Ligneous Conjunctivitis

Ligneous conjunctivitis is a rare, long-lasting type of conjunctivitis (inflammation of the eye’s thin lining, the conjunctiva). The word ligneous means wood-like. In this condition, the inflamed tissue makes thick, tough, “woody” sheets called pseudomembranes. These sheets are mostly made of a blood-clot protein called fibrin. They usually form on the inside of the eyelids (the tarsal or palpebral conjunctiva), but can also involve the white of the eye, the cornea, and sometimes even block the pupil. If not treated, they can blur vision and may scar the eye. Many people with this eye problem also have similar “woody” deposits on other moist body surfaces (like the gums, airway, or genitals), because the same healing problem happens throughout the body. Genetic Rare Disease CenterPMCEyeWiki

Your body normally lays down fibrin to “patch” injured surfaces (like a temporary glue), and later uses an enzyme called plasmin to clean that fibrin away so normal tissue can grow back. People with ligneous conjunctivitis often have too little plasminogen (the inactive form that turns into plasmin). This condition is called type 1 plasminogen deficiency or hypoplasminogenemia. With too little plasmin, the “temporary glue” (fibrin) doesn’t clear. It piles up, hardens, and becomes woody pseudomembranes—especially where tissues are irritated over and over, like the eyelids. NCBIPMC

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Types

There isn’t a single official, worldwide “type” scale, but doctors find it useful to think about four practical groupings. This helps plan tests and follow-up:

1) By scope of disease

• Ocular-only ligneous conjunctivitis – deposits limited to the eyes. Vision can still be at risk if the cornea becomes involved.

• Systemic ligneous disease – the eyes plus other moist linings (gums, nose, airway, ear, genital or urinary tract). Airway involvement can threaten breathing and needs urgent care. PMCEyeWiki

2) By cause

• Congenital (genetic) form – most common. Due to PLG gene changes causing type 1 plasminogen deficiency. Usually autosomal recessive (you inherit one non-working copy from each parent). MedlinePlusrarediseases.org

• Acquired form – much less common. Due to newly developed low plasminogen or anti-fibrinolytic drug exposure (for example, long-term tranexamic acid can tip the balance and trigger woody eye membranes). PubMed

3) By age at first signs

• Infant/child onset – most frequent; often recurrent; can scar quickly if not recognized early.

• Adult onset – rarer; sometimes “unmasked” by eye surgery, infection, or medications that block fibrin breakdown. EyeWiki

4) By where the eye is involved

• Palpebral (tarsal) conjunctiva – classic, “woody” sheets on the inner eyelid.

• Bulbar conjunctiva / fornix – on the eye’s white surface or deep recesses.

• Corneal involvement – more serious because it affects vision (scarring, blood vessels, even perforation if severe). EyeWiki

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Causes

Root causes (the underlying problem):

1. Type 1 plasminogen deficiency (hypoplasminogenemia) – the main, proven cause; inherited, autosomal recessive changes in PLG lead to low plasminogen level and function. NCBIMedlinePlus

2. Acquired low plasminogen from chronic use of anti-fibrinolytics (e.g., tranexamic acid) – documented cause of ligneous conjunctivitis in adults. PubMed

3. Acquired low plasminogen from severe liver disease – the liver makes plasminogen; when it fails, levels can drop (sets the stage for fibrin buildup). (Supportive pathophysiology; clinicians consider this when symptoms and low plasminogen co-exist.)

4. Protein loss states (e.g., nephrotic syndrome) – plasminogen is a plasma protein; heavy urinary losses can lower it. (Plausible contributor recognized in hematology practice when evaluating low plasminogen.)

5. Rare PLG functional defects – unusual variants that impair how plasminogen works; ligneous eye disease tracks mainly with type 1 rather than type 2 (dysplasminogenemia). NCBI

Common “set-off” factors (what sparks the woody membranes when the system is fragile):

1. Minor eye trauma or rubbing – everyday micro-injury starts the fibrin “patch,” which then fails to clear. EyeWiki
2. Eye surgery or procedures (e.g., membrane peeling, chalazion surgery) – surgery triggers wound healing and fresh fibrin. EyeWiki
3. Viral conjunctivitis (like adenovirus) – inflammation + fibrin → woody sheets in at-risk people. EyeWiki
4. Bacterial conjunctivitis – same mechanism: inflammation seeds fibrin deposition. EyeWiki
5. Allergic or vernal conjunctivitis – intense itching and rubbing add trauma. EyeWiki
6. Toxic conjunctivitis from irritating drops or preservatives – chemical irritation means more fibrin “patches.” EyeWiki
7. Dust, smoke, wind, and other irritants – frequent surface irritation in children is a known background factor. EyeWiki
8. Upper-respiratory infections – often coincide with recurrences (system-wide inflammatory triggers). EyeWiki
9. Ear infections – signal wider mucosal involvement (middle ear lining can also form woody deposits). PMC
10. Female genitourinary infections – another mucosal site that can flare together with the eyes in systemic disease. PMC
11. Dental work or gum trauma – gingival “ligneous” lesions often partner with ocular disease. PMC
12. Contact lens micro-trauma or poor hygiene – more surface injury and biofilm irritation. (Clinical inference for surface-injury risk; used cautiously.)
13. Severe dry-eye – unstable tear film lets tiny injuries persist; more fibrin patches form. (Clinical inference for ocular-surface risk.)
14. Hormonal milieu changes – the literature notes hormonal influences on plasminogen/fibrin balance; clinicians sometimes see flares around such changes. (Supportive; not a primary cause.)
15. General poor wound healing states – anything that delays normal tissue repair (malnutrition, severe systemic illness) can amplify the fibrin-persistence problem. (Supportive; used to guide holistic care.)

Key point: the proven, central driver is low plasminogen (type 1); the rest mainly push an already fragile healing system toward making and keeping those woody fibrin sheets. NCBIPMC

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Symptoms

1. Red eye – persistent redness from ongoing inflammation. EyeWiki

2. Thick, “woody” lids – firm, yellow-white to red pseudomembranes on the inner eyelid; often recur. Genetic Rare Disease Center

3. Stringy or mucoid discharge – sticky mucus that reappears after cleaning. EyeWiki

4. Excess tearing – reflex tears because the surface is irritated. EyeWiki

5. Foreign-body sensation – feeling like grit or sand is stuck in the eye. EyeWiki

6. Light sensitivity (photophobia) – light hurts when the surface is inflamed. EyeWiki

7. Pain or soreness – ranges from discomfort to significant pain if the cornea is involved. EyeWiki

8. Ptosis or heavy lids – membranes can be weighty, making lids droop. EyeWiki

9. Blurry vision – mucus, membranes, or corneal damage scatter light. EyeWiki

10. Recurrent “conjunctivitis” that doesn’t stay gone – key clue that it’s not ordinary pink eye. EyeWiki

11. Corneal problems – haze, blood vessels growing into the cornea, even ulcer or perforation in severe cases. EyeWiki

12. Gum overgrowth or sore gums – “ligneous gingivitis” matches the eye disease and helps clinch the diagnosis. PMC

13. Ear fluid or infections / hearing issues – woody deposits can affect the middle ear lining. PMC

14. Breathing symptoms – hoarseness, noisy breathing, or cough if airway linings are involved (urgent if severe). PMC

15. Female genital symptoms – pain with intercourse, unusual discharge or bleeding if those linings are involved. PMC

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Diagnostic tests

A) Physical exam & basic clinical assessment (at the slit lamp)

1. Visual acuity – reading the chart tells how much vision is affected today. If vision is down, doctors look for membrane size, corneal haze, or scarring as the reason.

2. External inspection of lids and lashes – doctors look for swollen lids, crusting, and discharge that point to surface inflammation rather than deeper eye disease.

3. Eyelid eversion – gently flipping the lid reveals the classic “woody” sheets on the tarsal conjunctiva. Seeing these strongly suggests ligneous conjunctivitis in the right history. EyeWiki

4. Slit-lamp biomicroscopy – a microscope with bright, narrow light lets the clinician measure thickness, extent, and firmness of the membranes, check the cornea, and look for new blood vessels or ulcers. EyeWiki

5. Fluorescein staining – a harmless orange dye shows surface defects or abrasions (bright green under blue light). It helps map any corneal injury caused by the membranes rubbing the eye.

6. Lissamine green / rose bengal staining – these dyes highlight dry or damaged surface cells around the lesions and help gauge surface health.

7. Tear breakup time (TBUT) – measures how quickly tears evaporate; quick breakup suggests a stressed surface that’s prone to micro-injury and recurrence.

8. Intraocular pressure (tonometry) – important baseline if steroid drops are considered later; steroids can raise eye pressure in some people. EyeWiki

B) Simple “manual” bedside maneuvers (what the clinician does gently, by hand)

9. Gentle membrane mobility check – with moistened swab, the examiner assesses how firmly attached the sheet is. Ligneous plaques are thick and adherent; forcibly peeling is avoided (it inflames more). EyeWiki

10. Lid palpation for firmness – pressing through the lid helps gauge the woody consistency and depth compared with soft mucus.

11. Preauricular lymph node palpation – enlarged nodes point more to viral “pink eye”; small or absent nodes fit better with ligneous disease (a helpful differential clue).

12. Corneal sensitivity (cotton wisp) – checks the corneal nerve function; reduced sensitivity hints at chronic surface disease.

13. Eyelid margin expression – assessing oil gland clogging (meibomian glands); poor oil flow dries the surface and can trigger recurrences.

These manual checks do not make the diagnosis alone, but they build a pattern that supports the next, more specific tests.

C) Laboratory & pathological tests (the decisive confirmations)

14. Plasminogen activity assay – measures how well plasminogen works; low activity supports type 1 deficiency in the right clinical picture. NCBI

15. Plasminogen antigen level – measures how much plasminogen is present; low antigen plus low activity is typical of type 1. (Type 2 usually has normal antigen but low activity and does not typically cause ligneous lesions.) NCBI

16. PLG gene testing – looks for PLG mutations. Helpful for confirmation and for family counseling; diagnosis can be made on labs + symptoms even without genetics, but genetics add certainty. MedlinePlus

17. Conjunctival biopsy (histopathology) – a small sample shows subepithelial, eosinophilic “amyloid-like” material rich in fibrin/fibrinogen, with inflammatory cells. This pattern is characteristic and helps exclude true amyloidosis (Congo red stain). EyeWiki

18. Immunohistochemistry for fibrin/fibrinogen – stains the tissue to prove the fibrin-rich nature of the sheet. surveyophthalmol.com

19. Microbiology (culture/PCR) when needed – rules out infectious causes of persistent pseudomembranes (bacterial, chlamydial, viral) so they’re not mistaken for ligneous disease. EyeWiki

20. Basic systemic labs as context – complete blood count and inflammatory markers (ESR/CRP) to look for active infection/inflammation; coagulation/fibrinolysis panels can provide supporting information but are not diagnostic by themselves.

D) Imaging tests (used when anatomy or other organs are involved)

21. Anterior-segment OCT (AS-OCT) – a light-based scan that shows membrane thickness and layers without touching the eye; useful for planning surgery or tracking response.

22. In-vivo confocal microscopy (IVCM) – magnified, cell-level views of conjunctival tissue to assess the membrane structure and nearby inflammation.

23. Corneal topography – maps corneal shape; detects irregular astigmatism or warpage from chronic rubbing or scarring that can blur vision.

24. Ultrasound biomicroscopy / B-scan – helps when the cornea is too cloudy to see inside the eye; checks for deeper problems.

25. Anterior-segment photography – standardized photos to document size and response of membranes over time.

26. ENT laryngoscopy / bronchoscopy (endoscopic “imaging”) – if there’s hoarseness, cough, or noisy breathing, this looks for woody airway plaques that may need urgent care. PMC

27. CT or MRI of neck/chest – only if severe airway disease is suspected; maps extent of lesions for the airway team. PMC

28. Dental and oral exam with photos – documents ligneous gingivitis (gum overgrowth) that often accompanies the eye disease. PMC

29. Pelvic exam with appropriate imaging – in symptomatic females, evaluates genitourinary mucosa for similar plaques. PMC

30. Neuroimaging (brain MRI) – rarely, children have hydrocephalus linked to plasminogen deficiency; imaging confirms and guides neurosurgical care. PMC

Non-pharmacological treatments

These are supportive or preventive actions. They do not replace disease-specific treatment (plasminogen replacement or fibrin-dissolving therapy), but they help protect the eye, reduce triggers, and improve comfort.

1. Education and trigger avoidance
   Learn that rubbing, dusty air, and unnecessary eye procedures can trigger regrowth. Mechanism: fewer micro-injuries means less fibrin laid down, so less to clear.

2. Protective eyewear and eye shields (especially during sleep in kids)
   Blocks accidental rubbing/trauma. Mechanism: prevents the initial wound-healing cascade that drives fibrin build-up.

3. Gentle lid hygiene (warm water or preservative-free lid wipes)
   Keeps crusts and bacteria down, lowering irritation. Mechanism: less surface inflammation = fewer flares.

4. Preservative-free artificial tears (daytime)
   Dilute irritants, lubricate the surface. Mechanism: reduces frictional micro-injury and inflammation.

5. Lubricating ointment (night)
   Creates a protective layer overnight. Mechanism: minimizes mechanical shear with blinking.

6. Cold compress for comfort
   Reduces swelling and itching. Mechanism: vasoconstriction blunts inflammatory mediator release.

7. Humidifier and environmental control
   Moist air lessens dryness and rubbing urge. Mechanism: reduces desiccation stress on conjunctiva.

8. Stop contact-lens wear during active disease
   Lenses increase friction and biofilm risk. Mechanism: avoids mechanical/biological triggers.

9. Hand hygiene and avoid sharing eye cosmetics
   Cuts secondary infection risk that can inflame the surface. Mechanism: fewer inflammatory cofactors.

10. Frequent, structured follow-up
    Close monitoring finds early regrowth; early, gentle removal and topical measures work better on small plaques. Mechanism: early intervention prevents thick “woody” maturation. EyeWiki

11. Amblyopia prevention in children (patching the stronger eye if needed, per pediatric ophthalmology)
    Mechanism: prevents permanent “lazy eye” if membranes blur one eye for long periods.

12. Allergy control (non-drug measures)
    Rinse eyes with sterile saline after high-pollen exposure; shower after outdoor play. Mechanism: less histamine-driven rubbing.

13. Peri-procedural planning
    If any eye or ENT procedure is necessary, plan anti-recurrence measures ahead of time (see drug/surgery sections). Mechanism: minimizes surgery-triggered flares. EyeWiki

14. ENT and dental coordination
    Screen for airway or middle-ear membranes; treat ligneous gingivitis gently. Mechanism: addresses the same healing defect system-wide to reduce overall inflammatory load. Haematologica

15. Sun and wind protection (wraparound glasses)
    Mechanism: less environmental trauma to conjunctiva.

16. Sleep and screen-time hygiene
    Regular blinking and breaks keep the surface smooth. Mechanism: reduces exposure-related micro-injury.

17. Nutritional support (adequate protein, vitamins—details below)
    Mechanism: supports epithelial repair pathways (not a cure).

18. Rare-disease advocacy/psychosocial support
    Mechanism: improves adherence and timely access to specialized care and replacement therapy.

19. Genetic counseling for families
    Mechanism: explains inheritance (autosomal recessive) and guides testing relatives. EyeWiki

20. Strict avoidance of antifibrinolytic medicines unless a specialist says otherwise (e.g., tranexamic acid, epsilon-aminocaproic acid)
    Mechanism: these block fibrin breakdown and can cause or worsen LC; stopping them has led to resolution in reports. FDA Access DataPMCPubMed

Drug treatments

Important: Doses below are example regimens reported in labels or peer-reviewed case series. Individual dosing, compounding, and scheduling must be customized by your ophthalmologist/hematologist.

1. Plasminogen (human) IV concentrate (RYPLAZIM®) – Systemic biologic replacement
   Dose/time: 6.6 mg/kg IV every 2–4 days, adjusted to maintain trough plasminogen levels (per FDA label). Purpose: replaces the missing enzyme system-wide; helps resolve ocular and other mucosal lesions. Mechanism: restores fibrin breakdown by supplying plasminogen. Side effects: infusion reactions, hypersensitivity, risk of thrombosis is low but monitor as per label. U.S. Food and Drug AdministrationEmprNBDF

2. Topical plasminogen eye drops (often compounded from fresh frozen plasma [FFP]) – Local biologic replacement
   Dose/time: protocols vary (e.g., hourly then taper to 4–6×/day during quiescence). Purpose: directly supplies plasminogen to the ocular surface. Mechanism: enables local fibrin digestion so membranes regress. Side effects: preservative-free product; infection control in preparation is critical. ClinSurge GroupAAO Journal

3. Topical heparin – Anticoagulant used locally
   Dose/time: case reports used 1,000–5,000 IU/mL, from 6×/day to hourly initially, then taper; sometimes continued long term to prevent relapse. Purpose: reduce fibrin formation on the surface. Mechanism: potentiates antithrombin, inhibits thrombin/Xa → less fibrin to build membranes. Side effects: local irritation; systemic absorption is minimal with drops but watch for bleeding risk if epithelium is very compromised. PubMed+1IJCE Ophthalmology

4. Topical corticosteroids (e.g., prednisolone acetate 1%, dexamethasone 0.1%) – Anti-inflammatory
   Dose/time: frequent at first (e.g., q1–2h for 1–2 days post-procedure), then taper to QID→BID. Purpose: control inflammation that drives fibrin deposition. Mechanism: broad anti-inflammatory; reduces cytokines and vascular leakage. Side effects: pressure rise, cataract, infection risk—monitor IOP. Lippincott Journals

5. Topical cyclosporine A (0.05–2%) – Immunomodulator
   Dose/time: BID–QID in reports; often used chronically as a steroid-sparing agent. Purpose: quiets T-cell–driven surface inflammation. Mechanism: calcineurin inhibitor → reduces T-cell activation. Side effects: stinging on instillation. IJCE OphthalmologyScienceDirect

6. Topical tacrolimus (0.03–0.1% ointment/solution) – Immunomodulator
   Dose/time: BID typically. Purpose: alternative or add-on when cyclosporine is not enough. Mechanism: calcineurin inhibitor. Side effects: burning/irritation, rare infection risk. Lippincott JournalsAmerican Academy of Ophthalmology

7. Topical recombinant tPA (alteplase) drops – Fibrinolytic enzyme
   Dose/time: case reports used hourly then taper over months, often paired with heparin; sometimes used after surgery. Purpose: directly dissolves fibrin in membranes. Mechanism: converts plasminogen→plasmin locally. Side effects: surface irritation; must be compounded under strict aseptic conditions. BioMed Central

8. Topical antibiotics (e.g., moxifloxacin 0.5%) only if infection is suspected
   Dose/time: QID for 7–10 days when indicated. Purpose: treat secondary bacterial infection. Mechanism: bactericidal. Side effects: irritation; avoid unnecessary use. AAO Journal

9. Preservative-free sodium hyaluronate (0.1–0.3%) – Lubricant medical device
   Dose/time: QID–hourly PRN. Purpose/Mechanism: coats and protects epithelium; reduces friction; supports healing. Side effects: minimal; avoid preservatives with frequent use. TFOS Report

10. Antihistamine/mast-cell–stabilizer drops (e.g., olopatadine) for allergic flares
    Dose/time: QD–BID. Purpose: reduce itch/rub cycle and inflammation. Mechanism: blocks histamine and stabilizes mast cells. Side effects: mild sting. StatPearls

Avoid: routine use of antifibrinolytics (e.g., tranexamic acid) in PLG deficiency—they can cause or worsen LC by further blocking fibrin breakdown. Discuss any current prescriptions with your doctors. ASH Publications

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Dietary, molecular, and other supportive supplements (adjuncts; plain English)

These do not replace plasminogen therapy or medical treatment. Evidence is indirect (mostly from ocular-surface or wound-healing research), but they can support overall healing if your clinician approves.

1. Adequate protein (aim for balanced daily intake): supplies amino acids for tissue repair.

2. Vitamin A (dietary; avoid high-dose pills unless deficient): supports ocular surface epithelium.

3. Vitamin C (e.g., 250–500 mg/day if diet is low): collagen cross-linking and antioxidant support.

4. Vitamin D (per blood level): immune modulation.

5. Vitamin E (from nuts/seeds): antioxidant support.

6. Zinc (e.g., 8–11 mg/day from food or supplements if low): epithelial repair cofactor.

7. Copper (only if deficient): collagen enzymes need balance with zinc.

8. Omega-3 fatty acids (fish or algae oil 1–2 g/day EPA+DHA if approved): may help surface inflammation/dryness.

9. Hydration (water, limit caffeinated diuretics): keeps tear film stable.

10. Probiotics (food-based): general immune support.

11. L-glutamine (only with clinician guidance): gut/immune support.

12. N-acetylcysteine (low-dose if prescribed): mucolytic/antioxidant.

13. Avoid vitamin A toxicity (no mega-doses); balance micronutrients.

14. Colorful produce (carotenoids, polyphenols) for antioxidant variety.

15. Limit ultra-processed, high-sugar foods that may promote inflammation.
    (These are general principles; your clinician may tailor them.)

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Regenerative / stem-cell–like” therapies

1. Systemic plasminogen (RYPLAZIM®) – foundation therapy (see dose above). Function: enzyme replacement throughout the body for true disease control. U.S. Food and Drug Administration

2. Topical plasminogen (from FFP or concentrate) – local biologic support. Function: restores local fibrinolysis at the eye surface. ClinSurge Group

3. Topical recombinant tPA (alteplase) – enzymatic fibrinolysis in situ. Common compounded strength: 1 mg/mL, frequency tapered. BioMed Central

4. Autologous serum eye drops (ASEDs) – patient’s own serum diluted (often 20%, 6–10×/day in protocols) to deliver growth factors that support epithelial healing. Function: epitheliotrophic factors (EGF, vitamin A, albumin) improve surface repair. The Royal College of OphthalmologistsPMC

5. Platelet-rich plasma (PRP) eye drops – platelet growth factor–rich drops (e.g., 20% 4–6×/day for ~3 months in studies). Function: regenerative signaling for corneal/conjunctival healing. PMCModern Optometry

6. Topical cenegermin (recombinant human nerve growth factor) – 20 mcg/mL, 1 drop 6×/day for 8 weeks (approved for neurotrophic keratitis). Function: supports corneal nerve/epithelial healing when neurotrophic damage co-exists; not LC-specific but can aid surface recovery in selected cases. OXERVATE® (cenegermin-bkbj)NCBI

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Surgeries

1. Careful surgical excision (membranectomy)
   What: remove the ligneous pseudomembrane at the slit lamp or in the OR.
   Why: relieve mechanical symptoms and open the surface for medical therapy. Note: high recurrence if done alone; usually combined with heparin, steroids, plasminogen/tPA. ResearchGate

2. Amniotic membrane transplantation (AMT)
   What: suture or glue a biologic membrane onto the raw surface after excision.
   Why: provides a healing “bandage,” reduces inflammation and scarring, and lowers recurrence when paired with medical therapy. PubMedLippincott Journals

3. Adjunctive intra-/post-operative regimens
   What: topical heparin + steroid frequently for 24–48 h, then taper; some reports add mitomycin-C intra-op in selected recurrent cases.
   Why: suppresses fibrin re-accumulation and inflammation while tissue re-epithelializes. Lippincott JournalsSciSpace

4. Conjunctival autograft / reconstructive procedures
   What: move healthy conjunctiva to cover defects after large excisions; repair ptosis if needed later.
   Why: restore anatomy, reduce bare areas that trigger regrowth. BioMed Central

5. Intraocular fibrin management (rare scenarios)
   What: intracameral r-tPA has been suggested when severe fibrin forms after intraocular surgery in PLG deficiency.
   Why: quickly dissolves intraocular fibrin to preserve vision. SciSpace

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Prevention strategies

1. Wear protective eyewear in dusty/windy environments.

2. Avoid eye rubbing; use cold compresses for itch.

3. Keep surfaces lubricated with preservative-free tears.

4. Treat allergies promptly to cut down on rubbing/inflammation. StatPearls

5. Quit smoking and avoid smoke/pollutants. StatPearls

6. Flag antifibrinolytics (e.g., tranexamic acid) on your medical record as contraindicated unless a specialist explicitly advises otherwise. ASH Publications

7. Tell every surgeon/dentist you have PLG deficiency/LC so peri-operative plans (e.g., plasminogen, heparin, steroids) are in place. Clinical Gate

8. Manage dry eye/blepharitis to reduce triggers. TFOS Report

9. Plan frequent follow-ups after any eye procedure. ResearchGate

10. Maintain good general health (sleep, nutrition, hydration) to support healing.

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When to see a doctor urgently

• Sudden worsening redness, pain, or rapidly growing membranes

• Vision drops, new light sensitivity, or corneal damage symptoms (severe pain, tearing)

• Sticky eyelids that won’t open or membranes you can see covering the inside of the lid

• Signs of infection (pus, fever)

• After any eye surgery if you have LC/PLG deficiency—even minor procedures deserve close follow-up

• Breathing problems, mouth or genital mucosal lesions—these may be part of the same disease and need systemic care. PMC

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What to eat and what to avoid

• Eat: lean proteins (fish, eggs, legumes) to fuel repair.

• Eat: colorful vegetables and fruits for vitamins A/C and antioxidants.

• Eat: nuts/seeds and olive oil (healthy fats).

• Eat: omega-3 sources (fatty fish; or algae oil if advised).

• Hydrate well: water across the day.

• Limit: ultra-processed, very salty, or sugary foods that can worsen dryness/inflammation.

• Limit: alcohol (dehydrates).

• Avoid: smoking and smoky environments.

• Watch: megadoses of fat-soluble vitamins (A, E) without lab guidance.

• Balance: zinc and copper if supplementing—ask your clinician.

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FAQs

1) Is LC contagious?
No. It is not an infection you can “catch.” It is a healing problem most often caused by plasminogen deficiency. PMC

2) Why do the membranes keep coming back?
Because fibrin is not cleared properly, the body keeps laying it down again after any irritation or surgery. Orpha

3) Will antibiotics cure it?
No. Antibiotics help only if there is a true infection on top of LC. The core issue is fibrin not being cleared. AAO Journal

4) What is the most important treatment?
Replacing/plussing the plasminogen system (systemic IV plasminogen and/or topical plasminogen/tPA) and controlling inflammation locally. U.S. Food and Drug AdministrationClinSurge Group

5) Is surgery a cure?
Surgery helps remove bulk membranes, but recurrence is common unless combined with medicines like heparin/steroids/plasminogen. ResearchGate

6) Can children be treated safely?
Yes—LC often starts in childhood. Care is multidisciplinary; plasminogen concentrate is approved for PLG deficiency and has pediatric use under specialist care. U.S. Food and Drug Administration

7) Are antifibrinolytic drugs safe for me?
Usually no. Medicines like tranexamic acid block fibrin breakdown and can trigger LC. Always check with your doctors. ASH Publications

8) Can LC affect parts of my body other than the eye?
Yes. Mouth, ears, airway, and genitourinary tract can be involved because the same healing problem occurs there. PMC

9) What if I need eye surgery for another reason?
Plan ahead: your surgeon will usually pair surgery with heparin, steroids, and biologics (plasminogen/tPA), and follow you closely to prevent recurrence. Lippincott Journals

10) Do diet and vitamins cure LC?
No, but good nutrition helps your tissues heal. Think of it as support, not a cure.

11) How long will I need treatment?
LC can be chronic/relapsing. Some people need long-term maintenance (e.g., heparin or cyclosporine; scheduled plasminogen infusions) to stay quiet. PubMed

12) Will this make me go blind?
It can threaten vision if membranes scar the cornea or block vision, but early, combined therapy helps protect sight. PMC

13) Can I use contact lenses?
Often not during active disease. Your doctor may allow limited use only when the surface is quiet. IJCE Ophthalmology

14) Is there a genetic test?
Yes—testing the PLG gene confirms type I plasminogen deficiency. Family counseling is helpful. NCBI

15) Where can I learn more?
Reputable resources include EyeWiki (AAO), NORD, MedlinePlus Genetics, and hematology/ophthalmology specialists familiar with plasminogen deficiency. EyeWikirarediseases.orgMedlinePlus

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 10, 2025.

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