Uveitis Masquerade Syndromes

Uveitis masquerade syndromes are eye problems that look like uveitis (inflammation inside the eye) but are not true autoimmune uveitis. In other words, the eye shows cells, haze, redness, or fluid that resemble inflammation, yet the underlying cause is something different—for example, a cancer cell infiltration, a retinal tear with bleeding, a detached retina, an infection, or a foreign body. Because the surface picture is similar to uveitis, doctors may start steroids or immunosuppressants, but the condition does not improve as expected or improves only briefly and relapses. That poor or paradoxical response is a critical clue that the “uveitis” might actually be a masquerade.

Uveitis masquerade syndromes (UMS) are conditions that look like uveitis (inflammation inside the eye) but are not true uveitis. In real uveitis, the eye is inflamed because the immune system is reacting to infection, injury, or an autoimmune disease. In UMS, the eye mimics that appearance—there may be floaters, cloudy fluid, “cells” and “flare” in the front chamber or vitreous haze in the back—but the underlying cause is different, such as cancer inside the eye, a retinal detachment, leaking lens material, a retained foreign body, or another problem that only looks like inflammation.

A helpful way to think about it is: true uveitis = immune inflammation; masquerade = look-alike. The eye reacts because something abnormal is present, but the driver is not an autoimmune process. This distinction matters, because the right treatment for a masquerade syndrome is to find and fix the hidden cause (remove a tumor, repair a tear, extract retained lens material, treat an infection, etc.), rather than only quieting the immune system. Delays in recognizing a masquerade can lead to vision loss or missed systemic disease (for example, lymphoma).

Key general clues for a masquerade include: atypical age (e.g., new “uveitis” after age 50), unusual pattern of inflammation (lots of vitreous cells but quiet front of the eye), poor steroid response, repeated relapse when tapering steroids, unilateral chronic disease, unexplained bleeding, retinal detachment signs, or systemic “B symptoms” (fever, night sweats, weight loss).

---

Types

Experts group uveitis masquerade syndromes by what is doing the masquerading:

1. Neoplastic (tumor-related) masquerade
   Cancer cells infiltrate the eye and mimic chronic uveitis, most famously primary vitreoretinal lymphoma (a type of diffuse large B-cell lymphoma). Leukemia or metastatic cancers can do the same. These often show persistent floaters, hazy vitreous, subtle creamy lesions, and little pain. Steroids may briefly “clarify” the view but the disease returns.

2. Structural/degenerative masquerade
   Rhegmatogenous retinal detachment, retinal tears, vitreous hemorrhage, intraocular foreign bodies, or retained lens fragments can release cells and pigments that look like intraocular inflammation. The eye is reacting to debris, traction, or fluid shifts—not autoimmune inflammation.

3. Infectious masquerade
   Some infections mimic noninfectious uveitis, such as syphilis, tuberculosis, Lyme disease, toxocariasis, or endophthalmitis. These are truly inflammatory, but the driver is a microbe, so they masquerade if they are misdiagnosed and treated only with steroids (which can worsen infection).

4. Vascular and exudative retinal disorders
   Conditions like Coats disease (leaky retinal vessels in children) or severe ischemic retinopathies can produce exudates and cells that resemble uveitis but are primarily vascular leakage problems.

5. Drug- or procedure-related masquerade
   Certain medications (e.g., checkpoint inhibitors, bisphosphonates, rifabutin) or post-surgical states can create intraocular cells and fluid that imitate uveitis. The mechanism is not classic autoimmune uveitis and often revolves around toxicity, lens material, or altered barriers.

6. Hereditary/retinal dystrophy masquerade
   X-linked retinoschisis and some retinal degenerations may present with cystic changes, vitreous veils, or vascular sheathing that can be mistaken for uveitis, especially when onset is in childhood or adolescence.

The unifying theme: the eye “looks inflamed,” but the underlying driver is different, so steroids alone do not solve the root cause.

---

Causes

1. Primary vitreoretinal lymphoma (PVRL)
   A lymphoma that starts in the vitreous and retina. It causes floaters, hazy vision, and creamy subretinal lesions. Often little pain, and steroids help only temporarily. Close link with central nervous system lymphoma.

2. Secondary intraocular lymphoma/leukemia
   Blood cancers can travel to the eye and produce persistent cells in the vitreous and retinal infiltrates. Might occur with known systemic disease or be the first sign.

3. Metastatic carcinoma to the uvea (e.g., breast, lung)
   Cancer cells seed the choroid or retina, creating exudative detachments, cells, and blurred vision. May present as “uveitis” before metastasis is recognized.

4. Uveal melanoma with inflammatory spillover
   A choroidal tumor can cause fluid leakage and mild inflammatory reaction that camouflages the mass, especially if small or masked by vitreous haze.

5. Retinoblastoma (children)
   A pediatric eye tumor that can show white pupil (leukocoria), vitreous seeding, or pseudo-hypopyon. It may be mistaken for uveitis if not carefully imaged.

6. Rhegmatogenous retinal detachment
   A tear in the retina allows fluid underneath, causing photopsias, floaters, curtain-like shadow, and pigment “tobacco dust” cells that can imitate uveitis.

7. Chronic tractional or exudative retinal detachment
   Long-standing detachments cause cells and protein in the vitreous and vascular changes, appearing “inflammatory” but driven by retinal architecture failure.

8. Vitreous hemorrhage
   Blood in the vitreous from a tear, diabetic eye disease, or trauma can be seen as cells and haze like uveitis, especially when the view is limited.

9. Intraocular foreign body
   Tiny metal, glass, or organic material inside the eye can produce chronic irritation and cells, often with a poor steroid response until the object is removed.

10. Retained lens fragments / lens-induced inflammation
    After cataract surgery or trauma, lens material can leak and provoke cells and flare. Looks like uveitis but responds only after removal of the lens material.

11. Endophthalmitis (postoperative or endogenous)
    A bacterial or fungal infection inside the eye with pain, redness, hypopyon, and vision loss. If misread as noninfectious uveitis and treated with steroids alone, it worsens.

12. Ocular syphilis
    A systemic infection that can mimic any uveitis pattern (anterior, intermediate, posterior, panuveitis). Needs serologic testing and antibiotics, not steroids alone.

13. Ocular tuberculosis
    Causes granulomas, vasculitis, and choroidal lesions. It can look like chronic uveitis but needs anti-TB therapy.

14. Lyme ocular disease
    Borrelia infection can present with vitritis, retinal vasculitis, or neuro-ophthalmic signs, masquerading as immune uveitis in endemic regions.

15. Toxocariasis (children, young adults)
    Parasitic granuloma causes white elevated lesions, vitreous bands, or traction that may be misread as uveitis, especially when unilateral.

16. Coats disease
    Abnormal retinal vessels leak lipid-rich fluid causing yellow exudates and exudative detachment, simulating inflammatory exudation.

17. Ischemic retinopathies (e.g., severe diabetic, sickle cell)
    Capillary nonperfusion and neovascularization introduce cells, hemorrhage, and exudates that can resemble a vasculitic uveitis.

18. X-linked retinoschisis
    Splitting of the retinal layers in boys/young men results in cystic macular changes, peripheral veils, and vitreous strands that look “inflammatory”.

19. Drug-related uveitis-like reactions (e.g., checkpoint inhibitors, rifabutin, bisphosphonates)
    Medications can trigger intraocular cells/edema that mimic autoimmune uveitis. Correct management involves drug review and coordination with the prescriber.

20. Masquerade from ocular surface or adnexal tumors (e.g., conjunctival lymphoma, sebaceous carcinoma) with intraocular spillover
    Tumors near the eye can lead to secondary intraocular reaction, appearing as “recurrent uveitis” until the adnexal source is found.

---

Common symptoms

1. Blurred or hazy vision
   The most common complaint, caused by vitreous cells, macular fluid, or media haze.

2. Floaters (spots, cobwebs, moving shadows)
   Cells, blood, tumor debris, or vitreous strands cast shadows that the brain perceives as floaters.

3. Photophobia (light sensitivity)
   Light entering an eye with cells or irritated tissues triggers discomfort or glare.

4. Eye redness
   Superficial conjunctival vessels dilate in response to internal irritation or infection.

5. Mild or absent pain
   Many masquerades, especially lymphoma, cause little pain, which can be a clue against severe autoimmune uveitis.

6. Vision fluctuating with steroid use
   Temporary improvement with steroids followed by relapse suggests a non-immune driver.

7. Peripheral shadow or curtain
   Suggests retinal detachment rather than pure inflammation.

8. Distortion (straight lines look wavy)
   Macular edema, schisis, or subretinal fluid distort the retinal architecture.

9. Sudden onset floaters with light flashes
   Points toward retinal tear or posterior vitreous detachment with pigment cells masquerading as inflammation.

10. Reduced night vision or color vision
    Indicates macular or photoreceptor involvement, seen in lymphoma or retinal dystrophies.

11. Unilateral persistent symptoms
    Long-standing one-eye disease with poor steroid response should raise suspicion.

12. Systemic “B symptoms” (fever, weight loss, night sweats)
    Point to lymphoma or systemic infection masquerading as uveitis.

13. Headache or neurological symptoms
    In PVRL, there may be CNS involvement causing headaches, confusion, or neurologic deficits.

14. Recurrent red eye after eye surgery or trauma
    Suggests retained lens material or foreign body.

15. Poor response or paradoxical worsening with steroids
    A red flag for infection or neoplastic infiltration.

---

Diagnostic tests

A) Physical examination (whole-person clues)

1. Vital signs and general examination
   Fever or weight loss support infection or cancer. Cachexia or night sweats matter.

2. Skin and mucous membrane check
   Rashes, nodules, ulcers, or mucosal lesions may point to syphilis, TB, or lymphoma.

3. Lymph node and organ palpation
   Enlarged nodes, liver, or spleen suggest hematologic malignancy or systemic infection.

4. Neurologic screening
   Cranial nerve deficits or cognitive changes can accompany CNS lymphoma or neuro-infectious disease.

5. Respiratory and cardiovascular review
   Cough, chest pain, or abnormal chest findings can support TB, metastatic disease, or sarcoid-like processes.

B) Manual/clinical eye tests (at the slit lamp and clinic)

6. Best-corrected visual acuity and pinhole
   Quantifies central vision and separates refractive blur from true retinal/macular disease.

7. Pupillary reactions (look for APD)
   An afferent pupillary defect hints at optic nerve or widespread retinal dysfunction, common in lymphoma or detachment.

8. Intraocular pressure (tonometry)
   Elevated IOP can occur with inflammatory debris, steroid response, or tumor-related angle changes; low IOP may signal ciliary shutdown in severe disease.

9. Color vision and Amsler grid
   Detects macular dysfunction (metamorphopsia, scotomas) seen with macular edema, subretinal fluid, lymphoma infiltration.

10. Confrontation visual fields
    Screens for peripheral defects from retinal detachment or mass lesions.

11. Slit-lamp biomicroscopy with anterior chamber cell/flare grading
    SUN grading helps quantify front-of-eye inflammation; in masquerade, the front may be quiet while the vitreous is very active.

12. Gonioscopy
    Looks for angle neovascularization, tumor seeding, or lens material, clarifying mechanisms of pressure rise or cells.

13. Dilated fundus exam with scleral depression
    Essential to find retinal tears, detachments, subtle tumors, vitreous hemorrhage, or infiltrates—core causes of masquerade.

C) Laboratory and pathological tests (getting to the root cause)

14. Complete blood count (CBC) with differential and peripheral smear
    Detects anemia, leukocytosis, blasts, or other hematologic clues for leukemia/lymphoma or infection.

15. Inflammatory markers (ESR, CRP) and LDH
    High ESR/CRP support inflammation/infection; LDH can be elevated in lymphoma or tissue turnover.

16. Serologic tests for infections (syphilis, TB, Lyme, toxocara, HIV)
    VDRL/RPR + treponemal test, IGRA/PPD, Lyme ELISA/Western blot, toxocara IgG, HIV testing—identify infectious masqueraders.

17. Vitreous/aqueous sampling for cytology and flow cytometry
    The definitive test for intraocular lymphoma: looks for atypical B-cells, monoclonality, and malignant morphology.

18. Molecular tests on ocular fluid (IgH gene rearrangement, MYD88 L265P, pathogen PCR)
    Clonality assays and MYD88 mutation support PVRL; PCR for pathogens (e.g., Toxoplasma, HSV/VZV, TB) identifies infections.

19. Serum ACE/lysozyme, autoimmune screens (ANA, ENA, RF, HLA typing) when relevant
    Helpful to exclude mimics and coexisting conditions, recognizing that a high ACE/lysozyme leans toward sarcoidosis (a true uveitis cause) but still part of the workup to avoid mislabeling.

D) Electrodiagnostic tests (functional testing of retina and optic pathway)

20. Full-field ERG, multifocal ERG, VEP, and EOG (grouped explanation)

• ERG evaluates photoreceptor and bipolar cell function; a reduced b-wave may point to retinoschisis or diffuse retinal dysfunction as seen with lymphoma infiltration.

• mfERG maps macular function, helpful in macular edema vs. infiltrative disease.

• VEP tests the optic pathway, flagging optic nerve involvement or retrobulbar processes.

• EOG assesses retinal pigment epithelium function, sometimes altered in infiltrative or degenerative masquerades.

E) Imaging tests (seeing what the eye is hiding)

21. Optical coherence tomography (OCT)
    High-resolution cross-sections show macular edema, subretinal fluid, schisis, infiltrative nodules, or vitreoretinal traction—key to separating inflammation from structural disease.

22. OCT-angiography (OCT-A)
    Visualizes blood-flow maps without dye, detecting capillary nonperfusion, neovascularization, or choriocapillaris dropout typical of ischemic or infiltrative disorders.

23. Fundus fluorescein angiography (FFA)
    Highlights leakage patterns (diffuse capillary leak in inflammation vs. focal tumor-related leakage or ischemic nonperfusion). Useful in Coats disease and diabetic retinopathy masquerades.

24. Indocyanine green angiography (ICGA)
    Penetrates deeper into the choroid, helpful for choroidal tumors, lymphoma, or TB granulomas with late-phase hypocyanescent spots.

25. Fundus autofluorescence (FAF)
    Maps RPE health; hyper/hypo-autofluorescence patterns can hint at infiltrative lesions, lipid exudation, or degeneration.

26. B-scan ocular ultrasonography
    Essential when media are hazy. Detects masses (melanoma, retinoblastoma), retinal detachment, vitreous debris, or foreign bodies.

27. Ultrasound biomicroscopy (UBM)
    High-frequency ultrasound of anterior segment to find ciliary body tumors, retained lens fragments, or angle abnormalities that drive cells and IOP changes.

28. MRI of brain and orbits with contrast
    Looks for CNS lymphoma, optic nerve involvement, orbital masses, or spread of systemic cancers.

29. CT chest/abdomen/pelvis (when indicated)
    Searches for primary tumors, lymphadenopathy, TB, or metastases that explain the eye findings.

30. PET-CT (oncologic staging)
    Detects metabolically active disease throughout the body in suspected lymphoma or metastatic cancer, guiding biopsy sites and treatment.

Non-Pharmacological Treatments (therapies and others)

(Each item includes Description, Purpose, and Mechanism in very simple terms.)

1. Accurate diagnostic pathway
   Description: Follow a structured checklist: rule out infection and tumor early, then consider structural causes.
   Purpose: Avoid harmful steroids and target the real cause fast.
   Mechanism: Systematic testing reduces missed diagnoses and wrong treatment.

2. Observation with frequent review
   Description: Short, close follow-up before strong immunosuppression when cancer/infection is possible.
   Purpose: Watch for clues (new lesions, systemic signs) to guide workup.
   Mechanism: Time reveals disease patterns that mimic inflammation.

3. Protective eye care
   Description: Lubrication, UV protection, and avoiding eye rubbing.
   Purpose: Reduce surface stress and symptom flare.
   Mechanism: Lowers irritation that can add “noise” to the picture.

4. Treat the source (cause-directed procedures)
   Description: If lens leakage or foreign body is the cause, fix that (see surgeries).
   Purpose: Remove the trigger, not just calm inflammation.
   Mechanism: Correcting structure stops the mimic.

5. Nutritional optimization
   Description: Balanced diet with antioxidants and adequate vitamin D/omega-3.
   Purpose: Support ocular tissues and general immunity.
   Mechanism: Reduces oxidative stress and supports barrier function.

6. Infection control measures
   Description: Prompt STI testing/treatment, TB evaluation when risk exists.
   Purpose: Catch infectious mimics early.
   Mechanism: Breaks pathogen-driven inflammation.

7. Oncologic coordination
   Description: Early oncology referral for suspected lymphoma/leukemia/metastasis.
   Purpose: Start tumor-directed therapy promptly.
   Mechanism: Cancer treatment removes the masquerade source.

8. Systemic health screening
   Description: Age-appropriate cancer screening; review medications.
   Purpose: Find hidden systemic diseases or drug triggers.
   Mechanism: Upstream detection prevents eye relapse.

9. Smoking cessation
   Description: Support to stop smoking.
   Purpose: Improve ocular perfusion and immune health.
   Mechanism: Reduces oxidative and vascular stress.

10. Vaccination up-to-date
    Description: Influenza, zoster, and others as indicated.
    Purpose: Lower infection risk that can mimic/worsen uveitis.
    Mechanism: Primed immunity prevents triggers.

11. Stress and sleep management
    Description: Sleep hygiene, relaxation, counseling when needed.
    Purpose: Reduce flare-promoting hormonal stress.
    Mechanism: Balanced cortisol and immune signaling.

12. Blood pressure and glucose control
    Description: Optimize BP and diabetes care.
    Purpose: Protect retina and reduce microvascular stress.
    Mechanism: Stabilizes retinal metabolism and barrier integrity.

13. Safe contact lens practice (if any)
    Description: Proper hygiene or pause use during active disease.
    Purpose: Prevent superimposed keratitis.
    Mechanism: Reduces microbial load.

14. UV-blocking eyewear
    Description: Sunglasses outdoors.
    Purpose: Reduce photic irritation and retinal stress.
    Mechanism: Lowers light-induced oxidative damage.

15. Allergen/environment control
    Description: Manage dust/mold/pollen if relevant.
    Purpose: Reduce surface inflammation that confuses the picture.
    Mechanism: Fewer mast-cell triggers.

16. Medication audit
    Description: Review drugs that can mimic uveitis (e.g., checkpoint inhibitors).
    Purpose: Identify and manage drug culprits with prescriber.
    Mechanism: Removing trigger stops recurrence.

17. Low-vision aids (if needed)
    Description: Magnifiers, contrast tools during recovery.
    Purpose: Maintain function while disease is treated.
    Mechanism: Compensates for temporary visual deficits.

18. Infection exposure counseling
    Description: Safe sex, TB precautions, travel health advice.
    Purpose: Prevent high-risk exposures.
    Mechanism: Interrupts transmission chains.

19. Adverse-effect education
    Description: Teach warning signs of steroid or chemo toxicity.
    Purpose: Early reporting prevents complications.
    Mechanism: Rapid response limits harm.

20. Shared decision-making
    Description: Clear discussion of diagnostic steps and options.
    Purpose: Improve adherence and timely consent for biopsy if needed.
    Mechanism: Patient engagement speeds correct care.

---

Drug Treatments

Important: These are examples for education. Actual dosing varies by patient, kidney/liver function, pregnancy, drug interactions, and regional protocols.

1. Intravitreal Methotrexate (antimetabolite chemo) for PVRL
   Dose/Timing: Commonly 400 micrograms/0.1 mL intravitreal, weekly for an induction phase, then tapered (protocols vary).
   Purpose: Kill lymphoma cells in the eye.
   Mechanism: Inhibits dihydrofolate reductase, blocking DNA synthesis in rapidly dividing cells.
   Side effects: Corneal epitheliopathy, cataract progression, rare retinal toxicity.

2. Rituximab (anti-CD20 monoclonal antibody) for B-cell lymphoma
   Dose/Timing: 375 mg/m² IV weekly x4 (regimens vary) ± intravitreal/intrathecal use in select centers.
   Purpose: Target B-cells driving lymphoma.
   Mechanism: Binds CD20 on B-cells → cell death.
   Side effects: Infusion reactions, infection risk, hepatitis B reactivation (screen before use).

3. High-dose Methotrexate (systemic) ± Cytarabine for PVRL/CNS involvement
   Dose/Timing: Specialist oncology protocols (e.g., 3–8 g/m² IV with leucovorin rescue).
   Purpose: Treat intraocular + CNS disease.
   Mechanism: Cytotoxic to lymphoma cells.
   Side effects: Myelosuppression, mucositis, renal toxicity (needs monitoring).

4. Ibrutinib or Zanubrutinib (BTK inhibitors) for select B-cell lymphomas
   Dose/Timing: Ibrutinib 420–560 mg orally once daily; Zanubrutinib 160 mg twice daily (indications vary).
   Purpose: Target B-cell receptor signaling.
   Mechanism: Blocks Bruton’s tyrosine kinase.
   Side effects: Bleeding risk, atrial fibrillation (ibrutinib), infections.

5. Penicillin G (for ocular syphilis / neurosyphilis)
   Dose/Timing: Aqueous crystalline penicillin G 18–24 million units/day IV (3–4 million units q4h) for 10–14 days; alternatives per guidelines if allergic.
   Purpose: Eradicate Treponema pallidum.
   Mechanism: Inhibits bacterial cell wall synthesis.
   Side effects: Jarisch–Herxheimer reaction, allergy, GI upset.

6. Anti-tubercular therapy (RIPE) when ocular TB is diagnosed
   Dose/Timing: Isoniazid + Rifampin + Pyrazinamide + Ethambutol (weight-based) for 2 months, then continuation phase (usually INH+RIF 4–7 months) per national guidelines.
   Purpose: Cure tuberculosis driving ocular disease.
   Mechanism: Multi-drug kill prevents resistance.
   Side effects: Hepatotoxicity, optic neuritis (ethambutol—monitor vision), drug interactions (rifampin).

7. Pyrimethamine + Sulfadiazine + Leucovorin (toxoplasmosis)
   Dose/Timing: Pyrimethamine 50–75 mg loading, then 25–50 mg daily; Sulfadiazine 1–1.5 g four times daily; Leucovorin 10–25 mg several times weekly to protect bone marrow; often 4–6 weeks or longer.
   Purpose: Treat Toxoplasma gondii retinochoroiditis.
   Mechanism: Folate pathway inhibition in parasite.
   Side effects: Bone marrow suppression (hence leucovorin), rash, GI upset.

8. Trimethoprim–Sulfamethoxazole (TMP-SMX) as alternative for toxoplasmosis
   Dose/Timing: 160/800 mg (DS) twice daily; duration varies (often 4–6 weeks).
   Purpose: Alternative regimen or maintenance prophylaxis in recurrences.
   Mechanism: Sequential folate inhibition.
   Side effects: Rash, hyperkalemia, cytopenias.

9. Valacyclovir / Acyclovir (HSV/VZV retinitis)
   Dose/Timing: Valacyclovir 1 g three times daily (oral) for HSV; for VZV or necrotizing herpetic retinitis, higher/IV acyclovir (10 mg/kg IV q8h) may be required initially; specialist guidance essential.
   Purpose: Control herpes viruses.
   Mechanism: Viral DNA polymerase inhibition.
   Side effects: Renal issues (ensure hydration), GI upset, headache.

10. Corticosteroids (topical/systemic) only after infection and tumor are reasonably excluded
    Dose/Timing: Topical prednisolone acetate 1% as per ophthalmologist; systemic prednisone often 0.5–1 mg/kg/day short-term if noninfectious inflammation confirmed.
    Purpose: Calm inflammation that is secondary to structural issues or post-treatment inflammation.
    Mechanism: Broad anti-inflammatory action.
    Side effects: High IOP, cataract, immunosuppression, hyperglycemia; can worsen infections and mask cancers if used blindly.

(Note: For leukemia-related ocular disease, systemic chemotherapy per hematology is primary; for metastasis, systemic therapy and/or ocular radiotherapy are used.)

---

Dietary Molecular Supplements

(Always review safety, drug interactions, pregnancy, and kidney/liver status with a clinician. These support eye health; they do not treat cancer or infections.)

1. Omega-3 (EPA+DHA)
   Dose: 1–2 g/day combined EPA+DHA.
   Function: Anti-inflammatory support; tear film stability.
   Mechanism: Competes with arachidonic acid pathways → fewer inflammatory mediators.

2. Lutein + Zeaxanthin
   Dose: Lutein 10 mg/day + Zeaxanthin 2 mg/day.
   Function: Macular pigment support; antioxidant.
   Mechanism: Filters blue light; quenches reactive oxygen species.

3. Vitamin D3
   Dose: 800–2000 IU/day (adjust per level).
   Function: Immune modulation and general health.
   Mechanism: Nuclear receptor signaling shaping immune responses.

4. Vitamin C
   Dose: 500–1000 mg/day (split doses).
   Function: Antioxidant; collagen support.
   Mechanism: Electron donor neutralizing free radicals.

5. Vitamin E (alpha-tocopherol)
   Dose: Up to 200 IU/day (avoid very high doses).
   Function: Lipid antioxidant in membranes.
   Mechanism: Breaks lipid peroxidation chains.

6. Zinc
   Dose: 10–25 mg elemental/day (short courses unless deficient).
   Function: Enzyme cofactor; retinal health.
   Mechanism: Supports antioxidant enzymes (e.g., superoxide dismutase).

7. Selenium
   Dose: 55–100 mcg/day (do not exceed upper limits).
   Function: Antioxidant enzyme cofactor.
   Mechanism: Component of glutathione peroxidases.

8. Curcumin (with piperine or optimized formulations)
   Dose: 500–1000 mg/day curcumin equivalents.
   Function: Adjunct anti-inflammatory.
   Mechanism: NF-κB pathway modulation; antioxidant.

9. Green tea extract (EGCG)
   Dose: 250–400 mg EGCG/day (avoid on empty stomach; monitor for rare liver issues).
   Function: Antioxidant/anti-inflammatory.
   Mechanism: Polyphenol signaling effects; free radical scavenging.

10. Resveratrol
    Dose: 100–250 mg/day.
    Function: Antioxidant adjunct.
    Mechanism: Sirtuin activation and anti-oxidative pathways.

---

Regenerative / stem cell” therapies

There is no standard “stem cell drug” for UMS. Some advanced therapies are used for the underlying diseases that masquerade as uveitis:

1. Hematopoietic Stem Cell Transplant (HSCT)
   Dose/Logistics: Oncologic procedure (conditioning chemo then stem cell infusion).
   Function: Curative intent for certain leukemias/lymphomas.
   Mechanism: Replaces diseased marrow with healthy hematopoiesis and immune system.

2. CAR-T cell therapy (anti-CD19, for select B-cell malignancies)
   Dose/Timing: Single-episode infusion after lymphodepletion, per oncology protocol.
   Function: Engineered T cells target malignant B-cells.
   Mechanism: Chimeric antigen receptor recognizes CD19 → tumor cell kill.
   Note: Ocular involvement management is individualized.

3. Rituximab (immune-targeted biologic)
   As above. Targets B-cells in PVRL/systemic disease. Considered immune-directed rather than “regenerative.”

4. BTK inhibitors (Ibrutinib/Zanubrutinib)
   As above. Targeted, immune-pathway-modifying cancer therapy.

5. Lenalidomide (IMiD) in select lymphoma settings
   Dose/Timing: Commonly 10–25 mg oral daily on cycles (varies).
   Function: Immunomodulatory anti-cancer agent.
   Mechanism: Affects cytokines, angiogenesis, and tumor microenvironment.
   Caution: Thrombosis risk; needs specialist oversight.

6. Proton/charged-particle or plaque brachytherapy for ocular tumors
   Dose/Timing: Radiation oncology protocols.
   Function: Local tumor control (e.g., melanoma, lymphoma focus).
   Mechanism: DNA damage to tumor cells with eye-sparing planning.

Warning: “Intravitreal stem cell injections” from unregulated clinics have caused severe, permanent blindness. They are not a treatment for UMS.

Surgeries/Procedures

1. Diagnostic Pars Plana Vitrectomy (PPV) with vitreous biopsy
   Procedure: Remove a sample of vitreous gel for cytology, flow cytometry, PCR, IL-10/IL-6, MYD88 testing.
   Why: Gold-standard to diagnose PVRL or infections that masquerade as uveitis.

2. Endoretinal/retinochoroidal biopsy
   Procedure: Targeted retinal/RPE biopsy when vitreous is nondiagnostic.
   Why: Increases diagnostic yield for lymphoma or unusual tumors.

3. Cataract extraction (lens removal) for lens-induced masquerade
   Procedure: Phacoemulsification with IOL (or without if indicated).
   Why: Removes leaking/provocative lens proteins causing “pseudo-uveitis.”

4. Retinal detachment repair (PPV, scleral buckle, or pneumatic retinopexy)
   Procedure: Reattach the retina using gas/oil/laser and/or buckle.
   Why: Chronic detachment can mimic inflammation with floaters/haze.

5. Ocular tumor-directed procedures
   Procedure: Plaque brachytherapy, proton beam, or, rarely, enucleation for blind, painful eyes with uncontrollable tumor.
   Why: Control or remove the masquerading tumor.

---

Preventions

1. Do not start strong steroids before basic infectious and neoplastic workup if red flags exist.

2. Keep vaccinations current (flu, zoster, others per age/health).

3. Practice safer sex and get STI screening when at risk (syphilis).

4. TB screening in high-risk settings or before immunosuppression.

5. Use eye protection at work/sports to prevent foreign bodies and trauma.

6. Avoid unregulated “stem cell” or injection therapies to the eye.

7. Medication review whenever starting new systemic drugs that can affect the eye.

8. Cancer screening as advised for age and history.

9. Control diabetes and hypertension for retinal health.

10. Early referral to uveitis/retina oncology specialists when patterns are atypical, asymmetric, or steroid-refractory.

---

When to see a doctor urgently

• Sudden vision loss, a “curtain” over vision, or many new floaters.

• Eye pain, light sensitivity, or severe redness.

• Unequal pupils, new double vision, or headache with visual change.

• Symptoms not improving or returning quickly after steroid treatment.

• Systemic signs (fever, weight loss, night sweats, neurologic symptoms) suggesting infection or malignancy.

• New eye symptoms while on cancer therapy or immunosuppression.

---

What to eat and what to avoid

What to eat (supportive):

• Colorful vegetables and fruits (spinach, kale, peppers, berries) for lutein/zeaxanthin and antioxidants.

• Fatty fish (salmon, sardines) or omega-3 supplements for anti-inflammatory support.

• Nuts and seeds (walnuts, flax, chia) for healthy fats.

• Lean proteins and whole grains to maintain general health and healing.

• Adequate vitamin D (diet and safe sun) as guided by testing.

What to avoid or limit:

• Smoking and vaping (harms retinal blood flow).

• Excess alcohol (optic and systemic toxicity risk).

• Ultra-processed foods, trans fats, and excess sugar (systemic inflammation).

• Megadoses of fat-soluble vitamins (A, E) without indication (toxicity risk).

• Unregulated supplements claiming to “cure” eye disease.

---

Frequently Asked Questions (FAQs)

1) Is a masquerade syndrome the same as uveitis?
No. It looks like uveitis but is caused by other problems like lymphoma, retinal detachment, lens leakage, or infections.

2) Why can steroids be dangerous in UMS?
Steroids can temporarily improve the appearance but worsen infections and hide cancers, delaying the correct treatment.

3) How do doctors prove it is UMS?
By combining history, exam, ocular imaging, targeted blood tests, and sometimes biopsy of the eye’s fluid for cytology/flow/PCR/IL-10/IL-6/MYD88.

4) What is vitreoretinal lymphoma (PVRL)?
A B-cell lymphoma that grows in the retina/vitreous and may link with brain lymphoma. It often presents with persistent vitreous cells and blurred vision.

5) What is the IL-10/IL-6 ratio and MYD88 test?
Markers measured in eye fluid that support lymphoma diagnosis (high IL-10 or MYD88 L265P mutation suggests PVRL).

6) Can infections “masquerade”?
Yes. Syphilis, TB, toxoplasmosis, herpes viruses can mimic noninfectious uveitis. They require specific antimicrobials, not steroids alone.

7) When is surgery needed?
When diagnosis requires biopsy, when lens leakage is the cause, when retina is detached, or when a tumor needs local therapy.

8) Will I lose vision?
Vision depends on the cause and speed of correct treatment. Early diagnosis often means better outcomes.

9) Do supplements cure UMS?
No. Supplements can support general eye health but do not treat cancer or infections.

10) Is radiation used inside the eye?
Yes, plaque brachytherapy or proton beam can treat certain ocular tumors that masquerade as uveitis.

11) Can UMS occur in both eyes?
Yes. Lymphoma and some infections may involve one or both eyes; patterns vary.

12) What are red flags for tumor-related UMS?
Older age, steroid-refractory haze, clumped vitreous cells, sub-RPE lesions on OCT, neurologic symptoms.

13) Will I need brain imaging?
Often yes, if PVRL is suspected, because of the link with CNS lymphoma.

14) Are “stem cell injections” into the eye helpful?
No. Unregulated intravitreal stem cell injections have caused severe blindness and are unsafe.

15) What should I do if my “uveitis” keeps coming back?
Ask for a re-evaluation specifically to rule out a masquerade syndrome and consider biopsy if advised.

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 29, 2025.