Relentless Placoid Chorioretinitis (RPC)

Relentless placoid chorioretinitis is a rare eye inflammation that affects the layer under the retina (the choroid and the retinal pigment epithelium). Doctors also call it ampiginous choroiditis. It is part of the “white-dot syndromes,” which are inflammatory diseases that leave many pale spots in the back of the eye. RPC often involves both eyes, spreads widely across the retina (including the mid-periphery), and keeps coming back over months if it is not controlled. Lesions are usually at different stages at the same time—some are new and creamy white, and others are older and dark or scarred. Because of this persistent or relapsing course, the disease can threaten central vision if the macula becomes involved. EyeWikiPubMedJAMA Network

Relentless Placoid Chorioretinitis (RPC) is a rare eye inflammation that affects the layer under the retina (the choroid) and the retinal pigment epithelium (RPE). “Placoid” means the spots doctors see are flat and creamy-white; “relentless” means the disease keeps coming back or stays active for many months. RPC usually involves both eyes, starts in young to middle adulthood, and behaves like cousins in the same “white-dot syndrome” family (especially APMPPE and serpiginous choroiditis), but it runs longer, often with many more lesions scattered toward the periphery of the retina. Diagnosis is clinical and imaging-based after ruling out infections (like syphilis or TB) and other causes of posterior uveitis. With timely steroids and immune therapy, most people keep good central vision, but untreated or frequently relapsing disease can scar and reduce sight. EyeWiki

RPC sits on a spectrum with two other placoid conditions: APMPPE (acute posterior multifocal placoid pigment epitheliopathy) and serpiginous choroiditis. RPC shares features with both but behaves more relentlessly than APMPPE and is more widespread than classic serpiginous disease. Recognizing this pattern matters because the long, recurrent course may require strong anti-inflammatory management. EyeWikiAAO-HNSPubMed Central

The exact cause is not fully known. The main idea is that the body’s immune system mistakenly attacks the outer retina, the retinal pigment epithelium, and the underlying choriocapillaris. Sometimes this may be triggered by an infection or follow a viral illness, but many patients have no clear trigger. Doctors also work hard to rule out infections that can mimic RPC (like tuberculosis or syphilis), because those need different treatment. PubMed Central+2PubMed Central+2

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Types

There is no official, rigid subtype system for RPC. Clinicians describe patterns that help with day-to-day care. Think of these as phenotypes rather than strict types:

1. Classic bilateral RPC
   This is the common picture. Both eyes show many scattered placoid lesions in the posterior pole and mid-periphery. New and old spots coexist. The disease smolders and relapses. PubMed

2. Pan-retinal RPC
   Lesions spread very widely, including far peripheral retina. This wide distribution is a key reason the disease is called “relentless.” PubMed

3. Macula-predominant RPC
   Some patients show early or heavy macular involvement. This pattern has higher risk for central vision problems and needs close monitoring. (This is a practical label used by clinicians when macula is threatened.) EyeWiki

4. Peripheral-predominant RPC
   Lesions favor the mid-periphery and periphery. Central vision may be spared at first, but the disease can march inward over time. retina-specialist.com

5. APMPPE-like RPC (overlap pattern)
   The lesions and early story look like APMPPE, but the disease does not burn out in weeks. Instead, it recurs, spreads, or persists—so it behaves like RPC. EyeWiki

6. Serpiginous-like RPC (overlap pattern)
   The lesions show some serpiginous features (geographic, creeping edges) but are more multifocal and widespread than typical serpiginous choroiditis. AAO-HNS

7. Pediatric- or young-adult-onset RPC
   RPC can present in teenagers or young adults and still follow a prolonged, relapsing course. PubMed Central

Note: These patterns reflect how RPC presents and behaves in clinics and publications; they are not formal subtypes set by a governing body. They help doctors explain risk and plan tests. EyeWiki

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Causes

RPC’s true cause is unknown, so it is more accurate to list suspected immune triggers and conditions that can look similar (mimics) and must be tested for. Doctors check all of these carefully before deciding on treatment.

1. Post-viral immune response
   Some patients develop placoid disease after a flu-like illness. The immune system may attack the outer retina after the infection has passed. PubMed CentralEyeWiki

2. COVID-19–related trigger (rare, reported)
   There are case reports of APMPPE that later behaved like RPC after COVID-19 infection. This supports an immune trigger in some people. PubMed Central

3. Tuberculosis (mimic/trigger)
   TB can cause serpiginous-like choroiditis that resembles placoid disease. It must be ruled out because management differs. PubMed Central

4. Syphilis (mimic)
   Syphilis can produce placoid lesions in the posterior pole and must always be excluded. Cybersight

5. Toxoplasmosis (mimic)
   Ocular toxoplasmosis can involve the retina and RPE with active white lesions; testing is important when the picture is atypical. PubMed Central

6. Bartonella (mimic)
   Bartonella infections can cause chorioretinitis that may resemble white-dot diseases in some phases. Cybersight

7. Lyme disease (mimic)
   Lyme can involve the back of the eye; serology is checked when history or geography fit. Cybersight

8. Herpesviruses (HSV/VZV/EBV) (mimic/possible trigger)
   Herpetic disease can affect the choroid and retina or trigger immune responses; it is part of the standard rule-out list. retina-specialist.com

9. Fungal infections (mimic)
   Fungal chorioretinitis can appear with creamy lesions; it is uncommon but important in the right clinical setting. PubMed Central

10. Sarcoidosis (mimic/systemic association)
    Sarcoid can inflame the choroid and RPE and create multifocal lesions. Serum ACE, lysozyme, and chest imaging help evaluate this. Cybersight

11. Autoimmune predisposition (general)
    RPC behaves like an immune-mediated outer retinal and choriocapillaris attack; immune predisposition is suspected even when a trigger is not found. PubMed Central

12. Genetic HLA background (extrapolated from related placoid diseases)
    APMPPE and serpiginous choroiditis have reported HLA associations (e.g., HLA-B7). While a specific HLA link for RPC is not firmly established, this supports an immune-genetic background for placoid chorioretinitides. EyeWikiPubMed CentralAAO-HNS

13. Vaccination as a rare trigger (reported in placoid spectrum)
    Occasional reports link placoid-type inflammation to recent vaccination, but causation is uncertain. Clinicians interpret these cautiously. (General white-dot literature). PubMed Central

14. Immune checkpoint inhibitors (drug-related uveitis/placoid chorioretinitis)
    Cancer immunotherapy can cause posterior uveitis with placoid features; the mechanism is immune activation. Lippincott Journals

15. Overlap with APMPPE (disease continuum)
    Some “APMPPE” cases evolve into a relentless, recurrent course compatible with RPC, suggesting a spectrum rather than separate causes. PubMed Central

16. Overlap with serpiginous choroiditis (disease continuum)
    Serpiginous-like features may appear in RPC, again supporting shared immune pathways. AAO-HNS

17. Retinal vasculitis as an associated finding
    Some RPC patients show vasculitis; this signals vascular immune involvement rather than a distinct cause. ResearchGate

18. CNS/neurologic associations in placoid spectrum (rare)
    In the broader placoid family, neurologic symptoms can occur (better described in APMPPE). This drives careful systemic review in atypical cases. EyeWiki

19. Environmental or undetected infectious triggers
    White-dot syndromes sometimes follow nonspecific illnesses and may reflect an immune response to an unknown antigen. PubMed Central

20. Idiopathic (no identified cause)
    Many patients have no clear trigger even after a thorough work-up. The disease is still real and immune-mediated in behavior. PubMed Central

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Symptoms

1. Blurred vision
   Vision may go in and out of focus because the inflamed outer retina cannot process light normally. This can be mild or severe. EyeWiki

2. Central or paracentral scotoma
   A small dark or gray area may block part of your central vision, especially when macular lesions are active. EyeWiki

3. Metamorphopsia
   Straight lines may look bent or wavy when the macula is affected. This reflects disturbed photoreceptors. EyeWiki

4. Photopsias (flashes or shimmering lights)
   Inflamed outer retina can misfire, creating flickers or sparks of light. PubMed Central

5. Light sensitivity (glare)
   Bright light may feel harsh, and recovery after glare can be slow. This often tracks with active lesions. PubMed Central

6. Reduced contrast sensitivity
   Grays and subtle textures are harder to see because the outer retina is disturbed. PubMed Central

7. Color desaturation
   Colors, especially reds, can look washed out when macula is involved. Color plates help detect this. PubMed Central

8. Floaters
   Clumps of inflammatory cells can drift in the vitreous, causing moving specks. EyeWiki

9. Peripheral blind spots
   Mid-peripheral lesions can create gaps at the edge of vision. Patients may notice bumping into objects. retina-specialist.com

10. Difficulty reading fine print
    Small letters require perfect macular function; inflammation reduces clarity and speed. EyeWiki

11. Poor night vision or delayed dark adaptation
    Inflamed photoreceptors recover slowly after light exposure. PubMed Central

12. Headache or viral-like prodrome
    Some placoid cases start after a “flu-like” episode with headache; in part of the spectrum this has been reported. EyeWiki

13. Vision fluctuates over weeks
    RPC is relapsing. Vision may improve as lesions heal and worsen when new ones appear. PubMed

14. Both eyes involved (not always symmetric)
    One eye can start first, but the fellow eye is usually involved over time. PubMed Central

15. Eye discomfort (usually mild)
    True pain is not a major feature, but some patients feel mild ache or pressure with inflammation. EyeWiki

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Diagnostic Tests

Goal of testing:

1. Confirm that the problem sits in the outer retina/RPE/choroid with a placoid pattern.

2. Map how active and widespread it is.

3. Exclude infections and systemic diseases that mimic RPC (because treatment differs).

4. Track recovery or relapse over time.

A) Physical exam tests

1. Best-corrected visual acuity
   This measures central clarity. It sets the baseline and tracks change with each visit. EyeWiki

2. Pupil exam (look for a relative afferent pupillary defect)
   This checks whether one eye’s retina/optic nerve is underperforming. A new RAPD in unilateral or asymmetric disease suggests significant dysfunction. PubMed Central

3. Slit-lamp biomicroscopy
   The doctor inspects the front of the eye and the vitreous for inflammatory cells. Vitreous cells support an inflammatory cause. EyeWiki

4. Dilated fundus examination
   With lens and light, the doctor directly sees the creamy placoid lesions and the pigment changes of healing and scarring. Extent and location are documented each visit. EyeWiki

B) Manual / functional chair-side tests

5. Amsler grid
   You look at a grid to check for missing spots or wavy lines that signal macular involvement. This is simple and repeatable at home. PubMed Central

6. Color vision plates (Ishihara or similar)
   Desaturated color perception can track macular function. This is quick and catches subtle macular changes. PubMed Central

7. Photostress recovery time
   After a bright light, recovery time reflects macular photoreceptor health; prolonged recovery suggests outer retinal dysfunction. PubMed Central

C) Laboratory and pathologic tests

8. Syphilis serology
   A non-treponemal test (RPR/VDRL) with a treponemal confirmatory test (FTA-ABS/TPPA) is essential in any unexplained posterior uveitis with placoid lesions. Cybersight

9. Tuberculosis testing (IGRA/QuantiFERON or TST)
   TB can cause serpiginous-like choroiditis. A positive result changes management and prompts chest imaging and infectious-disease input. PubMed Central

10. Bartonella serology
    Considered when history suggests cat exposure or compatible systemic symptoms. Cybersight

11. Lyme disease serology
    Checked in endemic areas or with a supportive clinical story. Cybersight

12. Sarcoid markers (ACE, lysozyme) and serum calcium
    These support evaluation for ocular sarcoidosis when the picture is atypical or when lungs/skin are involved. Cybersight

13. General inflammation work-up (CBC, ESR, CRP; consider ANA/ANCA/HIV as guided)
    These help screen for systemic inflammation, autoimmune disease, and infection risks before immunosuppression. PubMed Central

D) Electrodiagnostic tests

14. Full-field ERG (electroretinography)
    Measures global retinal function. In outer retinal inflammatory disease, ERG may show reduced photoreceptor responses, which can improve as inflammation settles. PubMed Central

15. Multifocal ERG
    Samples many tiny regions of central retina. It can map localized dysfunction from individual placoid lesions and track change over time. PubMed Central

16. EOG (electro-oculogram)
    Assesses retinal pigment epithelium function. White-dot literature shows EOG can be more persistently abnormal than the ERG in outer retinal/RPE disorders. TTUHSC

E) Imaging tests

17. Optical Coherence Tomography (OCT; include enhanced-depth when possible)
    OCT gives cross-sectional “slices” through the macula showing outer retinal disruption, RPE changes, and sometimes choriocapillaris signals. It is the best day-to-day tool to track lesion activity and macular risk. PubMed CentralBioMed Central

18. Fluorescein Angiography (FA)
    FA shows the retinal circulation and the staining/blocking pattern of placoid lesions over time. It helps separate active edges from old scars and checks for vasculitis or leakage. PubMed Central

19. Indocyanine Green Angiography (ICGA)
    ICGA images the choroidal circulation and highlights the choriocapillaris involvement typical of placoid diseases; it often shows more extensive disease than FA. PubMed Central

20. Fundus Autofluorescence (FAF)
    FAF maps lipofuscin signals from the RPE. In RPC, lesions commonly appear hypo-autofluorescent with hyper-autofluorescent borders during activity and then evolve. FAF is a sensitive way to follow new versus healing spots. Frontiers

Non-pharmacological treatments (therapies & others)

These do not replace medicines; they support recovery, protect vision, and reduce relapse risk. Each item includes description, purpose, and likely mechanism.

1. Rapid specialist care and scheduled follow-up
   What: See a retina/uveitis specialist promptly and keep regular visits.
   Purpose: Catch new lesions early; adjust treatment before vision is harmed.
   Mechanism: Frequent checks with OCT/FAF/FA/ICGA detect silent activity and guide safe steroid tapering. EyeWiki

2. Baseline infectious work-up before immunosuppression
   What: Lab tests for syphilis, TB, etc., as directed.
   Purpose: Avoid masking an infection with steroids/IMT.
   Mechanism: Exclusion testing prevents iatrogenic worsening of undiagnosed infections. EyeWiki

3. Written flare plan
   What: A simple plan (who to call, what imaging, when to increase drops or come in).
   Purpose: Shortens time to care during a new scotoma/photopsia.
   Mechanism: Faster evaluation → faster inflammation control → less scarring.

4. Light management and UV protection
   What: Sunglasses/hat outdoors; reduce glare; use screen night-mode.
   Purpose: Comfort and visual function during active lesions.
   Mechanism: Lowers photophobia and reduces retinal light stress while inflamed.

5. Low-vision aids (if lesions scar)
   What: High-contrast lighting, magnifiers, large-print settings.
   Purpose: Maintain reading/driving safety if paracentral scotomas persist.
   Mechanism: Optimizes remaining retinal function despite scars.

6. Amsler grid or simple self-monitoring
   What: Check a grid/straight lines daily with each eye.
   Purpose: Early detection of new distortions near the center.
   Mechanism: Prompts quicker clinic review for macular-threatening activity.

7. Cardiometabolic health optimization
   What: Control blood pressure, glucose, weight, lipids with your PCP.
   Purpose: General anti-inflammatory benefits and surgical readiness.
   Mechanism: Systemic inflammation and vascular stress can worsen ocular disease course.

8. Smoking cessation
   What: Stop cigarettes/vaping; get counseling/nicotine replacement if needed.
   Purpose: Smoking worsens ocular and immune outcomes broadly.
   Mechanism: Reduces oxidative and inflammatory load at the choroid/RPE.

9. Sleep regularity and stress reduction
   What: 7–9 hours sleep; mindfulness, CBT, or relaxation training.
   Purpose: Better immune regulation and adherence.
   Mechanism: Sleep/stress pathways influence cytokines that drive uveitis.

10. Vaccination review (before biologics)
    What: Update non-live vaccines (e.g., influenza); avoid live vaccines once on biologics unless specialist clears it.
    Purpose: Prevent infections during immunosuppression.
    Mechanism: Reduces infection-triggered flares and treatment interruptions. EyeWiki

11. Nutrition for inflammation balance (see food section below)
    What: Mediterranean-style eating rich in omega-3, colorful produce.
    Purpose: Support immune balance and antioxidant defenses.
    Mechanism: Modulates Th1/Th17 responses and oxidative stress (preclinical/associative evidence). PubMed Central+1

12. Hydration and limiting alcohol
    What: Regular water intake; avoid heavy drinking.
    Purpose: General vascular/immune support; avoid drug interactions.
    Mechanism: Decreases systemic stressors that complicate therapy.

13. Safe physical activity
    What: Moderate exercise most days.
    Purpose: Reduces systemic inflammation; supports mood and sleep.
    Mechanism: Lowers CRP/IL-6; improves steroid-related metabolic effects.

14. Medication adherence coaching
    What: Pillbox, reminders, pharmacist counseling.
    Purpose: Prevents missed doses that invite relapse.
    Mechanism: Maintains steady immune suppression to keep lesions quiet.

15. Sun-sensitive drug counseling
    What: If using photosensitizing meds, add extra sun protection.
    Purpose: Comfort and safety during outdoor exposure.
    Mechanism: Minimizes photophobia and UV-related irritation.

16. Bone and stomach protection during steroids
    What: Calcium/vitamin D (if indicated), PPI/H2 blocker when appropriate.
    Purpose: Reduce steroid side effects that derail treatment.
    Mechanism: Prevents osteoporosis and gastritis that limit steroid use. (Drug specifics below.)

17. Glaucoma and cataract surveillance
    What: Regular pressure checks and lens exams.
    Purpose: Detect steroid-induced IOP rise and cataract early.
    Mechanism: Allows timely drops or surgery if needed to protect vision. FDA Access Data

18. Driving and workplace adjustments
    What: Avoid night driving during flares; request screen/lighting accommodations.
    Purpose: Safety and productivity while vision fluctuates.
    Mechanism: Reduces accident risk and eye strain.

19. Infection-prevention habits on IMT
    What: Hand hygiene, avoid sick contacts, prompt treatment of febrile illness.
    Purpose: Reduce interruptions to immunotherapy.
    Mechanism: Lowers infection risk while immunosuppressed. EyeWiki

20. Patient education & support groups
    What: Learn RPC/uveitis basics; connect with others.
    Purpose: Empower self-care and resilience.
    Mechanism: Better understanding improves adherence and outcomes.

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Drug treatments

⚠️ Doses below are typical ranges used for noninfectious posterior uveitis; your own dose/taper must be set by your uveitis specialist based on weight, labs, and response.

1. Systemic corticosteroids (Prednisone PO)
   Class: Glucocorticoid anti-inflammatory.
   Dose/time: Commonly 0.5–1 mg/kg/day short term, then slow taper over weeks–months once a steroid-sparing agent takes effect.
   Purpose: Rapidly shut down active choroid/RPE inflammation.
   Mechanism: Broad cytokine suppression (T-cell, macrophage).
   Key side effects: Weight gain, mood/insomnia, hyperglycemia, hypertension, cataract, glaucoma, infection risk. EyeWiki+1

2. IV methylprednisolone “pulse”
   Class: High-dose steroid.
   Dose/time: 500–1,000 mg IV daily for 3 days in severe sight-threatening flares, then oral taper.
   Purpose: Rescue therapy for macula-threatening lesions.
   Mechanism/SE: Same as steroids; short high-dose burst. EyeWiki

3. Cyclosporine
   Class: Calcineurin inhibitor (IMT).
   Dose/time: ~2–5 mg/kg/day (divided), with trough-level and renal/BP monitoring.
   Purpose: Steroid-sparing control of relapsing RPC.
   Mechanism: Blocks T-cell activation (IL-2 pathway).
   Side effects: Hypertension, renal dysfunction, tremor, gingival hyperplasia. Note: Combination with prednisone reduced recurrences in reports, though some cases were refractory. EyeWiki+1

4. Azathioprine
   Class: Antimetabolite (IMT).
   Dose/time: ~1–2 mg/kg/day; check TPMT/NUDT15; monitor CBC/LFTs.
   Purpose: Steroid-sparing maintenance.
   Mechanism: Purine antagonism → reduced lymphocyte proliferation.
   Side effects: Cytopenias, hepatotoxicity, infection risk. EyeWiki

5. Mycophenolate mofetil
   Class: Antimetabolite (IMT).
   Dose/time: Often 1–1.5 g twice daily; monitor CBC/LFTs.
   Purpose: Alternative steroid-sparing agent; evidence mixed in RPC but widely used in NIU.
   Mechanism: Inhibits inosine monophosphate dehydrogenase in lymphocytes.
   Side effects: GI upset, cytopenias, infection. EyeWikiReview of Ophthalmology

6. Methotrexate
   Class: Antimetabolite (IMT).
   Dose/time: 7.5–25 mg once weekly + folic acid; monitor CBC/LFTs.
   Purpose: Long-term control, especially if other agents not tolerated.
   Mechanism: Anti-proliferative/anti-inflammatory; shifts cytokine balance.
   Side effects: Liver toxicity, cytopenias, oral ulcers; avoid in pregnancy. Review of Ophthalmology

7. Adalimumab (anti-TNF-α)
   Class: Biologic.
   Dose/time: 80 mg loading; 40 mg at week 1; then 40 mg every other week (NIU labeling).
   Purpose: For refractory RPC to allow steroid taper; case series show success.
   Mechanism: Neutralizes TNF-α, dampens T-cell inflammation.
   Side effects: Infection risk (TB reactivation screening needed), injection reactions; avoid live vaccines. ScienceDirect

8. Infliximab (anti-TNF-α, IV)
   Class: Biologic.
   Dose/time: ~5–10 mg/kg IV at 0, 2, 6 weeks then q4–8 weeks; adjust to response.
   Purpose: Option for severe refractory disease.
   Mechanism/SE: As above; infusion reactions, infection risk. (Used in NIU and reported in RPC literature.) Number Analytics

9. Tocilizumab (anti-IL-6R)
   Class: Biologic.
   Dose/time: 8 mg/kg IV monthly or 162 mg SC every 1–2 weeks (uveitis practice patterns).
   Purpose: Rescue for refractory inflammation or macular edema when anti-TNF fails.
   Mechanism: Blocks IL-6 signaling; reduces vascular leakage and inflammation.
   Side effects: Infection, liver enzyme rise, lipid changes. EyeWiki

10. Local steroid implants or injections (adjuncts)
    Options: Dexamethasone 0.7 mg (Ozurdex®); Fluocinolone acetonide 0.18–0.19 mg (Yutiq®/FAi); also intravitreal triamcinolone in selected cases.
    Dose/time: Single in-office injection; Ozurdex® lasts ≈3–6 months; Yutiq® ≈36 months.
    Purpose: Control local inflammation and macular edema; reduce systemic steroid need.
    Mechanism: Sustained intraocular steroid release.
    Key side effects: Intraocular pressure rise, cataract, rare infection. Evidence: Both Ozurdex® and FA implants are approved/validated for noninfectious posterior uveitis. FDA Access DataYUTIQPubMed Central

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Dietary “molecular” supplements

Always clear supplements with your doctor (interactions, surgery/biologic timing). Evidence ranges from animal/associational to small human studies in noninfectious uveitis, not specifically RPC.

1. Omega-3 (EPA/DHA) — ~1–2 g/day combined EPA+DHA
   Function: Anti-inflammatory lipid mediators (resolvins).
   Mechanism: Shifts Th1/Th17 responses; dampens dendritic-cell activation (preclinical). PubMed CentralPLOS

2. Vitamin D3 — often 1,000–2,000 IU/day (or per deficiency labs)
   Function: Immune modulation; bone protection on steroids.
   Mechanism: Links observed between low vitamin D and NIU; supplementation under study. PubMedJAMA Network

3. Curcumin (enhanced bioavailability forms) — 500–1,500 mg/day
   Function: Anti-inflammatory/antioxidant adjunct.
   Mechanism: NF-κB and cytokine modulation; small clinical signals in uveitis/mac-edema. PubMedEuropean Review

4. Lutein/Zeaxanthin — e.g., 10–20 mg lutein + 2–4 mg zeaxanthin/day
   Function: Macular pigment/antioxidant support.
   Mechanism: Quenches oxidative stress; experimental anti-inflammatory effects. PubMed Central+1

5. N-Acetylcysteine (NAC) — 600–1,200 mg/day
   Function: Glutathione precursor; antioxidant support.
   Mechanism: Redox balance that may limit oxidative damage during inflammation. (General ocular antioxidant rationale) PubMed Central

6. Resveratrol — 150–500 mg/day
   Function: Anti-oxidative/anti-inflammatory polyphenol.
   Mechanism: Sirtuin and NF-κB modulation (preclinical ocular data). PubMed Central

7. Green-tea catechins (EGCG) — 200–400 mg/day (caffeine-aware)
   Function: Anti-inflammatory/antioxidant support.
   Mechanism: Cytokine and oxidative stress modulation (preclinical). PubMed Central

8. Zinc — 10–25 mg elemental/day (short term unless deficient)
   Function: Immune and retinal enzyme cofactor.
   Mechanism: Supports antioxidant enzymes and immunity. (General ocular nutrition context) PubMed Central

9. Selenium — 100–200 mcg/day
   Function: Selenoprotein antioxidant activity.
   Mechanism: May support redox control during inflammation. (General antioxidant context) PubMed Central

10. Probiotics — product-dependent
    Function: Gut–immune axis support.
    Mechanism: May favor T-reg balance (preclinical uveitis data). (Conceptual support in immune modulation literature) Frontiers

Note: These supplements do not treat RPC by themselves. Use them, if at all, as carefully supervised adjuncts. Core therapy is steroid + immunomodulation.

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Regenerative” or immune-rebalancing therapies

These are not standard RPC treatments. They are discussed for completeness because you requested “hard immunity booster/regenerative/stem-cell drugs.” Use only in expert centers or trials.

1. Human umbilical cord–derived mesenchymal stem cells (HUC-MSCs, IV)
   Dose used in a small case series: ~1×10^6 cells/kg intravenously (single infusion).
   Function: Immune rebalancing in refractory noninfectious uveitis.
   Mechanism: Down-regulates Th1/Th17 responses; promotes regulatory T-cell effects.
   Evidence: 4-patient series reported fewer relapses and steroid tapering; still investigational for uveitis and not RPC-specific. PubMed Central

2. Bone-marrow–derived MSCs (IV; investigational)
   Dose: Protocols vary; often ~1×10^6 cells/kg.
   Function/Mechanism: Similar to HUC-MSC (systemic immune modulation); intravitreal MSCs have caused serious complications and are not recommended. PubMed Central

3. Autologous hematopoietic stem-cell transplantation (aHSCT)
   Use: Extremely refractory, life-threatening autoimmune disease (e.g., Behçet’s) when all else fails—not standard for RPC.
   Mechanism: Immune “reset” after conditioning chemotherapy.
   Evidence: Retrospective survey suggests feasibility in multi-refractory Behçet’s; again, not RPC care. ACR Meeting Abstracts

4. Intravenous immunoglobulin (IVIG)
   Typical dose: ~2 g/kg per cycle divided over 2–5 days, repeated by response.
   Function: Broad immune modulation; occasional use in refractory ocular inflammation.
   Mechanism: Fc-receptor blockade, cytokine modulation. Status: Special-case, off-label. EyeWiki

5. Interferon-α (IFN-α2a/2b)
   Typical regimens: e.g., 3–6 million IU SC several times weekly (varies by center).
   Function: Immunomodulatory; effective in some NIU (notably Behçet), but RPC data are limited and mixed.
   Mechanism/SE: Cytokine and cellular immunity modulation; flu-like symptoms, mood changes. EyeWiki

6. Regulatory T-cell (Treg)–based therapy or low-dose IL-2 induction (trial stage)
   Use: Experimental cellular therapy aiming to increase Tregs in autoimmune uveitis.
   Mechanism: Restores tolerance; dampens effector T-cell activity.
   Status: Early studies/clinical trials across autoimmune diseases; not clinical care for RPC yet. FrontiersClinicalTrials.gov

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Surgeries

1. Cataract extraction with intraocular lens
   Why it’s done: Treat steroid-induced or inflammation-related cataract to restore clarity.
   Evidence: Most uveitis eyes can reach good vision when inflammation is controlled pre-op; posterior uveitis eyes have more risk and need meticulous peri-op control. PubMed CentralAjo

2. Glaucoma surgery (trabeculectomy or tube shunt)
   Why it’s done: Control high eye pressure from steroids or uveitis (uveitic glaucoma) when drops/lasers fail.
   Evidence: Both trabeculectomy and tubes are used; outcomes vary by inflammation control and time. PubMed CentralMDPI

3. Retisert® (fluocinolone 0.59 mg) surgical implantation
   Why it’s done: Long-term local steroid delivery in chronic NIU to reduce relapses when systemic therapy isn’t suitable.
   Note: This is a minor ocular surgery done in the OR. PubMedAAO-HNS

4. Pars plana vitrectomy (PPV)
   Why it’s done: For non-clearing vitreous hemorrhage, dense vitreous opacities, or epiretinal membrane causing traction from complications.
   Mechanism: Removes hemorrhage/debris; allows membrane peel if needed. (General uveitis surgical practice.) PubMed Central

5. Glaucoma cyclophotocoagulation (select cases)
   Why it’s done: Lower pressure when filtering/tube options aren’t possible or have failed.
   Mechanism: Reduces aqueous production by treating ciliary body. (Advanced glaucoma management in uveitis.) SpringerOpen

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Prevention

There’s no proven way to prevent the first episode of RPC. Prevention focuses on reducing relapses and vision loss:

1. Keep regular specialist follow-ups and imaging (OCT/FAF) even when you feel fine. EyeWiki

2. Do not stop or taper steroids/IMT on your own; abrupt changes invite rebound inflammation. EyeWiki

3. Screen for infections before starting or changing immunosuppression. EyeWiki

4. Stay current on non-live vaccines before biologics; avoid live vaccines while on them unless cleared. EyeWiki

5. Report new visual symptoms immediately—even small wavy lines or gray spots. EyeWiki

6. Protect against steroid side effects (bone, stomach, glucose, pressure) so you can stay on the safest effective plan. EyeWiki

7. No smoking; it worsens inflammatory outcomes broadly.

8. Heart-healthy lifestyle (diet, exercise, sleep) to support immune balance. PubMed Central

9. Manage stress and maintain sleep to support immune regulation.

10. Carry a medication/imaging summary when traveling to speed urgent care if you flare away from home.

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When to see a doctor—urgent vs. routine

Seek urgent care now if you notice: new central blur; a new dark/gray spot; sudden distortion of straight lines; a shower of new floaters; flashing lights; eye pain; sudden drop in vision; or a severe headache with vision changes. These can signal an active macular lesion, macular edema, retinal vasculitis, or a complication that needs same-week treatment. EyeWiki

Routine but prompt: medication side effects (e.g., high sugars on steroids), rising eye pressure symptoms, steroid-related mood changes, or questions about vaccines/pregnancy while on IMT. EyeWiki

What to eat” and “what to avoid

Food supports general immune and vascular health; it doesn’t replace treatment.

1. Eat: Fatty fish (salmon/sardine) 2–3×/week → omega-3s. Avoid: Frequent deep-fried foods (pro-inflammatory oils). PubMed Central

2. Eat: Dark leafy greens, peppers, corn, eggs → lutein/zeaxanthin. Avoid: Ultra-processed snacks with dyes and additives. PubMed Central

3. Eat: Colorful fruits/veg (berries, citrus, tomatoes). Avoid: Sugary drinks and excess sweets (glycemic spikes).

4. Eat: Nuts, seeds, olive oil (Mediterranean fats). Avoid: Trans fats/partially hydrogenated oils.

5. Eat: Whole grains/legumes for fiber. Avoid: Refined white flours as staples.

6. Eat: Yogurt/kefir (if tolerated) for gut health. Avoid: Excess alcohol (immune and liver stress).

7. Eat: Spices like turmeric/ginger in meals. Avoid: High-salt fast foods (BP/edema). PubMed Central

8. Eat: Adequate protein (fish/lean meats/soy) for healing. Avoid: Extremely high-dose single supplements without medical advice.

9. Eat: Hydrating—water/unsweetened tea. Avoid: Energy drinks/high-caffeine if they worsen anxiety/insomnia on steroids.

10. Eat: Vitamin-D-rich foods (fortified dairy, oily fish) if low. Avoid: Skipping your lab-guided supplementation plan. PubMed

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Frequently Asked Questions (FAQ)

1) Is RPC contagious or caused by an infection?
No. RPC is considered a noninfectious inflammatory disease of the choroid/RPE. Infections are ruled out because treatments suppress immunity and would worsen an undiagnosed infection. EyeWiki

2) How is RPC different from APMPPE or serpiginous choroiditis?
They share placoid lesions and belong to the “white-dot” group, but RPC is typically more widespread, recurrent, and lasts >6 months, often with many peripheral lesions. EyeWiki

3) Will my vision recover?
With timely steroids and appropriate immunomodulators, long-term central vision is often good, but relapse or delayed treatment can leave scars or cause complications like macular edema or CNV. EyeWiki

4) What tests will I need?
Eye exam, OCT, fundus autofluorescence, fluorescein and sometimes ICG angiography; plus blood tests to exclude infections or systemic causes. EyeWiki

5) Do I need systemic treatment or can injections alone work?
Systemic therapy (steroids → IMT/biologic) is the backbone for RPC because it’s bilateral and relapsing. Local injections/implants can help macular edema or reduce systemic side effects. EyeWikiFDA Access DataYUTIQ

6) How long will I be on immunomodulatory therapy (IMT)?
Often many months to a few years. A common strategy is maintaining steroid-free quiescence for ≈2 years before a cautious IMT taper. EyeWiki

7) Are biologics like adalimumab safe?
They can be effective in refractory NIU/RPC but increase infection risk; TB/viral screening and vaccine planning are essential. ScienceDirect

8) Can RPC cause complications besides scars?
Yes—macular edema, choroidal neovascularization, epiretinal membranes, even retinal vein occlusion in rare cases. Regular monitoring is key. EyeWiki

9) I’m pregnant or planning pregnancy—what changes?
Some IMTs are unsafe in pregnancy; planning with your uveitis and obstetric teams allows safe alternatives and timing. (Do not stop meds abruptly.) EyeWiki

10) Are there cures or regenerative treatments?
No established cures. Experimental stem-cell or T-reg therapies are being studied for refractory uveitis—not standard RPC care. PubMed CentralFrontiers

11) Do sunglasses or screen filters help?
They improve comfort (less glare/photophobia) while inflamed; they do not treat inflammation. EyeWiki

12) Can diet or supplements replace medicines?
No. Nutrition can support overall health; core control needs steroids and immunomodulation. EyeWiki

13) How quickly should I report new symptoms?
Immediately—same day or next business day—for new scotoma, distortion, or sudden blur. Early steroid adjustment prevents scarring. EyeWiki

14) Are eye steroid implants safe?
They’re validated options for NIU but carry risks of cataract and high eye pressure; monitoring is mandatory. FDA Access DataPubMed Central

15) What is the long-term outlook?
Despite its name, many patients keep useful vision with the right plan. The “relentless” part means we respect the disease with close follow-up and steady therapy. EyeWiki

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 23, 2025.