Vogt–Koyanagi–Harada (VKH) Disease

Vogt–Koyanagi–Harada (VKH) disease is an autoimmune condition. “Autoimmune” means the body’s defense system gets confused and attacks its own cells. In VKH, the immune system mainly targets melanocytes—the pigment-making cells that give color to the eye, skin, hair, and parts of the inner ear and brain coverings (meninges). Because these pigment cells live in many places, VKH can cause eye inflammation (uveitis) with blurred vision, as well as headache, hearing problems, ringing in the ears, skin color changes (vitiligo), white eyelashes or scalp hair (poliosis), and hair loss (alopecia). It usually affects both eyes (often within days to weeks), and it tends to follow phases—an early flu-like phase, an acute eye-inflammation phase, and a convalescent or chronic phase where skin and hair findings appear and, if untreated, vision can be damaged.

Vogt-Koyanagi-Harada (VKH) disease is an immune-driven inflammation that mainly targets melanin-rich tissues—especially the eye (choroid/uvea)—and can also involve the inner ear, the coverings of the brain and spinal cord (meninges), and the skin/hair. In the eyes it causes a bilateral granulomatous panuveitis (inflammation throughout both eyes), which can lead to blurry vision, light sensitivity, and pockets of fluid under the retina (serous/exudative retinal detachments). Extra-ocular features may include headache, neck stiffness, hearing changes (tinnitus, muffled hearing), skin and hair depigmentation (vitiligo, poliosis), and alopecia. The disease often runs through four phases: prodromal (flu-like), acute uveitic, convalescent (depigmentation such as “sunset-glow fundus”), and sometimes chronic recurrent phases. Early, aggressive control of inflammation helps protect long-term vision. EyeWikiNCBIAmerican Academy of OphthalmologySpringerOpen

In VKH, specialized immune cells (especially T-cells of the Th1/Th17 type) target proteins found in melanocytes (for example tyrosinase-related proteins). This immune attack causes swelling and leakage in the eye’s uveal tract and retina, which can lead to serous (exudative) retinal detachments, optic disc swelling, and lots of inflammatory cells in the eye’s front (anterior chamber) and back (vitreous). Immune activity can also irritate the meninges (causing headache and neck stiffness) and affect the inner ear (causing tinnitus and hearing changes). Over time, if inflammation isn’t controlled early and fully, it can scar tissues and cause depigmentation of skin and hair.

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Types of VKH

Doctors describe “types” of VKH in a few practical ways. Think of them as different lenses for understanding the same disease.

A) By clinical phases (what the illness looks like over time)

1. Prodromal phase (flu-like phase):
   Lasts days. People feel headache, feverish, light-sensitive, with neck stiffness, ear ringing, and dizziness. It can look like a viral illness or meningitis.

2. Acute uveitic phase (eye-inflammation phase):
   Rapid bilateral eye involvement with blurry vision, floaters, eye pain/redness, and photophobia. The retina can leak fluid, forming serous detachments, and the optic disc may look swollen.

3. Convalescent phase (healing but pigment loss):
   Eye inflammation calms, but depigmentation shows up: vitiligo, poliosis, alopecia, and a characteristic “sunset-glow” fundus (the back of the eye looks pale/orange due to pigment loss).

4. Chronic recurrent phase (flares/relapses):
   Recurrent eye inflammation, often in the front of the eye. Without strong control, repeated flares raise the risk of cataract, glaucoma, macular changes, and vision loss.

B) By diagnostic certainty (how strictly it meets criteria)

5. Complete VKH:
   Typical eye findings plus skin/hair findings and no history of eye trauma or surgery (important to rule out sympathetic ophthalmia).

6. Incomplete VKH:
   Typical eye findings with some extra-ocular features (but not all).

7. Probable (ocular) VKH:
   Only eye findings, but pattern fits VKH and other causes are excluded.

C) By clinical behavior

8. Acute VKH (early-onset):
   Sudden, intense inflammation with exudative retinal detachments; vision can fall fast but may recover with prompt, high-dose treatment.

9. Chronic/recurrent VKH:
   Lower-grade but repeating inflammation; higher risk of complications due to cumulative damage.

10. Late-stage depigmenting VKH:
    Eye is quieter; skin/hair depigmentation and sunset-glow fundus are prominent; focus is on preventing relapses and managing long-term effects.

Key idea: Phases and labels can overlap. The “type” helps doctors plan treatment intensity and follow-up.

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Causes

VKH is fundamentally autoimmune. We do not think everyday injuries cause it. Instead, multiple influences increase risk or trigger the immune system to attack melanocytes. Evidence strength varies; some are strong (like genes), others are associations/case reports.

1. Autoimmune targeting of melanocytes:
   The core cause—immune cells misidentify pigment cells as “foreign” and attack them.

2. Genetic predisposition (HLA-DRB1*04:05 and related HLA class II types):
   Certain genes that shape immune responses make VKH more likely.

3. Other HLA/immune genes (e.g., DQA1/DQB1 variants):
   Additional immune gene combinations raise susceptibility.

4. Molecular mimicry after infections:
   An infection may carry proteins that look like melanocyte proteins, training the immune system to attack both.

5. Viral triggers (e.g., influenza, EBV, CMV, VZV, SARS-CoV-2) — association varies:
   Some people report VKH after viral illnesses; this is not proof, but suggests a trigger in prone individuals.

6. Recent vaccination (rare case reports):
   Very uncommon; thought to work via immune activation in those already genetically primed.

7. Immune checkpoint inhibitor therapy (e.g., nivolumab, pembrolizumab):
   Powerful cancer drugs that boost immunity can unmask autoimmune uveitis resembling VKH.

8. Skewed Th1/Th17 immune profile:
   A pro-inflammatory T-cell balance pushes the immune system toward tissue attack.

9. Breakdown of eye immune privilege (blood–ocular barrier):
   When the eye’s natural “low-inflammation zone” fails, immune cells gain access and sustain inflammation.

10. Ethnic susceptibility (more common in Asian, Hispanic/Latino, Middle Eastern, some Indigenous populations):
    Reflects gene pools and complex environmental interactions.

11. Female sex (slight predominance reported):
    Hormonal and immune differences can tilt risk.

12. Age 20–50 years (typical onset):
    Peak immune system activity years may align with VKH onset.

13. Family history of autoimmune disease:
    A family background of autoimmunity can raise overall risk.

14. Co-existing autoimmune conditions (e.g., thyroiditis, vitiligo):
    Having one autoimmune disease increases the chance of another autoimmune response.

15. Psychological stress (association, not proof):
    Stress hormones can modulate immunity, sometimes preceding flares.

16. Vitamin D insufficiency (association):
    Vitamin D influences immune balance; low levels may favor inflammation.

17. Smoking (general autoimmune risk factor):
    Smoking alters immune and vascular responses; it may worsen inflammatory eye disease.

18. High UV exposure (possible pigment-cell stress):
    UV can stress melanocytes and skin, possibly nudging immune attention in predisposed people.

19. Microbiome/viral “exposome” (emerging research):
    Life-long exposure to microbes may shape immune tolerance; changes might tilt toward autoimmunity.

20. Delayed or incomplete control of early inflammation (perpetuating factor):
    Not a root cause but an amplifier—ongoing inflammation keeps training the immune system to attack.

Takeaway: Genes set the stage; immune triggers start the play. VKH happens when a primed immune system focuses on melanocyte targets.

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Symptoms

1. Blurry vision (both eyes):
   Fluid and inflammation in the retina scatter light, so details look foggy.

2. Photophobia (light sensitivity):
   Inflamed eye tissues make bright light uncomfortable or painful.

3. Floaters (spots/strings in vision):
   Inflammatory cells and debris in the gel (vitreous) cast moving shadows.

4. Eye redness and ache:
   Blood vessels widen and the iris/ciliary body get sore and inflamed.

5. Sudden drop in vision quality (during acute phase):
   Fluid under the retina can warp the central seeing area (macula), reducing clarity.

6. Headache (often severe):
   Mild meningitis-like irritation causes diffuse head pain; neck may feel stiff.

7. Neck stiffness/meningism:
   Inflammation around the brain coverings makes bending the neck uncomfortable.

8. Tinnitus (ringing/buzzing in ears):
   Inner-ear involvement creates constant or intermittent sound without an external source.

9. Hearing changes (muffled or reduced hearing):
   Inflammation affects the inner ear, making sounds duller or uneven between ears.

10. Dizziness or imbalance:
    Ear involvement can disturb balance signals.

11. Vitiligo (skin depigmentation patches):
    Patches of skin lose pigment, turning lighter than surrounding areas.

12. Poliosis (white eyelashes/eyebrows) and/or alopecia (hair loss):
    Hair in pigment-rich areas turns white or thins.

13. “Sunset-glow” fundus (seen by the eye doctor):
    The back of the eye looks orange-pink as pigment fades.

14. General malaise/low-grade fever:
    The body’s immune activation makes you feel unwell and warm.

15. Visual distortion (straight lines look wavy):
    Macular swelling or sub-retinal fluid bends the image, so lines look curved (metamorphopsia).

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Diagnostic tests

Doctors combine history, exam, and tests to confirm VKH and rule out look-alike diseases (like sympathetic ophthalmia, sarcoidosis, syphilis, tuberculosis, lymphoma, and others). Below are common, practical tests with what they check and why they help.

A) Physical exam

1. Visual acuity testing (Snellen chart):
   Measures how clearly each eye sees at distance. Helps grade how much inflammation has affected vision and tracks recovery.

2. Slit-lamp examination (front of the eye):
   A microscope with a thin light beam shows cells and flare in the aqueous (signs of inflammation), keratic precipitates on the cornea, and iris changes—all classic uveitis signs.

3. Dilated fundus examination (indirect ophthalmoscopy):
   After dilating the pupil, the doctor looks at the retina and optic nerve. In VKH they may see serous retinal detachments, disc swelling, choroidal thickening, and later sunset-glow.

4. General skin/hair and neurologic exam:
   Checks for vitiligo, poliosis, alopecia, and signs of meningism (neck stiffness). These support VKH and help exclude other causes.

B) Manual/bedside functional tests

5. Amsler grid (at reading distance):
   A small grid reveals wavy lines or missing spots from macular swelling or sub-retinal fluid. Simple way to monitor central vision.

6. Ishihara color plates (color vision):
   Measures color discrimination, which can drop with macular or optic nerve inflammation.

7. Confrontation visual fields:
   Quick bedside screen for peripheral vision loss or blind-spot changes; can reflect retinal or optic nerve dysfunction.

Note: These bedside tests are fast and non-invasive, useful for tracking function between imaging visits.

C) Laboratory and pathological tests

8. Complete blood count (CBC), ESR, and CRP:
   Look for inflammation patterns and to exclude infection or blood malignancy that could mimic uveitis.

9. Infectious disease rule-outs (syphilis, TB, etc.):
   Syphilis serology (RPR/VDRL with treponemal confirmation) and TB testing (IGRA/Quantiferon or T-Spot, chest imaging if needed) are vital because these infections can look like VKH but need different treatment.

10. Autoimmune screening panel (ANA, ENA, etc.) as appropriate:
    Helps exclude connective-tissue diseases (e.g., lupus, sarcoidosis with ACE/lysozyme if suspected) that can also cause uveitis.

11. Cerebrospinal fluid (CSF) analysis via lumbar puncture (if not risky):
    Often shows lymphocytic pleocytosis in VKH’s early phase—supportive when neuro-meningeal symptoms are present; also helps rule out infections.

12. HLA typing (e.g., HLA-DRB1*04:05):
    Not diagnostic by itself, but a supportive genetic marker that raises VKH likelihood in the right clinical picture.

D) Electrodiagnostic/physiologic tests

13. Electroretinography (ERG):
    Measures the retina’s electrical response to light. In VKH, widespread choroidal/retinal involvement can reduce responses, informing extent and prognosis.

14. Visual evoked potentials (VEP):
    Tracks how visual signals travel from the eye to the visual cortex. Delays can indicate optic pathway involvement or macular dysfunction.

15. Auditory tests (pure-tone audiometry ± auditory brainstem response/ABR):
    Quantifies hearing loss and, with ABR, checks the neural pathway from ear to brain—useful when tinnitus or hearing changes occur.

E) Imaging tests

16. Optical coherence tomography (OCT):
    A light-based scan that shows microscopic cross-sections of the retina and choroid. In VKH it reveals sub-retinal fluid, macular edema, and choroidal thickening (often markedly thick in the acute phase).

17. Fluorescein angiography (FA):
    A fluorescent dye highlights retinal blood vessels. VKH classically shows multiple pinpoint leaks and pooling of dye under the retina (matching serous detachments), and sometimes optic disc leakage.

18. Indocyanine green angiography (ICGA):
    This dye images the choroidal circulation (deeper than FA). VKH shows hypofluorescent dark dots and diffuse choroidal inflammation—very helpful for monitoring disease activity.

19. B-scan ocular ultrasound:
    Sound waves measure choroidal thickness and detect exudative detachments, especially when media are cloudy or when OCT is hard to obtain.

20. MRI of brain and orbits with contrast (when neuro symptoms are present):
    Can show meningeal enhancement and optic nerve sheath changes, supporting VKH and helping exclude other neuro-inflammatory disorders.

Non-pharmacological treatments

(Each item = description • purpose • how it helps)

1. Urgent care with a uveitis specialist
   See an ophthalmologist quickly if VKH is suspected. Purpose: start high-dose steroids early to stop vision-threatening inflammation. Mechanism: early control prevents choroidal swelling and serous retinal detachments. EyeWiki

2. Sun/bright-light protection
   Wear dark sunglasses/hat. Purpose: reduce photophobia and retinal light stress. Mechanism: less light → less discomfort while the inflamed uvea heals.

3. Avoid contact lenses during flares
   Purpose: lower irritation/infection risk while the front of the eye is inflamed. Mechanism: keeps the cornea surface calm.

4. Eye-rest habits
   Short, frequent breaks from screens; larger text; artificial tears for comfort (non-medicated). Purpose: reduce strain; improve comfort with photophobia.

5. Sleep hygiene
   Regular sleep supports immune balance and healing; poor sleep worsens pain and inflammation.

6. Stress-reduction routine (breathing, mindfulness, gentle yoga)
   Purpose: lower stress hormones that can amplify immune activity; mechanism: reduced sympathetic drive can calm inflammatory signaling.

7. Smoke-free life
   Smoking worsens ocular inflammation and impairs healing. Quitting reduces relapse risk and steroid side-effects like high pressure and cataracts.

8. Vaccination planning
   Before starting strong immune drugs, complete non-live vaccines (e.g., influenza, pneumococcal, COVID-19). Avoid live vaccines while immunosuppressed; time shots with your team. Purpose: prevent serious infections during therapy. CDC+1

9. Infection-prevention habits
   Hand hygiene, food safety, mask in crowded settings when on strong therapy. Purpose: reduce infections that can interrupt eye treatment.

10. Bone protection
    Weight-bearing exercise + calcium/vitamin D foods support bones during steroid use; monitor bone density if on long-term steroids.

11. Blood pressure & sugar monitoring
    Home BP and periodic glucose checks while on steroids; low-salt diet if BP rises. Purpose: reduce steroid complications. Cleveland Clinic

12. Safe exercise
    Gentle, regular activity (walking, stretching). Purpose: anti-inflammatory effects, mood, and bone/muscle strength; avoid high-impact during acute headache/photophobia.

13. Audiology support
    If tinnitus/hearing changes occur, early audiology referral; hearing protection in loud settings to reduce inner-ear stress.

14. Dermatology/skin-care support
    Sun protection, cosmetic camouflage for vitiligo, scalp care for alopecia; purpose: comfort and confidence during recovery.

15. Medication-interaction awareness
    Avoid grapefruit products with cyclosporine/tacrolimus (raises drug levels). Avoid alcohol with methotrexate. Purpose: safety. PubMedDrugs.comUHCW

16. Pregnancy planning & reliable contraception
    Some drugs (e.g., methotrexate, mycophenolate) are not safe in pregnancy. Plan ahead with your doctors.

17. Regular dental care
    Healthy mouth lowers bloodstream bacteria risk while immunosuppressed.

18. Fall-risk reduction
    High-dose steroids can weaken muscles/bones → arrange home safety (lighting, slip-resistant rugs).

19. Headache safety
    For steroid-related insomnia/headache, prefer acetaminophen over frequent NSAIDs (NSAIDs can strain kidneys if on calcineurin inhibitors).

20. Flare diary & written plan
    Track vision changes, floaters, pain, headache, tinnitus; know whom to call and how urgently.

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Drug treatments

(Each: class • typical dose & timing • purpose • mechanism • key side effects — doses are common ranges; your doctor individualizes and monitors labs.)

1. Prednisone / Prednisolone (oral systemic corticosteroid)
   Dose/time: ~0.5–1 mg/kg/day at start, then slow taper over weeks to months.
   Purpose: first-line to quickly shut down panuveitis/choroiditis.
   Mechanism: broadly blocks multiple inflammatory pathways.
   Side effects: high BP/sugar, mood/sleep change, weight gain, cataract & glaucoma risk, osteoporosis—mitigate with the non-drug steps above. EyeWiki

2. Methylprednisolone IV “pulse”
   Dose/time: 500–1000 mg IV daily for 3 days for severe acute VKH, then oral taper.
   Purpose: rapid control of sight-threatening inflammation.
   Mechanism/risks: same as steroids, but faster effect; monitor BP/heart/glucose. EyeWiki

3. Methotrexate (antimetabolite DMARD)
   Dose/time: 15–25 mg once weekly (oral or subcutaneous) + folic acid; takes 4–8 weeks to work.
   Purpose: steroid-sparing maintenance to prevent relapses.
   Mechanism: inhibits folate pathways, calming immune cell activity.
   Side effects: nausea, mouth sores, liver enzyme rise, low blood counts; avoid alcohol; contraception needed. Taylor & Francis OnlinePMC+1

4. Mycophenolate mofetil (antimetabolite)
   Dose/time: 1–1.5 g twice daily; onset 4–8 weeks.
   Purpose: steroid-sparing, effective for posterior and panuveitis.
   Mechanism: blocks lymphocyte purine synthesis.
   Side effects: GI upset, leukopenia, infection risk; contraception required. PMCAmerican Academy of Ophthalmology

5. Azathioprine (antimetabolite)
   Dose/time: ~1–2 mg/kg/day; check TPMT/NUDT15 status if available.
   Purpose: alternative steroid-sparing agent.
   Mechanism: purine antagonist lowering lymphocyte proliferation.
   Side effects: low blood counts, liver issues; monitor labs. BioMed Central

6. Cyclosporine A (calcineurin inhibitor)
   Dose/time: ~2–5 mg/kg/day in divided doses; monitor trough, BP, kidney function.
   Purpose: powerful T-cell suppression for severe disease.
   Mechanism: blocks calcineurin → lowers IL-2/T-cell activation.
   Side effects: kidney strain, high BP, tremor; avoid grapefruit. PubMedNCBI

7. Tacrolimus (calcineurin inhibitor)
   Dose/time: often ~0.05–0.1 mg/kg/day in divided doses; monitor troughs, kidneys, potassium, BP.
   Purpose: option if cyclosporine not tolerated/effective.
   Mechanism/side effects: similar to cyclosporine; avoid grapefruit. PentaVisionDrugs.com

8. Adalimumab (anti-TNF-α biologic)
   Dose/time (adult NIU label): 80 mg once, then 40 mg every other week starting 1 week later (some need weekly).
   Purpose: steroid-sparing control of noninfectious panuveitis (including VKH) and prevention of relapse.
   Mechanism: neutralizes TNF-α, a key inflammation driver.
   Side effects: infection risk (screen TB/hep B), injection reactions. FDA Access Data

9. Infliximab (anti-TNF-α biologic, IV)
   Dose/time: 3–5 mg/kg IV at weeks 0, 2, 6; then every 4–8 weeks (some need 10 mg/kg).
   Purpose: rapid control in severe or refractory cases.
   Mechanism/side effects: TNF-α blockade; infusion reactions; infection risk—screen first. EyeWikiInfliximab

10. Tocilizumab (anti-IL-6 receptor biologic; IV or SC, off-label)
    Dose/time: IV 8 mg/kg monthly (or SC 162 mg weekly/every 2 weeks) used in trials/series for refractory NIU and uveitic macular edema.
    Purpose: for cases failing anti-TNF/antimetabolites.
    Mechanism: blocks IL-6 signaling.
    Side effects: ↑lipids/LFTs, infection risk; lab monitoring. PubMedPMC

Why so many medicines? VKH needs fast inflammation control (steroids) and long-term “steroid-sparing” therapy to keep vision safe with fewer steroid harms. Combination therapy early may improve long-term outcomes. PMC

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Dietary “molecular” supplements

Evidence ranges from observational to small trials; always review with your doctor, especially if you are pregnant or on immune drugs.

1. Vitamin D3 (e.g., 1000–2000 IU/day; adjust to blood 25-OH D level 30–50 ng/mL)
   Function: immune modulation; deficiency is linked with non-infectious uveitis risk/severity. Mechanism: supports regulatory T-cells. ScienceDirect

2. Omega-3 (EPA+DHA) (about 1–2 g/day combined)
   Function: anti-inflammatory lipid mediators; may reduce inflammatory cytokines and help macular physiology. Mechanism: pro-resolving mediators (resolvins). (Evidence in uveitis is limited but biologically plausible.)

3. Curcumin with piperine (e.g., 500 mg curcumin 1–2×/day with black pepper extract)
   Function: NF-κB inhibition; small clinical signals in ocular inflammation. Mechanism: down-regulates pro-inflammatory pathways. ScienceDirect

4. Probiotics (multistrain, ≥10^9 CFU/day)
   Function: gut–eye immune axis support; may modulate Th17/Treg balance. Mechanism: microbial metabolites signal to immune cells. (Emerging evidence; discuss if immunosuppressed.) PubMed

5. Lutein + Zeaxanthin (10 mg/2 mg daily)
   Function: macular antioxidants; general retinal support during recovery.

6. Zinc (10–20 mg/day elemental; short courses)
   Function: supports retinal enzymes and immune function; avoid excess (copper loss).

7. Selenium (50–100 mcg/day)
   Function: antioxidant enzyme cofactor (glutathione peroxidases).

8. Vitamin C (500 mg/day)
   Function: antioxidant support; helps collagen/uveal tissue healing.

9. EGCG (green tea extract) (250–300 mg/day; avoid if liver disease)
   Function: anti-inflammatory signaling; caution with hepatotoxicity risk.

10. Magnesium glycinate (200–400 mg at night)
    Function: sleep, headache/muscle cramp relief during steroid therapy.

Safety notes: Always screen for interactions (e.g., avoid high-dose antioxidants right around some surgeries; be cautious with herbs that alter liver enzymes). Grapefruit strongly interacts with calcineurin inhibitors; alcohol increases liver risk with methotrexate. U.S. Food and Drug AdministrationPMC

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Advanced” therapies (hard immunomodulators / regenerative & stem-cell–related)

(Used only in specialist hands for refractory VKH/uveitis; some are experimental.)

1. Rituximab (anti-CD20 B-cell biologic, IV)
   Dose: 1000 mg day 1 & 15 (or 375 mg/m² weekly ×4); may repeat in 6–12 months.
   How it helps: depletes B-cells that drive autoimmune cascades; used when anti-TNF/antimetabolites fail.
   Risks: infusion reactions, infections; vaccinate/timing guidance needed. PMC

2. Intravenous Immunoglobulin (IVIG)
   Dose (varies): ~2 g/kg/cycle split over 2–5 days, sometimes monthly.
   How it helps: pooled antibodies can neutralize autoantibodies and reset immune balance; used in selected refractory cases.
   Risks: headache, thrombosis risk; rare paradoxical uveitis reported. Centers for Medicare & Medicaid ServicesScienceDirectPMC

3. Anakinra (IL-1 blocker, SC)
   Dose: 100 mg daily (adjusted).
   How it helps: targets IL-1–driven inflammation; explored in refractory NIU.
   Risks: infection, neutropenia. CenterWatch

4. Tofacitinib (JAK inhibitor, oral)
   Dose: 5 mg twice daily (XR 11 mg once daily).
   How it helps: blocks JAK/STAT signaling downstream of many cytokines; case series show benefit in refractory uveitis.
   Risks: infections, zoster, lipids, clot risk—careful screening/monitoring. PMC+1

5. Baricitinib (JAK inhibitor, oral)
   Dose: 2–4 mg once daily (pediatric protocols differ).
   How it helps: similar pathway; pediatric trials under way/reported for uveitis.
   Risks: as above; hematology & liver monitoring. PMCPubMed

6. Cell-based approaches (research stage):
   a. Autologous hematopoietic stem-cell transplantation (AHSCT) — resets immune system; tried in other severe autoimmune diseases and rare ocular cases; high risk and reserved for trials/exceptional situations.
   b. Mesenchymal stem cells (MSC) / exosomes — preclinical/early human reports suggest anti-inflammatory effects in autoimmune uveitis; still experimental. FrontiersPMC

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Surgeries

1. Cataract surgery (phacoemulsification with IOL)
   Why: steroids and uveitis can cause cataracts; surgery improves cloudy vision once inflammation is quiet for several months.
   Notes: meticulous control before/after to prevent flare.

2. Glaucoma surgery — trabeculectomy or tube shunt (Ahmed/Baerveldt)
   Why: treat steroid-induced/uveitic glaucoma when drops fail; tube shunts are often favored in uveitis due to scar risk.
   Mechanism: creates a new path for fluid to lower eye pressure. PMCNature

3. Pars plana vitrectomy (PPV)
   Why: for non-clearing vitreous opacities, epiretinal membrane, or to aid diagnosis/complication repair.
   Mechanism: removes inflammatory vitreous; may help macular issues in selected cases. PentaVision

4. Fluocinolone acetonide intravitreal implant (Retisert®/Yutiq®)
   Why: provides years-long local steroid for chronic, relapsing posterior uveitis when systemic therapy is unsuitable.
   Mechanism: slow steroid release inside the eye. Risks: cataract, high pressure; may need glaucoma surgery. Bausch + LombPMC

5. Dexamethasone intravitreal implant (Ozurdex®)
   Why: treat relapsing posterior uveitis/macular edema; shorter-acting than fluocinolone.
   Mechanism: biodegradable implant releases steroid for months. Risks: pressure rise, cataract, rare infection. PMCEyeWiki

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Prevention tips

There is no proven way to prevent VKH from starting, but you can prevent flares and complications:

1. Start treatment early and do not stop suddenly. Follow the taper exactly. EyeWiki

2. Keep every follow-up; flares can be silent early—OCT/ICGA/FA can catch inflammation even if you feel okay. EyeWiki

3. Vaccinate smartly (non-live vaccines up to date; avoid live vaccines while immunosuppressed). CDC

4. Screen for TB and hepatitis before biologics; treat latent infections first. (Your team will arrange this.) CDC

5. Healthy bones, BP, sugar during steroid use (exercise, calcium/Vit-D foods, low salt, glucose checks). Cleveland Clinic

6. No smoking; limit alcohol (or avoid on methotrexate). UHCW

7. Avoid grapefruit with cyclosporine/tacrolimus; ask about other food–drug interactions. U.S. Food and Drug Administration

8. Protect eyes from bright light; rest eyes during flares.

9. Manage stress + sleep to support immune balance.

10. Have a flare plan in writing (who to call, same-day visit location).

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When to see a doctor now

• Sudden drop in vision, new shadows/curtains, or many new floaters.

• Severe eye pain, intense redness, or light intolerance.

• New severe headache/neck stiffness, ringing in ears, or hearing loss.

• Side-effects of medicines: fever, cough that won’t go away, severe stomach pain, yellowing eyes/skin, very high BP or sugar, swelling/weight gain on steroids. (Call your ophthalmologist or go to emergency if severe.)

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Things to eat and things to limit/avoid

(Supportive diet for steroid/immune therapy; customize for diabetes, kidney, or other conditions.)

Prefer / Eat more of:

1. Leafy greens & colorful veggies (antioxidants for retinal health).

2. Fatty fish (salmon/sardines) for omega-3s.

3. Eggs/yellow corn/greens (lutein/zeaxanthin).

4. Yogurt/fermented foods (probiotics) — if not contraindicated.

5. Citrus/berries (vitamin C) — but not grapefruit with specific drugs. U.S. Food and Drug Administration

6. Nuts/seeds (vitamin E, selenium, magnesium).

7. Lean proteins (healing; maintain muscle under steroids).

8. Whole grains & legumes (fiber; steadier sugars on steroids).

9. Low-fat dairy or fortified alternatives (calcium + vitamin D for bones).

10. Plenty of water (good for general health and some meds).

Limit / Avoid:

1. Grapefruit/pomelo/bitter orange if on cyclosporine or tacrolimus. PubMed+1

2. Alcohol with methotrexate (liver risk). uhleicester.nhs.uk

3. Very salty foods (steroids raise BP/fluid). Cleveland Clinic

4. Sugary drinks/sweets (steroid-induced high sugar). Cleveland Clinic

5. Undercooked/raw meats, unpasteurized dairy (infection risk while immunosuppressed).

6. High-dose herbal stimulants (unpredictable interactions).

7. Mega-dose supplements without medical advice.

8. NSAID overuse if on calcineurin inhibitors (kidney strain).

9. Energy drinks (BP/heart rate).

10. Smoking/vaping (worsens inflammation).

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FAQs

1. Is VKH contagious?
   No. It is an autoimmune disease. You cannot “catch” it.

2. Why are high-dose steroids used first?
   They quickly stop dangerous inflammation in the eye, protecting vision; then other drugs keep things quiet while steroids are tapered. EyeWiki

3. How long will I take medicines?
   Often months to years. Many people need a slow, careful taper plus a steroid-sparing medicine for long-term control. EyeWiki

4. Are biologics safe?
   They can be very effective and are generally well-tolerated with proper screening/monitoring; they do raise infection risk. ScienceDirect

5. Can I work or use screens?
   Yes, but during flares take frequent breaks, enlarge text, and use sunglasses/filters for comfort.

6. What about pregnancy?
   Some drugs (methotrexate/mycophenolate) are not safe in pregnancy; others may be used with specialist guidance. Plan ahead.

7. Can diet cure VKH?
   No. Diet supports your health and medication safety but does not replace immune-modulating therapy.

8. Why check TB and hepatitis before biologics?
   Because these drugs can “unmask” latent infections; screening protects you. CDC

9. Do vaccines trigger VKH?
   Uveitis after vaccines is rare; overall, vaccination is recommended for immunosuppressed patients, avoiding live vaccines during therapy and timing non-live vaccines with your doctors. BMJ OpenCDC

10. Will I need surgery?
    Only if complications (cataract, glaucoma, persistent vitreous opacities or macular issues) arise, and usually after inflammation is quiet. PMC

11. Why avoid grapefruit?
    It raises blood levels of drugs like cyclosporine/tacrolimus → toxicity. U.S. Food and Drug Administration

12. Can I drink alcohol?
    Avoid with methotrexate; otherwise ask your team, especially if liver tests are abnormal. uhleicester.nhs.uk

13. How do JAK inhibitors fit in?
    They are oral options for refractory uveitis under specialist care; evidence is growing. PMC

14. Are stem cell therapies available now?
    Mostly experimental; consider only within clinical trials at expert centers. PMC

15. What causes VKH?
    Likely a T-cell immune response against melanocyte antigens in genetically susceptible people; it can also be “VKH-like” after some cancer immunotherapies.

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 30, 2025.