Melanoma-Associated Retinopathy (MAR) is an autoimmune eye condition linked to melanoma (usually cutaneous skin melanoma, sometimes uveal/eye melanoma). “Autoimmune” means the body’s defense system mistakenly attacks its own tissues. In MAR, the immune system makes antibodies that recognize proteins in the retina—especially in bipolar cells that carry signals from rods and cones to the next layer. This attack disrupts vision even though the retina may look close to normal early on. People typically notice painless, progressive changes: night vision gets poor, sparkling or flickering lights appear, and visual fields shrink or get patchy. The eye doctor confirms the problem with an ERG, which shows a reduced b-wave with a relatively preserved a-wave (an “electronegative” ERG), fitting injury to ON-bipolar cells. EyeWikiPMC+1
MAR is a rare, cancer-related (paraneoplastic) eye condition in which your immune system—activated by melanoma—mistakenly attacks parts of your retina (the light-sensing layer at the back of the eye). This causes night-vision trouble (nyctalopia), shimmering lights (photopsias), and visual field loss, sometimes with relatively normal eye exams early on. Doctors confirm it with specialized electrical tests of the retina (electroretinography). EyeWiki
In many people with MAR, the immune system makes antibodies to TRPM1, a protein found both in melanoma cells and in the retina’s ON-bipolar cells (the neurons that carry “light-on” signals). Those antibodies disrupt ON-bipolar cells, so the retina’s “relay” signal weakens even though photoreceptors may still work. PMCPNAS
Why this happens: melanoma cells can display or “mimic” retinal proteins. The immune system learns to attack these proteins and then cross-reacts with the same proteins inside the eye. A key protein is TRPM1 (Transient Receptor Potential Melastatin-1), found in retinal ON-bipolar cells (and also in melanocytes). Many patients with MAR have anti-TRPM1 antibodies. Journal of Neuroscience+1PMC
Timing: MAR can appear before, with, or after the cancer diagnosis. Sometimes it even leads doctors to discover a hidden melanoma during the work-up for visual symptoms. PMC
How MAR works
Step 1 – Tumor “flags” the immune system: Melanoma cells can express fragments of retinal proteins (or altered versions of them). The immune system recognizes these as foreign. PMC
Step 2 – Antibodies form: The body makes antibodies against these proteins. One well-studied target is TRPM1, a channel that helps ON-bipolar cells turn light signals into electrical signals. Blocking or binding this channel silences part of the retinal pathway. Patients’ blood often contains anti-TRPM1 antibodies. Journal of NeurosciencePMC
Step 3 – Friendly fire in the eye: These antibodies cross the blood-retina barrier and bind to retinal cells, especially ON-bipolar cells, disrupting signal transmission from photoreceptors. ERG shows the hallmark electronegative pattern (small b-wave). Journal of Neuroscience
Step 4 – Variable retinal damage: Early on, the fundus may look normal. Over time, imaging can show inner nuclear layer changes; patients feel night-blindness, shimmering lights, and field defects. EyeWiki
Immune therapy link: Modern immune checkpoint inhibitors (ICIs) (e.g., nivolumab, pembrolizumab, ipilimumab) used for melanoma can trigger or unmask MAR-like autoimmune retinopathy in some patients. BMJ OphthalmologyPMC
Types” of MAR
There isn’t a formal universal subtype list in textbooks. Clinically, doctors see patterns that help with thinking and testing:
Classic MAR: Bilateral symptoms in a patient with known or soon-to-be-found cutaneous melanoma; electronegative ERG; anti-TRPM1 often present. EyeWikiJournal of Neuroscience
Uveal-melanoma-associated MAR: Same mechanism but melanoma in the eye (choroid/ciliary body/iris). EyeWiki
Metastatic-melanoma MAR: Visual symptoms arise in the setting of widespread melanoma; work-up may uncover metastasis if not already known. PMC
ICI-triggered MAR: MAR-like retinopathy during or after checkpoint inhibitor therapy (nivolumab, pembrolizumab, ipilimumab, or combinations). BMJ OphthalmologyPMC
Seronegative MAR: Typical ERG and clinical picture with melanoma history, but no antibody detected (limits in testing sensitivity or different target). aes.amegroups.org
Unilateral MAR (rare): Symptoms and ERG changes mainly in one eye; reported in case literature. PMC
Early/occult MAR: Normal-looking fundus initially; ERG abnormal; later imaging shows inner retinal changes. EyeWiki
MAR overlapping with broader Autoimmune Retinopathy (AIR): MAR sits within the AIR spectrum; some patients show mixed antibody profiles or features resembling CAR (cancer-associated retinopathy). aes.amegroups.org
TRPM1-dominant MAR: Laboratory proves anti-TRPM1 reactivity; helps clinch the mechanism. Journal of Neuroscience
Post-melanoma-remission MAR: Visual symptoms emerge after cancer control due to lingering/primed immunity. (Pattern recognized in AIR/MAR reviews.) PMC
Causes” and contributors
Important note: The core cause is autoimmunity linked to melanoma. The 20 items below describe situations, triggers, or mechanisms that can lead to MAR or MAR-like autoimmune retinopathy in people with melanoma. Evidence strength varies; I’ll note when data are case-based or from broader AIR literature.
Cutaneous melanoma (skin melanoma): the most common setting for MAR. EyeWiki
Metastatic melanoma: higher tumor load can heighten autoimmunity. PMC
Uveal melanoma (melanoma in the eye): can also be associated with MAR. EyeWiki
Tumor expression of retinal proteins (antigen mimicry), prompting autoimmune attack. PMC
TRPM1 autoantibodies that target ON-bipolar cells. Journal of Neuroscience
Altered/TRPM1 splice variants in melanoma that may drive antibody formation. PMC
Immune checkpoint inhibitors (ICIs) such as nivolumab triggering MAR-like retinopathy. PMC
Other ICIs (e.g., pembrolizumab, ipilimumab) as potential immunologic triggers. (AIR reported with ICIs in melanoma.) BMJ Ophthalmology
Combination ICI therapy, which amplifies immune activation (case reports). BMJ Ophthalmology
Antigen “spreading”: immune response widens from tumor antigens to retinal antigens (concept from paraneoplastic retinopathies). aes.amegroups.org
Occult (hidden) melanoma: MAR symptoms appear first and lead to detection of malignancy. PMC
Melanoma cell lines expressing retinal proteins (lab evidence supporting cross-reactivity). PMC
General autoimmune predisposition (family or personal history)—plausible contributor noted across AIR; data specific to MAR are limited. aes.amegroups.org
Prior ocular inflammation in AIR literature as a possible priming event (rare, nonspecific). PMC
Breakdown of the blood-retina barrier allowing antibodies to enter the eye (mechanistic model in paraneoplastic retinopathies). aes.amegroups.org
Melanoma progression/recurrence rekindling immune activity and symptoms. (Observed pattern in AIR/MAR series.) PMC
TRPM3 cross-reactivity (some MAR sera recognize TRPM3 in RPE; may explain varied symptoms). PMC
Host immune genetics (e.g., HLA background) likely modulates risk, though specific HLA-MAR links remain under study. aes.amegroups.org
Paraneoplastic immune complexes and complement activation within the retina (general paraneoplastic mechanism). aes.amegroups.org
Timing with cancer therapy (e.g., steroid tapers, tumor lysis, vaccine-like priming from therapy) may coincide with onset—reported in case narratives. BMJ Ophthalmology
Symptoms
Night blindness (nyctalopia): trouble seeing in dim light or at dusk. This is very common in MAR. PMC
Photopsias: seeing flashes, sparkles, shimmering, flickering, or pulsating lights even when nothing is there. PMC
Patchy blind spots (scotomas): missing islands in the visual field that make reading or walking in crowds hard. PMC
Peripheral field loss: tunnel-vision-like narrowing; bumping into objects on the side. PMC
Reduced central clarity: letters look faded or broken; fine print is harder. PMC
Poor contrast sensitivity: gray-on-gray details vanish; faces or steps are hard to pick out. EyeWiki
Color vision changes (dyschromatopsia): colors look washed out or “wrong,” especially in dim settings. EyeWiki
Glare and light sensitivity (photophobia): bright light feels harsh; recovery after glare is slow. EyeWiki
After-images and light trails: lingering images after looking away from a bright source. PMC
Slow dark adaptation: extra minutes needed to adjust when lights go off. EyeWiki
Difficulty driving at night: headlights halo, road edges disappear. (A practical result of night blindness + glare.) PMC
Reading fatigue: words fade or “jump,” especially under low light. EyeWiki
Visual snow-like static in some patients (a fine, television-snow sensation). Case-based descriptions. PMC
Depth-perception problems: steps and curbs are tricky because contrast and field are impaired. EyeWiki
Often painless with quiet-looking eyes: the eye exam may not show dramatic changes early on despite major symptoms. EyeWiki
Diagnostic evaluation
Diagnosis is multifactorial: symptoms + careful exam + ERG + imaging + antibody testing + cancer work-up. There is no single gold-standard test that proves MAR by itself every time; doctors combine results. Athenaeum Scientific Publishers
A) Physical-exam–based tests (done in clinic without machines beyond standard tools)
Best-corrected visual acuity (VA): letter chart (e.g., Snellen). MAR may lower VA, especially later; early VA can be near normal. Explains central function. EyeWiki
Pupil exam: checks the light reflex and looks for a relative afferent pupillary defect (RAPD) if one eye is worse; pupils are often normal in early, bilateral MAR. Helps rule other causes. EyeWiki
Confrontation visual fields: a bedside way to spot field defects (missing areas). Guides formal perimetry. PMC
Color vision plates (Ishihara) or D-15: simple check for dyschromatopsia (color errors). MAR often affects color perception. EyeWiki
Amsler grid at near: lines look wavy, missing, or dim where scotomas or distortion exist; useful home monitor, too. PMC
Brightness acuity/glare testing: simulates bright glare to show how light sensitivity degrades vision, common in MAR. EyeWiki
B) “Manual/functional” psychophysical tests (simple tools but standardized measures)
Automated perimetry (e.g., Humphrey/Goldmann): maps visual fields precisely; MAR often shows peripheral constriction or patchy scotomas. PMC
Dark-adaptation testing: measures rod recovery after light; MAR patients typically adapt slowly, matching nyctalopia. EyeWiki
Contrast sensitivity (e.g., Pelli-Robson): quantifies the ability to see low-contrast targets—often reduced in MAR. EyeWiki
Photostress test: time to read again after bright light; prolonged times fit retinal dysfunction. (Supportive, not diagnostic.) aes.amegroups.org
Low-luminance VA / reading performance: simulates dim conditions where MAR patients struggle; objectifies complaints. EyeWiki
C) Laboratory and pathological tests
Serum anti-retinal antibody panel with anti-TRPM1: detects antibodies against retinal antigens (especially TRPM1) by immunoblot/ELISA. A positive supports MAR in the right clinical context; a negative does not exclude MAR. Journal of NeuroscienceAthenaeum Scientific Publishers
Confirmatory assays for TRPM1 epitopes/splice variants: research or reference labs can map where antibodies bind; work shows short intracellular TRPM1 segments are targeted. PMC
Broader paraneoplastic autoantibody screen: looks for other cancer-related antibodies; useful in differential diagnosis (e.g., CAR vs MAR). aes.amegroups.org
Oncology labs (e.g., LDH): indirectly reflect melanoma activity; not MAR-specific but help stage/monitor the cancer that drives the autoimmunity. aes.amegroups.org
Repeat serology over time: antibodies can fluctuate; serial testing can help when initial results are equivocal. (Practice point from AIR reviews.) Athenaeum Scientific Publishers
D) Electrodiagnostic tests (the core objective evidence)
Full-field ERG (scotopic/photopic): signature test. MAR shows reduced b-wave with relatively preserved a-wave—an electronegative ERG—pointing to ON-bipolar cell dysfunction. This is high-yield for diagnosis. Journal of NeuroscienceEyeWiki
ON–OFF ERG protocols: isolate ON vs OFF retinal pathways; in MAR the ON pathway is disproportionately affected. Journal of Neuroscience
Multifocal ERG (mfERG): maps localized cone-system dysfunction across the macula, correlating with central scotomas or shimmering zones. aes.amegroups.org
Pattern ERG / Photopic Negative Response (PhNR): ancillary tests to characterize inner-retinal function; patterns can support the diagnosis and track change. (Supportive literature within AIR/MAR reviews.) aes.amegroups.org
E) Imaging tests (to document structure and find the cancer driver)
Optical Coherence Tomography (OCT): cross-section images of the retina. MAR can show inner nuclear layer and outer plexiform changes; sometimes OCT is near-normal early. EyeWiki
Fundus photography (including widefield): records baseline; early photos can look surprisingly normal despite symptoms. EyeWiki
Fundus autofluorescence (FAF): highlights metabolic stress in photoreceptors/RPE; patterns may be subtle or patchy. EyeWiki
Fluorescein angiography (FA): often unremarkable in early MAR (helps exclude inflammatory mimics). EyeWiki
OCT-Angiography (OCT-A): evaluates retinal capillary layers; generally used to rule out vascular causes of field loss. aes.amegroups.org
Whole-body cancer imaging (e.g., PET-CT): not an eye test, but crucial to find hidden or recurrent melanoma when MAR is suspected—sometimes the eye work-up leads to the discovery of metastases. PMC
Non-pharmacological treatments (therapies & “other” care)
Important: These approaches support vision and quality of life. They don’t replace medical therapy for melanoma or immune modulation when indicated.
Treat the melanoma promptly (team coordination)
Close coordination with oncology to control tumor burden (surgery/radiation/systemic therapy) may reduce the trigger for autoantibodies. Mechanism: lowers antigen load driving the autoimmune response. EyeWikiTherapeutic plasma exchange (TPE/plasmapheresis)
Removes circulating autoantibodies; sometimes used in MAR/AIR with variable benefit. Mechanism: physically lowers pathogenic antibody titers. EyeWikiLow-vision rehabilitation
Training and devices (magnifiers, e-readers, contrast enhancement) to maximize remaining vision.Tinted/filtered lenses (e.g., FL-41, blue-blocking)
Reduce photopsias and glare by limiting problematic wavelengths; improves comfort and function.Task lighting optimization at home/work
Bright, even lighting and flexible task lamps reduce strain when ON-pathway is impaired.Night-driving restriction & mobility training
Nyctalopia makes night driving risky; mobility specialists teach safer strategies.Orientation & mobility (O&M) therapy
Skills for safe navigation (white cane training, route planning) maintain independence.Contrast-rich environmental modifications
High-contrast labels, bold edge-marking on stairs, and color-coded organization cut accidents.Digital accessibility tools
Screen readers, large-text modes, high-contrast themes, and voice assistants reduce visual load.Occupational therapy (OT)
Adapts tasks and environments for cooking, finances, and work to preserve productivity.Psychological support / CBT
Helps manage anxiety, sleep disruption, or depression that photopsias and vision change can cause.Sleep hygiene
Consistent schedule, dark cool room, and minimizing nocturnal screen glare can lessen symptom burden at night.Regular aerobic exercise
Supports general immune regulation and mood; helps with fatigue from systemic cancer care.Smoking cessation
Improves ocular and systemic vascular health; supports melanoma and overall cancer outcomes.UV/sun protection
Broad-spectrum sunscreen, hats, and protective clothing—core melanoma prevention and recurrence-reduction practices.Dietary pattern: anti-inflammatory emphasis
Plenty of vegetables, fruits, legumes, whole grains, fish/omega-3s; minimizes ultra-processed foods. (Supplements listed later.)Glycemic and blood-pressure control
Keeps retinal circulation healthy and reduces additive damage risks.Falls-prevention home safety check
Decluttering, grab bars, non-slip mats; especially important when peripheral fields shrink.Baseline and periodic ERG/field/OCT monitoring
Early detection of change allows faster treatment adjustments (objective tracking). EyeWikiPatient support groups / rare-disease resources
Education and peer support improve coping, adherence, and access to trials; NORD maintains MAR resources. EyeWiki
Drug treatments
Notes: There is no single proven “cure” for MAR. Most therapies are off-label and backed by case reports/series or AIR reviews. Doses below are typical starting points—must be individualized by specialists (ocular immunology/retina + oncology). Some agents can interact with cancer immunotherapy; decisions should be made jointly with the oncology team.
High-dose corticosteroids (class: glucocorticoid)
Dose/time: IV methylprednisolone 500–1000 mg daily × 3 days, then oral prednisone ~0.5–1 mg/kg/day with slow taper if responsive.
Purpose: Calm the autoimmune attack quickly.
Mechanism: Broad immunosuppression; reduces antibody-mediated inflammation.
Key side effects: Hyperglycemia, mood change, infection risk, bone loss, glaucoma/cataract with chronic use. Evidence of lasting benefit in MAR is limited. EyeWikiIntravenous immunoglobulin (IVIG) (immune modulator)
Dose/time: 2 g/kg per cycle, spread over 2–5 days; often repeated monthly for several months if helpful.
Purpose: Modulate dysregulated immunity; neutralize pathogenic antibodies.
Mechanism: Fc-receptor blockade, anti-idiotype effects, complement inhibition.
Side effects: Headache, thrombotic risk, aseptic meningitis (rare); high cost. Mixed results in reports; some improvement in fields/symptoms. EyeWikiPlasmapheresis / therapeutic plasma exchange (TPE) (procedure, non-drug but often paired with drugs)
Dose/time: Typical series 3–5 exchanges over 1–2 weeks.
Purpose/mechanism: Rapid removal of circulating autoantibodies; sometimes used as a bridge to longer-acting immunotherapy.
Risks: Line infection, hypotension, electrolyte shifts; benefit inconsistent. EyeWikiRituximab (anti-CD20 B-cell–depleting monoclonal antibody)
Dose/time: 375 mg/m² weekly × 4, or 1 g on day 1 & day 15; may repeat based on response.
Purpose: Reduce autoantibody production by depleting B-cells.
Mechanism: Targets CD20 on B-lymphocytes.
Side effects: Infusion reactions, infection risk, HBV reactivation (screen first). Case reports/series—including triple therapy—showed meaningful visual/ERG improvements in MAR. PubMedJohns Hopkins UniversityMycophenolate mofetil (MMF) (antimetabolite immunosuppressant)
Dose/time: 1.0–1.5 g twice daily; onset over weeks.
Purpose: Steroid-sparing maintenance.
Mechanism: Inhibits lymphocyte guanine nucleotide synthesis.
Side effects: GI upset, leukopenia, infection risk; monitor CBC/LFTs. Used across autoimmune retinopathies. PMCAzathioprine (antimetabolite)
Dose/time: ~1–2 mg/kg/day; check TPMT activity; adjust for leukopenia.
Purpose: Steroid-sparing control.
Mechanism: Purine analog blocking lymphocyte proliferation.
Side effects: Cytopenias, liver toxicity, infection risk. EyeWikiMethotrexate (low-dose weekly) (antimetabolite)
Dose/time: 10–25 mg once weekly with folic acid supplementation.
Purpose: Maintenance immunosuppression in AIR spectrum.
Mechanism: Dihydrofolate reductase inhibition; immunomodulation.
Side effects: Stomatitis, liver enzyme elevation (avoid alcohol), marrow suppression (monitor). (AIR review evidence.) aes.amegroups.orgCyclophosphamide (alkylator; cytotoxic immunosuppressant)
Dose/time: Oral 1–2 mg/kg/day or IV pulses (e.g., 500–750 mg/m² monthly) in refractory cases.
Purpose: Rescue therapy when others fail.
Mechanism: Depletes rapidly dividing immune cells.
Side effects: Cytopenias, hemorrhagic cystitis (hydrate/mesna), infertility risk. (More evidence in CAR/AIR; used selectively.) Spandidos PublicationsIntravitreal corticosteroid (e.g., triamcinolone; dexamethasone implant)
Dose/time: Office-based injection; may repeat based on effect.
Purpose: Reduce intraocular inflammation/symptoms (e.g., photopsias); part of triple therapy in MAR case report.
Risks: IOP rise, cataract; sterile endophthalmitis (rare). PubMedSymptomatic agents (e.g., gabapentin for photopsias)
Dose/time: Gabapentin 100–300 mg at night, then titrate.
Purpose: Damp down distressing shimmering/paresthesia-like visual sensations.
Mechanism: Central neuronal modulation.
Side effects: Sedation, dizziness; renal dosing. (Not disease-modifying.) EyeWiki
Special oncology note: Immune checkpoint inhibitors (ICIs) such as nivolumab and ipilimumab are mainstays for melanoma and dramatically improve survival—but they can sometimes trigger or unmask autoimmune retinopathies, and ocular monitoring is essential. Decisions about steroids or other immunosuppression during ICI therapy need careful, shared oncology–ophthalmology planning. PMCResearchGateFrontiers
Dietary / molecular supplements
Big caution: Supplements do not treat MAR, and some antioxidants may interact with cancer care. Always clear supplements with your oncologist first—especially during immunotherapy. Evidence below is general/adjunctive (ocular neuroprotection or systemic health), not MAR-specific.
Omega-3s (EPA/DHA) — 1000–2000 mg/day combined EPA+DHA.
Rationale: Neuroprotective and anti-inflammatory fatty acids that support retinal cell membranes.Lutein/Zeaxanthin — 10 mg lutein + 2 mg zeaxanthin/day.
Rationale: Macular pigments with antioxidant/blue-light filtering; may aid contrast sensitivity.Vitamin D3 — 1000–2000 IU/day (adjust to serum level).
Rationale: Immune modulation; deficiency is common during chronic illness.Vitamin B12 (methylcobalamin) — 1000 µg/day or per labs.
Rationale: Nerve health; corrects deficiency-related neuropathy-like symptoms.Folate (as methylfolate) — 400–800 µg/day unless on methotrexate (then use folic acid per clinician).
Rationale: Supports cellular metabolism; avoid high doses without guidance.Magnesium — 200–400 mg/day (glycinate/citrate).
Rationale: May help sleep quality and reduce neurosensory irritability.Coenzyme Q10 (Ubiquinol) — 100–200 mg/day.
Rationale: Mitochondrial support; sometimes used in retinal/neural health contexts.Alpha-lipoic acid — 300–600 mg/day.
Rationale: Antioxidant with neural support; discuss with oncology during active treatment.N-acetylcysteine (NAC) — 600 mg once or twice daily.
Rationale: Glutathione precursor; consider only with oncology input due to conflicting data on antioxidants in cancer settings. ResearchGateCurcumin (with piperine or phytosomal form) — 500–1000 mg/day.
Rationale: Anti-inflammatory; potential immunomodulation (drug interactions possible).Resveratrol — 100–250 mg/day.
Rationale: Antioxidant; theoretical retinal neuroprotection.Taurine — 500–1000 mg/day.
Rationale: Abundant retinal amino acid with neuro-supportive roles.Zinc — 10–25 mg/day (balance with copper).
Rationale: Retinal enzyme cofactor; avoid high doses long-term.Vitamin C — Diet first; supplement only if deficient.
Rationale: Common deficiency during immunotherapy has been documented; high-dose IV vitamin C is investigational and not standard—discuss with oncology. MDPIBioMed CentralProbiotics (general gut support) — product-dependent.
Rationale: Gut–immune axis support; choose cautiously during immunosuppression.
Reminder: The oncology literature on antioxidants during active cancer therapy is mixed. Some reviews suggest possible synergy with ICIs or no harm, others urge caution; decisions should be personalized. Embo Press
Regenerative / stem-cell” drugs & approaches
There are no approved regenerative or stem-cell drugs for MAR. Below are contextual therapies you may hear about; they are either oncology immunotherapies (treat the cancer, not MAR directly) or experimental retinal cell therapies for other diseases. Any use should be within regulated clinical trials.
Nivolumab (PD-1 inhibitor) + Ipilimumab (CTLA-4 inhibitor) — oncology backbone for advanced melanoma; profound 10-year survival benefits in many patients. In some cases, ICIs can worsen autoimmune retinopathy, so ophthalmic monitoring is essential. PMCResearchGate
Pembrolizumab (PD-1 inhibitor) — similar oncologic role; same ocular monitoring caveats. EyeWiki
Targeted melanoma therapy (e.g., BRAF/MEK inhibitors) — for BRAF-mutant melanoma; goal is tumor cytoreduction, possibly lowering antigen drive behind autoantibodies. (Oncology-directed use; ocular side-effects monitoring applies.)
Human retinal progenitor cells (hRPC, “jCell/famzeretcel”) — for retinitis pigmentosa, not MAR; clinical trials show safety signals and exploratory functional gains, but not indicated for MAR. Avoid unregulated “stem-cell clinics.” ClinicalTrials.govBioMed Central
Autologous CD34+ bone-marrow–derived cells (experimental intravitreal) — Phase-I feasibility in retinal disease; not MAR therapy; risks and benefits remain under study. ophthalmologyscience.org
General warning about “stem-cell injections” outside trials — The FDA and case reports have documented severe, sometimes blinding complications from unapproved intravitreal stem-cell injections; do not pursue outside regulated studies. PMCBioMed Central
Surgeries (procedures & why they’re done)
Surgery is not for MAR itself; it’s for melanoma control or ocular complications.
Wide local excision (cutaneous melanoma)
Removes primary skin tumor with adequate margins; reduces tumor antigen load and guides staging.Sentinel lymph-node biopsy / lymphadenectomy
Maps and removes first draining nodes for staging/control—critical for melanoma management.Metastasectomy (selected cases)
Surgical removal of metastatic deposits (e.g., lung, liver) when feasible—aim: cytoreduction.Plaque brachytherapy (uveal melanoma)
A radiation “seed” is sutured to the eye over the tumor; preserves eye while controlling local disease. AAOEnucleation (advanced uveal melanoma)
Eye removal for large, painful, or visionless eyes or when tumor control requires it. EyeWiki
Prevention points
There’s no proven way to prevent MAR itself. Prevention focuses on melanoma risk reduction, surveillance, and fast action if new visual symptoms emerge.
Sun/UV protection (sunscreen, hats, clothing).
Skin self-checks and dermatology visits (ABCDE rule).
Follow oncology surveillance exactly (scans/visits).
Report new visual symptoms immediately (photopsias, night blindness).
Baseline eye exam before starting ICIs and periodic checks during therapy. EyeWiki
Avoid unregulated stem-cell injections of the eye. PMC
Don’t smoke; maintain healthy weight and fitness.
Manage blood pressure, glucose, and lipids.
Healthy, anti-inflammatory diet (see below).
Medication reconciliation at every visit to catch interactions (especially with immunotherapies).
When to see a doctor
Urgently (same day / ER if needed): sudden big drop in vision, new dark “curtain,” eye pain with vision change, or dramatic peripheral field loss.
Promptly (within days): new shimmering lights, worsening night vision, or new field defects—especially if you have current or past melanoma or are starting immunotherapy. EyeWiki
What to eat and what to avoid
Emphasize: Colorful vegetables and fruits, leafy greens (lutein/zeaxanthin), legumes, whole grains, nuts, seeds, olive oil, and fish (omega-3s).
Hydrate and balance protein (especially important during cancer care).
Limit/avoid: Ultra-processed foods, excess sugar, trans fats, and heavy alcohol.
Supplements: Only with oncology/ophthalmology approval; see cautions above about antioxidants during active cancer treatment. Embo Press
Frequently asked questions
Is MAR the same as “cancer-associated retinopathy (CAR)”?
No. Both are autoimmune retinopathies linked to cancer, but MAR typically targets ON-bipolar cells (anti-TRPM1) and shows an electronegative ERG, whereas CAR more often damages photoreceptors with both a- and b-waves reduced. EyeWikiCan MAR appear years after melanoma?
Yes. It often follows the melanoma diagnosis and can signal recurrence—that’s why new visual symptoms in melanoma patients warrant prompt evaluation. EyeWikiWhat test “proves” MAR?
There’s no single perfect test. Doctors use a triad: (1) typical symptoms and fields, (2) electronegative ERG/ON-pathway dysfunction, and (3) serum antiretinal antibodies (often anti-TRPM1). EyeWikiIf my eye exam looks normal, can I still have MAR?
Yes—early fundus can be normal; ERG and fields are far more sensitive. EyeWikiDo steroids fix MAR?
They sometimes help symptoms short-term but don’t reliably stop the disease. Long-term control often needs other immunotherapy and melanoma control. EyeWikiWhat about IVIG, rituximab, or “triple therapy”?
Case reports—including rituximab + IVIG + intravitreal steroid—show meaningful improvements in some patients. Responses vary; care must be individualized. PubMedWill melanoma immunotherapy (like nivolumab/ipilimumab) help or hurt MAR?
ICIs dramatically improve melanoma survival, which is crucial overall. But they can worsen autoimmune eye problems in some patients—so you’ll need coordinated oncology-ophthalmology monitoring and shared decisions about steroids/immunosuppression. PMCResearchGateAre there vitamins that treat MAR?
No. Nutrients may support general health, but supplements don’t treat MAR. Discuss any supplements with your oncology team to avoid therapy interactions. Embo PressIs surgery ever done for MAR?
Not for MAR itself. Surgery targets the melanoma (e.g., excision, lymph nodes, plaque radiotherapy, enucleation in uveal disease) to control cancer. AAOEyeWikiCan MAR be one-sided?
It’s usually both eyes, but early or atypical cases can present unilaterally—especially in reports tied to immunotherapy. PMCWhat does OCT show in MAR?
OCT may be normal early; in autoimmune retinopathies it can later show subtle inner retinal changes/thinning. ERG + fields detect dysfunction earlier. PMCHow often will I need follow-up?
Typically every 1–3 months early on, then tailored based on stability and treatments, with ERG/fields/OCT to track objective change.Can MAR go into remission?
Sometimes symptoms stabilize, especially if melanoma is controlled and immune therapy is effective; others need long-term immunomodulation.Is MAR painful?
No—vision changes are painless. Eye pain suggests a different problem that needs urgent evaluation.Where can I learn more / find community?
The AAO’s EyeWiki overview and NORD resources are good starting points; your retina specialist can point to trial options if appropriate. 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 13, 2025.
