Linear Interstitial Keratitis (LIK)

Linear interstitial keratitis (LIK) is a non-ulcerative, line-shaped inflammatory streak inside the cornea’s stromal layer. It looks like a straight, pale or hazy stripe at the slit lamp. The epithelium (the skin of the cornea) is usually intact, so there is no open sore. The endothelium (the inner lining) is also not the primary problem. Many patients feel light sensitivity, tearing, and blurred vision while the line is active. On modern scans (AS-OCT), the line shows up as a bright band limited to the anterior stroma; on in-vivo confocal microscopy, tiny needle-like reflective structures and activated stromal cells may be seen. Doctors usually diagnose it clinically and exclude infections; steroid drops commonly settle the inflammation. The overall cause is unclear—older reports speculated about infections like syphilis, but newer case series show no consistent infectious trigger. PMCPubMed

Linear Interstitial Keratitis is a very rare type of corneal inflammation where a thin, straight, horizontal line of haze or opacity appears inside the stroma (the middle, transparent layer) of the cornea. Unlike “ulcer” problems that break the surface, LIK happens within the cornea and usually does not involve the outer skin (epithelium) or the inner lining (endothelium). People often notice blurred vision, light sensitivity, tearing, redness, and a scratchy feeling. Doctors see a linear (line-like) white haze in the stroma, sometimes with tiny new blood vessels and mild inflammation inside the front of the eye. In published case series, topical steroid drops usually calm it down, but relapses can occur, and a faint scar may remain off the visual axis. Imaging tests (like anterior segment OCT) often show that the opacity sits mainly in the anterior stroma, and in-vivo confocal microscopy may show needle-like hyper-reflective structures in the same region. PMC

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Types

Because LIK is so rare, “types” are descriptive rather than official categories. These labels help clinicians think and communicate clearly:

1. Idiopathic LIK
   This is the most common label: the line-shaped stromal inflammation appears without a proven cause after history, exam, and testing. Some cases are non-migratory (the line stays put), others migratory (the line slowly shifts with time). MalaCards

2. Immune-flavored LIK
   The patient’s history, associated autoimmune features, or the way the eye responds to steroids makes doctors suspect an autoimmune mechanism, even if a single named disease is not proven. (This is a working hypothesis rather than a settled fact.) PMC

3. LIK with a recent trigger
   Occasionally, LIK appears after a recent corneal event (e.g., a prior abrasion or refractive surgery in the broader IK literature). When timing fits and no organism is found, clinicians may treat it as a sterile, immune reaction that happens to take a linear form. (Case reports include an LIK patient with a history of LASIK.) PMC

4. Anterior-predominant vs. pan-stromal
   Most cases show an anterior stromal band on AS-OCT; some confocal studies show wider stromal involvement even when the OCT band looks superficial. This type distinction comes from imaging findings and helps guide follow-up, not treatment. PubMedjuniperpublishers.com

5. Unilateral vs. (rarely) bilateral
   LIK is usually one-sided. Broader IK can be bilateral in certain systemic diseases, but true bilateral linear IK is unusual.

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Causes to consider

Important: For LIK, a single, proven cause is often absent. The list below blends what we know about general interstitial keratitis causes with case-series insights about linear presentations. Doctors use history, exam, and tests to rule these in or out.

1. Idiopathic (no identifiable cause) – After careful evaluation, some patients have no infection, no systemic disease, and no exposure that explains the line. These still respond to steroids. PMC

2. Immune reaction after minor corneal injury – A small scratch or prior irritation may “wake up” local immunity and create a linear stromal response rather than a round patch.

3. Autoimmune tendency without a named disease – Family or personal history hints at autoimmunity; the eye behaves like an immune-driven keratitis and quiets with steroids. PMC

4. Herpes simplex–related stromal keratitis (immune-mediated) – Classic IK cause; prior fever blisters or unilateral, recurrent episodes raise suspicion, even if PCR is negative during LIK. EyeWiki

5. Varicella-zoster (shingles)–related IK – After zoster affecting the eye/forehead, the cornea can develop immune stromal inflammation. EyeWiki

6. Syphilis (congenital or acquired) – Historically the leading cause of IK; today, still checked because it’s treatable and sometimes missed. (Recent LIK case series generally show negative syphilis tests, but clinicians still screen.) EyeWikiPMC

7. Lyme disease – In tick-endemic areas, Borrelia infection can drive IK; testing is guided by exposure history. EyeWiki

8. Tuberculosis – Rare in many regions, but possible via immune mechanisms; more likely to be considered with risk factors or compatible systemic signs. EyeWiki

9. Leprosy (Hansen disease) – Can involve the cornea with IK changes, especially in endemic settings. EyeWiki

10. Epstein–Barr virus and other viral exposures – Some viral antigens may set off stromal inflammation without active surface infection. EyeWiki

11. Cogan syndrome – A rare autoimmune disease linking IK with inner-ear symptoms (vertigo, tinnitus, hearing loss); if a patient with IK also has new hearing issues, doctors think about Cogan syndrome. NCBIEyeWiki

12. Sarcoidosis – A multi-system inflammatory disease that can inflame the cornea’s stroma as part of widespread granulomatous disease. EyeWiki

13. Granulomatosis with polyangiitis (Wegener’s) – A systemic vasculitis that can inflame the eye; peripheral stromal disease may extend inward. EyeWiki

14. Rheumatoid arthritis–associated ocular inflammation – Severe peripheral corneal inflammation can spill inward to the stroma, resembling IK. EyeWiki

15. Relapsing polychondritis – Autoimmune attacks on cartilage sometimes include corneal involvement with IK-like changes.

16. Parasitic disease (onchocerciasis) – In endemic regions, sclerosing keratitis and related stromal inflammation can occur; not typically linear, but IK mechanisms overlap. EyeWiki

17. Acanthamoeba – Classically causes ulcerative keratitis, but deep stromal immune reactions may mimic IK in atypical cases; confocal microscopy helps. EyeWiki

18. Leptospirosis / brucellosis – Uncommon, but listed IK causes in appropriate exposure contexts. EyeWiki

19. Contact lens–associated immune keratitis – Usually peripheral and non-infectious; rarely could present in unusual patterns. EyeWiki

20. Heavy metal/intracorneal foreign material reactions – Rare immune responses to embedded particles can produce stromal inflammation that may look band-like. EyeWiki

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Common symptoms

1. Blurred vision – The linear haze scatters light and makes images less sharp.

2. Light sensitivity (photophobia) – Inflamed corneal nerves make bright light uncomfortable.

3. Tearing – The eye makes more tears to soothe irritation.

4. Eye redness – Surface blood vessels dilate because of nearby inflammation.

5. Eye pain or ache – From inflamed corneal nerves and ciliary spasm.

6. Foreign-body sensation – It may feel like grit even without a surface scratch.

7. Glare and halos – Light spreads around the linear haze, especially at night.

8. Reduced contrast – Whites and grays look washed out near the line.

9. Monocular “double” or ghost images – The line bends light unevenly, creating a shadow image.

10. Variable vision during the day – Tear film changes and pupil size make vision fluctuate.

11. Headache around the eye – From squinting and ciliary muscle strain.

12. Soreness with eye movement – Inflammation can make focusing and moving the eye uncomfortable.

13. Difficulty reading – The line across the pupil reduces clarity for small letters.

14. Reduced night driving confidence – Glare and halos are worse in low light.

15. Recurrent episodes – Symptoms may come, settle with treatment, and return months or years later (a known behavior in LIK series). PMC

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Diagnostic tests

Doctors don’t run all of these for every patient. They choose based on history, exam, and local disease patterns. The aim is to confirm the pattern, document depth, and screen for treatable causes (especially syphilis/herpes/Cogan syndrome).

A) Physical exam–based tests (done at the slit lamp and in clinic)

1. Best-corrected visual acuity
   Measures how much the line affects clarity with proper glasses; tracks recovery over time. EyeWiki

2. External and conjunctival inspection
   Looks for redness pattern, lid issues, or blepharitis that might aggravate symptoms. EyeWiki

3. Pupil assessment
   Rules out deeper inflammation affecting the iris (rare in LIK but relevant if ache and photophobia are severe). EyeWiki

4. Intraocular pressure (IOP) measurement
   Establishes a baseline, since steroid treatment—which LIK often needs—can raise IOP. EyeWiki

5. Dilated fundus examination
   Ensures no posterior eye disease is masquerading as a corneal problem or coexisting with it. EyeWiki

B) Manual/bedside corneal tests

6. Slit-lamp biomicroscopy (detailed corneal mapping)
   The key test to see the straight stromal band, check if the epithelium is intact (usually yes), and look for neovascularization or thinning. This clinches the working diagnosis. EyeWiki

7. Fluorescein staining
   Dye highlights any surface defect; in LIK the surface is typically intact, which supports an interstitial (not ulcerative) process. EyeWiki

8. Corneal pachymetry
   Ultrasound or optical measurements check for localized thinning along the line; helpful for monitoring over time. EyeWiki

9. Corneal esthesiometry (sensation testing)
   A wisp of cotton or specialized device checks corneal nerve sensitivity; reduced sensation hints at herpetic disease even if tests are negative.

10. Schirmer’s test / tear breakup time
    Assesses tear film; dryness won’t cause LIK but can worsen discomfort and blur layered on top of the stromal line.

C) Laboratory & pathological tests (ordered selectively)

11. Syphilis screen (RPR or VDRL) and confirmation (TP-PA or FTA-ABS)
    Syphilis remains important to exclude in any IK because it’s treatable and sometimes silent. (Many LIK cases test negative, but screening is still recommended.) EyeWiki

12. HSV/VZV testing (PCR from tears/surface if a defect, or paired serology when helpful)
    Aimed at confirming or supporting a herpetic background when history suggests it; negative results don’t rule out an immune stromal process. EyeWiki

13. TB testing (IGRA or tuberculin skin test) with chest imaging if positive
    Used when risk factors, travel, or systemic symptoms are present. EyeWiki

14. Lyme serology (ELISA with confirmatory Western blot)
    Chosen in tick-exposed patients or endemic regions. EyeWiki

15. Autoimmune panel (ANA, ANCA, RF, ESR/CRP)
    Screens for systemic inflammatory diseases (e.g., GPA/Wegener’s, rheumatoid arthritis, connective tissue disease) that can underlie IK-like corneal inflammation. EyeWiki

16. Angiotensin-converting enzyme (ACE) ± lysozyme
    Considered if sarcoidosis is suspected from history or imaging. EyeWiki

D) Electrodiagnostic tests (occasionally used)

17. Visual evoked potential (VEP)
    Rarely needed for LIK itself; used if vision loss seems out of proportion and clinicians want to ensure the visual pathway beyond the cornea is functioning.

18. Full-field electroretinogram (ERG)
    Again, not routine; used when doctors must exclude retinal dysfunction in complex cases with unexplained vision loss.

(These electrical tests help when the clinical picture doesn’t add up; most LIK patients never need them.)

E) Imaging tests (document depth, location, and cell-level detail)

19. Anterior segment optical coherence tomography (AS-OCT)
    Shows a hyper-reflective linear band limited to the anterior stroma in many LIK cases, helping confirm the pattern and monitor thinning or resolution. PMC

20. In-vivo confocal microscopy (IVCM)
    Offers microscope-level images of living cornea; in LIK, it may show activated stromal cells and needle-like hyper-reflective structures along the band—useful for research, classification, and ruling out atypical infections. PubMed

Non-pharmacological treatments

1. Education and early follow-up: LIK can relapse; quick steroid re-start under supervision limits scarring. PMC

2. Sunglasses / UV protection: reduces photophobia and UV-driven inflammation.

3. Contact lens holiday: if you wear contacts, pausing use removes a trigger for immune keratitis and infection risk. EyeWiki

4. Lid hygiene (warm compress + lid scrubs): calms blepharitis/meibomian disease that worsens surface inflammation.

5. Humidifier / blink breaks: supports tear film, reduces glare and discomfort.

6. Avoid eye rubbing: rubbing ramps up inflammation and can worsen thinning/scar.

7. Nighttime shield: prevents accidental trauma to a sensitized cornea.

8. Manage systemic diseases: coordinate with rheumatology/ID for suspected syphilis, TB, Cogan syndrome, sarcoid, GPA—treating the root lowers eye relapse risk. CDCPMCBioMed Central

9. Cool compresses: reduces surface hyperemia and discomfort.

10. Blue-blocking/tinted lenses: practical help for light sensitivity.

11. Workstation ergonomics: larger fonts, frequent breaks to reduce strain.

12. Smoking cessation: smoking impairs ocular surface healing and promotes neovascularization.

13. Allergen control: reduce itch/rub cycle that fuels inflammation.

14. Treat dry eye contributors: warm compresses, environment tweaks; improves comfort and optical quality.

15. Nutritional optimization: adequate vitamin A, C, D, zinc, omega-3 supports immune balance and epithelial healing (see supplements below).

16. Scleral lens (later, when quiet): vaults over scars to improve optics without touching the cornea (fit only after inflammation is controlled).

17. Photography tracking: periodic slit-lamp photos to document improvement or recurrence.

18. Psychological support: flare-ups are stressful—brief counseling reduces anxiety and improves adherence.

19. Protective eyewear at work/sport: prevents minor traumas that can re-ignite inflammation.

20. Sun/light management plan: hats, wide-brim caps, shaded work areas to cut glare during recovery.

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Drug treatments

Safety note: Doses below are typical adult examples; clinicians individualize for you.

1. Topical corticosteroid (first-line for LIK/immune IK)
   Example: Prednisolone acetate 1% q1–2h while awake for several days, then taper over weeks as the line fades; or loteprednol 0.5% qid for milder cases or steroid-response risk.
   Purpose/Mechanism: Blunts stromal immune inflammation, limits scarring and neovascularization.
   Side effects: ↑IOP, cataract over time, infection risk if surface is broken—so doctors monitor pressure and healing. EyeWiki

2. Cycloplegic drop (for pain/iritis)
   Example: Homatropine 2% bid–tid, or Atropine 1% once–twice daily.
   Purpose: Relieves ciliary spasm pain and photophobia.
   Side effects: Blurred near vision, light sensitivity from dilation. (Common uveitis practice.)

3. Antiviral therapy when herpetic disease is suspected or proven (use with steroid)
   Example active treatment: Acyclovir 400 mg orally 5×/day 7–10 days, or Valacyclovir 500 mg tid (alternatives per clinician).
   Prophylaxis in recurrent HSV stromal keratitis: Acyclovir 400 mg bid reduces recurrences.
   Purpose/Mechanism: Suppresses HSV replication while steroids treat immunity.
   Side effects: GI upset, renal dose adjustments in kidney disease. EyeWiki

4. Topical antiviral (only if epithelial HSV is present)
   Example: Trifluridine 1% up to 8–9×/day short term.
   Purpose: Surface antiviral when there is an epithelial lesion.
   Side effects: Surface toxicity if prolonged. EyeWiki

5. Doxycycline (anti-collagenase & anti-inflammatory)
   Example: 50–100 mg bid for several weeks if thinning, lipid keratopathy, or MGD co-exists.
   Purpose/Mechanism: Inhibits matrix metalloproteinases, calms meibomian inflammation.
   Side effects: GI upset, photosensitivity; avoid in pregnancy. (Supported widely for ocular surface/keratolysis.)

6. Topical calcineurin inhibitors (steroid-sparing, off-label)
   Examples: Cyclosporine A 0.05–0.1% bid; Tacrolimus 0.03–0.1% drops/ointment qhs–bid.
   Purpose: Long-term immune modulation to reduce steroid dependence.
   Side effects: Initial stinging; rare infection reactivation—used by specialists. (Supported in ocular surface inflammation literature.)

7. Anti-VEGF therapy for corneal neovascularization (off-label)
   Examples: Topical bevacizumab 1% qid for ~3–4 weeks, or subconjunctival bevacizumab 2.5 mg/0.1 mL monthly × up to 3 injections if vessels threaten vision or graft survival.
   Purpose/Mechanism: Shrinks new corneal vessels to reduce haze/scar and improve graft prognosis.
   Side effects: Epithelial healing delay is possible; use by cornea specialists. Evidence from clinical trials and meta-analyses supports benefit. PMCWJGNet

8. Antibiotic coverage (topical) if an epithelial defect coexists (to prevent superinfection)
   Example: Moxifloxacin 0.5% qid until re-epithelialized.
   Purpose: Prevent secondary bacterial keratitis when the surface is open.
   Side effects: Surface irritation possible.

9. Systemic therapy for ocular syphilis (when testing is positive)
   Example: Aqueous crystalline penicillin G 18–24 million units/day IV (3–4 million units q4h or continuous) for 10–14 days.
   Purpose: Eradicates Treponema pallidum; ocular syphilis is treated as neurosyphilis.
   Side effects: Jarisch–Herxheimer reaction; allergy considerations. CDC+1

10. Antitubercular therapy (ATT) for suspected ocular TB
    Example (drug-susceptible TB): 2 months HRZE + 4 months HR (total 6 months) or other guideline-supported regimens; coordinated with TB/ID specialists.
    Purpose: Treats systemic/extrapulmonary TB driving ocular inflammation.
    Side effects: Hepatotoxicity (INH/RIF/PZA), optic neuritis (EMB)—monitored by specialists. CDCNCBI

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Dietary, molecular, and supportive supplements

Important: These support the ocular surface and immune balance; they do not replace medical therapy. Discuss with your clinician for interactions.

1. Vitamin A (2,500–5,000 IU/day, avoid excess in pregnancy): supports epithelial healing and mucins.

2. Omega-3 (EPA/DHA) (1–2 g/day): improves tear film quality and anti-inflammatory eicosanoid balance.

3. Vitamin C (500–1,000 mg/day): collagen synthesis and antioxidant defense in healing stroma.

4. Vitamin D3 (1,000–2,000 IU/day): immune modulation; deficiency is common.

5. Zinc (10–20 mg/day, with copper 1–2 mg/day if used >2–3 months): cofactor for wound repair enzymes.

6. N-Acetylcysteine (NAC) (600 mg bid): antioxidant; reduces mucous strands on ocular surface.

7. Curcumin (500 mg bid with piperine): NF-κB modulation, anti-inflammatory.

8. Quercetin (250–500 mg bid): mast-cell stabilizing antioxidant; may reduce surface inflammation.

9. EGCG (green tea extract) (200–400 mg/day): antioxidant; moderates cytokine signaling.

10. Selenium (100 mcg/day): antioxidant cofactor (glutathione peroxidase).

11. Probiotics (e.g., Lactobacillus/Bifidobacterium daily): gut–eye immune axis balance.

12. Lutein/Zeaxanthin (10/2 mg daily): ocular antioxidants for long-term retinal and surface health.

13. Hyaluronic acid (oral) (~200 mg/day): may support mucosal hydration.

14. L-carnitine (500 mg bid): mitochondrial support; studied in dry eye fatigue.

15. Lactoferrin (250 mg/day): antimicrobial/anti-inflammatory glycoprotein supporting tear defense.

(These have variable evidence—strongest for omega-3 and vitamin A in epithelial health/dry eye; others are supportive/adjunctive.)

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Regenerative / stem-cell–adjacent” therapies

1. Topical Cyclosporine A (0.05–0.1% bid): steroid-sparing immunomodulator for chronic surface inflammation after LIK quiets—reduces T-cell–driven cytokines.

2. Topical Tacrolimus (0.03–0.1% qhs–bid, off-label): similar T-cell effect when cyclosporine is not enough.

3. Systemic immunosuppressants for immune-associated IK (e.g., Cogan syndrome): Methotrexate (10–25 mg weekly), Azathioprine, Mycophenolate, or biologics (e.g., adalimumab, infliximab, certolizumab). Used by rheumatology/uveitis specialists when corneal inflammation is part of a systemic autoimmune picture. BioMed CentralFrontiersReumatología Clínica

4. Autologous serum tears (20–50% QID–8×/day): patient’s own serum provides growth factors and vitamins to promote epithelial/stromal healing; widely used in severe ocular surface disease. OXERVATE® (cenegermin-bkbj)

5. Platelet-rich plasma (PRP) eye drops (e.g., 20% QID–6×/day): concentrated platelet growth factors to boost regeneration; growing evidence for persistent defects. Lippincott Journals

6. Cenegermin (recombinant nerve growth factor 0.002% 6×/day for 8 weeks): for neurotrophic keratitis; considered if corneal nerves are compromised. (Indication-specific; used by specialists.) ScienceDirect

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Surgeries

1. Amniotic membrane transplantation (AMT): A biologic “bandage” placed on the cornea to calm inflammation, reduce scarring, and speed epithelial healing when defects persist or inflammation is stubborn. Multiple reviews support its safety and usefulness across ocular surface diseases. PMC+1

2. Superficial keratectomy (SK): Gentle polish/excision of superficial scar tissue to smooth the corneal surface when the line leaves irregularity near the surface after the eye is quiet. Frontiers

3. Phototherapeutic keratectomy (PTK): Excimer laser removes a very thin layer of anterior stroma to reduce haze/irregularity and improve optics if the residual linear scar sits superficially and causes blur. Known pros, cons, and indications are well described. PMCBlue Cross Blue Shield of Rhode Island

4. Deep anterior lamellar keratoplasty (DALK): Layered corneal transplant (replaces scarred stroma but keeps your endothelium) when scarring is deep but endothelium is healthy; reduces rejection risk versus full-thickness graft.

5. Penetrating keratoplasty (PK): Full-thickness corneal transplant for advanced scarring or perforation unresponsive to other measures; outcomes are good with careful follow-up, but rejection risk is higher in inflamed, vascularized corneas. NCBI

(Transplant is generally delayed until the eye has been quiet for months to minimize rejection and recurrence.) EyeWiki

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Prevention tips

1. Prompt eye exam if you develop redness/light sensitivity/blur.

2. Stick to the taper for steroid drops; don’t stop suddenly. EyeWiki

3. Antiviral prophylaxis (e.g., acyclovir 400 mg bid) if you have recurrent HSV stromal disease, per your doctor. EyeWiki

4. Treat systemic diseases (syphilis, TB, autoimmune) fully to lower future eye flares. CDC+1

5. Contact lens hygiene (or pause use) to avoid immune flares and infections. EyeWiki

6. UV and wind protection (sunglasses, hat).

7. Quit smoking; avoid secondhand smoke.

8. Hand/eye hygiene; avoid rubbing.

9. Manage blepharitis (warm compresses/lid hygiene).

10. Nutrition/hydration (see diet below).

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When to see a doctor urgently

• Sudden blur, severe light sensitivity, or increasing pain—especially if you see a white spot, new blood vessels, or the line looks wider/darker.

• Any relapse of previous symptoms (LIK can recur and is best treated early). PMC

• If you’re on steroids and vision worsens or you get halos (possible pressure rise). EyeWiki

• If you tested positive for syphilis or TB or have fever, rash, cough, weight loss, or new hearing/balance issues with eye symptoms (think Cogan syndrome). CDCPMCBioMed Central

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Foods to favor— to limit/avoid

Eat more of:

1. Fatty fish (salmon/sardine/mackerel) for omega-3.

2. Orange/yellow veggies (carrots, pumpkin, sweet potato) for vitamin A precursors.

3. Leafy greens (spinach, kale) for lutein/zeaxanthin.

4. Citrus/berries/kiwi for vitamin C.

5. Eggs (yolk carotenoids) if your cholesterol plan allows.

6. Nuts/seeds (walnut, flax, chia) for plant omega-3 and minerals.

7. Legumes (zinc/antioxidants).

8. Whole grains (steady energy, micronutrients).

9. Lean proteins (healing).

10. Plenty of water (tear film).

Limit/avoid:

1. Smoking (strongly).

2. Excess alcohol (slows healing).

3. Ultra-processed snacks (pro-inflammatory oils).

4. Very high-salt foods (dehydrating).

5. Sugary drinks (glycemic spikes worsen inflammation).

6. Trans fats (packaged/fried foods).

7. Excess vitamin A supplements (toxic in high doses).

8. Unhygienic street foods if you wear contacts.

9. Allergy-trigger foods (if they make your eyes itch/rub).

10. Energy drinks (drying caffeine load).

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FAQs

1) Is LIK contagious?
No. LIK itself isn’t an infection. Doctors still screen for infections that can mimic it (like HSV, syphilis, TB) because those need specific treatment. EyeWiki

2) Does LIK always come back?
No—but recurrences are reported. Early evaluation and a guided steroid taper reduce scarring risk. PMC

3) Will steroid drops harm my eye?
They’re the main treatment. Your doctor will monitor eye pressure and taper to the lowest effective dose to minimize side effects. EyeWiki

4) Why add antivirals with steroids?
If HSV/VZV is suspected, antivirals protect against viral flare while steroids calm inflammation. EyeWiki

5) What if syphilis testing is positive?
Ocular syphilis is treated with IV penicillin for 10–14 days, coordinated with infectious-disease care. CDC

6) What if TB testing is positive and the eye fits TB?
Doctors may start ATT per national/WHO guidance; this lowers relapse risk of TB-related uveitis/keratitis. CDCPMC

7) Will I need a corneal transplant?
Usually no. Most LIK responds to medical therapy. Transplant (DALK/PK) is reserved for dense scarring or perforation after inflammation is quiet. EyeWikiNCBI

8) How do doctors track improvement?
With slit-lamp photos, AS-OCT (to see the line fade), and symptom checks. PMC

9) Can diet or supplements cure LIK?
No, but good nutrition supports healing and comfort. They’re adjuncts, not replacements.

10) Is anti-VEGF safe on the cornea?
In specialist hands, topical or subconjunctival bevacizumab can reduce new vessels. Doctors weigh benefits vs. epithelial-healing risks. PMCWJGNet

11) Are calcineurin-inhibitor drops a replacement for steroids?
They’re steroid-sparing long-term helpers once the eye is quiet—not for acute, severe flares.

12) Can I keep wearing my contact lenses?
Pause during active inflammation; discuss a careful re-fit later. EyeWiki

13) Why test for hearing or balance problems?
If Cogan syndrome is suspected (IK plus audiovestibular signs), early systemic treatment protects hearing. EyeWikiBioMed Central

14) How long does each flare last?
With prompt therapy, weeks—but tapers can take a month or more to prevent rebound. PMC

15) What’s the long-term outlook?
Good, if treated early—many patients keep useful vision; scars that impair vision can be treated with PTK or, rarely, transplant. PMCNCBI

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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