Peripheral Ulcerative Keratitis (PUK)

Peripheral Ulcerative Keratitis (PUK) is a serious eye condition where the edge of the cornea (the clear front window of the eye) becomes inflamed, thins out, and forms a crescent-shaped ulcer very close to the limbus (the border between the cornea and the white part of the eye). This inflammation can eat away the corneal tissue (called “melting”), sometimes quickly, and can lead to a hole in the cornea (perforation) if not treated fast. PUK can be caused by autoimmune diseases (the body’s immune system attacking its own tissues), infections, or can be idiopathic (no clear cause), as in Mooren’s ulcer. Because the peripheral cornea sits next to many tiny blood vessels and immune cells, it is especially vulnerable to immune-driven damage, and that is why PUK tends to happen at the edge, not in the center. Early recognition is critical because perforation is an emergency and PUK can be the first sign of a dangerous whole-body disease like rheumatoid arthritis or vasculitis. NCBIReview of OphthalmologyPMC

Peripheral ulcerative keratitis (PUK) is a serious inflammation that eats away at the edge of the clear front window of the eye (the cornea). “Peripheral” means it happens along the rim of the cornea, near the white of the eye (the limbus). “Ulcerative” means there is an open sore in the surface skin of the cornea (the epithelium) together with loss of the supporting corneal tissue underneath (the stroma). Over time, this inflammation can thin the cornea so much that it can bulge, form an irregular shape, or even perforate (make a hole). PUK is not just an eye problem—very often it is a warning sign that the immune system is attacking the body, such as in rheumatoid arthritis (RA) or ANCA-associated vasculitis like granulomatosis with polyangiitis (GPA). Because the edge of the cornea is rich in tiny blood vessels and immune cells, inflammation can be very aggressive in this location. Prompt diagnosis and treatment are essential to protect sight and, sometimes, to uncover and control a dangerous whole-body disease. NCBIEyeWikiRush University System for Health

How PUK damages the eye

Think of the cornea like a clear, layered shield. At the edge, this shield lies next to a dense network of blood vessels and immune tissue in the conjunctiva and the white of the eye (sclera). When the immune system is overactive or misdirected (autoimmunity), it sends inflammatory chemicals and cells into this rim area. These chemicals (including enzymes called collagenases and proteases) break down the corneal scaffold in the periphery. The surface skin of the cornea can peel off (epithelial defect), and the deeper layers start melting (stromal lysis). Because the edge is mechanically important for the cornea’s shape, this melting quickly causes thinning, warpage (irregular astigmatism), and risk of perforation. Infections can also trigger similar melting. All of this explains the classic crescent-shaped ulcer close to the limbus, with redness, pain, and light sensitivity. NCBIPMC

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Types of PUK

1. PUK linked to systemic autoimmune disease
   This is the most common and most dangerous group. The eye inflammation is part of a wider body inflammation (vasculitis or connective tissue disease). Common links are rheumatoid arthritis and ANCA-associated vasculitis (e.g., GPA). In RA, PUK usually appears years after the arthritis and can signal a severe, blood-vessel-based complication; in GPA, it can even be the first clue to the disease. avehjournal.orgNCBI

2. PUK without a known systemic disease (Mooren’s ulcer)
   Mooren’s ulcer is a special pattern: a painful, crescent-shaped, peripheral ulcer that is by definition not tied to a known systemic autoimmune disease. It tends to creep around the corneal edge and can be very stubborn. Because its appearance overlaps with early autoimmune PUK, careful systemic evaluation is still needed to avoid missing a dangerous body-wide condition. EyeWikiEyeWorld

3. Infectious PUK (peripheral microbial keratitis)
   Less common but critical to recognize, this includes bacterial, viral (HSV/VZV), fungal, or mycobacterial infections that particularly involve the periphery. Infection-related ulcers look similar but need antimicrobial therapy, not just immune suppression. Corneal scrapings and cultures guide treatment. NCBI+1

4. PUK secondary to ocular surface inflammation or trauma
   Severe blepharitis, chronic contact-lens-related inflammation, exposure problems (poor eyelid closure), or chemical injury can create a local inflammatory loop at the corneal edge that leads to ulceration and thinning. Surgery near the limbus can sometimes trigger PUK in susceptible people. WebEye

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Causes

Below are twenty believable, evidence-anchored causes or associations that can set off or worsen PUK. Each item is explained in plain English so you can recognize the pattern.

1. Rheumatoid arthritis (RA)
   RA is the leading systemic association. Long-standing RA can evolve into a blood-vessel inflammation (vasculitis) that targets the corneal edge. When PUK shows up in RA, it often means the disease is severe and needs prompt systemic control. avehjournal.org

2. Granulomatosis with polyangiitis (GPA; ANCA-associated vasculitis)
   PUK may be the first sign of GPA. Patients may also have sinus problems, cough, or kidney issues. A positive PR3/c-ANCA supports the diagnosis. avehjournal.org

3. Microscopic polyangiitis (MPA; ANCA-associated)
   Similar to GPA but often without granulomas. p-ANCA/MPO positivity is common. Eye disease can include PUK. NCBI

4. Polyarteritis nodosa (PAN)
   A medium-vessel vasculitis that can rarely present with PUK as part of widespread vessel inflammation. NCBI

5. Systemic lupus erythematosus (SLE)
   SLE can inflame small vessels and the ocular surface, occasionally leading to PUK, especially when disease is active. NCBI

6. Sjögren’s syndrome
   Severe dryness and immune activity can damage the corneal edge, predisposing to ulceration and melt. NCBI

7. Inflammatory bowel disease (ulcerative colitis or Crohn’s)
   Eye inflammation can occur alongside gut flares. PUK is rare but reported. NCBI

8. Relapsing polychondritis
   Inflammation of cartilage (ears, nose, airway) can be accompanied by ocular surface inflammation and PUK. NCBI

9. Sarcoidosis
   Granulomatous inflammation can affect the eye; PUK is uncommon but possible. NCBI

10. Hepatitis B or C-related vasculitis
    Virus-related immune complex vasculitis may involve the eye and predispose to PUK. NCBI

11. Mooren’s ulcer (idiopathic peripheral autoimmune keratitis)
    An eye-only, severe, creeping peripheral ulcer with no proven systemic driver. It behaves like a local autoimmune attack on the corneal edge. EyeWiki

12. Severe staphylococcal blepharitis with marginal keratitis
    Chronic lid inflammation can cause immune “hot spots” at the corneal edge; if aggressive, these can ulcerate and thin like PUK. EyeWiki

13. Bacterial keratitis (peripheral)
    Organisms like Staphylococcus aureus or Pseudomonas can infect the corneal rim, producing a true infectious ulcer that can mimic or trigger PUK-like melting. NCBI

14. Herpes simplex or varicella-zoster keratitis
    These viruses can inflame and thin the cornea, sometimes in the periphery, and can be confused with autoimmune PUK. NCBI

15. Fungal keratitis (peripheral)
    Especially after plant-related trauma or in warm climates, fungi can infect the corneal edge and cause ulceration and melting. NCBI

16. Contact lens–related inflammation or infection
    Overwear, poor lens hygiene, or tight lenses can inflame the periphery and occasionally ulcerate or invite infection. NCBI

17. Exposure keratopathy (poor lid closure, facial nerve palsy)
    The corneal edge may dry out and break down first, leading to peripheral epithelial defects and secondary melting. NCBI

18. Ocular surgery near the limbus
    Surgical incisions or sutures at the corneal edge can rarely trigger a localized immune melt in predisposed patients. WebEye

19. Chemical injury
    Alkali injuries in particular can set off a cascade of inflammation and enzyme activity that thins the peripheral cornea. NCBI

20. Tuberculosis or syphilis (systemic infections with ocular involvement)
    These infections can drive immune complex disease or direct infection that contributes to peripheral corneal ulceration. Always consider them in the right risk setting. NCBI

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Common symptoms

1. Eye pain — often sharp or aching because exposed nerve endings and inflamed tissues are very sensitive.

2. Redness — the white of the eye flushes with blood due to active inflammation at the limbus. PMC

3. Light sensitivity (photophobia) — inflamed cornea and iris react strongly to light, causing discomfort. PMC

4. Tearing (watering) — the eye tries to wash and protect the injured cornea.

5. Foreign-body sensation — the rough ulcer edge feels like grit in the eye.

6. Blurred or fluctuating vision — the cornea loses its smooth shape; irregular astigmatism and scarring reduce clarity. PMC

7. Mucous discharge — inflamed surface cells and glands produce stringy mucus.

8. Tenderness to touch — the inflamed surface and adjacent sclera can be sore.

9. Worsening with dryness or wind — a dry surface exposes more nerve endings and slows healing.

10. Localized sectoral redness next to the ulcer — often most intense at the exact area of disease on the corneal edge. WebEye

11. Peripheral thinning signs — patients may notice a greyish rim or an arc near the edge if they look closely, sometimes with an overhanging inner edge.

12. Glare and halos at night — irregular corneal shape scatters light.

13. Reduced contact lens tolerance — lenses become painful or impossible to wear.

14. Symptoms of adjacent scleritis — deep, boring pain that may radiate to the brow or jaw, worse at night; PUK and scleritis often run together. WebEye

15. Sudden worsening if a tiny hole develops (perforation) — vision drops and pain spikes; this is an emergency.

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Diagnostic tests

A) Physical exam (at the slit lamp and in the clinic)

1. Visual acuity (Snellen chart)
   This basic test measures how well you see. In PUK, vision may drop due to an irregular surface, scarring, or swelling. Tracking acuity helps judge severity and response to treatment. NCBI

2. External exam of lids, lashes, and glands
   The doctor looks for blepharitis (lid margin inflammation), crusting, and meibomian gland blockage. These problems can fuel corneal edge inflammation and must be treated if present. EyeWiki

3. Conjunctival and scleral exam
   A careful look for sectoral redness, nodules, or deep tenderness suggests episcleritis or scleritis, which commonly accompanies PUK and signals a stronger immune drive. WebEye

4. Pupil and iris check
   Inflammation can spread inside the eye (iritis). Light reactions and signs inside the anterior chamber are assessed.

5. Intraocular pressure (IOP) check by tonometry
   PUK itself may not raise pressure, but treatment (like steroids) and associated inflammation can change it; baseline IOP guides safe care.

6. General physical exam for systemic disease
   The clinician looks for arthritic joints, nasal crusting/bleeding, cough or breathing issues, skin rashes or purpura, and blood-pressure or kidney concerns—clues to RA or vasculitis. NCBI

B) Manual/bedside ocular surface tests

7. Slit-lamp biomicroscopy with fluorescein dye
   A cobalt-blue light shows the ulcer as a bright green area and highlights the exact shape, depth, and location. The doctor also looks for a “Seidel sign” (leak of aqueous through a micro-perforation). This is the cornerstone bedside test for PUK. NCBI

8. Seidel test (perforation check)
   A concentrated stripe of fluorescein is painted over the thinnest spot. If it washes out in a stream, there is a leak—an emergency needing protection and urgent treatment. NCBI

9. Corneal sensation testing (Cochet-Bonnet esthesiometer or gentle wisp)
   Low sensitivity suggests herpetic disease or severe surface damage—and changes treatment choices. NCBI

10. Eyelid eversion and fornix sweep
    The lids are flipped to rule out a hidden foreign body, trichiasis (misdirected lashes), or giant papillae that rub the corneal edge.

11. Tear breakup time (TBUT)
    A small drop of fluorescein helps measure how fast the tear film breaks up. A short TBUT points to dry eye, which worsens PUK and slows healing. NCBI

12. Schirmer test (tear production)
    Filter paper strips measure basic tear output. Poor tear production means the surface is unprotected and at risk for ulceration and melt. NCBI

C) Laboratory and pathological tests (find the “why”)

13. Complete blood count (CBC), ESR, and CRP
    These tests look for inflammation and anemia of chronic disease. High ESR/CRP suggest active systemic inflammation. NCBI

14. Rheumatoid factor (RF) and anti-CCP antibodies
    These help detect RA. Anti-CCP is specific and, if positive with compatible symptoms, strengthens the RA link to PUK. NCBI

15. ANCA testing (c-ANCA/PR3 and p-ANCA/MPO)
    Positive ANCA supports ANCA-associated vasculitis (like GPA or MPA), important when PUK is the first clue and there are sinus, lung, or kidney features. NCBI

16. ANA and complement levels
    These screen for connective tissue diseases such as SLE or mixed connective tissue disease that can drive ocular surface vasculitis. NCBI

17. Infection screening: corneal scrapings for Gram/fungal stains, cultures, and PCR (e.g., HSV)
    If infection is possible, the clinician gently scrapes the ulcer edge to send samples to the lab. Results separate infectious ulcers from immune-driven PUK and guide antibiotics/antivirals/antifungals. NCBI

18. Systemic infection tests (TB IGRA/PPD, syphilis serology; hepatitis B/C)
    These uncover infectious triggers or vasculitis drivers, shaping both eye and systemic treatment. NCBI

19. Urinalysis and kidney profile
    Microscopic blood or protein in urine can signal kidney vasculitis in ANCA diseases; this is a crucial safety check when PUK may be only the “tip of the iceberg.” NCBI

20. Histopathology (if tissue is removed in surgery or debridement)
    Rarely, removed tissue is examined under a microscope to confirm inflammation pattern or rule out unusual infections.

D) Electrodiagnostic tests (rarely used in PUK—explained)

Electrodiagnostic studies are not routine for diagnosing PUK because the disease is at the corneal edge and can be seen directly. They are listed here for completeness because some patients undergo broader nervous-system testing when a systemic vasculitis is suspected.

21. Visual evoked potential (VEP)
    Measures electrical signals from the visual pathway to the brain. Only used if visual loss seems out of proportion to corneal findings or if there is concern for optic nerve involvement from a systemic process. (Again, not a standard PUK test.) NCBI

22. Electroretinogram (ERG)
    Checks retinal function. Considered only when retinal disease is suspected alongside systemic vasculitis; not part of routine PUK care. NCBI

23. Nerve conduction studies/EMG (systemic work-up)
    If a person with suspected vasculitis has numbness or weakness in the limbs, these tests can confirm peripheral nerve involvement. This does not diagnose PUK but supports the systemic diagnosis that often travels with PUK. NCBI

E) Imaging tests (to map thinning, track healing, and check systemic disease)

24. Anterior segment optical coherence tomography (AS-OCT)
    This painless scan creates cross-section images of the corneal edge to measure exact thickness, show where the tissue is melting, and monitor healing over time. AS-OCT findings can even help stage PUK (acute, healing, healed) in a consistent way. It is one of the most helpful modern tools for PUK. PMC+1EyeWiki

25. Corneal topography/tomography (e.g., Pentacam)
    Maps the cornea’s shape and thickness across the surface to show irregular astigmatism and peripheral thinning. This helps explain fluctuating vision and guides protective lenses or surgery planning. MDPI

26. Ultrasound biomicroscopy (UBM)
    High-frequency ultrasound images the corneal periphery and the front part of the sclera, useful when the view is limited or when deep scleral involvement is suspected.

27. B-scan ocular ultrasound
    If the front of the eye is too inflamed to see through, a B-scan checks the deeper eye to rule out other problems (e.g., posterior scleritis).

28. Clinical photography
    Serial photos document the size and depth of the ulcer and provide an objective record of healing or worsening.

29. Chest imaging (X-ray or CT) when systemic vasculitis is suspected
    Helps detect sinus disease, lung nodules, or infiltrates seen in GPA and other vasculitides that may present with PUK. avehjournal.org

30. Sinus CT (if GPA suspected)
    Evaluates chronic sinus inflammation, bone changes, or masses that fit with ANCA-associated disease. avehjournal.org

Non-pharmacological treatments

1. Protective lubrication (preservative-free tears/gel/ointment, very frequent)
   Purpose: keep the cornea wet and comfortable.
   Mechanism: dilutes inflammatory mediators in the tear film and reduces friction on the thin edge. WebEye

2. Moisture chamber goggles / humidifier
   Purpose: reduce evaporation.
   Mechanism: keeps a humid micro-environment to slow desiccation and allow epithelial cells to migrate.

3. Lid hygiene & warm compresses (blepharitis control)
   Purpose: reduce bacteria and toxins at the lid margin that trigger peripheral inflammation.
   Mechanism: unclogs meibomian glands and decreases staph antigens that can fuel marginal/peripheral keratitis. EyeWiki

4. Bandage contact lens (soft)
   Purpose: protect the ulcer surface and reduce pain.
   Mechanism: a smooth shield that decreases lid shear over the ulcer while epithelium heals. (Used carefully when infection is excluded.) Lippincott Journals

5. Scleral lens / PROSE device
   Purpose: vaults over the cornea, creating a fluid reservoir that nourishes and shields the surface.
   Mechanism: liquid bandage that promotes re-epithelialization and reduces mechanical trauma from blinking. PMC+1

6. Protective eye shield at night
   Purpose: prevent accidental rubbing or pressure that could perforate a thin cornea.
   Mechanism: physical barrier, particularly useful during sleep. Review of Ophthalmology

7. Temporary punctal occlusion (plugs) or cautery
   Purpose: keep tears on the eye longer.
   Mechanism: reduces tear drainage, helping hydration and epithelial migration. EyeWiki

8. Cyanoacrylate glue (office procedure)
   Purpose: urgently seal micro-perforations or areas of extreme thinning.
   Mechanism: polymerizes to form a tectonic patch, blocking entry of inflammatory mediators and giving structural support. Often combined with a (temporary) bandage lens. WebEyeAAO

9. Conjunctival resection around the ulcer
   Purpose: remove nearby inflammatory tissue feeding the melt.
   Mechanism: cuts off blood-borne enzymes and cells arriving via adjacent conjunctiva. (Preferred in Mooren’s ulcer.) PMC

10. Amniotic membrane graft (biologic dressing)
    Purpose: cover and heal the ulcer, reduce inflammation, and provide growth factors.
    Mechanism: amnion acts as a scaffold with anti-inflammatory effects and promotes epithelialization. PMCBioMed Central

11. Tarsorrhaphy (partial eyelid closure)
    Purpose: protect and hydrate the cornea when exposure worsens the ulcer.
    Mechanism: decreases evaporation and friction by reducing palpebral fissure.

12. Discontinue contact lens wear
    Purpose: remove mechanical stress and biofilm risk.
    Mechanism: halts micro-trauma and reduces infection risk during healing.

13. UV and wind protection outdoors
    Purpose: reduce irritation and evaporation.
    Mechanism: physical shield to limit triggers.

14. Treat eyelid malposition (entropion/ectropion) if present
    Purpose: stop lashes or lid edges from scraping the ulcer.
    Mechanism: surgical or procedural lid correction reduces corneal trauma.

15. Nutritional optimization
    Purpose: support collagen and epithelial repair.
    Mechanism: adequate protein and vitamin C aid collagen synthesis.

16. Smoking cessation
    Purpose: improve ocular surface healing and reduce inflammation.
    Mechanism: smoking impairs microcirculation and collagen repair.

17. Manage systemic triggers (coordinate with rheumatology)
    Purpose: control the root autoimmune disease to stop the eye melt.
    Mechanism: systemic disease control reduces immune attack on the cornea. Review of Ophthalmology

18. Eyelid taping or moisture patch at night (if lagophthalmos)
    Purpose: prevent overnight drying.
    Mechanism: maintains closed, moist environment.

19. Careful avoidance of topical NSAIDs
    Purpose: reduce risk of corneal melt associated with NSAIDs in vulnerable corneas.
    Mechanism: NSAIDs can impair epithelial healing in some cases. ScienceDirect

20. Close, frequent follow-up
    Purpose: monitor thinning and catch perforation early.
    Mechanism: serial exams with AS-OCT and slit-lamp allow timely escalation. (Imaging supports.)

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Drug treatments

Important note on steroids: Sources differ on topical steroid use in PUK. Many cornea specialists avoid topical steroids during active melting for fear of accelerating keratolysis, preferring lubrication, antibiotics, doxycycline, vitamin C, and systemic immunosuppression; others may use carefully in selected cases. Systemic steroids and steroid-sparing immunomodulators are central when autoimmune disease is driving PUK. Review of OphthalmologyEyeWiki

1. Prednisone (systemic corticosteroid)
   Class/Dose: 0.5–1 mg/kg/day orally; in severe cases, IV methylprednisolone 1 g/day ×3 days then oral taper.
   Purpose: quickly suppress immune attack to stop melting.
   Mechanism: broad anti-inflammatory and anti-lytic effects.
   Side effects: hyperglycemia, hypertension, mood change, infection risk, osteoporosis, GI irritation; taper slowly. EyeWiki

2. Methotrexate (antimetabolite, steroid-sparing)
   Dose: 10–25 mg once weekly PO/SC with folic acid daily (except MTX day).
   Purpose: long-term control in RA/vasculitis-associated PUK.
   Mechanism: inhibits dihydrofolate-dependent pathways, dampening lymphocyte activity.
   Side effects: liver toxicity, cytopenias, stomatitis; avoid in pregnancy. EyeWiki

3. Azathioprine (antimetabolite)
   Dose: 1–2 mg/kg/day PO.
   Purpose: steroid-sparing control of autoimmune PUK.
   Mechanism: purine analog; reduces lymphocyte proliferation.
   Side effects: leukopenia, hepatotoxicity; TPMT testing helpful. EyeWiki

4. Mycophenolate mofetil (antimetabolite)
   Dose: 1–1.5 g twice daily PO.
   Purpose: alternative steroid-sparing agent.
   Mechanism: blocks inosine monophosphate dehydrogenase to suppress T/B cells.
   Side effects: GI upset, infection risk. EyeWiki

5. Cyclophosphamide (alkylator)
   Dose: 1–2 mg/kg/day PO or IV pulses under specialist care.
   Purpose: severe, vision-threatening, vasculitis-linked PUK.
   Mechanism: profound lymphocyte suppression.
   Side effects: cytopenias, cystitis, infertility; requires close monitoring. EyeWiki

6. Cyclosporine A (calcineurin inhibitor) — topical and/or systemic
   Topical dose: 0.05%–2% drops, 2–4×/day.
   Purpose: calm local surface inflammation; adjunct to systemic therapy.
   Mechanism: calcineurin inhibition reduces T-cell cytokines.
   Side effects: stinging; systemic CsA has renal/HTN risks. WebEyeScienceDirect

7. Tacrolimus (calcineurin inhibitor) — often topical 0.03% ointment
   Dose: apply 1–2×/day to lids/ocular surface as directed (compounded drops also used).
   Purpose: steroid-sparing control of surface inflammation and some refractory PUK/Mooren’s cases.
   Mechanism: calcineurin inhibition like CsA, often stronger at T-cell suppression.
   Side effects: burning; rare HSV reactivation reported in atopic eyes (monitor). PMCophed.com

8. Doxycycline (tetracycline class)
   Dose: 50–100 mg once or twice daily PO.
   Purpose: anti-collagenase/MMP effect to slow melting; also improves meibomian function.
   Mechanism: down-regulates MMPs and inflammation.
   Side effects: photosensitivity, GI upset; avoid in pregnancy/children. PMCReview of Ophthalmology

9. Vitamin C (ascorbate)
   Dose: commonly 500 mg 1–2×/day PO.
   Purpose: supports collagen synthesis during corneal repair.
   Mechanism: co-factor for collagen cross-linking enzymes.
   Side effects: GI upset at high doses; caution in renal stones. Review of OphthalmologyScienceDirect

10. Topical prophylactic antibiotic (e.g., moxifloxacin 0.5% QID while epithelial defect persists)
    Purpose: prevent superinfection on an open ulcer.
    Mechanism: kills or suppresses bacteria during healing.
    Side effects: surface irritation; prolonged fluoroquinolone use may upregulate MMPs—use judiciously. WebEye

Caution: Topical NSAIDs are generally avoided in melting corneas due to reported association with worsening keratolysis. ScienceDirect

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Dietary molecular supplements

These can support ocular surface healing but do not replace urgent medical and surgical care.

1. Vitamin C — 500 mg 1–2×/day.
   Function: collagen support; Mechanism: co-factor in collagen synthesis. Review of Ophthalmology

2. Omega-3 fatty acids (EPA/DHA) — 1–2 g/day combined EPA+DHA.
   Function: anti-inflammatory support for meibomian/tear function; Mechanism: shifts eicosanoids toward pro-resolving mediators.

3. Vitamin D3 — 1000–2000 IU/day (personalized).
   Function: immune modulation; Mechanism: vitamin D receptors on immune cells can temper inflammatory responses.

4. N-Acetylcysteine (oral) — 600 mg 1–3×/day.
   Function: antioxidant and mucolytic; Mechanism: reduces oxidative stress and may modulate MMP activity (topical NAC also described). EyeWiki

5. Zinc — 10–25 mg/day.
   Function: epithelial repair co-factor; Mechanism: protein and DNA synthesis support.

6. L-lysine — 500–1000 mg/day.
   Function: HSV-prone patients sometimes use it; Mechanism: may counter arginine-dependent HSV replication (evidence mixed).

7. Curcumin (turmeric extract) — 500–1000 mg/day with pepper extract for absorption.
   Function: systemic anti-inflammatory; Mechanism: NF-κB pathway modulation.

8. Collagen peptides/gelatin — 5–10 g/day.
   Function: substrate for collagen building; Mechanism: provides amino acids for extracellular matrix.

9. Riboflavin (B2) — 100–200 mg/day.
   Function: cellular energy; Mechanism: co-factor in oxidative metabolism; topical riboflavin+UVA is a procedure (cross-linking), not a supplement.

10. Multinutrient ocular surface formulas (vitamins A/E, trace minerals) — as labeled.
    Function: fills dietary gaps; Mechanism: supports epithelial integrity.
    Always check interactions (e.g., anticoagulants with omega-3/curcumin) and individual health status.

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Regenerative / biologic” therapies

1. Rituximab (anti-CD20 monoclonal antibody, biologic)
   Dose: 1000 mg IV on days 1 & 15 (RA regimen) or 375 mg/m² weekly ×4; repeat per rheumatology.
   Function: for refractory RA- or ANCA-associated PUK.
   Mechanism: depletes B-cells that drive auto-antibody inflammation.
   Notes: infection risk; screen for hepatitis/TB. PMC

2. Infliximab (anti-TNF-α monoclonal antibody)
   Dose: 3–5 mg/kg IV at weeks 0, 2, 6, then every 8 weeks.
   Function: shuts down severe immune-driven melts (including IBD-related).
   Mechanism: blocks TNF-α, a key inflammatory cytokine.
   Notes: TB/hepatitis screening; infusion reactions possible. PMC

3. Adalimumab (anti-TNF-α, SC)
   Dose: 40 mg subcutaneously every 2 weeks (autoimmune uveitis/RA schedules).
   Function: steroid-sparing control of systemic inflammation driving PUK.
   Mechanism: neutralizes TNF-α. Review of Ophthalmology

4. Tocilizumab (anti-IL-6 receptor biologic)
   Dose: per rheumatology protocol (e.g., 162 mg SC weekly/biweekly or IV).
   Function: option in refractory autoimmune cases.
   Mechanism: blocks IL-6 signaling to reduce inflammation. MDPI

5. Autologous Serum Eye Drops (ASED)
   Dose: commonly 20%–50% serum, 4–8×/day (compounded).
   Function: regenerative tear substitute rich in growth factors and vitamins.
   Mechanism: mimics natural tears to promote epithelial healing and reduce surface inflammation. PMCIOVS

6. Platelet-Rich Plasma (PRP) eye drops
   Dose: protocol-specific (often 4–8×/day).
   Function: concentrated platelet growth factors speed epithelial closure.
   Mechanism: delivers PDGF, TGF-β, EGF, and others to stimulate repair; helpful in non-healing ulcers. PMCLippincott Journals

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Surgeries or procedures

1. Cyanoacrylate tissue adhesive (“glue”)
   Procedure: small drop of glue is placed on the thin or perforated spot (often <3 mm), usually with a bandage lens.
   Why: immediate tectonic support to stop leak and buy time for healing and systemic control. WebEyeLippincott Journals

2. Conjunctival resection (peritomy) around the ulcer
   Procedure: remove a ring of conjunctiva adjacent to the melt.
   Why: cuts off inflammatory supply from conjunctival vessels and immune cells; especially useful in Mooren’s ulcer. PMC

3. Amniotic membrane transplantation (AMT)
   Procedure: one or multiple layers of amnion are sutured or glued onto the ulcer.
   Why: biologic bandage to reduce inflammation and promote regrowth; also adds tectonic strength in thinning. PMCBioMed Central

4. Lamellar/tectonic patch graft (corneal or corneoscleral graft)
   Procedure: partial-thickness corneal (or scleral) patch to restore thickness.
   Why: treats advanced melts or perforations when glue/membrane are insufficient. EyeWiki

5. Temporary tarsorrhaphy
   Procedure: partly sew eyelids together to protect the cornea.
   Why: reduces exposure and speeds epithelial recovery in severe surface disease.

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Prevention tips

1. Treat and monitor the underlying autoimmune disease with a rheumatologist. Review of Ophthalmology

2. Address lid disease (blepharitis, MGD) with hygiene and warm compresses. EyeWiki

3. Avoid contact lenses during active disease; resume only with specialist approval.

4. Use preservative-free lubrication frequently if you have dry eye tendencies.

5. Protect eyes from wind/UV and dusty environments.

6. Stop smoking and limit irritants that slow healing.

7. Avoid topical NSAIDs in a thinning cornea unless a cornea specialist advises them. ScienceDirect

8. Eat a nutrient-rich diet (adequate protein, vitamin C, and omega-3s).

9. Manage systemic infections and get screened for TB/hepatitis before immunosuppression. Review of Ophthalmology

10. Keep close follow-up appointments for early detection of re-thinning or superinfection.

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When to see a doctor

• Immediately if you have severe eye pain, sudden vision drop, or a “leak” (water running from the eye after staining) — this may indicate perforation.

• Urgently (same day) for new redness, light sensitivity, tearing, or a crescent-shaped gray edge on the cornea.

• Promptly if you have RA, vasculitis, or other autoimmune disease and you notice any new eye symptoms — PUK can be the first sign of a serious flare. NCBI

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What to eat and what to avoid

1. Eat protein-rich foods (eggs, fish, legumes, lean meats) to supply amino acids for repair.

2. Eat vitamin-C-rich foods (citrus, guava, kiwi, pepper) to support collagen.

3. Eat omega-3-rich foods (fatty fish, flax/chia) to help calm surface inflammation.

4. Hydrate well — adequate fluids support tear production.

5. Include colorful vegetables/fruits (antioxidants) to reduce oxidative stress.

6. Limit ultra-processed, high-sugar foods that can promote inflammation.

7. Limit excessive alcohol, which can dehydrate and impair healing.

8. Avoid smoking and vaping (they reduce oxygen and slow repair).

9. Discuss supplements (vitamin D, omega-3, vitamin C, NAC) with your clinician to personalize dosage.

10. Be cautious with herbal “immune boosters” — some conflict with immunosuppressants; always check with your doctor.

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Frequently asked questions (FAQs)

1) Is PUK contagious?
No. Non-infectious PUK is an immune problem, not an infection. But infection can mimic or complicate PUK, so doctors often culture first if unsure. EyeWiki

2) Why the edge of the cornea, not the center?
The peripheral cornea sits next to blood and lymphatic vessels and many immune cells, so immune attacks and enzyme release hit the edge first. Review of Ophthalmology

3) Can PUK make me blind?
Yes, if not treated. Rapid melting can cause perforation, scarring, or infection. Immediate care greatly reduces this risk. NCBI

4) What is Mooren’s ulcer?
A PUK-like ulcer with no proven systemic autoimmune disease — an idiopathic immune attack on the cornea itself. NCBI

5) Do I need a rheumatologist?
Often yes. Over half of PUK cases link to systemic autoimmune disease, and coordinated care improves outcomes. Review of Ophthalmology

6) Are topical steroids safe?
Controversial in active melting: many specialists avoid them initially because they may worsen keratolysis; systemic steroids and immunomodulators are preferred when autoimmune disease is active. Decisions are individualized by your cornea specialist. Review of OphthalmologyEyeWiki

7) Why doxycycline and vitamin C?
Doxycycline reduces MMPs (enzyme-driven melting). Vitamin C supports collagen to rebuild the cornea. PMCReview of Ophthalmology

8) What does glue do?
Cyanoacrylate glue makes an instant patch over a thin spot or small hole, buying time for healing or later grafting. WebEye

9) What is amniotic membrane?
A biologic dressing from donated placenta that reduces inflammation and speeds epithelial growth. PMC

10) Will I need a corneal transplant?
Only if thinning or perforation is too advanced for glue or amnion. Even then, systemic immunosuppression helps prevent recurrent melts and graft failure. MDPI

11) Are scleral lenses just for vision?
They also protect and bathe the cornea in fluid, which promotes healing of stubborn defects. PMC

12) Can PUK come back?
Yes. Recurrences can occur if the underlying immune disease flares or if local risk factors return. Regular follow-up matters. Scholars@Duke

13) How fast can PUK worsen?
Sometimes very fast — hours to days in aggressive cases. Seek care immediately for worsening pain or vision. NCBI

14) What tests will I need before biologics or strong immunosuppressants?
Screening for TB and hepatitis is standard. Your team will also check blood counts and liver/kidney function. Review of Ophthalmology

15) What’s the prognosis?
With prompt diagnosis, systemic control, and surface protection, many eyes stabilize. Prognosis depends on severity, presence of scleritis, and control of the systemic disease. NCBI

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 21, 2025.