Birdshot Lesions

Birdshot lesions” are many small, cream-colored spots in the deeper eye layers (the choroid and retina). They are usually oval and radiate out from the optic disc toward the mid-periphery, often in both eyes. Doctors now group these findings under birdshot chorioretinopathy (also called birdshot retinochoroiditis or HLA-A29 uveitis), a rare, chronic, non-infectious inflammation strongly linked to HLA-A29. The lesions reflect ongoing inflammation that can damage photoreceptors and the retinal pigment epithelium, causing night vision trouble, color vision changes, floaters, glare, and gradual vision loss if untreated. Multimodal imaging (indocyanine green angiography, OCT, and autofluorescence) helps detect active versus “burnt-out” (inactive) spots and monitor treatment. Early, sustained control of inflammation is key to protect vision. EyeWiki+2NCBI+2

“Birdshot lesions” are the pale, cream-colored spots that doctors see at the back of the eye in a rare eye disease called birdshot chorioretinopathy (also called birdshot uveitis or HLA-A29 uveitis). These lesions sit deep in the eye wall (the choroid and the retina) and tend to be oval, slightly elongated, and radiate outward from the optic nerve in both eyes. They reflect ongoing inflammation in those tissues. The disease is usually long-lasting (chronic), often affects adults in mid-life, and is strongly tied to a genetic marker named HLA-A29. Vision can be affected by blurred vision, floaters, night-vision problems, flashes of light, blind spots, and loss of contrast. Diagnosis is clinical and imaging-based, supported by HLA-A29 testing, and by excluding infections and other causes of uveitis. Frontiers+3EyeWiki+3NCBI+3

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Other names

Birdshot lesions appear in the disease known by several names:

• Birdshot chorioretinopathy (BSCR)

• Birdshot retinochoroidopathy / birdshot retinochoroiditis

• Birdshot uveitis

• HLA-A29 uveitis (emphasizing the genetic association)

• Vitiliginous chorioretinitis (older term) bjo.bmj.com+1

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Types

1. Typical “birdshot” pattern
   Many, cream-colored, oval lesions in both eyes, most dense around the optic nerve and mid-periphery, with relative sparing of the very center (fovea) at the start. AAO

2. Active vs. inactive (scarred) lesions
   “Active” lesions look slightly fuzzy or ill-defined and come with leakage on angiography; “inactive” lesions look sharper and more depigmented as scars. PubMed

3. ICGA-positive choroidal “dark dots”
   On indocyanine green angiography (ICGA), doctors often see many more “silent” hypofluorescent dots than are visible clinically—this reveals deeper choroidal disease. IOVS+1

4. Macular-edema–predominant vs. atrophy-predominant
   Some patients mainly show macular edema (swelling) early; others progress toward outer retinal and choroidal atrophy with thinning on OCT if inflammation persists. PMC

5. HLA-A29–positive classic disease vs. “birdshot-like” cases
   The classic entity is HLA-A29–positive. Rare “birdshot-like” pictures without HLA-A29 exist and need careful work-up for mimics. Frontiers+1

6. Early vs. late functional involvement
   Even when visual acuity looks okay, electroretinography (ERG) can show widespread retinal dysfunction; later, vision and fields decline. PMC+1

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Causes

Important note: The exact cause is unknown. The strongest, proven factor is the HLA-A29 genetic marker. Everything else below are plausible contributors or reported associations, with varying levels of evidence. PMC

1. HLA-A29 genetic predisposition — the key risk factor; most patients are HLA-A29–positive. Frontiers+1

2. HLA-A*29:02 subtype and antigen presentation — a specific HLA-A29 subtype and how it presents peptides to T cells likely matter. Frontiers

3. ERAP-mediated peptide trimming pathway — variants in antigen-processing genes (e.g., ERAP) may shape autoimmunity. Frontiers

4. T-cell–driven autoimmune response — misdirected immunity toward retinal/choroidal antigens is suspected. PMC

5. Molecular mimicry after infections (hypothesis) — a microbe peptide resembling a self-peptide could trigger disease in a predisposed host. PMC

6. Choroidal innate-immune activation — chronic activation of the choroid’s immune cells may sustain inflammation. PMC

7. Gut microbiome dysbiosis (theory) — altered gut flora may modulate HLA-linked uveitis risk; data are early. Frontiers

8. Age-related immune changes — disease usually starts in mid-life; immunosenescence may contribute. EyeWiki

9. Genetic background of Northern European ancestry (epidemiology) — higher prevalence has been reported; ancestry is a risk pattern, not a cause. EyeWiki

10. Environmental triggers (unknown) — some outside trigger probably sets off disease in a genetically primed person. PMC

11. “Birdshot-like” HLA-A29-negative pathways — rare cases suggest other, as-yet-uncertain mechanisms can mimic the picture. MDPI

12. Breakdown of ocular immune privilege — chronic inflammation can persist once local immune tolerance fails. PMC

13. Microvascular stress in the choroid — imaging shows choroidal involvement; vascular inflammation may perpetuate damage. Nature

14. Macular edema biology — inflammatory cytokines increase retinal vascular leakage, adding morbidity though not the root cause. PMC

15. Oxidative stress from chronic inflammation — long-standing immune activity may harm photoreceptors. PMC

16. Epitope spreading over time — immune targets may broaden, worsening disease chronicity. PMC

17. Reduced regulatory T-cell control (hypothesis) — inadequate immune “brakes” can allow autoreactivity. PMC

18. Cytokine network imbalance — shifts in inflammatory mediators (e.g., Th1/Th17) likely fuel activity. PMC

19. Host factors linked to reported associations — hypertension, vitiligo, and hearing loss have been reported with BSCR in some series; these are associations, not proven causes. EyeWiki

20. Combined “gene–environment–immune” model — most experts believe multiple small factors stack on a strong HLA-A29 base. PMC

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Symptoms

1. Blurred vision — especially during flares, and sometimes steadily over years if inflammation is not controlled. EyeWiki

2. Floaters — dark specks or strands due to inflammatory cells in the vitreous. EyeWiki

3. Night-vision trouble (nyctalopia) — trouble seeing in dim light is very common. EyeWiki

4. Flashes of light (photopsias) — brief light streaks from retinal irritation. EyeWiki

5. Color vision changes (dyschromatopsia) — colors look washed out or off-tone. EyeWiki

6. Glare and light sensitivity — bright light feels harsh and vision seems hazy. EyeWiki

7. Loss of contrast — fine shades of gray are harder to see, making reading and face recognition difficult. ScienceDirect

8. Patchy blind spots (scotomas) — small areas of missing vision in the center or near-center. PMC

9. Distorted vision (metamorphopsia) — straight lines may look wavy when the macula is swollen. PMC

10. Peripheral field loss — side vision may shrink over time. ScienceDirect

11. Trouble reading — from combined effects of contrast loss, blind spots, and macular edema. ScienceDirect

12. Eye discomfort — a sense of pressure or ache (severe pain is less typical unless complications). NCBI

13. Vision that fluctuates — better and worse days, often tracking inflammation or edema. NCBI

14. Gradual progression — without control, function may worsen slowly and steadily. NCBI

15. Both eyes involved — symptoms almost always affect both eyes. AAO

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Diagnostic tests

A. Physical examination in the eye clinic

1. Best-corrected visual acuity (BCVA)
   Measures how clearly you see letters on a chart with your best glasses. In birdshot, acuity can be normal early and later fall, so BCVA is essential but not the whole story. ScienceDirect

2. Pupil exam and RAPD check
   A swinging-flashlight test looks for a relative afferent pupillary defect, which can suggest asymmetric retinal or optic-nerve dysfunction. NCBI

3. Intraocular pressure (IOP)
   Measured with tonometry. Steroid treatment or inflammation can change IOP; tracking it prevents optic-nerve damage from pressure. NCBI

4. Slit-lamp exam with dilated funduscopy
   The doctor inspects anterior chamber cells/flare, vitreous cells, and the classic cream-colored lesions in the posterior pole and mid-periphery of both eyes. AAO

B. Simple manual/bedside visual-function tests

5. Amsler grid
   A handheld grid that reveals central distortions or small blind spots you may not notice otherwise; useful to monitor macular edema or paracentral scotomas. NCBI

6. Confrontation visual fields
   Quick in-office check of side vision; if abnormal, it prompts formal perimetry. NCBI

7. Color vision testing (e.g., Ishihara plates)
   Screens for color loss (dyschromatopsia), which is common in BSCR. EyeWiki

8. Contrast sensitivity (e.g., Pelli-Robson)
   Detects reduced ability to see faint targets—a sensitive measure that often declines before standard acuity drops. ScienceDirect

C. Laboratory / pathological tests (mainly to support diagnosis and exclude mimics)

9. HLA-A29 typing
   A blood test that detects the HLA-A29 antigen. A positive result strongly supports the diagnosis in the right clinical setting. Frontiers

10. Syphilis serology (non-treponemal + treponemal)
    Rules out syphilitic uveitis, a key mimic that can resemble many posterior uveitides. NCBI

11. Tuberculosis screening (IGRA such as QuantiFERON)
    Done to exclude TB-related posterior uveitis in appropriate risk settings. NCBI

12. Sarcoidosis markers (ACE and/or lysozyme) and basic autoimmune screen
    Help exclude sarcoid uveitis and systemic autoimmune causes when history suggests them. NCBI

D. Electrodiagnostic tests (measure electrical responses of the retina/visual pathway)

13. Full-field ERG
    Assesses global rod and cone function. In birdshot, 30-Hz flicker implicit times often delay and amplitudes may fall, even when vision looks okay. It tracks disease activity over time. PMC

14. Multifocal ERG (mfERG)
    Maps cone-mediated function across the macula. Abnormal rings or depressed responses correlate with OCT changes and microperimetry defects. ajo.com+1

15. Electro-oculography (EOG)
    Evaluates the retinal pigment epithelium (RPE) and can be abnormal when RPE is affected by inflammation. PMC

16. Visual evoked potentials (VEP)
    Assesses the pathway from retina to visual cortex; useful if optic-nerve involvement is suspected or to complement ERG in complex cases. PMC

E. Imaging tests (show inflammation, leakage, and structural change)

17. Optical coherence tomography (OCT)
    Cross-section images of the retina. Detects macular edema, outer-retinal thinning, ellipsoid-zone loss, and later atrophy; key for follow-up. PMC

18. Fluorescein angiography (FA)
    Highlights retinal blood-vessel leakage, optic-disc leakage, and vasculitis; active lesions may show late staining. PubMed

19. Indocyanine green angiography (ICGA)
    Best for choroid. Shows many hypofluorescent “dark dots”—often more than the visible lesions—and is highly sensitive for subclinical activity and relapse. PubMed+2PMC+2

20. Fundus autofluorescence (FAF)
    Maps lipofuscin at the level of the RPE; shows hyper- or hypo-autofluorescent patches that mirror RPE stress or loss near birdshot lesions. PMC

Non-pharmacological treatments (therapies & others)

Each item includes: description (~brief), purpose, and mechanism. These support medical care but do not replace immunosuppressive treatment your ophthalmologist prescribes.

1. Disease education & close monitoring
   Learning what birdshot lesions mean, how flares feel, why appointments, labs, and imaging matter, and when to call for help improves adherence and outcomes. Keeping a symptom diary (glare, night vision, color shifts), doing Amsler grid checks, and attending scheduled OCT/FAF/ICGA helps catch active disease early so treatment can be adjusted before vision is harmed. Educated patients tend to achieve earlier inflammation control and maintain function better over time. Purpose: empower self-management and early reporting. Mechanism: earlier recognition of inflammatory activity → timely therapy → less structural damage. NCBI

2. Smoking cessation
   Smoking worsens ocular perfusion and oxidative stress, which can amplify inflammatory eye disease and impede healing after injections or surgery. Stopping smoking reduces vascular and inflammatory burdens, supporting better macular and optic nerve health over time. Purpose: lower modifiable risk that can aggravate inflammation or surgical risk. Mechanism: reduces systemic pro-inflammatory cytokines and improves microvascular function. (General uveitis guidance.) NCBI

3. UV/blue-light protection
   Wraparound sunglasses and anti-glare lenses can ease photophobia and reduce scatter that worsens visual discomfort in active uveitis. Purpose: symptom relief and comfort. Mechanism: reduces retinal light stress and glare, improving contrast sensitivity in inflamed eyes. NCBI

4. Optimized home/work lighting
   Bright, even, indirect lighting, task lights, and reduced nighttime glare help compensate for night blindness and contrast loss. Purpose: safety and functional vision. Mechanism: improves signal-to-noise for the retina when rod/dark adaptation is impaired by inflammation. EyeWiki

5. Low-vision rehabilitation
   If vision reduces, referral for magnifiers, high-contrast materials, electronic readers, large-print devices, and training preserves independence. Purpose: maintain daily living and reading. Mechanism: assistive optics and training bypass reduced contrast and field defects from lesions. NCBI

6. Nutrition pattern for eye/immune health
   A generally anti-inflammatory eating pattern (more fruits/vegetables, fish, nuts; less ultra-processed foods) supports vascular and retinal health. This does not treat flares but supports overall status and steroid side-effect mitigation (weight, glucose, bone). Purpose: systemic risk reduction. Mechanism: lowers systemic oxidative and inflammatory load; supports metabolic health during steroids. NCBI

7. Exercise plan (as tolerated)
   Regular aerobic and resistance activity improves cardiometabolic health, mood, and steroid-related risks (osteopenia, weight, blood pressure). Purpose: counter medication effects and improve resilience. Mechanism: anti-inflammatory myokines and improved insulin sensitivity help systemic health during long immunotherapy. NCBI

8. Stress-reduction & sleep hygiene
   Mindfulness, CBT techniques, and 7–9 hours of sleep support immune balance and coping with a chronic condition. Purpose: reduce flare-perceived severity and improve adherence. Mechanism: dampens hypothalamic–pituitary–adrenal stress activation that can modulate immune responses. NCBI

9. Vaccination planning (with your doctors)
   Keeping up with non-live vaccines (e.g., influenza) is important before/while using immunosuppression. Coordinate timing with your ophthalmologist/rheumatologist. Purpose: infection risk reduction. Mechanism: lowers preventable infections that can interrupt uveitis control. NCBI

10. Bone & stomach protection during steroids
    Calcium/vitamin D, fall-prevention, weight-bearing exercise, and (when appropriate) PPIs lessen common systemic steroid harms while you taper to a safer maintenance dose. Purpose: mitigate steroid toxicity. Mechanism: supports bone mineralization and gastric mucosal protection during corticosteroid use. Review of Ophthalmology

11. Blood pressure, glucose, and lipid control
    Managing these reduces vascular stress on the retina and helps tolerate steroids and calcineurin inhibitors. Purpose: reduce complications. Mechanism: better microvascular health protects macula/optic nerve during chronic therapy. NCBI

12. Fall and driving-safety adjustments
    Anti-glare night driving strategies, up-to-date glasses, and home de-cluttering reduce injury risk from reduced contrast and night vision. Purpose: safety. Mechanism: minimizes consequences of impaired scotopic vision and field defects. EyeWiki

13. Digital ergonomics
    High-contrast mode, larger fonts, reduced screen glare, and frequent breaks reduce eye strain in symptomatic periods. Purpose: comfort and productivity. Mechanism: fewer triggers of glare/photopsia during active disease. EyeWiki

14. Allergy/irritant avoidance
    Limiting ocular surface triggers (wind, smoke, allergens) can help comfort even though birdshot is posterior. Purpose: reduce additive irritation. Mechanism: fewer surface symptoms improve adherence to drops after procedures. NCBI

15. Support groups & counseling
    Chronic uveitis can be isolating; peer and mental-health support improve coping and adherence. Purpose: psychosocial resilience. Mechanism: lowers distress → better treatment follow-through. NCBI

16. Medication adherence tools
    Use phone reminders and blister packs for complex systemic regimens (weekly MTX, twice-daily MMF, etc.). Purpose: consistent control. Mechanism: reduces missed doses that risk flares. clinexprheumatol.org

17. Sunlight scheduling
    Plan outdoor activity with sunglasses/hat at lower-glare times. Purpose: symptom relief. Mechanism: reduces photophobia-related discomfort. EyeWiki

18. Surgery-timing discipline
    If cataract or glaucoma surgery is needed, ensure uveitis is quiet for ~3 months beforehand whenever feasible, as outcomes are better. Purpose: fewer complications; better vision. Mechanism: less perioperative inflammation. EyeWiki+1

19. Written flare plan
    Agree with your clinician on who to call and what to adjust at first sign of CME or increased floaters. Purpose: faster escalation. Mechanism: earlier anti-inflammatory control prevents structural damage. NCBI

20. Regular imaging-guided care
    Serial OCT/FAF/ICGA and visual fields guide dose-tapering and detect subclinical activity. Purpose: objective control. Mechanism: imaging shows edema or choroidal hypofluorescence before vision drops. NCBI+1

Drug treatments

Birdshot chorioretinopathy is a non-infectious posterior uveitis; long-term control usually requires steroid-sparing immunomodulatory therapy. Below, FDA-approved labels for uveitis itself are explicitly cited; other agents are widely used off-label in non-infectious uveitis based on clinical studies and expert practice. Always individualize dosing and monitoring with your uveitis specialist.

1. Prednisone (systemic corticosteroid) — induction & bridge
   Class: corticosteroid. Typical dose/time: 0.5–1 mg/kg/day, taper to ≤7.5 mg/day once steroid-sparing therapy takes effect. Purpose: rapid control of intraocular inflammation/CME. Mechanism: broad cytokine suppression (NF-κB/AP-1). Side effects: weight gain, glucose/BP rise, mood change, cataract, glaucoma, osteoporosis; use bone/GI protection. (General uveitis practice for induction/bridge.) NCBI+1

2. Dexamethasone intravitreal implant (OZURDEX® 0.7 mg)
   Class: intraocular corticosteroid (biodegradable). Dose/time: single office injection; effect ~3–6 months; repeat PRN. Purpose: treat non-infectious posterior-segment uveitis and uveitic macular edema. Mechanism: local steroid release to the vitreous, suppressing inflammatory mediators. Side effects: IOP rise, cataract, injection risks (endophthalmitis, retinal tear). FDA-label: indicated for non-infectious posterior uveitis. FDA Access Data+1

3. Fluocinolone acetonide intravitreal implant (YUTIQ® 0.18 mg)
   Class: intraocular corticosteroid (non-bioerodible). Dose/time: in-office injection; releases ~0.25 µg/day for up to 36 months; reduces posterior uveitis recurrences. Purpose: long-term control with fewer re-injections. Mechanism: sustained steroid micro-dose to posterior segment. Side effects: cataract, IOP rise; monitor and treat as needed. FDA-label & review: approved for chronic non-infectious uveitis affecting the posterior segment. FDA Access Data+1

4. Fluocinolone acetonide surgical implant (RETISERT® 0.59 mg)
   Class: intraocular corticosteroid (surgically sutured). Dose/time: OR implantation; releases steroid for ~30 months; strong control of posterior uveitis. Purpose: durable suppression in severe/refractory disease. Mechanism: high local steroid levels in posterior segment. Side effects: high rates of cataract and IOP rise (often need surgery); surgical risks. FDA-label: indicated for chronic non-infectious posterior uveitis. FDA Access Data+2FDA Access Data+2

5. Adalimumab (HUMIRA® and biosimilars, e.g., HULIO®) — FDA-approved for non-infectious uveitis
   Class: anti-TNF-α biologic. Dose/time (adult uveitis): 80 mg loading, then 40 mg every other week; some need weekly dosing under specialist care. Purpose: steroid-sparing systemic control of intermediate/posterior/panuveitis, including birdshot. Mechanism: neutralizes TNF-α to prevent inflammatory cascades. Side effects: infection risk (TB/hep B screening), injection site reactions; rare demyelination. FDA-label: approved for non-infectious uveitis with dosing above. FDA Access Data+2FDA Access Data+2

6. Mycophenolate mofetil (MMF) (off-label in uveitis)
   Class: antimetabolite. Dose/time: commonly 1–1.5 g twice daily; titrate to effect and labs. Purpose: steroid-sparing long-term control of posterior/panuveitis. Mechanism: inhibits inosine monophosphate dehydrogenase (lymphocyte proliferation). Side effects: GI upset, leukopenia; teratogenic—avoid in pregnancy. Evidence: multiple series show effectiveness for non-infectious uveitis. PMC+2cda-amc.ca+2

7. Methotrexate (MTX) (off-label)
   Class: antimetabolite/DMARD. Dose/time: 15–25 mg once weekly (oral or subcutaneous) with folic acid; lab monitoring. Purpose: steroid-sparing control; useful if MMF not tolerated. Mechanism: dihydrofolate-related anti-proliferative and adenosine-mediated anti-inflammatory effects. Side effects: liver enzyme elevation, cytopenias, stomatitis; avoid pregnancy; monitor CBC/LFTs. Evidence: widely used in non-infectious uveitis; expert dosing consensus. clinexprheumatol.org+1

8. Azathioprine (off-label)
   Class: purine analog. Dose/time: ~1–2(–3) mg/kg/day; TPMT/NUDT15 testing guides safety. Purpose: steroid-sparing alternative; helpful in intermediate/posterior uveitis. Mechanism: blocks lymphocyte proliferation. Side effects: leukopenia, liver toxicity, infection risk; avoid with allopurinol unless dose-adjusted. Evidence: moderate efficacy in ocular inflammatory diseases. PMC+1

9. Cyclosporine (CsA) (off-label; classic for birdshot)
   Class: calcineurin inhibitor. Dose/time: often 2.5–5 mg/kg/day in divided doses with BP/renal monitoring. Purpose: potent steroid-sparing control; long track-record in birdshot. Mechanism: inhibits calcineurin → blocks IL-2/T-cell activation. Side effects: nephrotoxicity, hypertension, tremor. Evidence: low-dose CsA ± azathioprine effective in birdshot series. PubMed+1

10. Tacrolimus (off-label)
    Class: calcineurin inhibitor. Dose/time: individualized low oral doses; trough monitoring. Purpose: alternative to cyclosporine when side effects limit use. Mechanism: FKBP-12/calcineurin inhibition → T-cell blockade. Side effects: nephrotoxicity, diabetes risk, tremor. Evidence: used across non-infectious uveitis as a CsA alternative. NCBI

11. Infliximab (IV anti-TNF-α) (off-label)
    Class: monoclonal antibody to TNF-α. Dose/time: e.g., 5–10 mg/kg IV at weeks 0, 2, 6, then every 4–8 weeks. Purpose: rapid control of severe/refractory uveitis or CME. Mechanism: systemic TNF-α neutralization. Side effects: infusion reactions, infection risk, TB/hep B screening. Evidence: widely reported benefit in refractory non-infectious uveitis. NCBI

12. Tocilizumab (anti-IL-6R) (off-label)
    Class: biologic. Dose/time: IV or SC per rheumatology regimens. Purpose: recalcitrant uveitic CME or TNF-refractory disease. Mechanism: IL-6 pathway blockade. Side effects: infection risk, liver enzymes, lipids. Evidence: case series and trials in NIU with CME. NCBI

13. Sirolimus (intravitreal or systemic) (off-label for NIU control)
    Class: mTOR inhibitor. Dose/time: intravitreal dosing per protocol or low-dose oral under specialist care. Purpose: steroid-sparing option in refractory cases. Mechanism: inhibits T-cell proliferation via mTOR. Side effects: ocular inflammation (local), systemic lipids/oral ulcers (systemic). Evidence: studied in NIU cohorts. NCBI

14. Cyclophosphamide (off-label; selected refractory cases)
    Class: alkylator. Dose/time: oral or IV “pulses,” short-term due to toxicity. Purpose: rescue therapy when vision-threatened and other agents fail. Mechanism: suppresses proliferating lymphocytes. Side effects: cytopenias, gonadotoxicity, hemorrhagic cystitis; oncology-style monitoring. NCBI

15. Rituximab (anti-CD20) (off-label)
    Class: B-cell depleting monoclonal antibody. Dose/time: lymphoma-style or RA-style cycles with premedication. Purpose: B-cell-mediated or refractory uveitis. Mechanism: depletes CD20+ B-cells, dampening autoimmune loops. Side effects: infusion reactions, infection risk, rare PML. NCBI

16. Acetazolamide (off-label adjunct for cystoid macular edema)
    Class: carbonic anhydrase inhibitor. Dose/time: e.g., 250 mg 2–4×/day if tolerated; monitor electrolytes. Purpose: reduce CME in selected cases. Mechanism: improves fluid transport across RPE to dry the macula. Side effects: paresthesias, metabolic acidosis, kidney stones; avoid in sulfa allergy. NCBI

17. Suprachoroidal triamcinolone (XIPERE®)
    Class: corticosteroid delivered to suprachoroidal space. Dose/time: 4 mg (0.1 mL of 40 mg/mL) via microinjector for macular edema associated with uveitis. Purpose: targeted steroid for CME with lower anterior segment exposure. Mechanism: high posterior-segment levels, relatively sparing the anterior chamber. Side effects: IOP rise, cataract, injection risks. FDA review/approval docs available. FDA Access Data+2FDA Access Data+2

18. Periocular (sub-Tenon) triamcinolone (procedure; off-label)
    Class: corticosteroid depot. Dose/time: single injection with repeat PRN. Purpose: treat posterior inflammation/CME when systemic therapy is undesirable. Mechanism: depot steroid diffuses to macula/choroid. Side effects: IOP rise, ptosis, globe perforation (rare). NCBI

19. Topical corticosteroids & cycloplegics (adjunct)
    Class: anti-inflammatory and ciliary spasm relief. Use: limited for posterior disease but helpful for anterior spillover symptoms and peri-op control. Mechanism: surface anti-inflammatory; atropinic agents ease photophobia from ciliary spasm. Side effects: IOP rise, delay wound healing (steroids). NCBI

20. Combination immunomodulatory therapy
    Class: e.g., CsA + AZA or MTX + anti-TNF. Use/time: for incomplete control with monotherapy. Purpose: achieve steroid-free remission and protect visual fields. Mechanism: targets multiple immune pathways to prevent flares. Evidence: birdshot series and broader NIU cohorts support combination strategies when monotherapy fails. JAMA Network+1

Dietary molecular supplements

Evidence in birdshot specifically is limited. These do not replace anti-inflammatory drugs. They may support general ocular/immune health.

1. Omega-3 (EPA/DHA) — 1–2 g/day combined EPA+DHA. Supports retinal cell membranes and has systemic anti-inflammatory effects that may modestly reduce inflammatory mediators; can help dry eye symptoms that complicate care. Monitor for bleeding with anticoagulants. NCBI

2. Lutein & zeaxanthin — e.g., 10 mg + 2 mg/day. Macular carotenoids filter short-wavelength light and support antioxidant defenses; widely used for retinal health though not birdshot-specific. NCBI

3. Vitamin D — dose to maintain sufficiency per labs (often 800–2000 IU/day). Low vitamin D is common in chronic illness; adequate levels support immune regulation and bone health during steroids. Avoid excess. Review of Ophthalmology

4. Curcumin (with piperine or phytosomal forms) — ~500–1000 mg/day equivalents. Has anti-NF-κB activity; small ocular surface and systemic studies suggest anti-inflammatory potential; interactions/bleeding risk possible. NCBI

5. N-Acetylcysteine (NAC) — 600–1200 mg/day. Antioxidant/precursor to glutathione; studied as adjunct in oxidative retinal conditions; may help tolerate oxidative stress from chronic inflammation. NCBI

6. Alpha-lipoic acid — 300–600 mg/day. Antioxidant that recycles glutathione and vitamins C/E; caution with diabetes meds (hypoglycemia risk). NCBI

7. Coenzyme Q10 — 100–200 mg/day. Mitochondrial antioxidant; general retinal/optic nerve support proposed. Limited direct evidence in birdshot. NCBI

8. Quercetin — 500 mg/day. Flavonoid with anti-inflammatory signaling effects; theoretical ocular benefits; watch drug interactions. NCBI

9. Green-tea catechins (EGCG) — standardized extract supplying ~200–300 mg EGCG/day. Anti-oxidative/anti-inflammatory; avoid with liver disease and limit caffeine. NCBI

10. Resveratrol — 100–250 mg/day. Polyphenol with anti-inflammatory signaling effects; human ocular data limited; consider only as physician-approved adjunct. NCBI

Drugs for immunity boosting / regenerative / stem-cell” concepts

There are no proven “immunity boosters” for birdshot. Care relies on carefully reducing overactive immunity. Below are therapies sometimes discussed in regenerative or immune-modulating contexts—not replacements for standard care.

1. Intravitreal fluocinolone micro-dose (YUTIQ®) — 0.18 mg implant releases steroid for up to 36 months, providing long-term local immune dampening and reducing recurrences; helps macular structure recovery. Risks: cataract, IOP rise; needs monitoring. FDA Access Data+1

2. Dexamethasone implant (OZURDEX®) — biodegradable steroid gives months of local control; can allow the retina to repair edema-related damage. Monitor IOP/cataract. FDA Access Data

3. Suprachoroidal triamcinolone (XIPERE®) — targeted steroid delivery to the suprachoroidal space for uveitic CME; may lower anterior segment exposure versus intravitreal delivery. FDA Access Data

4. Adalimumab — systemic biologic that re-balances immune pathways (anti-TNF-α), often enabling steroid withdrawal and retinal recovery when inflammation quiets. FDA Access Data

5. Sirolimus (intravitreal investigational/selected use) — mTOR inhibition locally modulates T-cell–driven inflammation; used in refractory NIU under specialist protocols. NCBI

6. Future/experimental cellular therapies — At present, stem-cell therapies are not established for birdshot; participation should be limited to IRB-approved clinical trials. Standard immunomodulation remains the evidence-based path. NCBI

Surgeries (procedures & why they’re done)

1. Fluocinolone implant surgery (RETISERT®)
   A small device is sutured to the sclera in the OR to release steroid long term. Why: very durable control when disease is severe or injections fail. Notes: high cataract/IOP risks; plan for glaucoma care, and often cataract surgery later. FDA Access Data+1

2. Office-based steroid implants (OZURDEX®, YUTIQ®)
   Micro-injections place biodegradable or non-bioerodible implants into the vitreous. Why: treat posterior uveitis/CME without systemic immunosuppression. Notes: IOP/cataract monitoring essential. FDA Access Data+1

3. Cataract surgery (phacoemulsification with IOL)
   Chronic inflammation and steroids often cause cataract. Surgeons usually wait until uveitis has been quiet for ~3 months to lower complication risks and improve outcomes. Why: restore vision once inflammation is controlled. EyeWiki+1

4. Glaucoma surgery (trabeculectomy or tube shunt)
   Steroids and uveitis can raise IOP. If drops fail, filtering (trabeculectomy) or drainage devices can control pressure. Why: protect the optic nerve from high IOP. Notes: effectiveness similar on average, safety profiles differ; decision individualized. PubMed+1

5. Pars plana vitrectomy (PPV)
   Micro-incision vitrectomy removes inflammatory vitreous gel, may aid diagnosis, clear opacities, improve CME, and sometimes reduce systemic immunosuppression needs in selected NIU cases. Why: vision rehabilitation and inflammation control in complicated cases. PMC+1

Preventions

1. Keep all follow-ups and imaging; flare control prevents new lesions. NCBI

2. Report new floaters, glare spikes, or blurry central vision promptly. NCBI

3. Taper steroids only as your specialist directs; abrupt changes risk flares. Review of Ophthalmology

4. Vaccinate (non-live) before/during immunotherapy per clinician advice. NCBI

5. Control BP, glucose, and lipids to protect the macula and optic nerve. NCBI

6. Use sunglasses/hat outdoors for comfort and function. EyeWiki

7. Stop smoking; avoid secondhand smoke. NCBI

8. Keep a written medication/imaging plan for emergencies. NCBI

9. Address mental health; chronic disease care is a marathon. NCBI

10. Discuss pregnancy plans early; some drugs require months-ahead planning. clinexprheumatol.org

When to see doctors (now vs. routine)

See your uveitis/retina specialist urgently for new or rapidly worsening floaters, flashes, a “gray curtain” (possible detachment), sudden blur, severe eye pain/redness, or a big jump in glare or night-vision problems. Routine care means sticking to scheduled visits and labs while on immunomodulators; many therapies need regular blood tests (CBC, LFTs, renal function), IOP checks, and OCT to watch for macular edema. If you’re planning surgery (cataract or glaucoma), coordinate timing when inflammation is quiet for best vision results and fewer complications. NCBI+1

What to eat and what to avoid

1. Emphasize vegetables, fruits, legumes, whole grains, fish, and nuts—an anti-inflammatory pattern that supports overall health during long-term therapy. Avoid ultra-processed foods and excess sugar that worsen weight/glucose on steroids. Review of Ophthalmology

2. Adequate calcium + vitamin D for bone health if on steroids; use doses your doctor recommends. Avoid megadoses without labs. Review of Ophthalmology

3. Hydrate well, especially if taking acetazolamide; avoid high-salt diets that can worsen edema and BP. NCBI

4. Fish (omega-3s) 2–3×/week or physician-approved supplements; avoid if contraindicated. NCBI

5. Limit alcohol (interacts with MTX and raises liver risk). clinexprheumatol.org

6. Caution with grapefruit if you take cyclosporine or tacrolimus (raises drug levels). PMC

7. Consistent protein to maintain muscle while tapering steroids; avoid crash diets. Review of Ophthalmology

8. Coffee/tea okay in moderation; watch for insomnia/anxiety if on steroids. Review of Ophthalmology

9. Discuss herbs/supplements (curcumin, NAC, etc.) with your doctor for interactions (anticoagulants, immunosuppressants). NCBI

10. Food safety: immunosuppression raises infection risk—avoid undercooked meats/unpasteurized products. NCBI

FAQs

1) Are birdshot lesions permanent?
Active spots can quiet with treatment, but structural changes may persist. The goal is to prevent new lesions and protect function with long-term control. NCBI

2) Do I need treatment if my vision is still 20/20?
Yes—this is a chronic, progressive disease; early immunomodulation prevents irreversible damage even before vision drops. JAMA Network

3) What is first-line therapy?
Often systemic steroids to gain control, then a steroid-sparing agent (e.g., MMF, MTX, CsA) or an FDA-approved option like adalimumab or intravitreal steroid implants depending on disease pattern. FDA Access Data+2FDA Access Data+2

4) How long will I be on treatment?
Many patients need years of therapy; doses may be tapered once inflammation is quiet and imaging stable. Relapses require prompt escalation. JAMA Network

5) Is adalimumab really approved for this?
Yes—for non-infectious intermediate, posterior, and panuveitis in adults (uveitis label). Birdshot falls within this group. FDA Access Data

6) What about eye injections instead of pills?
OZURDEX® and YUTIQ® are FDA-labeled for posterior uveitis; they can control inflammation and CME locally, sometimes avoiding systemic side effects. FDA Access Data+1

7) Will I get cataracts or high eye pressure?
Steroids (systemic and intraocular) can cause cataract and glaucoma; your team monitors IOP and lens changes and treats proactively if needed. FDA Access Data

8) Can surgery fix birdshot?
Surgery treats complications (cataract, glaucoma, dense vitreous opacities) or delivers implants; it does not cure the immune disease. Medical control remains central. EyeWiki+1

9) Is this caused by infection?
No—birdshot is non-infectious and autoimmune-mediated; infectious causes must be excluded before immunosuppression. NCBI

10) Are there lifestyle cures?
No. Healthy habits support your overall health, but drug therapy is essential to quiet inflammation and prevent vision loss. NCBI

11) Could I go blind?
Untreated disease can cause major, permanent vision loss. With modern immunomodulation and implants, many patients maintain useful vision long term. JAMA Network

12) Are supplements helpful?
Supplements are optional adjuncts with limited direct evidence in birdshot; discuss risks and interactions first. They do not replace immunotherapy. NCBI

13) How often do I need imaging?
Your doctor tailors OCT/FAF/ICGA frequency to disease activity; more often during flares or tapers, less often in stable remission. NCBI

14) Can I get pregnant on these medicines?
Some agents are unsafe (e.g., MTX, MMF). Plan pregnancy with your team; safer alternatives and timing are available. clinexprheumatol.org

15) Is birdshot really “HLA-A29 uveitis”?
Yes—HLA-A29 is strongly associated, and many experts prefer this name because it reflects the disease mechanism and typical testing. Wikipedia

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: October 27, 2025.