Mooren’s ulcer is a rare, very painful sore at the edge of the cornea (the clear front window of the eye). It starts near the limbus (the border where the white of the eye meets the clear cornea) and slowly eats away at the peripheral cornea. It usually spreads around the edge (circumferentially) and can creep toward the center over time. Doctors see a crescent-shaped ulcer with a sharp “overhanging edge” and thinning of the cornea on the slit lamp exam. By definition, it is not caused by an infection and is not due to a systemic autoimmune disease—so it is a diagnosis of exclusion (you have to rule other causes out first). EyeWikiWebEyePMC
Mooren’s ulcer is a rare, painful, sight-threatening disease where the outer edge of the cornea (the clear front window of the eye) develops a crescent-shaped ulcer that gradually eats into (thins) the cornea. It usually begins at the periphery, often with a sharp overhanging edge, and can spread around the rim and toward the center. Importantly, it is considered idiopathic and autoimmune (the body’s immune system attacks corneal tissue) and is not caused by a systemic vasculitis like rheumatoid arthritis—those other causes are classified separately as “PUK due to systemic disease.” Mooren’s ulcer is therefore a diagnosis of exclusion: doctors first rule out infection and systemic autoimmune causes, then treat the corneal-only (Mooren’s) form aggressively to prevent melt and perforation. NCBIWebEyeEyeWiki
The best current explanation is autoimmunity triggered by exposed corneal proteins after a “provocation” such as minor trauma, surgery, or infection. In genetically susceptible people, the immune system can then mount a harmful response against the cornea; studies show auto-antibodies to corneal stromal antigens and HLA (tissue type) associations (e.g., HLA-DR17(3)/DQ2). Some regions (Africa, Indian subcontinent) report more cases, and small studies note associations with hepatitis C (ulcers improved when hepatitis C was treated). Mechanisms include activated T-cells, B-cells, and enzymes (MMPs) that digest corneal collagen. PubMed+1PMCLippincott JournalsEyeWiki
The exact cause is unknown. The best current idea is that it’s an autoimmune attack focused on the cornea: the body’s immune system mistakes corneal tissue for an enemy and keeps the inflammation going. Some people seem genetically predisposed (certain HLA types show up more often). Eye injuries or surgeries may “unmask” corneal proteins and trigger the reaction later. A few infections (like hepatitis C or hookworm) have been reported alongside Mooren’s ulcer in some series, but the evidence is mixed, so doctors test for them but do not say they are proven causes for everyone. PubMed+3PubMed+3PubMed+3PMC
Types
Doctors have described two–three clinical patterns. The most widely used are:
Limited/Benign type
Usually one eye, tends to occur in older adults, and responds better to treatment. Uveitis.org | OIUFWebEyeAtypical/Malignant (progressive) type
Often both eyes (bilateral), more aggressive, more painful, and harder to control, classically in younger patients. Estimates suggest bilateral disease occurs in ~25% of benign cases and ~75% of malignant cases. PMC+1
Some authors (Watson) further note a “bilateral indolent” subtype—both eyes, slower “guttering” at the edge, often in middle-aged patients. Not every center uses this extra label, but you may see it. SciSpaceLippincott Journals
Causes/triggers/risk factors
Mooren’s ulcer is idiopathic (no single known cause). The list below includes immune mechanisms, predispositions, and reported triggers/associations doctors look for—mainly to rule out other diseases and to calm the immune system if a trigger is found.
Autoimmune misfire against corneal proteins – the immune system attacks the peripheral cornea. PubMed
Helper-T-cell–driven inflammation and auto-antibodies to corneal/conjunctival tissue. Uveitis.org | OIUF
Genetic susceptibility (HLA-DR17(3), HLA-DQ2)—seen more often in Mooren’s ulcer patients. PubMed+1
Prior corneal surgery (e.g., cataract, pterygium, keratoplasty) can unmask corneal antigens and “prime” the immune system. Lippincott Journals+1
Recent ocular trauma—injury can expose hidden corneal proteins. Lippincott Journals
Hepatitis C virus (HCV)—reported association in case series (controversial—some studies find no link). PubMedNature
Hookworm/helminth infections—association reported in endemic regions. PMC
Geographic clustering (Southern/Central Africa, India, parts of China) suggests environmental or genetic influence. PMC
Severe local inflammation at the limbus (episclera/conjunctiva) that “feeds” the corneal ulcer. EyeWiki
Matrix-degrading enzymes (collagenases) driven by inflammation contribute to stromal “melt.” OUCI
Circulating immune complexes detected in some patients (further evidence of immune drive). Uveitis.org | OIUF
Low immune “brakes” (regulatory/suppressor T-cell imbalance) seen in older studies. Medscape
Coexisting ocular surface disease (e.g., active pterygium) occasionally co-reported with Mooren’s ulcer. PMC
Post-glaucoma filtering implant surgery (rare case reports). ScienceDirect
Older age (for limited/benign type) as an epidemiologic risk pattern—not a cause by itself. Uveitis.org | OIUF
Younger age (for progressive/malignant type) as another pattern—not a cause by itself. WebEye
Male sex predominance noted in some series—again, not causal but a pattern. PMC
Prior infectious keratitis (non-active now) as a theorized “priming” event. EyeWiki
Auto-inflammatory comorbidities rarely co-reported (e.g., pyoderma gangrenosum)—shared immune features. EyeWiki
Nutritional/parasite interplay in endemic areas (hookworm + environment) posited in some epidemiologic work. PMC
Common symptoms
Severe eye pain—often worse than the redness looks.
Red eye, especially near the edge of the cornea.
Tearing/watering.
Light sensitivity (photophobia).
Blurred vision.
Foreign-body sensation (scratchy, gritty).
Worsening pain with eye movement or wind.
Tenderness at the limbus (edge of the cornea).
Burning.
Blepharospasm (difficulty keeping the eye open).
Glare and halos from irregular corneal shape.
Headache around the eye from sustained pain.
Pain at night (tearing/photophobia can disturb sleep).
Reduced vision from irregular astigmatism as the cornea thins.
Fear of light/excessive squinting because it hurts to open the eye.
(These reflect classic PUK/Mooren features—pain, redness, photophobia, tearing, reduced vision—plus common pain behaviors patients report.) PMC
Diagnostic tests doctors
(grouped by category; explained in simple terms)
Important: Mooren’s ulcer is a diagnosis of exclusion. Tests aim to (a) confirm the corneal pattern and thinning, and (b) rule out infection or a body-wide autoimmune disease that can imitate Mooren’s. WebEye
A) Physical examination
Visual acuity (Snellen chart) – measures how clearly you see; gives a baseline and tracks change over time. EyeWiki
Pupil exam and light reflex – checks for nerve problems; severe corneal pain may cause light sensitivity but pupils should react normally. EyeWiki
Intraocular pressure (IOP) check – too low may hint at a microscopic leak; too high can complicate healing. EyeWiki
External inspection – looks for intense redness near the limbus and swelling of the conjunctiva/episclera. EyeWiki
Slit-lamp biomicroscopy – the key exam: doctors look for a peripheral crescent ulcer, overhanging edge, and corneal thinning that can spread around and inward. EyeWikiPMC
B) “Manual” chair-side tests
Fluorescein staining – orange dye glows under blue light to outline the ulcer.
Seidel test – uses fluorescein to see if aqueous fluid is leaking from a very thin spot (a “green waterfall”).
Corneal esthesiometry (Cochet-Bonnet) – a thin nylon filament touches the cornea to check sensation; very low sensation suggests herpetic disease rather than Mooren’s.
Applanation tonometry – a device gently flattens the cornea to measure pressure; helpful when the cornea is thin and at risk of perforation.
Lid eversion & fornix sweep – turns the lid to look for a hidden foreign body or papillae that could worsen surface inflammation.
(These bedside tests complement the slit-lamp exam and help screen for leaks, altered sensation, pressure changes, and mechanical irritants.) EyeWiki
C) Laboratory & pathological tests
Corneal scraping for Gram/KOH stain and cultures – rules out bacterial, fungal, or Acanthamoeba infection (Mooren’s is noninfectious, but infection can mimic it). WebEye
HSV/VZV PCR (when suspected) – checks for herpetic keratitis, another mimic that reduces corneal sensation. EyeWiki
Autoimmune screening to exclude systemic PUK – RF, ANA, ANCA, ESR, CRP (to screen for diseases like rheumatoid arthritis or granulomatosis with polyangiitis that can cause PUK with scleritis—not Mooren’s). NCBI
Hepatitis C testing (antibody and RNA) – because some reports link HCV with Mooren-type ulcers; still controversial, so it’s checked and treated if present. PubMedNature
Stool exam for ova/parasites (in endemic areas) – looks for hookworm, which has been associated with Mooren’s ulcer in case-control work. PMC
HLA typing (e.g., HLA-DR17, HLA-DQ2) – occasionally done for academic interest or research, showing a susceptibility pattern, not a yes/no diagnosis. PubMed+1
D) Electrodiagnostic tests
Visual Evoked Potential (VEP) – measures electrical signals from the brain when you look at patterns; helps confirm the optic pathway is working if vision is worse than the corneal findings suggest.
Electroretinography (ERG) – checks retinal function; rarely needed, but can rule out retinal disease if symptoms don’t match the corneal picture.
(These help be sure the vision loss is from the cornea and not the retina/optic nerve; they aren’t Mooren-specific.)
E) Imaging tests
Anterior Segment OCT (AS-OCT) – a light-based “microscope scan” that maps corneal layers and quantifies thinning and depth of the ulcer; very useful for tracking healing or planning surgery. NCBIPMC
Corneal tomography/topography or pachymetry – maps the shape and thickness of the cornea (irregular astigmatism, thinnest point, progression). Ultrasound biomicroscopy (UBM) may be added if doctors need to check there’s no scleral involvement, which helps separate Mooren’s from other PUK. NCBI
Non-pharmacological treatments
(Each item: What it is – Purpose – How it helps)
Protective eye shield or glasses – Prevents accidental rubbing or trauma while the cornea is fragile; mechanical protection reduces risk of sudden perforation.
Frequent preservative-free lubricating drops & gel/ointment at night – Keeps the surface moist, reduces friction from blinking, and supports epithelial healing.
Moisture-chamber goggles/humidifier – Retains humidity around the eye; dryness worsens epithelial defects, so more moisture supports healing. PMC
Stop contact lens wear (unless used therapeutically by your doctor) – Regular lenses can irritate; therapeutic bandage lenses may be prescribed only under close supervision (see #10). AAO
UV and wind protection outdoors – Sunglasses/hat reduce wind-shear and light sensitivity, easing pain and microtrauma.
Lid hygiene if blepharitis is present – Warm compress + gentle lid cleaning can reduce inflammatory load and toxins at the lid margin that aggravate the ocular surface.
Avoid topical anesthetics at home – They delay healing and can cause severe complications if misused. (Doctors may use them briefly in-clinic.) EyeWiki
Avoid/stop topical NSAID eye drops – In thinning corneas, they can worsen melts and raise perforation risk; they’re generally avoided in Mooren’s ulcer. Review of Optometry
Cycloplegic drops (in-clinic prescription) – Not painkillers, but they rest the ciliary muscle, reducing spasm-related pain; non-pharm mechanism (lens/iris relaxation). AAO Journal
Bandage soft contact lens (BCL) – Placed by the doctor to splint the epithelium, reduce pain, and protect against lid shear; must combine with antibiotic cover and close follow-up. AAOPMC
Scleral lens (PROSE device) – Vaults over the cornea in a liquid reservoir, shields the surface and can promote epithelial healing in persistent defects; specialist fitting required. PMCAjo
Nutritional optimization (protein, vitamin A, C, zinc; see supplement section) – General wound-healing support helps the cornea re-epithelialize.
Treat any coincident dry eye disease – Lid-warming, meibomian gland care, and controlled environment improve tear film and surface stability. PMC
Manage triggers – Tell your clinician about recent trauma, surgery, infections, or hepatitis C; treating triggers (e.g., HCV) can help. Lippincott Journals
Strict infection control – If epithelium is open, avoid swimming/hot tubs; follow clean-hand and drop-hygiene rules to prevent secondary infection.
Cold compresses for comfort – Brief cold compress can reduce surface inflammation and pain (avoid pressure).
Eye-rest strategies – Frequent breaks, controlled screen time, blink exercises reduce ocular surface stress.
Smoking cessation – Smoking impairs wound healing and tear quality; quitting supports corneal recovery.
Allergen control – If allergic eye disease coexists, minimizing allergens reduces rubbing and inflammation.
Careful follow-up – Early, frequent slit-lamp checks let clinicians catch new thinning or leaks fast—key to saving vision. (This frequent-monitoring need in early care is emphasized in clinical case guidance.) WebEye
Drug treatments
Important: Doses are typical ranges used in corneal inflammatory disease; your ophthalmologist will individualize. Many are off-label for Mooren’s ulcer. Evidence is largely case series/observational; RCTs are lacking. PMC
Topical corticosteroid (e.g., prednisolone acetate 1% hourly, then taper)
Purpose: Rapidly suppress local inflammation to stop immune attack.
Mechanism: Blocks multiple inflammatory pathways.
Side effects: ↑ eye pressure, cataract risk, delayed epithelial healing if overused; needs close medical supervision. WebEyeOral corticosteroid (e.g., prednisone 0.5–1 mg/kg/day, then taper over weeks)
Purpose: Calms aggressive/bilateral disease or progression.
Mechanism: Systemic immunosuppression.
Side effects: Glucose elevation, mood/sleep changes, infection risk, osteoporosis with long use. NCBITopical cyclosporine A (e.g., 0.05%–1% twice to four times daily)
Purpose: Steroid-sparing control of local immune activity.
Mechanism: Calcineurin inhibitor—reduces T-cell activation and cytokines.
Side effects: Burning/irritation; rare infection risk. (Clinical reports include 1% drops used adjunctively in PUK/Mooren’s.) MDPIPMCTopical tacrolimus (e.g., 0.03%–0.1% ointment or compounded drops once–twice daily)
Purpose: Alternative local calcineurin inhibitor when cyclosporine is not enough.
Mechanism: T-cell suppression via calcineurin blockade.
Side effects: Stinging/irritation; use is off-label in corneal inflammation (specialist use). PMCDoxycycline (100 mg twice daily, often 2–4 weeks then taper)
Purpose: Anti-collagenase support to slow “melt.”
Mechanism: Inhibits MMPs and reduces inflammatory proteases that digest corneal collagen.
Side effects: Stomach upset, photosensitivity; avoid in pregnancy/children. ScienceDirectTopical N-acetylcysteine (NAC) 5–10% drops (e.g., 4–6×/day)
Purpose: Additional collagenase inhibition to reduce melt.
Mechanism: MMP inhibition and mucolytic action; used off-label in non-infectious keratolysis.
Side effects: Burning, conjunctival irritation. ResearchGateMethotrexate (10–25 mg once weekly + folic acid)
Purpose: Steroid-sparing systemic immunosuppressant for persistent disease.
Mechanism: Anti-metabolite that dampens T-cell activity and cytokines.
Side effects: Liver enzyme elevation, cytopenias; requires blood-test monitoring. (Part of PUK/Mooren’s immunomodulation toolkits.) NCBIMycophenolate mofetil (1 g twice daily)
Purpose: Alternative steroid-sparing agent.
Mechanism: Inhibits lymphocyte purine synthesis.
Side effects: GI upset, leukopenia; lab monitoring needed. NCBICyclophosphamide (1–2 mg/kg/day oral, or IV pulses in severe cases)
Purpose: Stronger immunosuppressant in aggressive, refractory melts.
Mechanism: Alkylating agent—suppresses rapidly dividing immune cells.
Side effects: Cytopenias, hemorrhagic cystitis (hydrate), infection risk; specialist oversight essential. NCBITopical interferon-α2a (compounded; dosing varies, e.g., 1–6×/day in reports)
Purpose: Adjunct immunomodulation when standard therapy fails or cannot be used.
Mechanism: Modulates immune signaling locally.
Evidence: Small case reports document improvement; overall evidence is limited.
Side effects: Irritation; access via compounding only. PubMedPMC
Often combined: A prophylactic topical antibiotic (e.g., moxifloxacin) is added if the epithelium is open to guard against infection; not to treat Mooren’s directly. Bandage/scleral lens use is paired with antibiotic cover and strict follow-up. AAO
Regenerative/biologic options
These are typically reserved for refractory cases under cornea + uveitis/immunology teams.
Rituximab – B-cell depleting monoclonal antibody
Dose (common regimens): 375 mg/m² IV weekly ×4, or 1,000 mg IV on days 1 & 15.
Function/Mechanism: Removes antibody-producing B-cells to reduce autoimmune attack.
Evidence: Case series in PUK show promise; used when conventional agents fail.
Notes: Infusion monitoring; infection risk. PMCInfliximab (anti-TNF-α) – Biologic anti-inflammatory
Dose: 5 mg/kg IV at weeks 0, 2, 6, then every 8 weeks.
Use: Refractory Mooren’s ulcer has improved in reports.
Risks: Screen for TB/hepatitis; risk of serious infection. PubMedScienceDirectAdalimumab (anti-TNF-α) – Subcutaneous biologic
Dose: Common ocular regimen 40 mg SC every 2 weeks (specialist adjusts).
Use: Extrapolated from PUK cases; used when other agents fail.
Risks: Similar to infliximab (TB/hepatitis screening). PMCTocilizumab (anti-IL-6 receptor) – Biologic immunomodulator
Dose: IV or SC schedules per rheumatology; specialist-directed.
Use: Sparse reports in PUK where other therapies failed.
Risks: Infection, lab monitoring. PMCIVIG (intravenous immunoglobulin) – Immune modulation
Dose: Often 2 g/kg over 2–5 days (varies).
Use: Case-based use in refractory immune corneal melts; evidence limited.
Risks: Headache, thrombosis risk; high cost. IOVSCenegermin (rh-NGF, Oxervate®) – regenerative biologic for epithelial healing
Dose: 20 mcg/mL 1 drop 6×/day for 8 weeks (FDA-approved for neurotrophic keratitis, not for Mooren’s; occasionally considered off-label to help stubborn epithelial defects).
Function/Mechanism: Nerve growth factor promotes corneal nerve recovery and epithelial healing.
Evidence: Strong RCT evidence in neurotrophic keratitis; off-label if used in non-neurotrophic melts. FDA Access DataNCBI
Surgeries
Conjunctival resection (peritomy) around the ulcer
What: A ring of conjunctiva adjacent to the ulcer is excised and lightly cauterized.
Why: The adjacent conjunctiva can harbor proteolytic enzymes and inflammatory cells that fuel melt; removing it cuts off this supply and helps the cornea stabilize. PubMed+1Lippincott JournalsCyanoacrylate tissue glue ± bandage contact lens
What: A tiny drop of medical-grade adhesive seals an impending leak or micro-perforation; a bandage lens protects it.
Why: Immediate tectonic support while immune therapy takes effect. AAO JournalAmniotic membrane transplantation (AMT)
What: A biological membrane is sutured or glued onto the ulcer.
Why: Provides scaffold and anti-inflammatory growth factors to help re-epithelialization and reduce pain; results vary by series. PubMedPMCLamellar (crescentic) keratoplasty / patch graft
What: A partial-thickness donor corneal “patch” reinforces the thinned rim.
Why: Restores strength and preserves globe integrity when thinning is advanced. BioMed CentralPenetrating keratoplasty (full-thickness corneal transplant)
What: Full-thickness graft if damage is deep or perforated.
Why: Tectonic + optical rehabilitation when other measures can’t restore structure. (Requires sustained immune control to prevent recurrence at graft edges.) BioMed Central
Avoid conjunctival flaps in active Mooren’s ulcer: case reports show worsening after flaps (likely because they carry inflammatory tissue over the melt). BioMed Central
Dietary / molecular & supportive supplements
(These support wound healing and tear film; they do not replace medical/surgical care. Discuss with your doctor, especially if pregnant, on blood thinners, or with kidney/liver disease.)
Protein (food goal ~1.2–1.5 g/kg/day) – Supplies amino acids for collagen and epithelium. PMC
Vitamin C (e.g., 500–1000 mg/day) – Collagen cross-linking cofactor; often used with doxycycline to slow melts. ScienceDirect
Vitamin A (diet and, if deficient, supervised supplementation) – Essential for epithelial health; deficiency causes corneal ulcers. (Avoid high-dose without supervision.) Wiley Online Library
Zinc (e.g., 15–30 mg/day) – Cofactor for tissue repair; don’t exceed recommended doses long-term. PMC
Omega-3 (EPA/DHA, e.g., 1–2 g/day total) – May improve tear film and surface comfort; evidence in dry eye is mixed but supportive for some patients. IOVS
Arginine (e.g., 3–9 g/day in divided doses) – Can support wound healing pathways in stressed tissues. PMC
Glutamine (e.g., 5–10 g/day) – Fuel for rapidly dividing epithelial cells (wound-healing data). PMC
Copper (small amounts via diet or multivitamin) – Needed for collagen enzymes; avoid excess.
Selenium (dietary range) – Antioxidant support; avoid high doses.
Hydration (2–3 L/day unless restricted) – Better tear volume and mucin function.
Taurine (low-dose) – Anti-oxidative/osmoprotective roles on the ocular surface (adjunctive; limited direct data in MU).
Probiotics (dietary) – Gut health may reduce systemic inflammation (general supportive rationale).
Vitamin D (e.g., 800–2000 IU/day if low) – Immune modulation; check levels first.
B-complex (RDA range) – Nerve and tissue metabolism support.
L-carnitine (dietary/low dose) – Osmoprotectant roles suggested in ocular surface stress.
Biologic eyedrops like autologous serum or platelet-rich plasma (PRP) are not standard supplements but blood-derived treatments used by specialists to promote epithelial healing when defects persist; numerous studies in ocular surface disease support benefit, though protocols vary and evidence quality ranges from moderate to low. PMC+1AAO Journal
When to see a doctor urgently
Sudden severe pain, light sensitivity, or drop in vision
New gray/white spot, crescent at the edge, or a visible thin “pinhole”
Any fluid leak (tears running with a salty taste after bending, or a positive “Seidel” test in clinic)
A contact lens glued on by discharge/pain or trauma to the eye
If you are on steroids and pain gets worse (possible infection or melt)
Early, frequent follow-up is critical in the first weeks. WebEye
Prevention tips (day-to-day)
No eye rubbing; use a clean tissue or artificial tears if itchy.
Protective eyewear during yard work, sports, windy/dusty days.
Manage blepharitis/dry eye to reduce surface stress. PMC
Avoid topical NSAID eye drops unless your cornea specialist specifically prescribes them. Review of Optometry
Sun/UV and wind protection (wrap-around glasses/hat).
Don’t swim or hot-tub with an open epithelial defect or bandage lens.
Quit smoking; it impairs wound healing.
Keep systemic infections under care (e.g., test/treat hepatitis C if indicated). Lippincott Journals
Medicines check – tell your doctor about all drops and pills; some can dry the eye or raise melt risk.
Regular follow-ups even when quiet; Mooren’s can relapse.
What to eat / what to avoid
Eat more: quality protein (fish, eggs, dairy/soy, legumes), vitamin-A–rich foods (leafy greens, carrots, eggs), vitamin C sources (citrus, berries), zinc (seafood, legumes, nuts), omega-3–rich fish (salmon, sardines), and plenty of water. Wiley Online LibraryPMC
Limit/avoid: Smoking and second-hand smoke; excess alcohol (impairs healing); very spicy/irritating foods if they worsen reflux/tearing; ultra-processed high-salt snacks if they dehydrate you; megadose supplements without labs/medical advice.
FAQs
Is Mooren’s ulcer an infection?
No. It’s mainly autoimmune. Doctors still check for infection because open ulcers can get secondarily infected. NCBIHow is it different from other “PUK” ulcers?
Mooren’s has no systemic vasculitis; other PUK often comes with diseases like rheumatoid arthritis. That’s why doctors do a systemic work-up first. NCBICan it affect both eyes?
Yes. One-eye disease can be milder; bilateral cases are often more aggressive and need systemic therapy early. EyeWikiWhy do doctors start steroids so quickly?
To stop the immune attack and protect corneal thickness while additional treatments are added. WebEyeAre steroid-sparing drops helpful?
Yes—cyclosporine or tacrolimus drops can reduce steroid needs by calming T-cells at the surface. MDPIWhy doxycycline and vitamin C?
They slow collagen breakdown (melt) by inhibiting MMPs and supporting collagen synthesis. ScienceDirectWhat about interferon drops?
Small case reports show benefit in some patients; evidence is limited, and access is via compounding pharmacies. PubMedCan biologics like rituximab or anti-TNF help?
In refractory cases, case series report success; they require screening and specialist oversight. PMCPubMedAre bandage or scleral lenses safe?
They protect and splint the surface when used with antibiotic cover and close follow-up. Infection risk rises if used unsupervised. AAOIs amniotic membrane a cure?
It helps healing and pain as a biologic scaffold, but disease control still depends on immunosuppression; results vary among studies. PubMedPMCWhy avoid topical NSAIDs?
Because in a thinning cornea, NSAIDs can worsen melt and even perforation. Review of OptometryCan hepatitis C treatment help?
Some reports show ulcer improvement after HCV therapy, supporting a trigger role in some patients. Lippincott JournalsWill I need surgery?
Surgery is needed if thinning is severe or a leak/perforation is present. The aim is tectonic support while medical therapy controls the autoimmunity. AAO JournalCan Mooren’s come back?
Yes—relapses can happen, so long-term follow-up is important even after healing. PMCWhat’s my outlook?
With early recognition, aggressive medical therapy, and timely surgery when needed, many eyes stabilize and keep useful vision, but delays can lead to perforation and scarring. High-quality trials are limited, so care is individualized. PMC
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 13, 2025.
Monovision LASIK
