Eales Disease is a rare eye condition that mainly affects the small veins in the outer (peripheral) part of the retina, the light-sensing layer at the back of the eye. It usually happens in young adults, more often in men, and frequently in areas where tuberculosis is common (like India and Southeast Asia). The disease causes inflammation of retinal veins (periphlebitis), loss of blood flow (ischemia), and then abnormal new blood vessel growth (neovascularization). These abnormal vessels are fragile and tend to bleed into the vitreous (the gel inside the eye), causing sudden, painless vision loss. Because no single test can prove Eales Disease, doctors make the diagnosis by recognizing its characteristic signs and ruling out other causes of similar retinal vasculitis. Nature MDPI MalaCards
Eales Disease is a rare eye condition that affects the small veins in the peripheral retina. It is a kind of retinal vasculitis, which means the blood vessels in the retina become inflamed, especially the veins, leading to blockages, low oxygen (ischemia), and then abnormal new blood vessel growth (neovascularization). These fragile new vessels often bleed into the vitreous, causing floaters or sudden vision loss. The disease most commonly appears in otherwise healthy young adults, especially males, and is seen more frequently in the Indian subcontinent. The inflammation, vessel closure, and subsequent complications occur in overlapping stages—not always in a fixed order—making early detection and tailored therapy important. Evidence connects the disease to an immune reaction possibly triggered by Mycobacterium tuberculosis proteins, though the exact cause remains idiopathic in many cases. Definitions, mechanisms, and standard staging are reviewed in modern clinical summaries like StatPearls and ophthalmology literature. NCBI EyeWiki SpringerOpen
Pathophysiology and Etiology
Eales Disease begins with inflammation of retinal veins (periphlebitis). The inflamed vessel walls can become narrowed or blocked, resulting in areas of retinal ischemia. Ischemia drives the retina to produce growth signals (like VEGF), causing new but abnormal blood vessels to sprout. These vessels are fragile and prone to bleeding, leading to recurrent vitreous hemorrhage. A significant hypothesized trigger is hypersensitivity to tuberculoproteins—pieces of tuberculosis bacteria—which primes the immune system to attack retinal vessels, either from latent or past exposure, even without active systemic tuberculosis. Oxidative stress and lowered antioxidant levels (especially vitamins C and E) have been observed in patients, suggesting that free radical accumulation may worsen inflammation and vessel damage. PMCMDPIAuctores PubMed
Types / Classification (Stages)
Eales Disease is described in overlapping stages rather than sharply separated types, and multiple classification schemes exist. The most widely used modern description breaks the disease into three overlapping phases:
Inflammatory (periphlebitis) stage – inflammation of peripheral retinal veins, seen as white sheathing or exudates along the veins and superficial retinal hemorrhages. Nature
Ischemic (occlusive) stage – inflammation leads to blockage of retinal blood flow, causing capillary non-perfusion and retinal ischemia. This drives tissue distress because parts of the retina are not getting enough oxygen. MDPINature
Proliferative stage – ischemia stimulates production of growth factors (like VEGF), causing new fragile blood vessels to form (neovascularization), which easily bleed, producing recurrent vitreous hemorrhages and possible tractional retinal detachment. MDPINature
An earlier detailed evolutionary classification by Charmis and others subdivides the inflammatory stage into small and large vessel involvement and further refines progression, but contemporary practice usually refers to the three overlapping pathological phases above for diagnosis and management. Nature
Proposed or Associated Causes / Contributing Factors
Important framing: The exact single cause of Eales Disease is unknown; current evidence supports a multifactorial process where immune reactions, infections (especially tuberculosis), genetic susceptibility, and biochemical derangements intersect. The list below enumerates 20 factors that have been proposed, observed, or associated with its development or pathogenesis in the literature.
Hypersensitivity to tuberculoproteins (latent Mycobacterium tuberculosis exposure): Many patients with Eales Disease have evidence of prior exposure to tuberculosis; the immune system reacts to mycobacterial proteins leading to retinal vein inflammation. This immune hypersensitivity is considered a major driver. MDPIPMC
Presence of Mycobacterium tuberculosis DNA in ocular tissue: Polymerase chain reaction studies have detected M. tuberculosis DNA in epiretinal membranes of patients, suggesting that even if active infection is absent, residual antigenic material can stimulate inflammation. MDPI
Involvement of non-tuberculous mycobacteria (e.g., M. fortuitum): Some studies have found associations or suggested possible roles of other mycobacterial species, adding complexity to the infectious/antigenic triggers. MDPI
Autoimmune cross-reaction to retinal antigens: Retinal proteins such as retinal S-antigen and interphotoreceptor retinoid-binding protein-3 have been implicated in the disease, suggesting that abnormal immune recognition of self-retinal components contributes to inflammation. PMC
Genetic predisposition affecting immune regulation: Certain human leukocyte antigen (HLA) types and inherited immune response patterns are thought to make some individuals more susceptible to the inflammatory cascade seen in Eales Disease. Nature
Immune complex formation and deposition in retinal vessels: Deposition of circulating immune complexes in vessel walls can incite vasculitis and is part of proposed immune mechanisms. Nature
Elevated pro-inflammatory cytokines (e.g., IL-1β, TNF-α): Active disease shows increased levels of inflammatory mediators, perpetuating vessel wall inflammation and driving downstream ischemia and neovascularization. PMC
Oxidative stress and reduced antioxidant capacity: Patients with Eales Disease have been shown to have oxidative damage markers and decreased systemic antioxidant defenses, which injure vascular endothelium and amplify inflammation. PMC
Hyperhomocysteinemia: Elevated homocysteine levels can cause endothelial injury and oxidative stress, further weakening vascular integrity and contributing to the inflammatory milieu; supplementation with folate and B12 has been suggested when present. PMC
Imbalance of angiogenic regulators (VEGF/PEDF ratio): Ischemia and chronic inflammation disrupt the delicate balance between pro-angiogenic and anti-angiogenic factors, promoting pathological neovascularization. PMC
Endothelial dysfunction from lingering inflammation: Chronic low-grade vascular inflammation damages endothelial cells, reducing their ability to regulate blood flow and barrier function, which facilitates occlusion and abnormal vessel behavior. MDPIPMC
Coagulation abnormalities or prothrombotic tendencies: Individual or family predisposition to clotting may exacerbate venous occlusion in retinal microcirculation, compounding ischemia; case reports note coagulation history as a possible amplifier. MDPI
Substance abuse (e.g., cocaine): Vasoactive substances like cocaine can injure retinal vessels or provoke vasospasm and inflammation, and isolated cases have described Eales-like presentation in users without clear infectious triggers. MDPI
Demographic susceptibility – young adult age: Eales Disease predominantly affects healthy young adults, suggesting that age-related immune or vascular dynamics contribute to its expression. MDPI
Male sex predominance: Males are more commonly affected, which may reflect hormonal modulation of immune response or genetic factors influencing susceptibility. MDPI
Geographical and environmental background (endemic tuberculosis regions): Higher prevalence in India, Southeast Asia, and some other regions correlates with latent tuberculosis burden and possibly local environmental or infectious co-factors. MDPI
Chronic systemic inflammatory states: Other subclinical inflammatory conditions could prime or amplify retinal immune responses, making the retina more vulnerable to vasculitic cascades. MDPI
Molecular mimicry from unidentified microbial antigens: It is hypothesized that pathogens sharing structural similarity with retinal proteins could trigger cross-reactive immune responses, although direct pathogens beyond mycobacteria are not firmly established. PMC (inference based on immune cross-reactivity discussions)
Altered protein expression or structural retinal protein changes: Changes in three-dimensional structure of key proteins (mentioned as functionally relevant in pathogenesis studies) may modify local immune recognition or vascular responses. PMC
Combined multifactorial interaction (“idiopathic” component): In many patients, no single trigger is isolated; instead, a combination of mild immune dysregulation, latent infection, biochemical imbalance, and local retinal vulnerability creates the disease picture labeled idiopathic. MDPIPMC
Common Symptoms
Eales Disease can present with a variety of symptoms depending on the stage and complications. Many early cases may have no symptoms until a bleeding event. The 15 symptoms below are those that patients most often experience or that result from its known pathological processes:
Sudden, painless loss of vision: This is most often due to vitreous hemorrhage when fragile new vessels bleed into the vitreous cavity. PMC
Floaters: Patients see small moving spots or cobwebs, representing blood cells or debris floating in the vitreous from prior or active bleeding. MDPIPMC
Blurry or blurred vision: General decrease in visual clarity from hemorrhage, macular edema, or traction on the retina. MDPI
Visual field defects (especially peripheral): Areas of the retina deprived of blood or affected by neovascular complications can produce scotomas (blind spots) or loss of side vision. MDPI
Photopsia (flashes of light): Traction on the retina or irritation from vascular changes can produce perceptions of flashes. Nature
Distorted vision (metamorphopsia): Epiretinal membranes or macular involvement in advanced disease can warp the image perceived. Nature
Repeated episodes of vision change (waxing and waning): Multiple bleeding events lead to fluctuating levels of vision, with some spontaneous improvements followed by sudden deterioration. PMC
Asymptomatic early disease: In the inflammatory stage, patients may have no noticeable complaints until ischemia or bleeding occurs. MDPI
Dark or red shadows in vision: Persistent or settling hemorrhage can be interpreted as shadowing from the patient’s perspective. PMC
Decreased contrast sensitivity: Subtle retinal ischemia or mild edema may reduce the ability to distinguish fine differences in shading or color. (Clinical implication from retinal vascular dysfunction; inference based on known ischemic retinal effects.) MDPI
Double vision (rare, if tractional detachment distorts alignment): Significant structural distortion can alter visual input, sometimes interpreted as diplopia. (Less common; implied in advanced structural complications.) Nature
Symptoms from secondary glaucoma (pain/eye redness): If neovascularization extends to the angle causing neovascular glaucoma, patients may experience discomfort or elevated pressure signs. Nature
Difficulty seeing in low light (relative): Peripheral ischemia may degrade scotopic (night) vision subtly. (Expected from peripheral retinal ischemia; supported by general retinal ischemia physiology.) MDPI
Persistent blurry patches despite cleared hemorrhage: Residual damage, epiretinal membrane formation, or chronic ischemia can cause lasting visual degradation. Nature
Variable vision between the two eyes: The disease often affects both eyes but asymmetrically, causing different severity of symptoms in each eye. MDPI
Diagnostic Tests
Because Eales Disease is a diagnosis of exclusion, a combination of clinical observation and auxiliary tests are used—both to detect its characteristic retinal changes and to rule out other diseases. Below are 20 tests, grouped into the categories requested, with explanations.
A. Physical Examination / Clinical Evaluation
Visual acuity testing: Measures how well the patient sees at distance and helps quantify vision loss from hemorrhage, macular involvement, or other complications. PMC
Pupillary reflexes (including relative afferent pupillary defect assessment): Helps assess asymmetric optic pathway or severe retinal dysfunction; a RAPD can signal significant unilateral or asymmetric disease. MDPI
Intraocular pressure measurement: Screening for secondary complications like neovascular glaucoma which can elevate pressure and worsen prognosis if untreated. Nature
Slit-lamp examination: Evaluates anterior segment for signs of inflammation (cells/flare) that may coexist and helps differentiate from other uveitic causes. PMC
Dilated fundus examination: Direct visualization of the retina using wide pupil dilation to identify retinal periphlebitis, hemorrhages, neovascularization, and vitreous hemorrhage—central to the clinical diagnosis. NatureMDPI
B. Manual / Bedside Functional Tests
Confrontation visual field testing: A simple in-office test to detect peripheral field defects due to localized ischemia or structural distortion. MDPI
Amsler grid (central vision grid): Detects distortion or scotomas when macular or epiretinal involvement affects central vision, guiding further imaging. Nature
Color vision testing: Can reveal subtle macular dysfunction or neural pathway involvement when neovascular or ischemic changes approach the posterior pole. Nature
C. Laboratory and Pathological Tests
Mantoux skin test (tuberculin sensitivity test): Detects prior exposure to tuberculosis and supports the hypothesis of tubercular hypersensitivity, a common association. MDPI
Interferon-gamma release assays (e.g., QuantiFERON-TB Gold): More specific blood test to detect latent tuberculosis infection without cross-reactivity from BCG vaccination, used in the workup for potential tubercular linkage. ASM Journals
Chest imaging (chest X-ray or high-resolution CT): To look for active or healed pulmonary tuberculosis, which may coexist or support a presumptive tubercular etiology. MDPIPMC
PCR from ocular fluid (aqueous or vitreous) for Mycobacterium tuberculosis DNA: Detects mycobacterial DNA fragments, bolstering the link to tubercular antigenic stimulus even when cultures are negative. MDPI
Complete blood count (CBC): Rules out hematologic causes of retinal hemorrhage (like leukemia) that can mimic retinal vascular changes. MDPI
Erythrocyte sedimentation rate (ESR) / C-reactive protein (CRP): Non-specific inflammation markers that help evaluate systemic inflammation and aid differential diagnosis. MDPI
Blood sugar (glucose / HbA1c): To exclude diabetic retinopathy as a mimic or co-contributor when vascular retinal changes are present. MDPI
Hemoglobin electrophoresis: Rules out sickle cell retinopathy, which can present with peripheral ischemia and neovascularization similar to Eales Disease. MDPI
Syphilis serology (RPR/TPHA) and HIV testing: To exclude infectious etiologies that can manifest with retinal vasculitis and hemorrhages in the differential. jophthalmicrespract.org
D. Electrodiagnostic Tests
Electroretinography (ERG): Measures electrical responses of the retina; while not diagnostic for Eales Disease specifically, it helps assess generalized retinal function and rule out other diffuse retinal disorders. (Used to characterize functional impairment when structural findings are ambiguous.) Nature (inference from general retinal assessment principles)
Visual evoked potentials (VEP): Tests the integrity of the visual pathway from eye to visual cortex; used if there is concern for overlapping optic nerve involvement or to exclude other neurologically mediated vision loss. Nature
E. Imaging Tests
Fundus fluorescein angiography (FFA): Dye study that shows vessel wall inflammation, areas of non-perfusion (ischemia), leakage from neovascularization, and helps stage disease and plan laser therapy. MDPINature
Optical coherence tomography (OCT): Non-invasive cross-sectional imaging of the retina to evaluate macular edema, epiretinal membranes, or traction that may accompany or complicate Eales Disease. MDPI
B-scan ultrasonography: Useful when vitreous hemorrhage obscures the view; can detect retinal detachment or other posterior segment changes behind opaque media. MDPI
Wide-field fundus photography / ultra-widefield imaging: Captures the peripheral retina where Eales Disease predominantly manifests, enabling documentation and follow-up. Nature
Optical coherence tomography angiography (OCT-A): Non-invasive vascular imaging that can map neovascular networks and capillary non-perfusion without dye, helpful in subtle proliferative or ischemic changes. Nature
Non-Pharmacological Treatments
Observation with regular monitoring: In early or quiescent stages without active bleeding or significant ischemia, careful observation with frequent retinal exams helps track progression and avoid unnecessary interventions. The purpose is timely detection of worsening. MDPI
Laser photocoagulation (panretinal or sectoral): This uses focused laser burns to the ischemic peripheral retina to reduce VEGF drive and regress abnormal new vessels. The mechanism is destruction of hypoxic retina so it stops signaling for neovascularization, thereby preventing recurrent hemorrhage. PMCLippincott Journals
Anti-VEGF adjunctive procedural use (non-pharmacological context as injection-assisted regression): While anti-VEGF is a drug, its administration is a procedure that helps rapidly regress neovascular tissue before surgical or laser therapy, reducing intraoperative bleeding risk. PMCLippincott Journals
Control of systemic latent tuberculosis (screening and treatment as public health measure): Early identification of latent TB exposure (e.g., Mantoux/IGRA) and appropriate management reduces antigenic stimulus for hypersensitivity that may exacerbate retinal vasculitis. While drug-based, the strategic screening and public health surveillance is a non-pharmacological preventive framework. PMCSpringerOpen
Smoking cessation and avoidance of tobacco smoke: Smoking increases oxidative stress and vascular dysfunction; stopping smoking lowers inflammatory burden and supports retinal microcirculation health. Verywell Health
Optimizing general systemic health (nutrition, avoiding obesity, controlling blood pressure and glucose): Good metabolic control reduces systemic inflammatory tone and helps retinal vascular resilience. Though not disease-specific, overall health optimization supports better outcomes. Lippincott Journals
Antioxidant-rich diet and lifestyle (emphasis on natural sources): Using foods high in vitamins C, E, lutein, zeaxanthin, and zinc supports cellular defense against free radicals implicated in retinal inflammation. The mechanism is neutralizing oxidative damage that contributes to vessel injury. PubMedMDPI
Low vision rehabilitation and aids: For patients with permanent visual deficits from past hemorrhage or scarring, training in adaptive strategies, magnifiers, and visual rehabilitation helps maintain function and quality of life. Purpose is maximizing residual vision. Number Analytics
Avoidance of ocular trauma and exertion during active bleeding: Physical strain or trauma may precipitate or worsen vitreous hemorrhage; rest and protection during acute episodes limit further bleeding. ResearchGate
Stress reduction and sleep hygiene: Chronic stress can exacerbate systemic inflammation; improving sleep and stress management may lower inflammatory mediators indirectly affecting retinal vasculitis. Lippincott Journals
Photoprotection (UV-blocking sunglasses): Limiting UV-induced oxidative stress on ocular tissues reduces chronic micro-damage and supports retinal health. Verywell Health
Weight management through exercise: Moderate exercise improves vascular health globally and modulates inflammatory cytokines, supporting retinal microcirculation. Lippincott Journals
Hydration and avoidance of dehydration: Good blood viscosity and flow depend partly on hydration; avoiding thickened blood may help microvascular perfusion in marginal retinal areas. (Inference based on microvascular physiology.) Lippincott Journals
Education on symptom recognition: Teaching patients to recognize floaters, flashes, and sudden vision changes leads to earlier presentation and treatment, reducing vision loss risk. MDPI
Controlled gradual steroid tapering when used (procedural strategy): Even though steroids are drugs, the non-pharmacological approach of careful tapering avoids rebound inflammation and reduces side effects. ResearchGate
Use of periocular steroid injection technique optimization: Choosing appropriate delivery (e.g., posterior subtenon vs intravitreal) based on disease location and severity is a procedural non-drug tailoring to maximize anti-inflammatory effect while minimizing systemic exposure. MDPI
Regular follow-up scheduling (structured surveillance): Setting a follow-up interval (e.g., every 3–6 months when stable, more often if active) is a management strategy to catch progression early. ROQUE Eye Clinic | Eye.com.ph
Eye hygiene and avoiding infections: Preventing secondary anterior segment infections reduces overall intraocular inflammation that could aggravate the retinal condition. General ophthalmic care principles apply. Lippincott Journals
Use of systemic immunomodulatory planning (multidisciplinary decision-making): In refractory cases, counseling and planning with rheumatology/immune specialists to weigh when to escalate beyond steroids is a strategy for durable control. SAGE Journals
Adjunctive laser barrier techniques in complex detachments (surgical planning): Strategic placement of barrier laser to “wall off” areas of ischemia before hemorrhage or detachment worsens is a procedural decision that protects central vision. BioMed Central
Drug Treatments
Oral Corticosteroids (e.g., Prednisone): Class: systemic anti-inflammatory. Typical starting dose for active periphlebitis is around 1 mg/kg/day (up to ~60–80 mg) with gradual taper over weeks depending on response. Purpose is to suppress vessel inflammation and reduce macular edema. Mechanism: inhibits inflammatory cytokines, stabilizes vascular permeability. Side effects include weight gain, hypertension, blood sugar elevation, osteoporosis, mood changes, and increased infection risk. Tapering carefully is critical to avoid relapse. PentaVisionMDPIResearchGate
Periocular or Intravitreal Corticosteroid (e.g., Triamcinolone acetonide): Class: local steroid. Dosage: intravitreal injections often use 4 mg/0.1 mL; subtenon doses vary by preparation. Purpose: treat localized inflammation or macular edema with less systemic exposure. Mechanism: local suppression of inflammation, reduction of vascular leakage. Side effects include elevated intraocular pressure and cataract formation. MDPIResearchGate
Anti-tubercular Therapy (ATT) — Combination of Isoniazid, Rifampicin, Ethambutol, Pyrazinamide (with or without Streptomycin): Class: antibacterial/anti-mycobacterial. Standard regimen for presumed tubercular association is usually 6–9 months (often extrapolated from ocular TB protocols), with initial intensive phase of 2 months (HRZE) followed by continuation (HR) for 4–7 months depending on local guidelines. Purpose: eliminate latent or active mycobacterial antigenic stimulus, reducing hypersensitivity and progression. Mechanism: bactericidal activity against Mycobacterium tuberculosis. Side effects include hepatotoxicity, optic neuritis (ethambutol), neuropathy (isoniazid), and drug interactions. Close monitoring is needed. SpringerOpenIJMRR
Intravitreal Anti-VEGF Agents (e.g., Bevacizumab, Ranibizumab, Aflibercept): Class: biologic vascular endothelial growth factor inhibitors. Dosage: typically injected intravitreally every 4–6 weeks depending on response (off-label in many retinal vasculitis contexts). Purpose: regress neovascularization and reduce leakage, stabilizing or clearing vitreous hemorrhage tendency. Mechanism: neutralizes VEGF, stopping abnormal new vessel growth. Side effects: rare endophthalmitis, increased intraocular pressure, and transient inflammation. PMCLippincott JournalsResearchGate
Systemic Immunosuppressants (e.g., Azathioprine): Class: antimetabolite. Dosage: often 1–2 mg/kg/day orally, adjusted based on tolerance. Purpose: steroid-sparing control of chronic inflammation when prolonged steroids cause unacceptable side effects. Mechanism: inhibits purine synthesis lowering immune cell proliferation. Side effects include bone marrow suppression, liver enzyme elevation, and increased infection risk. SAGE Journals
Methotrexate: Class: folate antagonist immunosuppressant. Low-dose weekly oral or injectable regimen (e.g., 7.5–25 mg weekly) used to control chronic ocular inflammation. Purpose: alternative or adjunct to steroids in resistant vasculitis. Mechanism: inhibits dihydrofolate reductase affecting rapidly dividing immune cells. Side effects include liver toxicity, mucositis, and bone marrow suppression; folinic acid rescue is often used. SAGE Journals
Mycophenolate mofetil: Class: purine synthesis inhibitor. Dosage: 1–1.5 g twice daily orally for ocular inflammatory diseases. Purpose: steroid-sparing agent for long-term control. Mechanism: inhibits lymphocyte proliferation. Side effects include gastrointestinal upset and risk of infection. SAGE Journals
Oral Nonsteroidal Anti-inflammatory Drugs (NSAIDs) (adjunct, e.g., Indomethacin): Class: COX inhibitors. Generally used with caution; these do not treat the core vasculitis but may provide mild adjunctive relief of discomfort. Mechanism: reduction of prostaglandin-mediated inflammation. Side effects: GI irritation, kidney strain. Note: they are not primary therapy but sometimes used symptomatically. (Inference from general ocular inflammatory management practices.) Lippincott Journals
Systemic Anti-VEGF (experimental/adjunct in severe proliferative disease): Though less commonly used than intravitreal, systemic modulation of VEGF pathways (investigational) may be considered in refractory neovascularization; this remains largely off-label and under study. Side effects relate to systemic VEGF inhibition (hypertension, proteinuria). (Caution—experimental.) PMC
Topical IOP-lowering agents (e.g., Beta-blockers or Prostaglandin analogues): Class: ocular hypotensives. Purpose: manage steroid-induced intraocular pressure rise when intraocular steroids are used. Mechanism: reduce aqueous production or increase outflow. Side effects: local irritation, systemic effects depending on agent. (Supportive care for complications.) MDPI
Dietary Molecular Supplements
Vitamin C (Ascorbic Acid): Typical oral dose for ocular support ranges 500–1,000 mg daily. Function: antioxidant that scavenges free radicals. Mechanism: neutralizes reactive oxygen species that contribute to vascular and retinal inflammation. Side effects mild (GI upset at high doses). Evidence in retinal diseases suggests benefit in oxidative stress reduction. PubMedMDPI
Vitamin E (Alpha-tocopherol): Common dose 200–400 IU daily as part of antioxidant support. Function: lipid-soluble antioxidant protecting cell membranes. Mechanism: prevents lipid peroxidation in retinal cell membranes, reducing inflammatory signaling. High doses should be used cautiously (bleeding risk). PubMedMDPI
Lutein and Zeaxanthin: Dose often 10 mg lutein + 2 mg zeaxanthin daily (AREDS2-style levels). Function: macular pigment enhancement reducing blue light damage. Mechanism: filters light and provides antioxidant defense in the retina. Helpful in supporting retinal health under ischemic/inflammatory stress. MDPI
Zinc (Elemental): Supplemental dose 25–80 mg daily (with copper to avoid imbalance). Function: cofactor in antioxidant enzymes and retinal metabolism. Mechanism: stabilizes cell membranes and supports immune modulation, aiding in reducing oxidative damage. MDPI
Omega-3 Fatty Acids (DHA/EPA): Typical dose 1,000–2,000 mg combined EPA/DHA daily. Function: anti-inflammatory and membrane stabilizer. Mechanism: modulates inflammatory eicosanoid pathways, reducing chronic inflammation in microvasculature; supports retinal neuronal health. Verywell Health
Coenzyme Q10: Doses around 100–200 mg daily. Function: mitochondrial support and antioxidant. Mechanism: improves cellular energy and reduces oxidative damage within retinal cells. Evidence in retinal degenerative conditions shows potential neuroprotective effect. MDPI
Curcumin (Turmeric extract with enhanced bioavailability): Dose varies (e.g., 500–1,000 mg of bioavailable formulation daily). Function: anti-inflammatory and antioxidant. Mechanism: inhibits NF-kB and pro-inflammatory cytokines, reducing retinal inflammation. Use with black pepper extract (piperine) or formulated versions to increase absorption. Verywell Health
Resveratrol: Commonly 150–500 mg daily. Function: anti-inflammatory, antioxidant, and vascular protective. Mechanism: activates sirtuins, improves endothelial function, and reduces oxidative stress in retinal microvasculature. Lippincott Journals
N-Acetylcysteine (NAC): Dose about 600–1,200 mg twice daily. Function: precursor to glutathione, the body’s master antioxidant. Mechanism: replenishes glutathione and scavenges free radicals, potentially lowering oxidative-driven inflammation. Lippincott Journals (Inference from oxidative stress pathways in retinal disease.)
Bilberry Extract (Anthocyanins): Typical standardized extract doses 80–160 mg twice daily. Function: microvascular support and antioxidant. Mechanism: may improve capillary integrity and reduce oxidative damage through flavonoid activity. Evidence is mixed but often used adjunctively. Verywell Health
Regenerative / Stem Cell / “Hard Immunity” Experimental Therapies
Autologous CD34+ Stem Cell Intravitreal Injection: Derived from the patient’s own bone marrow, CD34+ cells have been tested in early-phase retinal degeneration trials, showing safety and some functional preservation. The proposed mechanism includes homing to damaged retinal areas, releasing trophic factors, and modulating inflammation. Doses vary by protocol; examples include single injections of autologous CD34+ cells in small-volume intraocular delivery. This is experimental and not standard for Eales but represents regenerative potential for damaged retinal vasculature. UC Davis Health
Mesenchymal Stem Cells (MSCs) Therapy: MSCs from bone marrow or umbilical sources can be delivered intravitreally or periocularly in trials for retinal disorders. They secrete anti-inflammatory cytokines, neurotrophic factors, and can modulate immune overactivity, potentially stabilizing retinal vasculitis and promoting repair. Dosages depend on preparation but early-phase studies use tens of millions of cells in a single administration. This remains investigational. PMCBioMed Central
Induced Pluripotent Stem Cell (iPSC)-Derived Retinal Progenitor Cells: These cells are engineered to become retinal lineage cells and hold promise for replacing damaged retinal tissues. Mechanism includes cell replacement and neuroprotection. Human trials are early-stage; use in inflammatory vascular diseases like Eales is theoretical and not yet established. PMC
Retinal Pigment Epithelium (RPE) Cell Transplantation (Stem Cell-Derived): Although more established in degenerative diseases (AMD), the trophic environment created by healthy RPE may indirectly benefit ischemic/inflammatory retina through support of outer retinal layers. Delivery is surgical/subretinal. Its application in Eales is speculative and experimental. PentaVision
Cell-Based Immunomodulatory Therapy (e.g., Regulatory T cell enhancement via cell therapy principles): Still preclinical, approaches aiming to induce immune tolerance (reducing hypersensitivity to tuberculoproteins) are being explored. Mechanism: balancing pro- and anti-inflammatory immune responses to prevent recurrent vascular inflammation. (Inference from broader immunoregulatory cell therapy research.) SAGE Journals
Neuroprotective Growth Factor Delivery via Cellular Vehicles: Using genetically modified cells or cell-derived exosomes to deliver VEGF inhibitors or anti-inflammatory growth factors locally to the retina is under study. Purpose: protect retina from ischemic injury while dampening pathologic vessel growth and inflammation. These are not yet standardized and remain in research phases. BioMed Central
Note: All regenerative/stem cell approaches for Eales Disease are experimental. Patients should only consider them in clinical trial settings with informed consent, and standard of care remains medical and surgical therapy. PMCBioMed Central
Surgical Procedures
Laser Photocoagulation (Panretinal or Sectoral): A non-incisional procedure where laser burns are applied to ischemic peripheral retina. It is done to reduce the stimulus for abnormal vessel growth by destroying hypoxic retina, thereby decreasing recurrent vitreous hemorrhage or neovascular complications. PMCLippincott Journals
Pars Plana Vitrectomy for Non-Clearing Vitreous Hemorrhage: This is a microsurgical removal of the cloudy vitreous containing blood when spontaneous clearing fails and vision remains significantly compromised. The purpose is to restore clarity and allow other treatments (e.g., laser) to be applied directly. retina-specialist.com
Vitrectomy with Membrane Peeling for Tractional Retinal Detachment: In advanced proliferative stages where scar tissue pulls the retina (traction), surgical removal of membranes and release of traction is required. Tamponade gases or silicone may be used to reattach the retina. This is performed to prevent permanent vision loss from detachment. Nature
Combined Surgery (Vitrectomy plus Endolaser and Anti-VEGF Injection): For complex cases with active neovascularization and hemorrhage, combining vitrectomy with intraoperative laser and sometimes anti-VEGF reduces rebleeding risk and stabilizes the eye long-term. ResearchGate
Scleral Buckling (adjunct for Rhegmatogenous Components): When Eales Disease leads to tears or breaks causing rhegmatogenous detachment (often in combination with traction), a scleral buckle may be placed externally to support the retinal reattachment. This is less common but used in mixed mechanism detachments. Nature
Preventions
Early screening for tuberculosis exposure and timely management reduces the antigenic stimulus that may drive hypersensitivity-related vasculitis. SpringerOpenIJMRR
Regular eye check-ups in at-risk populations (young adults in endemic areas or with prior ocular inflammation) allow early detection before complications. MDPI
Smoking cessation removes a modifiable source of oxidative and vascular stress. Verywell Health
Maintaining good general health (control of blood sugar and hypertension) minimizes systemic contributors to vascular stress and inflammation. Lippincott Journals
Nutrient-rich diet emphasizing antioxidants supports the body’s defenses against oxidative damage linked to vessel inflammation. MDPI
Avoiding self-medication with systemic steroids without supervision, which can mask disease activity and lead to rebound inflammation. Appropriate tapering and physician guidance prevent complications. ResearchGate
Prompt treatment of minor ocular complaints (floaters, blurring) to rule out early vasculitis and intervene before proliferation. MDPI
Education about signs of progression so patients don’t delay seeking care—knowing symptoms leads to earlier management. MDPI
Avoiding unnecessary ocular trauma and high-risk behaviors during active disease reduces secondary hemorrhage risk. ResearchGate
Structured follow-up regimen to ensure stable disease remains controlled and flare-ups are caught early. ROQUE Eye Clinic | Eye.com.ph
When to See a Doctor
You should see an ophthalmologist right away if you experience any sudden or new symptoms such as floaters (spots drifting in vision), flashes of light, sudden blurring of vision, dark shadows or curtain over vision (suggesting retinal detachment), recurrent bleeding in the eye, increasing redness or pain, or any unexplained changes in vision. Even mild persistent symptoms like slight blurring, peripheral vision defects, or recurrent dark spots warrant evaluation because early-stage inflammation or ischemia can be silent until complications arise. Timely care reduces risk of permanent vision loss. MDPI
What to Eat and What to Avoid
What to Eat:
Eat foods that nourish the retina and reduce inflammation. Include dark leafy greens (spinach, kale) for lutein/zeaxanthin; colorful fruits (berries, citrus) for vitamin C; nuts and seeds for vitamin E; fatty fish (salmon, sardines) for omega-3s; whole grains and legumes for steady glucose control; foods with zinc (shellfish, pumpkin seeds); turmeric-containing foods (with black pepper) for anti-inflammatory benefit; and foods rich in resveratrol like grapes or moderate dark chocolate. A Mediterranean-style diet supports both ocular and systemic vascular health. Verywell HealthMDPI
What to Avoid:
Avoid smoking and excessive alcohol, which increase oxidative stress and vascular damage. Limit high-sugar or highly processed foods that drive systemic inflammation. Avoid excessive saturated and trans fats, which impair microcirculation. Do not self-medicate with high-dose vitamin A or unregulated supplements without professional advice, as overdosing fat-soluble vitamins can cause harm. Avoid skipping monitoring when using steroids to prevent hidden side effects like elevated intraocular pressure or blood sugar spikes. Verywell HealthLippincott Journals
Frequently Asked Questions (FAQs)
What causes Eales Disease?
Eales Disease is believed to be due to an immune reaction, possibly against proteins from Mycobacterium tuberculosis, leading to inflammation of retinal veins. Exact causes remain unclear, and sometimes no definite trigger is found. SpringerOpenPMCIs Eales Disease contagious?
No, Eales Disease itself is not contagious. If associated with latent tuberculosis, the underlying TB exposure could be transmissible in active pulmonary disease, but the retinal vasculitis is immune-mediated. SpringerOpenIJMRRCan Eales Disease lead to blindness?
Yes, if untreated or if complications like tractional retinal detachment or recurrent massive vitreous hemorrhage occur, permanent vision loss can result. Early diagnosis and treatment preserve vision in most cases. retina-specialist.comNatureDoes everyone with Eales need anti-tubercular therapy?
Not always. If there is strong evidence of tuberculosis exposure or hypersensitivity (positive Mantoux/IGRA) or clinical suspicion, anti-tubercular therapy is often given, especially in proliferative stages. Decisions are individualized. SpringerOpenIJMRRWhy are steroids used, and are they safe?
Steroids reduce inflammation and prevent progression in active vascular inflammation stages. They are effective but have side effects, so dosing is carefully managed and tapered. Local injections limit systemic effects. MDPIResearchGateWhat is the role of laser treatment?
Laser photocoagulation reduces abnormal vessel growth by destroying ischemic retinal areas, decreasing the likelihood of bleeding and progression to proliferative disease. PMCLippincott JournalsCan the disease come back after treatment?
Yes, recurrence is possible, especially if underlying triggers persist or if regular follow-up is not kept. Continuous monitoring and sometimes maintenance therapy are needed. MDPIAre there lifestyle changes that help?
Yes. Improving general health—quitting smoking, eating antioxidant-rich foods, managing stress, and controlling systemic illnesses—supports retinal health and may reduce flare severity. Verywell HealthLippincott JournalsAre dietary supplements helpful?
Supplements like vitamins C and E, lutein/zeaxanthin, omega-3s, zinc, and CoQ10 can support the retina by fighting oxidative stress. They are adjuncts, not replacements for core treatment. MDPIVerywell HealthWhen is surgery needed?
Surgery is needed when there is non-clearing vitreous hemorrhage, tractional retinal detachment, or when laser and medical therapy fail to control proliferative complications. retina-specialist.comNatureIs stem cell therapy a cure?
Not yet. Stem cell and regenerative therapies are experimental for Eales Disease. They are being researched for retinal repair but are not established standard care; participation should be in the context of clinical trials. PMCBioMed CentralHow often should I follow up?
Follow-up depends on disease activity: active disease may require visits every few weeks, whereas stable quiescent disease might be monitored every 3–6 months. Your ophthalmologist will tailor frequency. ROQUE Eye Clinic | Eye.com.phCan both eyes be affected?
Yes. Although one eye may show earlier or more severe signs, the other eye can also develop inflammation or neovascularization, so both should be regularly examined. ResearchGateIs there a genetic risk?
There is no clear hereditary pattern; most cases appear sporadic. Geographic clustering (e.g., higher in South Asia) suggests environmental or infectious association more than direct genetic inheritance. AuctoresWhat is the long-term outlook?
With timely and appropriate therapy, most patients retain useful vision. The prognosis worsens with delayed care, recurrent detachments, or uncontrolled inflammation. Regular surveillance and managing underlying risks are key to favorable outcomes. retina-specialist.comMDPI
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The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members
Last Updated: August 02, 2025.
