Intermediate Uveitis

Intermediate uveitis is when the middle part of the eye (the vitreous gel and the pars plana just behind the iris) becomes inflamed. This means the tissues in that area swell up because of cells from your immune system. People often call it “pars planitis” when they see white clumps (“snowballs”) or deposits (“snowbanking”) on the edge of the retina. In intermediate uveitis, there is no inflammation in the front (iris) or back (retina/choroid) of the eye—just in the middle layer where the vitreous sits Taylor & Francis Online.

Intermediate uveitis is inflammation primarily involving the vitreous—the clear, gel-like substance filling the back of the eye—and the peripheral retina. In simple terms, immune cells infiltrate and irritate the middle part of the eye, causing floaters, blurred vision, and, if left untreated, sight-threatening complications like cystoid macular edema (CME) Wikipedia. It may occur on its own or herald systemic conditions such as multiple sclerosis or sarcoidosis Wikipedia. The defining hallmarks are “snowballs” (clumps of inflammatory cells in the vitreous) and “snowbanking” (whitish exudates along the pars plana) NCBI.

Anatomic Classification & Types

According to the Standardization of Uveitis Nomenclature (SUN) working group, uveitis is divided by where the inflammation happens. Intermediate uveitis involves mainly the vitreous and pars plana and includes three subtypes:

• Pars Planitis: Inflammation at the flat part of the ciliary body, often with “snowbanking” on the pars plana.

• Posterior Cyclitis: Inflammation primarily of the back part of the ciliary body, sometimes extending into the vitreous.

• Hyalitis: Inflammation limited mostly to the vitreous gel itself.
  Together, these three patterns make up intermediate uveitis PMCMD Searchlight.

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Types of Intermediate Uveitis

1. Pars Planitis
Pars planitis is a type of intermediate uveitis where white inflammatory deposits form on the pars plana, the flat part of the ciliary body behind the iris. These deposits look like snowbanks, and you may also see floating white clumps called snowballs. This form often affects young adults and children and can recur over time MD Searchlight.

2. Posterior Cyclitis
Posterior cyclitis means inflammation is deeper in the eye, at the back of the ciliary body. In this type, the vitreous may have scattered inflammatory cells, and the nearby retina can show mild swelling or blood vessel changes. Patients can have floaters and blurred vision when the cells leak into the gel Orpha.

3. Hyalitis
Hyalitis refers to inflammation confined mostly to the vitreous gel, without much visible change on the pars plana. The vitreous becomes hazy or cloudy, causing vision to be fuzzy. This type may not show snowbanking but still leads to floaters and decreased vision due to the cloudy gel American Academy of Ophthalmology.

4. Systemic disease–associated
This type occurs in patients with conditions like multiple sclerosis or sarcoidosis. The underlying disease triggers immune cells to inflame the vitreous, so treating the systemic disorder helps control eye inflammation ScienceDirect.

5. Infectious intermediate uveitis
Infections such as tuberculosis, Lyme disease, or syphilis can inflame the vitreous and peripheral retina. Identifying and treating the infection is key to preventing recurrent inflammation Verywell Health.

6. Masquerade syndrome
Rarely, cancers (e.g., intraocular lymphoma) mimic intermediate uveitis. In these cases, malignant cells infiltrate the vitreous, requiring biopsy or imaging to distinguish from true inflammation PMC.

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Causes of Intermediate Uveitis

Many times, doctors cannot find a clear reason for intermediate uveitis (idiopathic). But when a cause is known, it often links to infections, autoimmune disorders, or systemic illnesses. Below are 20 possible causes, each explained in very simple terms:

1. Idiopathic (Unknown Cause)
   Most patients (50–70%) have no clear trigger. Doctors call this “idiopathic.” It means cells leak into the vitreous for reasons we can’t see on tests Cleveland Clinic.

2. Multiple Sclerosis
   In some people with MS, the immune system attacks both nerves and eye tissues. About 15% of intermediate uveitis cases link to MS, causing inflammation in the vitreous PMC.

3. Sarcoidosis
   Sarcoidosis makes small clumps (granulomas) in organs, including the eye. Roughly 25% of people with sarcoidosis develop intermediate uveitis when these clumps form in the vitreous or pars plana EyeWiki.

4. Lyme Disease
   Caused by a tick bite carrying Borrelia bacteria, Lyme disease can trigger inflammation in the eye weeks or months after the bite, leading to floaters and blurred vision PMC.

5. Tuberculosis (TB)
   TB bacteria can spread from the lungs to the eye and cause scattered inflammation in the vitreous gel. Doctors look for TB by doing chest X-rays and blood tests PMC.

6. Syphilis
   The bacteria that cause syphilis can infect the eye, leading to white blood cells in the vitreous. Tests like VDRL or FTA-ABS help find this infection American Academy of Ophthalmology.

7. Toxoplasmosis
   A tiny parasite (Toxoplasma gondii) from undercooked meat or cat feces can inflame retinal tissue and vitreous, causing floaters and blurred spots.

8. Toxocariasis
   Roundworm larvae from pets can enter the eye, causing localized inflammation near the pars plana and in the vitreous.

9. Cat-Scratch Disease
   Bartonella henselae from a cat scratch can inflame eye tissues, including the vitreous, leading to intermediate uveitis symptoms.

10. HTLV-1 Infection
    Human T-lymphotropic virus type 1 can infect immune cells, sometimes causing ocular inflammation in the vitreous.

11. Epstein-Barr Virus (EBV)
    EBV, the virus that causes mononucleosis, can rarely trigger intermediate uveitis by attacking eye tissues.

12. Juvenile Idiopathic Arthritis (JIA)
    In children with JIA, the immune system attacks joints and can also attack eye tissues, causing intermediate uveitis without clear pain Cleveland Clinic.

13. Behçet’s Disease
    An autoimmune disease that inflames blood vessels can affect the uvea, causing repeated episodes of intermediate uveitis.

14. Wegener’s Granulomatosis
    Now called granulomatosis with polyangiitis, this disease damages small blood vessels and can inflame the vitreous.

15. Inflammatory Bowel Disease (IBD)
    Ulcerative colitis or Crohn’s disease can sometimes cause immune cells to attack the eye, including intermediate structures.

16. Leukemia/Lymphoma
    Cancer of blood cells can sometimes involve the eye, with malignant cells infiltrating the vitreous.

17. Intraocular Lymphoma
    A type of eye cancer that often looks like chronic uveitis, with cells in the vitreous.

18. Local Eye Injury
    A blunt injury or surgery can trigger inflammation deep in the eye, including the vitreous.

19. Medication-Induced
    Some drugs (like rifabutin or cidofovir) can cause uveitis as a side effect, inflaming the vitreous.

20. Viral Infections (Herpes Viruses)
    Herpes simplex or varicella-zoster viruses can spread to the vitreous, causing intermediate inflammation.

Symptoms of Intermediate Uveitis

Intermediate uveitis often comes on slowly and may last a long time. Here are 15 common symptoms, each explained in plain English:

1. Floaters
   Little dots or threads that seem to drift in your vision. They are clumps of white blood cells in the vitreous Moorfields Eye Hospital.

2. Blurred Vision
   Vision becomes fuzzy because the vitreous turns cloudy from inflammation Moorfields Eye Hospital.

3. Mild Eye Redness
   Unlike front-eye uveitis, the redness is often low-grade and may not be very noticeable Moorfields Eye Hospital.

4. Eye Pain
   A dull ache rather than sharp pain, felt deep in the eye.

5. Photophobia (Light Sensitivity)
   Bright lights seem too strong or uncomfortable, because the inflamed tissues react to light.

6. Decreased Night Vision
   It becomes harder to see in dim light, since inflammation scatters light inside the eye.

7. Vitreous Haze
   A grayish film over what you see, caused by proteins leaking into the vitreous.

8. Metamorphopsia
   Straight lines appear wavy, as inflammation near the retina alters light paths.

9. Scotoma
   A small blind spot in your vision, where inflammation blocks light.

10. Halos Around Lights
    Rings or colored circles around lamps or streetlights.

11. Color Vision Changes
    Colors look dull or washed out when inflammation affects retinal blood flow.

12. Difficulty Focusing
    It feels hard to keep things sharp, because the vitreous isn’t clear.

13. Eye Fatigue
    Your eyes get tired more quickly when they try to see through cloudy fluid.

14. Reduced Depth Perception
    Judging distances becomes harder, since light scattering blurs fine details.

15. Intermittent Symptoms
    Symptoms may improve or worsen over weeks to months, as inflammation flares or calms.

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Diagnostic Tests for Intermediate Uveitis

To find intermediate uveitis and its cause, eye doctors use a mix of physical checks, manual procedures, lab tests, electrodiagnostic measures, and imaging. Below are 20 key tests, grouped by type, each explained in very simple English:

A. Physical Exam

1. Visual Acuity Test
   Measures how well you can see letters on a chart from a set distance. A drop in acuity suggests inflammation.

2. Slit-Lamp Examination
   A bright light and microscope let the doctor see the front of your eye and the vitreous edge for cells or haze.

3. Intraocular Pressure (IOP) Measurement
   Checks fluid pressure inside your eye using a small puff of air or a gentle probe. Uveitis can lower or raise IOP.

4. Fundus Examination
   With special lenses, the doctor looks at the back of your eye (retina and vitreous) to spot cells or snowbanking.

B. Manual Procedures

5. Gonioscopy
   Uses a mirror lens on the eye to check the drainage angle; inflammation can narrow angles.

6. Indirect Ophthalmoscopy with Scleral Depression
   Pressing gently on the outside of the eye lets the doctor see peripheral retina and pars plana up close.

7. Ocular Motility Evaluation
   Checks eye movements to make sure muscles are fine and no hidden pain limits motion.

8. Digital Palpation of Globe
   Very gentle pressing on the eyelid to feel if the eye is tender or firmer than normal.

C. Lab & Pathological Tests

9. Complete Blood Count (CBC)
   Measures red and white blood cells; high white counts can hint at systemic infection or inflammation.

10. Erythrocyte Sedimentation Rate (ESR)
    A blood test that shows how fast red blood cells settle; higher rates mean more inflammation.

11. C-Reactive Protein (CRP)
    Another blood marker for inflammation; rises quickly when the body fights infection.

12. Antinuclear Antibody (ANA) Test
    Checks for antibodies linked to autoimmune diseases like lupus, which can underlie uveitis.

13. Syphilis Serology (VDRL/FTA-ABS)
    Blood tests to find syphilis, a treatable infection that can cause intermediate uveitis American Academy of Ophthalmology.

14. Vitreous Biopsy & Histopathology
    In rare cases, a small sample of vitreous fluid is taken to look for cancer or infection under a microscope.

D. Electrodiagnostic Tests

15. Electroretinography (ERG)
    Records electrical signals from the retina when light flashes, checking retinal cell health.

16. Visual Evoked Potential (VEP)
    Measures electrical activity in the brain’s vision centers when you see a pattern, testing the entire visual pathway.

17. Electrooculography (EOG)
    Tracks eye movement signals reflecting the health of the retinal pigment epithelium and the light-dark adaptation.

E. Imaging Tests

18. Optical Coherence Tomography (OCT)
    Like an ultrasound but with light, OCT creates a detailed picture of retinal and vitreous layers, showing swelling.

19. Fluorescein Angiography (FA)
    A special dye injected in your arm lights up blood vessels in your eye so the doctor can photograph leaks or blockages.

20. B-Scan Ultrasonography
    Sound waves create an image of the inside of the eye when the view is blocked by dense vitreous haze or cataract. Mayo Clinic

Non-Pharmacological Treatments (Therapies & Other Interventions)

1. Pars Plana Vitrectomy (PPV)
   Description: Microsurgical removal of the vitreous gel along with inflammatory debris.
   Purpose: Clears vitreous opacities, reduces cytokine load, and treats complications like CME and epiretinal membranes.
   Mechanism: By physically removing inflammatory cells and mediators, PPV promotes a more quiescent intraocular environment PMC.

2. Laser Photocoagulation
   Description: Application of focused laser burns to areas of retinal nonperfusion.
   Purpose: Prevents or treats neovascularization caused by ischemia.
   Mechanism: Laser destroys ischemic retina, reducing vascular endothelial growth factor (VEGF) drive and halting new vessel growth PubMed+1.

3. Cryotherapy
   Description: Freezing therapy applied to the peripheral retina.
   Purpose: Alternative to laser in treating peripheral neovascularization and snowbanking.
   Mechanism: Cryogenic injury induces scarring in snowbank areas, reducing inflammatory stimulus and neovascular drive PMC.

4. Low-Level Light Therapy
   Description: Infrared or red light applied externally to the eye.
   Purpose: Experimental reduction of inflammation.
   Mechanism: Photobiomodulation may modulate mitochondrial function and reduce reactive oxygen species.

5. Hyperbaric Oxygen Therapy
   Description: Breathing 100% oxygen at increased atmospheric pressure.
   Purpose: Alleviate retinal hypoxia.
   Mechanism: Increased dissolved oxygen in plasma improves retinal oxygenation, potentially reducing inflammatory drive in ischemic areas.

6. Acupuncture
   Description: Insertion of fine needles at specific body points.
   Purpose: Reduce ocular inflammation and associated symptoms.
   Mechanism: May modulate systemic immune response and neurogenic inflammation via endorphin release.

7. Mindfulness-Based Stress Reduction (MBSR)
   Description: Meditation and yoga program.
   Purpose: Decrease systemic stress, which can exacerbate autoimmune inflammation.
   Mechanism: Downregulation of hypothalamic–pituitary–adrenal (HPA) axis reduces proinflammatory cytokine production.

8. Smoking Cessation
   Description: Stopping tobacco use.
   Purpose: Lower risk of uveitis flares and improve treatment response.
   Mechanism: Eliminating smoking reduces systemic oxidative stress and vascular inflammation Wikipedia.

9. UV-Blocking Eyewear
   Description: Sunglasses or contact lenses filtering UVB/UVA.
   Purpose: Protects the anterior segment from UV-induced inflammatory injury.
   Mechanism: Blocking UV light reduces photochemical damage and immune activation in ocular tissues PMC.

10. Temperature Modulation (Warm/Cold Compresses)
    Description: Applying warm or cold packs to closed eyelids.
    Purpose: Provides symptomatic relief of ocular discomfort.
    Mechanism: Vasodilation (warm) or vasoconstriction (cold) may transiently reduce inflammatory mediator activity.

11. Dietary Counseling
    Description: Guidance on anti-inflammatory eating patterns.
    Purpose: Support systemic immune balance.
    Mechanism: Encouraging whole foods rich in antioxidants reduces systemic inflammation PMC.

12. Occupational Therapy
    Description: Ergonomic and lighting adjustments at work/home.
    Purpose: Minimize glare and eye strain.
    Mechanism: Reducing mechanical and photic stress can lessen ocular irritation.

13. Physical Therapy for Associated MS
    Description: Neuromuscular exercises if multiple sclerosis is present.
    Purpose: Improve mobility and possibly modulate autoimmune activity.
    Mechanism: Exercise-induced anti-inflammatory cytokine release may aid systemic control.

14. Biofeedback
    Description: Visual or auditory cues to control stress responses.
    Purpose: Enhance relaxation and reduce systemic inflammation.
    Mechanism: Autonomic regulation dampens inflammatory pathways.

15. Psychological Support/Counseling
    Description: Therapy for coping with chronic disease.
    Purpose: Lower stress-related exacerbations.
    Mechanism: Mental well-being correlates with improved immune regulation.

16. Chiropractic Adjustment
    Description: Spinal manipulation therapy.
    Purpose: Anecdotal calming of systemic inflammatory tone.
    Mechanism: Hypothesized modulation of neuro-immune axis.

17. Ocular Drainage Massage
    Description: Gentle manual eyelid massage.
    Purpose: Promote clearance of inflammatory exudates.
    Mechanism: Mechanical agitation may help redistribute snowbank material.

18. Yoga and Tai Chi
    Description: Mind-body movement practices.
    Purpose: Reduce stress and improve autonomic balance.
    Mechanism: Lowered cortisol and pro-inflammatory cytokines.

19. Photobiomodulation
    Description: Targeted near-infrared light to head/eyes.
    Purpose: Emerging therapy for ocular inflammation.
    Mechanism: Modulates mitochondrial oxidative stress in ocular cells.

20. Music Therapy
    Description: Listening to calming music.
    Purpose: Systemic stress reduction to support immune balance.
    Mechanism: Neuroendocrine modulation reduces inflammatory mediator release.

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Evidence-Based Drug Treatments

1. Prednisone (Oral)
   Class: Systemic corticosteroid
   Dosage: 1 mg/kg/day (max 60 mg) tapered over weeks
   Time: Morning administration to mimic diurnal cortisol
   Purpose: Rapid suppression of acute inflammation
   Mechanism: Inhibits phospholipase A₂, reducing prostaglandin and leukotriene synthesis
   Side Effects: Weight gain, hypertension, hyperglycemia, cataract, glaucoma Wikipedia.

2. Methotrexate
   Class: Antimetabolite (DMARD)
   Dosage: 15–25 mg SC weekly
   Time: Once weekly with folinic acid rescue
   Purpose: Steroid-sparing long-term control
   Mechanism: Inhibits dihydrofolate reductase, reducing lymphocyte proliferation
   Side Effects: Hepatotoxicity, cytopenias, mucositis Wikipedia.

3. Azathioprine
   Class: Purine analogue immunosuppressant
   Dosage: 1–2 mg/kg/day orally
   Time: Daily
   Purpose: Adjunct in chronic uveitis
   Mechanism: Interferes with purine synthesis, reducing lymphocyte DNA/RNA formation
   Side Effects: Myelosuppression, hepatotoxicity Wikipedia.

4. Mycophenolate Mofetil
   Class: Antimetabolite
   Dosage: 1 g twice daily orally
   Time: BID
   Purpose: Alternative steroid-sparing agent
   Mechanism: Inhibits inosine monophosphate dehydrogenase, blocking guanine synthesis in lymphocytes
   Side Effects: GI upset, leukopenia Wikipedia.

5. Cyclosporine
   Class: Calcineurin inhibitor
   Dosage: 3–5 mg/kg/day in two divided doses
   Time: BID
   Purpose: Refractory uveitis control
   Mechanism: Inhibits IL-2 transcription, reducing T-cell activation
   Side Effects: Nephrotoxicity, hypertension Wikipedia.

6. Tacrolimus
   Class: Calcineurin inhibitor
   Dosage: 0.05–0.1 mg/kg/day in two divided doses
   Time: BID
   Purpose: Alternative to cyclosporine
   Mechanism: Binds FKBP-12, inhibiting calcineurin and IL-2 synthesis
   Side Effects: Nephrotoxicity, neurotoxicity Wikipedia.

7. Infliximab
   Class: Anti-TNF-α chimeric mAb
   Dosage: 5 mg/kg IV at weeks 0,2,6 then q4–8 weeks
   Time: According to infusion schedule
   Purpose: Refractory non-infectious uveitis
   Mechanism: Neutralizes TNF-α, reducing inflammatory signaling
   Side Effects: Infusion reactions, infection risk PubMed.

8. Adalimumab
   Class: Anti-TNF-α human mAb
   Dosage: 40 mg SC every 2 weeks
   Time: Biweekly
   Purpose: FDA-approved for non-infectious intermediate/posterior uveitis
   Mechanism: TNF-α blockade, reducing uveitic flares
   Side Effects: Injection site reactions, infection risk PubMed.

9. Tocilizumab
   Class: Anti-IL-6 receptor mAb
   Dosage: 4–10 mg/kg IV monthly or 162 mg SC every week
   Time: Monthly IV or weekly SC
   Purpose: Refractory uveitic macular edema and systemic control
   Mechanism: Inhibits IL-6–mediated inflammation
   Side Effects: Elevated liver enzymes, lipid changes PubMed.

10. Intravitreal Dexamethasone Implant (Ozurdex®)
    Class: Corticosteroid implant
    Dosage: 0.7 mg single intravitreal injection
    Time: Effect lasts ~4–6 months
    Purpose: Control of localized intraocular inflammation and CME
    Mechanism: Sustained release of dexamethasone, inhibiting inflammatory mediators
    Side Effects: Intraocular pressure rise, cataract progression eyewiki.aao.org.

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Dietary Molecular & Herbal Supplements

1. Omega-3 Long-Chain Polyunsaturated Fatty Acids
   Dosage: 1–3 g/day of EPA/DHA
   Function: Anti-inflammatory mediator precursor
   Mechanism: Competes with arachidonic acid, reducing proinflammatory eicosanoids PMC.

2. Curcumin (Turmeric Extract)
   Dosage: 500 mg thrice daily
   Function: Broad anti-inflammatory agent
   Mechanism: Inhibits NF-κB and COX-2 pathways EBSCO.

3. Resveratrol
   Dosage: 150–500 mg/day
   Function: Antioxidant and anti-inflammatory
   Mechanism: Inhibits cyclooxygenase and TNF-α expression PubMed.

4. Quercetin
   Dosage: 500 mg twice daily
   Function: Mast cell stabilizer, antioxidant
   Mechanism: Scavenges free radicals, downregulates histamine release.

5. Vitamin D₃
   Dosage: 2,000 IU/day
   Function: Immune modulation
   Mechanism: Promotes T-regulatory cell function, reduces Th17 responses PMC.

6. Vitamin E (α-Tocopherol)
   Dosage: 400 IU/day
   Function: Lipid antioxidant
   Mechanism: Protects cell membranes from oxidative damage.

7. Lutein & Zeaxanthin
   Dosage: 10 mg lutein + 2 mg zeaxanthin daily
   Function: Macular protection
   Mechanism: Filters blue light, reduces oxidative stress.

8. Ginkgo Biloba
   Dosage: 120 mg/day standardized extract
   Function: Microcirculatory enhancer
   Mechanism: Improves ocular blood flow, antioxidant effects.

9. Green Tea (EGCG)
   Dosage: 300 mg EGCG/day
   Function: Antioxidant, anti-inflammatory
   Mechanism: Inhibits inflammatory cytokines.

10. Boswellia Serrata Extract
    Dosage: 300 mg thrice daily
    Function: 5-LOX inhibitor
    Mechanism: Reduces leukotriene synthesis.

11. Ashwagandha (Withania somnifera)
    Dosage: 300 mg twice daily
    Function: Adaptogen, immune modulator
    Mechanism: Lowers cortisol, modulates Th1/Th2 balance.

12. Cat’s Claw (Uncaria tomentosa)
    Dosage: 250 mg twice daily
    Function: Anti-TNF-α activity
    Mechanism: Blocks NF-κB activation.

13. Aloe Vera Gel
    Dosage: 100 mg/day
    Function: Anti-inflammatory
    Mechanism: Inhibits COX enzymes.

14. Methylsulfonylmethane (MSM)
    Dosage: 1,000 mg twice daily
    Function: Sulfur donor, anti-inflammatory
    Mechanism: Reduces cytokine production.

15. Alpha-Lipoic Acid
    Dosage: 300 mg/day
    Function: Potent antioxidant
    Mechanism: Regenerates other antioxidants, reduces oxidative stress.

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Advanced (Biologic/Regenerative/Stem-Cell) Therapies

1. Adalimumab
   Dosage & Route: 40 mg SC every 2 weeks
   Function: Anti-TNF-α biologic
   Mechanism: Blocks TNF-α–mediated inflammation PubMed.

2. Infliximab
   Dosage & Route: 5 mg/kg IV q4–8 weeks
   Function: Chimeric TNF-α inhibitor
   Mechanism: Neutralizes TNF-α, reducing uveitic flares PubMed.

3. Tocilizumab
   Dosage & Route: 4–10 mg/kg IV monthly or 162 mg SC weekly
   Function: IL-6 receptor antagonist
   Mechanism: Prevents IL-6–driven inflammatory cascade PubMed.

4. Rituximab
   Dosage & Route: 375 mg/m² IV weekly × 4 doses
   Function: Anti-CD20 B-cell depletion
   Mechanism: Eliminates pathogenic B-cells, reducing autoantibody and cytokine production PubMed.

5. Intravitreal Sirolimus
   Dosage & Route: 440 μg intravitreal injection
   Function: mTOR inhibitor
   Mechanism: Blocks T-cell proliferation locally, minimal systemic exposure PubMed.

6. Mesenchymal Stem Cell Therapy
   Dosage & Route: Experimental MSC infusion (50 µg exosomes or 5×10⁶ cells IV)
   Function: Regenerative immunomodulation
   Mechanism: MSCs and their secreted extracellular vesicles modulate T-cell responses, promote regulatory T-cells, and reduce ocular inflammation in preclinical models PubMed.

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Surgical & Procedural Interventions

1. Pars Plana Vitrectomy (PPV)
   Procedure: Removal of the vitreous gel via 23–27G ports.
   Why: Clears inflammatory cells, treats nonresolving CME, ERM, and vitreous opacities PMC.

2. Cataract Extraction
   Procedure: Phacoemulsification with intraocular lens implantation.
   Why: Restores vision in uveitic or steroid-induced cataract Wikipedia.

3. Glaucoma Filtration Surgery (Trabeculectomy or Tube Shunt)
   Procedure: Creation of a fistula or implant placement to drain aqueous humor.
   Why: Controls secondary uveitic glaucoma refractory to medications Wikipedia.

4. Laser Photocoagulation
   Procedure: Argon or panretinal laser to ischemic retina.
   Why: Treats retinal neovascularization to prevent hemorrhage and fibrovascular proliferation PubMed+1.

5. Fluocinolone Acetonide Intravitreal Implant
   Procedure: Surgical insertion of a 0.19–0.2 μg/day sustained-release steroid implant (ILUVIEN®/Retisert®).
   Why: Long-term prevention of uveitis relapses in chronic non-infectious posterior uveitis PMC+1.

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Key Prevention Strategies

1. Smoking Cessation
   Rationale: Smoking is a risk factor for non-infectious uveitis Wikipedia.

2. UV Protection
   Rationale: UVB promotes uveitic injury; blocking UV reduces inflammation PMC.

3. Control Systemic Diseases
   Rationale: Early management of MS, sarcoidosis, IBD may prevent ocular manifestations Wikipedia.

4. Avoid Ocular Trauma
   Rationale: Trauma can trigger sympathetic ophthalmia, a form of uveitis Wikipedia.

5. Vaccinate Appropriately
   Rationale: Prevent infectious triggers (e.g., varicella, rubella) that can lead to infectious uveitis.

6. Regular Ophthalmic Screening
   Rationale: Early detection of subclinical inflammation prevents complications.

7. Hand & Face Hygiene
   Rationale: Reduces ocular surface infections that can complicate or mimic uveitis.

8. Healthy Diet Rich in Antioxidants
   Rationale: Antioxidant intake (fruits, vegetables) may lower ocular inflammation PMC.

9. Stress Management
   Rationale: Psychological stress can exacerbate autoimmune flares.

10. Environmental Allergen Control
    Rationale: Reduces secondary ocular irritation that can worsen inflammation.

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When to See Your Doctor

– Sudden vision changes: Floaters, blurring, or loss of vision.
– Eye pain or redness: Even mild discomfort can signal a flare.
– Photophobia: Light sensitivity often accompanies active inflammation.
– New headaches with ocular symptoms: May reflect associated MS.
– Persistent ocular discomfort: Failure of home remedies.
– Complication signs: Glaucoma (halos around lights), cataract (gradual dimming).

Clinical signs include redness, pain, blurred vision, photophobia, and floaters Wikipedia.

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Foods to Eat & Avoid

Eat:

• Leafy greens & berries (antioxidants) PMC.

• Oily fish & flaxseed (omega-3) PMC.

• Turmeric (curcumin) EBSCO.

• Nuts & seeds (vitamin E).

• Yogurt (probiotics for gut–eye axis).

Avoid:

• Processed & fried foods (pro-inflammatory).

• High-sugar beverages (oxidative stress).

• Trans fats (vascular inflammation).

• Excess alcohol (immune dysregulation).

• Excess caffeine (ocular dryness).

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Frequently Asked Questions

1. What causes intermediate uveitis?
   It can be idiopathic or linked to systemic autoimmune (MS, sarcoidosis) or infectious triggers (Lyme, EBV) Wikipedia.

2. Is intermediate uveitis inherited?
   No clear Mendelian inheritance, but HLA associations (HLA-DR2, DR15) suggest a genetic predisposition NCBI.

3. Can intermediate uveitis resolve on its own?
   Mild cases may self-resolve, but chronic inflammation often requires treatment to prevent complications.

4. How long does treatment last?
   Acute flares: weeks to months; chronic management: years, often with steroid-sparing agents.

5. Will I go blind?
   With prompt, adequate therapy, permanent vision loss is uncommon; CME is the leading threat Wikipedia.

6. Can I drive during a flare?
   No—blurred vision and photophobia make driving unsafe.

7. Are there lifestyle modifications?
   Yes: UV protection, smoking cessation, stress reduction, anti-inflammatory diet.

8. What complications should I watch for?
   Cataract, glaucoma, CME, retinal detachment, epiretinal membrane.

9. Can children get intermediate uveitis?
   Yes—pediatric IU accounts for up to 25% of uveitis cases in referral centers Wikipedia.

10. Is immunosuppression safe long-term?
    When monitored, DMARDs and biologics have acceptable safety profiles compared to uncontrolled inflammation PubMed.

11. Can pregnancy worsen uveitis?
    Pregnancy often improves inflammation due to immune tolerance, but postpartum flares can occur.

12. Are alternative therapies effective?
    Some, like acupuncture or mindfulness, may help symptomatically but aren’t a substitute for medical therapy.

13. When is surgery needed?
    For complications: cataract removal, glaucoma surgery, PPV for nonresolving CME or vitreous opacities.

14. Can vaccinations trigger uveitis?
    Rarely—live vaccines pose higher risk; discuss timing with your specialist.

15. How often should I follow up?
    During active disease: every 1–4 weeks; quiescent: every 3–6 months, or sooner if symptoms recur.

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.

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Last Updated: August 07, 2025.

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