stabilizer (e.g., olopatadine 0.1–0.2%).
   Use: 1 drop 1–2×/day during allergy seasons.
   Purpose: Cut itch to prevent rubbing.
   Mechanism: Blocks histamine and calms mast cells.
   Side effects: Mild sting, dryness.

3. Short course topical corticosteroid (e.g., loteprednol 0.2–0.5%).
   Use: 1 drop 3–4×/day for 1–2 weeks, then taper (doctor-supervised).
   Purpose: Quiet surface inflammation after biopsy or during flare.
   Mechanism: Suppresses inflammatory pathways.
   Side effects: Pressure rise, cataract with long use; infection risk—requires monitoring.

4. Topical NSAID (e.g., ketorolac 0.5%)—selective, short term.
   Use: 1 drop 2–4×/day for brief periods if doctor advises.
   Purpose: Pain relief if surface is sore (post-procedure).
   Mechanism: Blocks prostaglandins.
   Side effects: Stinging, delayed healing with prolonged use.

5. Topical cyclosporine (0.05–0.1%).
   Use: 1 drop twice daily for chronic surface inflammation/dry eye.
   Purpose: Improves baseline comfort so the deposit irritates less.
   Mechanism: T-cell modulation reduces inflammatory tear cytokines.
   Side effects: Burning on instillation for 1–2 weeks.

6. Topical lifitegrast 5%.
   Use: 1 drop twice daily for inflammatory dry eye.
   Purpose: Similar goal as cyclosporine.
   Mechanism: Blocks LFA-1/ICAM-1 interaction to curb T-cell–mediated inflammation.
   Side effects: Taste disturbance, irritation.

7. Topical antibiotic ointment (e.g., erythromycin) after biopsy.
   Use: Thin ribbon at bedtime for a few days.
   Purpose: Prevents infection while the surface heals.
   Mechanism: Suppresses bacterial growth.
   Side effects: Mild blur, contact sensitivity (rare).

8. Hypertonic saline 5% (drops/ointment) for surface edema (select cases).
   Use: Drops during day, ointment at night for 1–2 weeks.
   Purpose: Pulls excess fluid from the surface if swollen.
   Mechanism: Osmotic effect.
   Side effects: Stinging.

9. Acetaminophen (paracetamol) for discomfort.
   Use: Typical adult dose 500–1,000 mg up to every 6–8 h (max per label/doctor).
   Purpose: Systemic pain control post-procedure.
   Mechanism: Central analgesic pathways.
   Side effects: Liver risk with overdose—follow medical guidance.

10. Avoid or adjust blood-thinning agents only with physician approval.
    Use: Cardiologist/physician may tweak aspirin/anticoagulants if recurrent bleeds and safe to do so.
    Purpose: Reduce eye-surface bleeding events.
    Note: Never stop these drugs on your own.

Dietary molecular supplements

Evidence that supplements change conjunctival amyloid is limited. These options may support general ocular surface health or inflammation balance. Always discuss with your clinician to avoid interactions.

1. Omega-3 fatty acids (fish oil: EPA+DHA 1,000–2,000 mg/day).
   Function: Supports tear oil layer and may reduce surface inflammation.
   Mechanism: Alters eicosanoid balance toward less-inflammatory mediators.

2. Flaxseed oil (ALA 1–2 g/day).
   Function: Plant-based omega-3 precursor for tear support.
   Mechanism: Partial conversion to EPA/DHA.

3. Vitamin D3 (as per blood level, often 800–2,000 IU/day).
   Function: Immune modulation; deficiency is common and can worsen dryness.
   Mechanism: Nuclear receptor signaling adjusts inflammatory gene expression.

4. Vitamin A (prefer beta-carotene forms; dose individualized).
   Function: Epithelial health for ocular surface.
   Mechanism: Retinoid pathways regulate mucin and epithelial differentiation.
   Caution: Excess preformed vitamin A is toxic—medical supervision needed.

5. Vitamin C (250–500 mg/day).
   Function: Collagen support and antioxidant defense.
   Mechanism: Scavenges reactive oxygen species.

6. Vitamin E (100–200 IU/day if appropriate).
   Function: Lipid-phase antioxidant.
   Mechanism: Protects cell membranes from oxidative stress.

7. Zinc (as part of a balanced multivitamin, ~8–11 mg/day).
   Function: Supports epithelial repair and immune function.
   Mechanism: Enzyme cofactor roles in healing.

8. Curcumin (typical 500–1,000 mg/day of standardized extract with piperine).
   Function: Systemic anti-inflammatory adjunct.
   Mechanism: NF-κB pathway modulation (note: evidence for conjunctival amyloid is theoretical).

9. N-acetylcysteine (NAC 600 mg 1–2×/day).
   Function: Mucolytic/antioxidant; may reduce filamentary debris in dry eye.
   Mechanism: Glutathione precursor and mucolysis.

10. Hyaluronic acid oral (per label).
    Function: May support tear film moisture and joint health.
    Mechanism: Hydrophilic glycosaminoglycan retains water.

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Advanced/biologic” options

There are no approved “immunity booster,” regenerative, or stem-cell drugs that treat conjunctival amyloid deposits. The items below are adjuncts for ocular surface health, used in other conditions, and sometimes considered around surgery. Transparency first:

1. Autologous serum tears (20–50%, 4–6×/day).
   Role: For severe surface disease after surgery or in coexisting dry eye.
   Mechanism: Patient’s own growth factors and vitamins support epithelial healing.
   Note: Compounded; off-label.

2. Platelet-rich plasma (PRP) tears (per protocol).
   Role: Similar to serum tears; higher platelet-derived growth factors.
   Mechanism: Promotes cell migration and healing; not specific to amyloid.

3. Topical cyclosporine 0.05–0.1% (b.i.d.).
   Role: Immune modulator for chronic inflammation, not an amyloid treatment.
   Mechanism: T-cell suppression to stabilize tear cytokines.

4. Topical lifitegrast 5% (b.i.d.).
   Role: Immune modulator for inflammatory dry eye.
   Mechanism: Blocks LFA-1/ICAM-1 adhesion.

5. Recombinant nerve growth factor (cenegermin) — not for PLCA.
   Role: Only for neurotrophic keratitis; included here because patients ask.
   Mechanism: Nerve regeneration; no evidence for amyloid.

6. Systemic anti–plasma-cell chemotherapy — only if systemic AL amyloidosis is diagnosed.
   Role: Hematology-directed therapy (e.g., bortezomib-based) for body-wide disease, not localized conjunctival deposits.
   Mechanism: Reduces production of amyloid light chains throughout the body. PubMed

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Surgical/office procedures

1. Excisional biopsy with surgical debulking.
   Procedure: Surgeon numbs the eye, removes as much of the deposit as safely possible, and sends tissue for Congo red staining.
   Why: Confirms the diagnosis and reduces bulk that causes bleeding, irritation, or eyelid droop. Recurrence can happen; hence follow-up. PMCEyeWiki

2. Liquid-nitrogen cryotherapy to the lesion bed (often with debulking).
   Procedure: After removing bulk, the surgeon freezes the base in brief cycles.
   Why: Freezing closes small feeder vessels and may lower recurrence risk in some reports. EyeWiki

3. Low-dose superficial radiotherapy (select, recurrent cases).
   Procedure: Precisely targeted radiation in a few sessions.
   Why: For stubborn, repeatedly recurring disease when other options are insufficient; not a first-line standard. EyeWiki

4. Ptosis repair (levator advancement).
   Procedure: Tightens or advances the eyelid-lifting tendon.
   Why: Corrects droopy lid when deposits or scarring change lid position; case reports show improvement. AAO Journal

5. Amniotic membrane–assisted conjunctivoplasty.
   Procedure: After debulking a large area, a biologic membrane is sutured or glued to cover the defect.
   Why: Speeds healing, reduces scarring, and restores a smooth surface for comfort.

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Prevention tips

1. You cannot “prevent” amyloid formation with certainty, but you can protect the surface.

2. Do not rub your eyes; treat itch promptly.

3. Use preservative-free tears to reduce friction if you feel grit.

4. Control allergies (environmental steps first; medicines if needed).

5. Wear eye protection in dusty/windy settings.

6. Keep lids clean to limit chronic irritation.

7. Quit smoking to reduce oxidative stress.

8. Stay hydrated and take screen breaks to maintain a healthy tear film.

9. Review blood thinners with your doctor if you have frequent eye bleeds.

10. Attend scheduled follow-ups; early tweaks prevent bigger problems.

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When to see a doctor urgently

• A new or rapidly enlarging conjunctival mass.

• Repeated spontaneous bleeds on the eye surface.

• Pain, vision change, or light sensitivity.

• Droopy lid that worsens or blocks vision.

• After any trauma to the eye with known amyloid.

• If you were told you have systemic amyloidosis or symptoms like unexplained weight loss, numbness, or heart/kidney issues—ask for a coordinated evaluation. PubMed

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What to eat and what to avoid

What to eat :

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

2. Leafy greens (spinach, kale) for carotenoids and antioxidants.

3. Colorful fruits/vegetables (berries, peppers) for vitamin C and polyphenols.

4. Nuts and seeds (walnuts, flaxseed) for healthy fats and micronutrients.

5. Plenty of water throughout the day.

What to avoid/limit :

1. Smoking and secondhand smoke.

2. Excess alcohol, which dries the surface.

3. Very salty ultra-processed foods that worsen dehydration.

4. High-sugar spikes, which may fuel inflammation.

5. Anything that triggers allergies for you (e.g., certain pollens or pets—use environmental controls).

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Frequently asked questions

1. Is PLCA cancer?
   No. It is a benign protein deposit. It can mimic tumors, which is why biopsy is important. Ajo

2. Will it go away on its own?
   Deposits usually persist or grow slowly. Comfort measures help; surgery removes bulk if needed. EyeWiki

3. How is the diagnosis confirmed?
   By biopsy with Congo red staining and apple-green birefringence under polarized light. PMCBMJ

4. Do I need whole-body testing?
   Doctors often order basic tests once to rule out systemic amyloidosis, even though PLCA is commonly localized. PubMed

5. What are the most common symptoms?
   A visible conjunctival mass, recurrent red bleeds, and sometimes droopy eyelid. BioMed Central

6. What is the standard treatment?
   Observation for mild cases; excision/debulking for symptomatic ones; cryotherapy may be added; radiotherapy is rarely used. EyeWiki+1

7. What is the chance it comes back after surgery?
   Recurrence is possible; published series suggest around 20–30% over time, hence follow-up. surveyophthalmol.com

8. Can eye drops dissolve amyloid?
   No. Drops help symptoms and healing but do not melt amyloid deposits. Surgery addresses the deposit. EyeWiki

9. Is cryotherapy safe?
   Reports suggest it can be helpful as an adjunct; your surgeon will weigh benefits vs. risks for your specific lesion. EyeWiki

10. Is radiotherapy a good option?
    Sometimes used in very stubborn cases; not a routine first-line treatment. EyeWiki

11. Will this affect my vision?
    Usually the surface and eyelid are involved; vision is fine unless the lesion distorts the surface, causes significant bleeding, or the lid droops over the pupil.

12. What about both eyes?
    PLCA is often unilateral, but bilateral cases exist—evaluation is the same. BioMed Central

13. Can diet cure it?
    No. Diet supports eye comfort and general health but doesn’t remove deposits.

14. How often should I follow up?
    Typically every 3–12 months depending on symptoms and whether you had surgery; your doctor will tailor the schedule.

15. What if my eyelid droops?
    If ptosis interferes with vision or daily life, ptosis repair can help after the surface is stabilized. AAO Journal

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

Last Updated: August 22, 2025.