Linear Interstitial Keratitis (LIK)

Linear interstitial keratitis is a very rare form of corneal inflammation in which a line-shaped streak appears inside the stroma (the middle, transparent layer of the cornea). The line is usually horizontal, can be single or parallel, and may leave a thin scar after it settles down. Unlike many other kinds of keratitis, the surface skin of the cornea (epithelium) and the inner lining (endothelium) are not the primary problem—the inflammation lives mostly inside the stroma. Doctors diagnose it mainly by looking at the eye under a slit-lamp and seeing that distinctive linear stromal opacity. Most reported cases improve with topical steroid drops, but relapses can happen. PMCEyeWiki

Linear interstitial keratitis (LIK) is a stripe-like inflammatory scar inside the corneal stroma. Unlike surface scratches or ulcers, LIK affects the middle layer (the “glass-like” collagen bed that gives the cornea its strength). Doctors recognize LIK because the inflamed area often looks like a sharp, horizontal line rather than a round patch. LIK sits under the surface skin (epithelium) and above the innermost liner (endothelium). Because the cornea must be crystal clear for sharp vision, even a thin linear scar can cause blur, glare, halos, and light sensitivity. LIK belongs to the wider group of interstitial keratitis, which is any non-ulcerating stromal inflammation, usually with new blood vessels growing into the normally vessel-free cornea. PMCEyeWiki

In broader terms, interstitial keratitis (IK) means non-ulcerating inflammation of the corneal stroma—that is, the tissue is inflamed but not melted or ulcerated, and the stroma is the main layer involved. IK can be caused by infections or immune reactions and often shows new blood vessels growing into the cornea (“stromal neovascularization”), which can lead to haze and scarring. LIK is a special, line-shaped subtype within this family. EyeWikiMerck Manuals

When the eye is examined, the cornea shows a pale, linear streak within the stroma. The surrounding area may look slightly swollen, and tiny new blood vessels sometimes creep toward the line from the edge of the cornea. People usually complain of light sensitivity, watering, redness, and blurred vision. On more advanced imaging, doctors often find that the opacity sits in the anterior (front) part of the stroma, and in-vivo confocal microscopy may show needle-like reflective structures within the tissue—clues that the stroma is actively inflamed. These cases typically respond to corticosteroid eye drops, though scars may remain once the flare calms. PMC

Historically, LIK was once suspected to be syphilis-related, but modern case series have found negative syphilis tests in many patients, and the current view is that the cause is usually unknown (idiopathic). Some authors have suggested an autoimmune basis, but this is not yet proven. EyeWikiPubMed

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Types of Linear Interstitial Keratitis

Because LIK is rare, doctors group it in practical ways based on how it behaves and what else is going on:

1. By cause (etiology)

   • Idiopathic (most common): no infection or systemic cause is found; responds to steroids; may recur. PMC

   • Possible immune-mediated association: suspected link with immune dysregulation; evidence is limited. EyeWiki

   • Historically suspected infectious association: early reports hinted at syphilis or Lyme disease, but modern testing often does not support this. EyeWiki

2. By depth in the cornea

   • Anterior stromal LIK (most reported): the line lies closer to the front of the cornea on imaging. PMC

   • Mid-stromal LIK (less often): the line sits deeper, sometimes with more haze.

3. By activity

   • Active (inflamed): redness, light sensitivity, and a brighter line.

   • Quiescent (scarred): symptoms settle, leaving a faint linear scar or ghost vessels.

4. By laterality

   • Unilateral (one eye) is typical; bilateral is unusual.

5. By course

   • Single episode vs recurrent attacks over time. Relapses have been described in the literature. PMC

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Causes

A key point first: in LIK, the most common real-world outcome of testing is “no clear cause found.” The list below blends what is known for interstitial keratitis in general with reported associations and plausible triggers for LIK. Your clinician uses the history, exam, and local disease patterns to decide which ones to test. EyeWiki

1. Idiopathic immune reaction — the body’s defense system inflames the corneal stroma for reasons we cannot yet pinpoint; this is the leading scenario in LIK case series. PMC

2. Herpes simplex–related immune keratitis — not an active surface ulcer, but a deeper immune response after HSV exposure; can mimic IK patterns. EyeWikieyerounds.org

3. Varicella-zoster–related stromal keratitis — a post-zoster immune reaction in the stroma. EyeWiki

4. Syphilis (historical link) — a classic cause of IK; however, most modern LIK patients test negative, so LIK is not reliably syphilitic. EyeWiki+1PubMed

5. Lyme disease — bacterial infection that can lead to IK in some settings. EyeWiki

6. Tuberculosis — either infection or immune reaction related to TB antigens. EyeWiki

7. Leprosy — chronic infection that can inflame the cornea’s stroma. EyeWiki

8. Brucellosis — systemic infection; rarely reaches the cornea but is on standard IK lists. EyeWiki

9. Leptospirosis — waterborne infection occasionally tied to IK. EyeWiki

10. Onchocerciasis — a parasitic disease (river blindness) that can cause stromal keratitis in endemic areas. EyeWiki

11. Acanthamoeba-related immune stromal disease — usually after contact lens exposure or water, sometimes with stromal inflammation that resembles IK. EyeWiki

12. Cogan syndrome (autoimmune) — a systemic autoimmune disorder that can present with interstitial keratitis and inner-ear problems. NCBI

13. Sarcoidosis (autoimmune/granulomatous) — can inflame the stroma as part of broader eye disease. EyeWiki

14. Granulomatosis with polyangiitis (ANCA-associated vasculitis) — rare, but on immune IK differentials. EyeWiki

15. Rheumatoid arthritis and related autoimmune disease — immune imbalance may involve the cornea. EyeWiki

16. Post-LASIK corneal immune reaction (association) — a case report series described LIK in a patient with prior LASIK; this does not prove causation, but it is a reported association. PMC

17. Hidradenitis suppurativa (association with IK) — rare reports link IK to this chronic inflammatory skin disease. PubMed

18. Contact lens–associated immune keratitis — a noninfectious reaction sometimes included in IK differentials. EyeWiki

19. Heavy metals or intracorneal foreign material (immune reaction) — included in IK differentials when exposure history fits. EyeWiki

20. Minor ocular surface triggers (e.g., recent irritation, a healed abrasion, new cosmetics) that coincide with onset in case descriptions—best viewed as possible triggers, not proven causes. PMC

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Symptoms

1. Blurred vision — the line and surrounding haze bend light and reduce sharpness. Merck Manuals

2. Sensitivity to light (photophobia) — bright light hurts and makes you squint. Merck ManualsMayo Clinic

3. Eye redness — the white of the eye looks injected. Mayo Clinic

4. Watery eye (tearing) — reflex tearing from irritation. Merck Manuals

5. Eye pain or ache — from inflammation in and around the cornea. Merck Manuals

6. Foreign-body sensation — feels like grit in the eye although nothing is there. Mayo Clinic

7. Glare and halos — especially at night due to light scatter through the haze.

8. Reduced contrast — letters look washed-out.

9. Trouble opening the eye in bright light or wind. Mayo Clinic

10. Headache or brow ache — from sustained squinting and ciliary spasm.

11. Eyelid tenderness — from rubbing or blepharospasm.

12. Intermittent sharp pains — “zings” as the surface dries then re-wets.

13. Visual fluctuation — vision changes with blinking or tear film quality.

14. A sense of dryness — even though tearing is present.

15. Relapsing episodes — symptoms may return after months and then settle again. PMC

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Diagnostic tests

Doctors do not order every test for every person. They start with history + slit-lamp exam, then pick specific tests based on the pattern and the most likely causes for your location and risk factors. The goal is to (1) confirm it is interstitial keratitis, (2) rule out surface ulcers or infections, and (3) look for a cause when it matters for treatment. EyeWiki

A) Physical examination (bedside assessments)

1. Visual acuity with and without pinhole
   What it is: Reading letters on a chart; the pinhole helps tell if blur is from focusing changes or from tissue haze.
   Why it matters: Haze and scarring from stromal inflammation reduce clarity; pinhole gives a quick sense of how much can improve with optics.

2. External inspection (lids, lashes, conjunctiva) and ocular alignment
   What it is: Looking for redness patterns, lid disease, discharge, or misalignment.
   Why it matters: Helps separate corneal disease from surface eyelid problems that can mimic irritation. EyeWiki

3. Pupil exam (direct/consensual light reflex and RAPD check)
   What it is: Shining a light and watching the pupils.
   Why it matters: Ensures no deeper optic nerve problem is hiding behind the corneal symptoms.

4. Slit-lamp biomicroscopy (white light and various beams)
   What it is: The core eye exam with a microscope and bright beam.
   What LIK looks like: a linear stromal opacity that’s typically anterior; there may be stromal edema, fine neovascularization, and sometimes mild iritis.
   Why it matters: This is how LIK is clinically diagnosed. EyeWiki

5. Dilated fundus examination
   What it is: Drops enlarge the pupil so the retina and optic nerve can be examined.
   Why it matters: Rules out posterior eye disease as a cause of reduced vision (important when symptoms are severe but corneal signs are modest).

B) Manual / office tests (simple tools and dyes)

6. Fluorescein staining (with cobalt blue light)
   What it is: A harmless dye that sticks to areas where the surface skin is missing.
   Why it matters: LIK is a stromal problem; the epithelium is usually intact. Staining suggests a different or additional diagnosis (like infectious epithelial keratitis). eyerounds.org

7. Seidel test
   What it is: A focused fluorescein test to see if any clear fluid is leaking from the cornea.
   Why it matters: Very rarely, severe inflammation can thin the cornea; this test checks safety when pain is intense or the cornea looks suspicious.

8. Corneal esthesiometry (Cochet-Bonnet)
   What it is: A fine filament touches the cornea to measure sensation.
   Why it matters: Reduced corneal sensation points toward herpetic disease or neurotrophic problems, which changes management. NCBI

9. Schirmer tear test
   What it is: Paper strips in the lower lids to measure tear production in 5 minutes.
   Why it matters: Dry eye can worsen pain and blur and complicate healing.

10. Tear break-up time (TBUT)
    What it is: Time until the tear film breaks into dry spots after a blink.
    Why it matters: Unstable tears aggravate light sensitivity and blur; fixing the tear film can ease symptoms while the stroma heals.

C) Lab & pathological tests (targeted blood tests and samples)

11. RPR or VDRL (nontreponemal syphilis screen)
    Why: Syphilis is a classic cause of IK and is easy to treat; still worth checking even though most LIK patients are negative. EyeWiki+1

12. FTA-ABS or TPPA (confirmatory treponemal test)
    Why: Confirms or refutes a positive screen so you don’t miss treatable disease. EyeWiki

13. Quantiferon-TB Gold or T-SPOT (TB testing)
    Why: Looks for tuberculosis exposure when the history or region suggests risk. EyeWiki

14. Lyme disease serology (ELISA with reflex Western blot)
    Why: On the IK differential in some regions; testing is guided by exposure risk. EyeWiki

15. ACE and/or lysozyme levels (sarcoidosis screen)
    Why: If there are systemic signs, these labs, alongside chest imaging, support or question sarcoidosis as a contributor. EyeWiki

Depending on the story, doctors may also check ANCA (vasculitis), ANA/RF/anti-CCP (autoimmunity), Brucella/Leptospira serology, or take corneal scrapings for PCR/culture if an infectious surface process is suspected. EyeWiki

D) Electrodiagnostic tests (used selectively)

16. Visual evoked potential (VEP)
    Why: If the vision is far worse than the cornea explains, VEP clarifies whether the optic nerve/brain pathway is at fault (rarely needed, but helpful in puzzling cases).

17. Electroretinography (ERG)
    Why: Similar logic—used when a retinal problem is suspected alongside corneal disease; not routine for LIK, but occasionally clarifies the picture.

E) Imaging tests (show where the line is and how the tissue is behaving)

18. Anterior segment optical coherence tomography (AS-OCT)
    What it shows: A cross-section “slice” of the cornea.
    Why it matters: In LIK, the opacity is usually anterior stromal with hyper-reflectivity, helping confirm the location and depth and guiding follow-up. PMC

19. In-vivo confocal microscopy (IVCM)
    What it shows: Microscopic, live images of corneal cells.
    Why it matters: LIK reports describe hyper-reflective, needle-like structures in the stroma; this supports active stromal inflammation and helps distinguish from other diseases. PMC

20. Specular microscopy (and/or corneal endothelial imaging)
    What it shows: The health of the endothelial cell layer.
    Why it matters: Confirms that the inner layer is relatively spared (fits IK) and documents any secondary changes; part of the broader work-up in corneal inflammation. PubMed

Other useful imaging/metrics your clinician may use include pachymetry (corneal thickness), corneal topography/tomography (shape maps), and serial slit-lamp photos to track healing or recurrence. EyeWiki

Non-pharmacological treatments (therapies and supports)

These do not replace cause-specific medicines (e.g., antibiotics for syphilis). They support healing, reduce symptoms, and protect vision.

1. UV-blocking glasses and a hat — Purpose: cut light sensitivity and UV-triggered inflammation. Mechanism: lowers phototoxic and inflammatory signaling.

2. Rest in dim light during flares — Purpose: comfort. Mechanism: reduces ciliary spasm and photophobia-related pain.

3. Preservative-free lubricating tears (hourly to q2–3h) — Purpose: dilute inflammatory mediators; smooth the optical surface. Mechanism: tear film stabilization; less scatter.

4. Cold compresses (10 minutes, few times/day) — Purpose: symptom relief. Mechanism: vasoconstriction → less swelling/nerve firing.

5. Protective eyewear / safety shields — Purpose: prevent micro-trauma and wind irritation. Mechanism: mechanical barrier.

6. Lid hygiene if blepharitis coexists — Purpose: calmer surface improves comfort. Mechanism: reduces bacterial load and meibum stagnation.

7. Humidifier and blink breaks — Purpose: reduce dryness. Mechanism: keeps tear film stable, lowering photic scatter.

8. Therapeutic bandage contact lens (short-term, monitored) — Purpose: pain relief if epithelium is irritable. Mechanism: shields corneal nerves; smooths micro-irregularities.

9. Scleral lens (when quiet, for visual rehab) — Purpose: restores quality of vision over a scar/irregular cornea. Mechanism: vaults the cornea with a liquid reservoir, creating a new smooth optical surface.

10. Punctal occlusion (temporary plugs) when dryness worsens symptoms — Purpose: keep tears longer. Mechanism: slows drainage.

11. Autologous serum tears (AST) — Purpose: bioactive lubrication in stubborn surface discomfort. Mechanism: growth factors and vitamins from your serum support epithelial healing.

12. Avoid contact lens wear during active inflammation — Purpose: reduce mechanical stress and infection risk. Mechanism: gives cornea recovery time.

13. Smoking cessation — Purpose: better corneal and immune healing. Mechanism: less oxidative stress/vasoconstriction.

14. Treat eyelid margin disease (warm compress/massage) — Purpose: improve tear lipid layer. Mechanism: better meibum quality → more stable tear film.

15. Manage systemic disease (rheumatology/ENT/ID co-care) — Purpose: quiet the driver (e.g., Cogan syndrome, TB, syphilis). Mechanism: source control. NCBIEyeWiki

16. Vaccinations up to date (measles/mumps, etc., per guidelines) — Purpose: prevent viral triggers that historically caused IK. Mechanism: immune priming.

17. Allergen control (if ocular allergy worsens symptoms) — Purpose: reduce itch/rub cycle. Mechanism: lower mast-cell activation.

18. Nutritional optimization (see supplements below) — Purpose: collagen and immune support. Mechanism: cofactors for stromal repair.

19. Stress-sleep hygiene — Purpose: immune resilience. Mechanism: cortisol balance and cytokine modulation.

20. Education on steroid safety (if prescribed) — Purpose: prevent steroid-response glaucoma and cataract. Mechanism: early pressure checks and taper compliance.

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Drug treatments

Medication choices depend on the confirmed cause. Never self-start or change doses without medical supervision.

1. Topical corticosteroids (e.g., prednisolone acetate 1%, loteprednol 0.5%)

   • When: immune-mediated stromal inflammation (NOT active epithelial HSV without antiviral cover).

   • Dose/time: commonly q4–6/day, then slow taper over weeks.

   • Purpose/mechanism: shuts down stromal immune inflammation.

   • Key side effects: eye pressure rise, cataract with prolonged use; infection risk—monitor IOP.

2. Oral corticosteroids (e.g., prednisone ~0.5–1 mg/kg/day, taper)

   • When: significant stromal inflammation, bilateral disease, or Cogan syndrome.

   • Mechanism: systemic immunosuppression.

   • Side effects: glucose, blood pressure, mood, bone loss; needs plan to taper. NCBIBioMed Central

3. Antiviral therapy for HSV (e.g., acyclovir 400 mg 5×/day acute; 400 mg BID prophylaxis)

   • When: suspected herpetic stromal keratitis or history of HSV keratitis with steroid use.

   • Mechanism: inhibits viral DNA polymerase; reduces recurrences.

   • Side effects: GI upset, renal dosing adjustment.

4. Antiviral for VZV (e.g., valacyclovir 1,000 mg TID for 7 days)

   • When: zoster-related eye disease.

   • Mechanism/risks: as above; hydration and renal function monitoring.

5. Antibiotics for syphilis (penicillin-based per guidelines; ocular syphilis is often treated like neurosyphilis with IV aqueous penicillin G for 10–14 days; late latent forms may receive benzathine penicillin G IM per protocol)

   • When: positive treponemal testing/ID confirmation.

   • Mechanism: eradicates Treponema pallidum.

   • Side effects: allergy, Jarisch–Herxheimer reaction; managed by ID specialist. EyeWiki

6. Anti-TB therapy (RIPE regimen)

   • When: IK with TB evidence.

   • Mechanism: multi-drug bacterial eradication.

   • Side effects: liver, vision (ethambutol), drug interactions; supervised by TB program.

7. Doxycycline 100 mg BID (adjunct)

   • When: chlamydial disease or for its anti-collagenase/anti-inflammatory effect in ocular surface disease.

   • Mechanism: reduces matrix metalloproteinases; antimicrobial.

   • Side effects: GI upset, photosensitivity; avoid in pregnancy.

8. Topical cycloplegics (e.g., atropine 1% daily or cyclopentolate TID)

   • When: light sensitivity and ciliary spasm pain.

   • Mechanism: relaxes iris/ciliary body; reduces ache.

   • Side effects: blurred near vision; light sensitivity.

9. Steroid-sparing immunomodulators (DMARDs) — methotrexate (10–25 mg weekly), azathioprine (1–2 mg/kg/day), mycophenolate mofetil (1–1.5 g BID)

   • When: autoimmune IK (e.g., Cogan syndrome) needing long-term control or steroid-intolerance.

   • Mechanism: dampens maladaptive immune response.

   • Side effects: liver/bone-marrow suppression; requires lab monitoring. BioMed Central

10. Biologic agents (e.g., infliximab, adalimumab) in selected severe autoimmune cases

• When: refractory Cogan syndrome or systemic vasculitis with ocular disease, under specialist care.

• Mechanism: targeted cytokine blockade (e.g., TNF-α).

• Side effects: infection risk, TB reactivation screening required. BioMed Central

Other helpful Rx often used alongside: preservative-free lubricants, short courses of topical antibiotic only if the epithelium is compromised or bandage lenses are used (infection prophylaxis), and intraocular pressure-lowering drops if there’s a steroid response.

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Regenerative” options

These are not first-line and are used selectively when standard care isn’t enough, or when systemic disease requires stronger control. I’ll note the intent and the mechanism in plain English.

1. Intravenous methylprednisolone pulses (e.g., 500–1,000 mg/day × 3 days)

   • Function: fast “reset” of severe autoimmune inflammation threatening vision.

   • Mechanism: rapid, high-dose steroid immunosuppression.

2. Rituximab (anti-CD20)

   • Function: steroid-sparing control in certain refractory autoimmune vasculitides.

   • Mechanism: depletes B-cells that help drive autoimmunity.

3. Cyclophosphamide (oral or IV)

   • Function: rescue therapy in severe systemic vasculitis with ocular involvement.

   • Mechanism: cytotoxic suppression of overactive immune cells.

4. Intravenous immunoglobulin (IVIG)

   • Function: modulates immune signaling when autoimmunity is active and other agents are unsuitable.

   • Mechanism: Fc-mediated immune “balancing.”

5. Autologous serum tears (biologic drop) at higher concentrations (e.g., 20–50%)

   • Function: supports epithelial and nerve health when discomfort persists.

   • Mechanism: patient’s own growth factors and vitamins.

6. Amniotic membrane therapy (sutureless device in clinic)

   • Function: biologic bandage to reduce inflammation and promote healing in surface irritation overlying stromal disease.

   • Mechanism: anti-inflammatory cytokines and a scaffold for epithelial repair.

(For true stem-cell approaches like limbal stem-cell transplantation, see “Surgeries” below; these are reserved for coexisting limbal stem-cell deficiency rather than LIK itself.)

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Surgeries

1. Deep anterior lamellar keratoplasty (DALK)

   • Procedure: replaces the diseased stromal layers while keeping the healthy endothelium.

   • Why: removes dense stromal scarring while lowering rejection risk compared with full-thickness graft.

2. Penetrating keratoplasty (PKP, full-thickness graft)

   • Procedure: replaces all corneal layers.

   • Why: for full-thickness scarring or when DALK isn’t possible.

3. Phototherapeutic keratectomy (PTK)

   • Procedure: excimer laser gently polishes superficial scars/irregularities.

   • Why: improves smoothness and vision when the linear scar is superficial.

4. Amniotic membrane transplantation (surgical)

   • Procedure: sutured graft to calm surface inflammation and aid epithelial recovery.

   • Why: persistent surface breakdown over a stromal scar.

5. Limbal stem-cell transplantation (autologous or allogeneic; highly specialized)

   • Procedure: replaces damaged stem cells at the corneal edge.

   • Why: only if limbal stem-cell deficiency coexists (not typical in pure LIK).

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Dietary, molecular, and supportive supplements

(These do not treat infections or replace prescription therapy; discuss with your clinician—doses are common adult ranges.)

1. Vitamin A (2,500–5,000 IU/day) — Function: epithelial health; Mechanism: retinoid signaling for surface healing.

2. Vitamin C (500–1,000 mg/day) — Function: collagen cross-link support; Mechanism: cofactor for collagen synthesis.

3. Vitamin D3 (1,000–2,000 IU/day, adjust to level) — Function: immune modulation; Mechanism: regulates innate/adaptive immunity.

4. Omega-3 fatty acids (EPA+DHA 1–2 g/day) — Function: anti-inflammatory milieu; Mechanism: pro-resolving lipid mediators.

5. Zinc (10–20 mg/day) — Function: immune and epithelial support; Mechanism: cofactor in repair enzymes; vitamin A metabolism.

6. N-acetylcysteine (600–1,200 mg/day) — Function: antioxidant; Mechanism: glutathione precursor; mucolytic/anti-collagenase effects on surface.

7. Curcumin (500–1,000 mg/day with pepper extract) — Function: adjunct anti-inflammatory; Mechanism: NF-κB pathway modulation.

8. Quercetin (250–500 mg/day) — Function: antioxidant mast-cell stabilizer; Mechanism: cytokine down-regulation.

9. L-lysine (500–1,000 mg/day) — Function: sometimes used by clinicians to reduce HSV recurrences; Mechanism: competes with arginine (evidence mixed).

10. Hyaluronic acid (oral 120–240 mg/day) — Function: supports hydration/tear quality; Mechanism: hydrophilic polymer dynamics.

11. Beta-carotene from diet (carrots, leafy greens) — Function: vitamin A precursor; Mechanism: converted to retinol as needed.

12. Collagen peptides (5–10 g/day) — Function: building blocks for stromal collagen; Mechanism: amino-acid supply.

13. Coenzyme Q10 (100–200 mg/day) — Function: mitochondrial support in healing tissues; Mechanism: electron transport antioxidant.

14. Magnesium (200–400 mg/day) — Function: nerve/immune support; Mechanism: cofactor in hundreds of reactions.

15. Probiotics (per label) — Function: gut–immune axis support; Mechanism: microbial immune modulation.

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Prevention tips

1. Prompt testing for syphilis in any IK — early treatment protects eyes. EyeWiki

2. Safe sexual practices and prenatal screening to prevent congenital/acquired syphilis. EyeWiki

3. Stay current with vaccines (measles/mumps) where recommended.

4. Manage systemic autoimmune disease with your specialists (rheumatology, ENT). NCBI

5. HSV-prone patients: discuss antiviral prophylaxis if your doctor recommends it.

6. Eye protection from UV/wind/dust to reduce flares.

7. Don’t rub your eyes during irritation; use cold compresses instead.

8. Quit smoking to improve healing.

9. Keep follow-up appointments (pressure checks on steroids; labs on DMARDs).

10. Treat eyelid disease (blepharitis) to calm the surface environment.

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When to see a doctor

• Same day / urgent if you have new eye pain, marked light sensitivity, sudden vision drop, a new “line” or haze in the cornea, halos around lights, or redness.

• Urgent if you have eye symptoms plus ear symptoms (dizziness, ringing, hearing loss) — this pattern raises concern for Cogan syndrome, which needs coordinated care. NCBI

• Promptly if you are on steroids and notice headache, haloes, or blurred vision (could be pressure rise).

• Promptly if you are pregnant or planning pregnancy and have positive syphilis testing or eye findings. EyeWiki

• Promptly if you are immunosuppressed or have TB exposure and develop eye inflammation.

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What to eat and what to avoid

Helpful to eat:

1. Colorful vegetables (carrots, spinach, kale) for carotenoids and vitamin C.

2. Citrus/berries for vitamin C (collagen support).

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

4. Nuts/seeds (walnuts, flax, chia) for plant omega-3s and magnesium.

5. Lean proteins (eggs, legumes, poultry) to supply collagen amino acids.

Better to limit/avoid:
6) Ultra-processed, high-sugar foods (pro-inflammatory).
7) Excess alcohol (poor immunity/healing).
8) Smoking/vaping (impairs corneal repair).
9) Very salty foods if steroids raise blood pressure/fluid retention.
10) Foods or supplements that interact with your medicines (e.g., alcohol with methotrexate; ask your clinician).

Most cases of LIK/IK quiet down with cause-directed therapy. Some people are left with a faint line or mild haze that causes glare or ghosting; many can reach good vision with scleral lenses. Surgery helps when scars are dense and centrally located. Because LIK is rare and often idiopathic, your care team will monitor closely and adjust the plan over time. EyeWiki

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Frequently asked questions (FAQ)

1) Is linear interstitial keratitis contagious?
No. The inflammation itself is not contagious. If it’s triggered by an infection like syphilis, the infection is contagious; the inflammation pattern in your cornea is your body’s response. EyeWiki

2) Will I need lifelong treatment?
Often, no. You may need a finite course of antimicrobials or a taper of steroids. Autoimmune cases sometimes need longer steroid-sparing care.

3) Can glasses fix the blur?
Sometimes. If the linear scar causes irregular optics, a scleral lens usually gives the best quality vision.

4) Are steroids safe for my eyes?
They’re effective but must be monitored. Your doctor will check eye pressure and taper slowly to avoid rebound.

5) Do I always need blood tests?
With IK/LIK, doctors usually screen for syphilis and other triggers because treatment changes based on the cause. EyeWiki

6) What imaging will I have?
Often AS-OCT and sometimes in-vivo confocal microscopy to map the lesion and track improvement. PMC

7) Can LIK come back?
Yes. If the underlying trigger re-activates (e.g., autoimmune flare or HSV recurrence), inflammation can return.

8) Does diet cure LIK?
No. Diet and supplements support healing but do not replace antibiotics, antivirals, or immunosuppressants when indicated.

9) Is surgery common?
No. Surgery is for stable, visually significant scars that don’t respond to non-surgical care.

10) Could this be Cogan syndrome?
If you also have ear symptoms (dizziness, ringing, hearing loss), your team will consider it and may involve ENT/rheumatology. NCBI

11) I had syphilis years ago; could LIK appear now?
Yes—late ocular syphilis and interstitial keratitis are well described; your team will test and treat per guidelines. EyeWiki

12) Are biologics ever needed?
Rarely, for refractory autoimmune cases under specialist care (e.g., infliximab/adalimumab in Cogan syndrome). BioMed Central

13) How is LIK different from a corneal ulcer?
LIK is non-ulcerative stromal inflammation; ulcers involve a surface defect with infection risk. EyeWiki

14) Can I wear contact lenses?
Avoid during active inflammation. Later, a scleral lens may greatly improve vision and comfort.

15) What follow-up do I need?
Early on: frequent visits (every 1–3 weeks) to track inflammation, IOP, and tapering. Later: maintenance visits to keep things stable.

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 11, 2025.

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