Ocular Graft-Versus-Host Disease (oGVHD)

Ocular graft-versus-host disease (oGVHD) is an eye problem that can happen only after an allogeneic stem cell or bone marrow transplant. In this transplant, blood-forming cells from a donor replace the recipient’s cells. The donor’s immune cells can sometimes see the patient’s tissues as foreign and attack them. When this attack targets the eyes and the tissues around the eyes, we call it ocular GVHD. The surface of the eye (the clear cornea and the pink conjunctiva), the tear glands (which make the watery part of tears), and the oil glands in the eyelids (which make the oily part of tears) can all be affected. When these structures are inflamed or scarred, the tear film becomes weak and unstable. This leads to dryness, burning, pain, blurred vision, and light sensitivity. oGVHD can be mild, moderate, or severe. It can show up early after transplant or many months later. It may get better with treatment or it may become long-lasting if scarring develops. Early recognition and steady, layered treatment usually help people feel and see better.

Ocular graft-versus-host disease (oGVHD) happens when immune cells from a donor attack the surface of the recipient’s eyes after an allogeneic stem-cell (bone-marrow) transplant. The attack targets the lacrimal (tear) glands, meibomian (oil) glands, conjunctiva, and cornea. That combination dries the eyes, inflames the surface, and—if untreated—can lead to erosions, ulcers, infection, scarring, and even perforation. Between roughly 40% and 90% of people with chronic GVHD develop eye symptoms, so it’s common and important to recognize early. EyeWiki

oGVHD usually presents like a severe, stubborn dry-eye disease, but it’s not “just dryness”—it’s an immune-driven surface disorder tied to your transplant. Quality of life can drop markedly (pain, light sensitivity, fluctuating or blurry vision). A team approach between your transplant clinicians and an eye specialist (preferably a cornea/ocular surface expert) gives the best outcomes. FrontiersPMC

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What happens in the eye

The donor immune cells attack small “target” areas in and around the eye. The lacrimal glands (tear-making glands) can become inflamed and then fibrose (harden), so they make fewer tears. The meibomian glands in the eyelids can get clogged and damaged, so they release less and poorer-quality oil. Without enough oil, tears evaporate too fast. The conjunctiva can lose goblet cells, which normally make mucin, the “gluey” part that helps tears spread smoothly over the eye. The cornea can develop surface damage and tiny breaks because it is not well covered or well lubricated. The eyelid margins may become inflamed (blepharitis), and the blinking pattern may change, so the eye is exposed even more. All of this creates a dry, inflamed, unstable tear film, which feels bad and blurs vision. If the inflammation continues, scarring can pull on the eyelids and the conjunctiva, making symptoms worse and harder to treat.

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Types of ocular GVHD

1. Aqueous-deficient dry eye type
   The main problem is low watery tear production because the lacrimal glands are inflamed or scarred. The eyes feel dry and gritty. Schirmer testing often shows low tear volume.

2. Evaporative dry eye type
   The main problem is meibomian gland dysfunction (MGD). The eyelid oil is thick, blocked, or poor quality, so tears evaporate quickly. The eyes may water reflexively even though they are dry.

3. Mixed dry eye type (aqueous + evaporative)
   Many people have both low tear production and poor oil layer. This is very common in oGVHD.

4. Cicatricial (scarring) conjunctivitis type
   The inner eyelids and conjunctiva develop scarring. The eyelids may turn inward or outward, and the tear ducts may narrow. Strings of mucus and surface breakdown are common.

5. Keratitis / epitheliopathy type
   The corneal surface shows punctate staining, filaments, or persistent epithelial defects. Light sensitivity and pain are prominent.

6. Limbal stem cell deficiency pattern (less common but serious)
   The edge of the cornea (the limbus) loses stem cells that renew the surface. Vision can drop and the corneal surface becomes unstable.

7. Exposure-related pattern
   Incomplete blinking, poor eyelid closure, or eyelid malposition increases exposure and worsens dryness and irritation.

8. Punctal stenosis / tear drainage scarring pattern
   The tiny tear drain openings can scar and narrow. Paradoxically, the eye may water constantly while still being inflamed and dry on the surface.

(These patterns often overlap in the same person.)

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Causes and strong risk/worsening factors

Important note: oGVHD happens only in people who have had an allogeneic stem cell or bone marrow transplant. The items below describe what causes oGVHD (the donor immune attack) and what increases risk or makes it worse.

1. Allogeneic transplant itself – donor immune cells may attack the eye tissues.

2. Chronic systemic GVHD elsewhere in the body – if GVHD is active in the skin, mouth, liver, or gut, the eyes are more likely to be involved.

3. Past acute GVHD – earlier GVHD episodes increase the chance of later eye involvement.

4. HLA mismatch between donor and recipient – more mismatch means more immune conflict risk.

5. Female donor to male recipient – sex-mismatch can raise risk due to minor antigen differences.

6. Older recipient age – older eyes and glands are more vulnerable to dryness and scarring.

7. Peripheral blood stem cell grafts – these grafts carry more mature immune cells, which can raise GVHD risk.

8. Intense conditioning (such as total body irradiation) – can injure tissues and set the stage for GVHD.

9. Rapid taper or withdrawal of systemic immunosuppression – GVHD can flare as medicines are reduced.

10. Pre-existing dry eye disease – a weak tear film before transplant makes oGVHD more likely and more symptomatic.

11. Meibomian gland dysfunction before or after transplant – poor eyelid oil worsens evaporation.

12. Eyelid margin inflammation (blepharitis) or Demodex mites – chronic lid irritation worsens surface inflammation.

13. Irritating environments – low humidity, air-conditioning, fans, smoke, dust, pollution, and wind increase evaporation.

14. Prolonged screen time and infrequent blinking – longer open-eye time dries the surface.

15. Systemic medicines that dry the eye – antihistamines, antidepressants, anticholinergics, some acne medicines (e.g., isotretinoin) reduce tear quantity or quality.

16. Poor nutrition or vitamin A deficiency – weak surface repair and poor mucin support.

17. Eye infections (bacterial or viral) – add inflammation and can trigger flares.

18. Contact lens overuse – mechanical stress on a fragile ocular surface.

19. Eye surgery after transplant – surgery can inflame the surface and provoke flares.

20. Other autoimmune-like features (e.g., Sjögren-like) – overlap can deepen tear gland damage.

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Common symptoms

1. Dryness – a feeling that the eyes do not have enough moisture.

2. Grittiness or “sand in the eye” – tiny rough spots on the cornea create a sandy sensation.

3. Burning or stinging – inflammation of the surface nerves causes a hot, stinging feel.

4. Foreign-body sensation – it feels like something is stuck under the eyelid even when nothing is there.

5. Redness – blood vessels widen because the surface is irritated and inflamed.

6. Watery eyes – reflex tears run because the surface is irritated, even though the baseline tear film is poor.

7. Light sensitivity (photophobia) – the damaged corneal surface and inflamed nerves make light uncomfortable.

8. Blurred or fluctuating vision – the tear film is the first “lens” of the eye; when it breaks, vision wavers.

9. Stringy or sticky mucus – loss of normal mucin and surface damage leads to thick strands.

10. Pain or soreness – from surface injury, lid-margin inflammation, or exposed nerves.

11. Itching – often from lid inflammation or allergic overlay.

12. Eye fatigue – reading, screen use, or driving feels tiring because the surface dries quickly.

13. Morning discomfort – the surface may stick to the eyelid overnight and feel sore on waking.

14. Contact lens intolerance – lenses feel uncomfortable or intolerable on a fragile surface.

15. Sensitivity to wind or air-conditioning – moving air increases evaporation and discomfort.

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Diagnostic tests

A) Physical exam tests

1. Visual acuity and refraction
   Reading the eye chart and checking for glasses needs. Fluctuations with blinking suggest an unstable tear film.

2. External exam and blink assessment
   The doctor looks at eyelid position, blink completeness, and how often you blink. Poor or incomplete blinks increase exposure and dryness.

3. Slit-lamp biomicroscopy
   A microscope with a bright light shows the eyelid margins, lashes, oil gland openings, tear meniscus (the small tear lake), the conjunctiva, and the cornea. The doctor looks for redness, scarring, filaments, and surface injury.

4. Fluorescein corneal staining
   A safe yellow dye highlights tiny scratches on the cornea. Patterns of dots, lines, or filaments show where the surface is breaking down.

5. Lissamine green (or rose bengal) conjunctival staining
   These dyes stain sick or unprotected cells on the white of the eye and the inner eyelids. Heavy staining points to mucin loss and surface stress.

B) Manual/bedside tear function tests

6. Schirmer test without anesthesia (Schirmer I)
   A small paper strip is placed under the lower lid for five minutes. The wet length shows how much watery tears are made at baseline. Very low numbers suggest tear gland damage.

7. Schirmer test with anesthesia
   Numbing drops reduce reflex tearing. The result shows true basal tear production. Low results strengthen the diagnosis of aqueous deficiency.

8. Phenol red thread test
   A tiny red-tipped thread is placed in the lower lid for about 15 seconds. It measures tear volume quickly and is helpful when Schirmer is uncomfortable.

9. Tear break-up time (TBUT) with fluorescein
   After a blink, the doctor times how long the tear film stays smooth before it “breaks.” A short time (e.g., under 10 seconds) means the tear film is unstable, often from poor oil or mucin.

10. Meibomian gland expression and scoring
    Gentle pressure on the lid margin expresses oil. Thick, toothpaste-like oil or little to no flow means gland blockage or damage.

C) Laboratory and pathological tests

11. Tear osmolarity
    A tiny sample of tears shows how salty and concentrated they are. High osmolarity means the tear film is stressed and dehydrated.

12. Tear MMP-9 point-of-care test
    MMP-9 is an enzyme that rises with inflammation. A positive test supports inflammatory dry eye, which is common in oGVHD.

13. Conjunctival impression cytology
    A small filter paper gently touches the eye surface to collect cells. Under the microscope, doctors can see loss of goblet cells and signs of surface cell stress and scarring.

14. Tear lactoferrin (and/or lysozyme) levels
    These tear proteins drop when the lacrimal gland is weak. Low levels support tear gland dysfunction.

15. Cultures or PCR from the ocular surface (when discharge or ulcers are present)
    Testing for bacteria or viruses helps tailor treatment if infection is suspected on top of oGVHD.

D) Electrodiagnostic or nerve-function–related tests

16. Visual evoked potentials (VEP) (selected cases)
    If vision is unusually poor and the surface findings do not explain it, VEP checks how signals travel from the eye to the brain. This helps rule out nerve pathway problems unrelated to the surface.

17. Electroretinography (ERG) (selected cases)
    If there is concern for retinal toxicity from medicines used after transplant or unexplained vision loss, ERG can evaluate retinal function. This is not routine for oGVHD but can be helpful in complex cases.

E) Imaging tests

18. Infrared meibography
    A special camera shows the structure of meibomian glands through the eyelid. Glands that are shortened, twisted, or missing suggest chronic damage.

19. In vivo confocal microscopy (IVCM)
    A high-magnification scanner looks at corneal nerves, cells, and even meibomian glands. It can show inflammation, nerve changes, and scarring at a microscopic level.

20. Anterior segment OCT (AS-OCT) for tear meniscus height and surface integrity
    This painless scan measures the tiny tear lake at the lid edge and can show epithelial defects. A low tear meniscus supports aqueous deficiency.

Non-pharmacological treatments

Each item lists what it is, purpose, and how it helps.

1. Education & trigger control — learn your flares; reduce AC/fans/smoke; blink fully on screens. Purpose: lower daily “evaporation load.” Mechanism: removes environmental stressors that destabilize tears. (Core DEWS II step-1 care.) tfosdewsreport.org

2. Room humidifier — aim for ~40–50% indoor humidity. Purpose: reduce evaporation. Mechanism: higher ambient moisture slows tear water loss. tfosdewsreport.org

3. Moisture-chamber glasses/goggles (day or sleep shields) — wraparound eyewear that traps humidity. Purpose: comfort, less evaporation, fewer flares outdoors. Mechanism: creates a local “mini-humid” zone around the eyes; clinical studies show improved stability and symptoms. PMCPubMed

4. Blink training & screen hygiene — 20-20-20 rule; purposeful full blinks. Purpose: restore oily layer spread. Mechanism: complete blinks express meibum and re-coat the tear film. tfosdewsreport.org

5. Warm compresses (10–15 min, 1–2×/day) — with lid massage. Purpose: liquefy thick meibum. Mechanism: heat melts gland oils → better tear film stability. tfosdewsreport.org

6. Lid hygiene (daily) — gentle cleanser along lashes. Purpose: decrease bacteria/biofilm that inflame the margin. Mechanism: fewer inflammatory by-products at the lid line. tfosdewsreport.org

7. Thermal pulsation (in-office) — e.g., LipiFlow®/similar. Purpose: deeper heat plus gland expression. Mechanism: clears obstructed glands to reduce evaporation; evidence is growing in MGD. ScienceDirect

8. Intense pulsed light (IPL) for MGD — Purpose: reduce vascular/inflammatory lid changes. Mechanism: photothermal effects quiet lid inflammation; useful in selected patients. (Evidence emerging in MGD.) ophthalmology360.com

9. Scleral lenses / PROSE — large vaulting lenses bathe the cornea in fluid all day. Purpose: powerful surface protection and optical quality. Mechanism: a liquid reservoir shields epithelium and smooths vision; widely used in severe oGVHD. PubMed

10. Bandage soft contact lenses — short-term surface protection. Purpose: promote epithelial healing. Mechanism: reduces friction from blinking. PMC

11. Nighttime ointment/gel + eyelid taping or sleep shields — Purpose: stop nocturnal exposure. Mechanism: keeps the surface lubricated and covered. tfosdewsreport.org

12. Punctal plugs (clinic procedure) — tiny plugs in tear drains. Purpose: keep more of your own tears on the eye. Mechanism: slows tear outflow; safe and effective in oGVHD but retention can be an issue. PMCPubMed

13. All-preservative-free drops regimen — even when using medicines, prefer PF versions. Purpose: avoid surface toxicity. Mechanism: benzalkonium chloride and similar preservatives aggravate the ocular surface. American Academy of Ophthalmology

14. Protective eyewear outdoors — wrap shades; avoid wind/dust. Purpose: reduce environmental injury. Mechanism: physical barrier against airflow. American Academy of Ophthalmology

15. Hydration & room ergonomics — drink water; avoid direct vents. Purpose: reduce hyperosmolar stress. Mechanism: supports basal tear water content. tfosdewsreport.org

16. Treat blepharitis and Demodex (as advised) — mechanical lid debridement/tea-tree-based care. Purpose: lower lid-margin inflammation. Mechanism: reduces mites/biofilm load driving MGD. tfosdewsreport.org

17. Smoking cessation — Purpose: remove a major ocular irritant. Mechanism: smoke increases oxidative stress & evaporation. tfosdewsreport.org

18. Cold compresses during flares — Purpose: soothe acute inflammation. Mechanism: vasoconstriction reduces burning/itching transiently. tfosdewsreport.org

19. Allergen control if applicable — Purpose: less histamine-driven surface inflammation. Mechanism: reducing allergen load reduces itch/rub cycle that injures epithelium. tfosdewsreport.org

20. Co-management of systemic GVHD — regular communication with your transplant team. Purpose: treat the root immune process. Mechanism: better systemic control often improves the eyes. PMC

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Drug treatments

1. Topical corticosteroids (e.g., loteprednol 0.5% 4×/day then taper; or short bursts of stronger steroids): calm flares fast. Mechanism: broad anti-inflammatory; Cautions: glaucoma, cataract, infection—so use short courses and monitor pressure. PMC

2. Topical cyclosporine A (e.g., 0.05–0.09% twice daily): disease-modifying immunomodulator that improves tear production and reduces inflammation over weeks to months; cornerstone long-term therapy in oGVHD. Side effects: burning on instillation. American Academy of OphthalmologyPMC

3. Topical tacrolimus (e.g., 0.03% ointment to lids once–twice daily, or compounded drops such as 0.02–0.05% BID): helpful when cyclosporine is not enough; RCTs show efficacy in oGVHD vs steroid. Caution: stinging; use under specialist guidance. PMCJournalAgent

4. Lifitegrast 5% (BID): blocks LFA-1/ICAM-1 to reduce T-cell–mediated inflammation; pilot studies show benefit in oGVHD. Side effects: taste disturbance, mild irritation. ScienceDirect

5. Perfluorohexyloctane (PFHO, Miebo) (QID): prescription drop for evaporative dry eye; forms a long-lasting layer that slows evaporation—useful when MGD/evaporation dominates. CRSToday

6. Varenicline nasal spray (0.03 mg/nostril BID): stimulates trigeminal parasympathetic pathways to increase basal tearing; non-ocular route can be helpful on sensitive surfaces. (Approved for DED; used case-by-case in oGVHD.) Wikipedia

7. Autologous serum/platelet-based drops (see “regenerative” section for details): biologic tears rich in growth factors; dosed often (e.g., 20–100% strength, QID–hourly) in severe disease. PubMed

8. Topical N-acetylcysteine 5–10% (QID): mucolytic helpful for filamentary keratitis on the oGVHD surface; compounded. (Specialist use.) PMC

9. Oral doxycycline (50–100 mg daily for 6–12 weeks): anti-inflammatory effects on meibomian glands; improves oil quality and lid inflammation. (Avoid in pregnancy/children; photosensitivity.) tfosdewsreport.org

10. Topical azithromycin 1% or short oral azithromycin courses for refractory MGD/blepharitis as directed. Mechanism: anti-inflammatory/antibacterial at the lid margin. tfosdewsreport.org

Important: Most chronic control comes from steroid-sparing agents (cyclosporine/tacrolimus/lifitegrast) ± scleral lenses and environmental control. Steroids are for flares under supervision. PMC

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Dietary molecular supplements

Evidence for nutrition in dry eye is mixed. Large trials show omega-3s don’t reliably improve symptoms over placebo, though some meta-analyses suggest benefits for certain signs or with higher doses and longer duration. Use these as add-ons after discussing with your clinicians—especially important if you’re on transplant medications that interact with supplements.

1. Omega-3s (EPA/DHA): 1–2 g/day total EPA+DHA. Function: anti-inflammatory lipid mediators; Mechanism: shifts eicosanoids toward resolvins; evidence mixed (DREAM trial negative for symptoms; meta-analyses show some sign improvements). New England Journal of MedicinePMC

2. Vitamin D3: 1000–2000 IU/day (or per lab guidance). Function: immune modulation; Mechanism: may lower ocular surface inflammation; Evidence: meta-analyses suggest improvement in signs/symptoms when deficient. PubMed

3. GLA (gamma-linolenic acid, e.g., evening primrose/borage): ~240–300 mg GLA/day. Function: anti-inflammatory prostaglandins; Evidence: RCTs show symptom/sign improvement in some DED groups. PubMed

4. Curcumin: 500–1000 mg/day (enhanced-bioavailability forms). Function: NF-κB/COX-2 modulation; Evidence: small trials suggest added symptom benefit with tears. PMCLippincott Journals

5. Lactoferrin: 250–350 mg/day. Function: tear protein with antimicrobial/anti-inflammatory roles; Evidence: small trials show improved TBUT/comfort. PMCAAO Journal

6. Antioxidant blends (vitamins C/E, lutein/zeaxanthin): label dose. Function: oxidative stress reduction; Evidence: supportive but not oGVHD-specific. tfosdewsreport.org

7. Probiotics/prebiotics: as labeled for 8–12 weeks. Function: gut–eye immune axis; Evidence: early RCTs suggest reduced DED severity; confirm with your transplant team before use. PMC

8. Hyaluronic acid (oral): 120–240 mg/day. Function: hydration/viscoelastic support; Evidence: limited but biologically plausible adjunct. tfosdewsreport.org

9. Zinc with vitamin A (RDA-level dosing). Function: epithelial health; Caution: avoid high-dose vitamin A without medical supervision. tfosdewsreport.org

10. Coenzyme Q10 (100–200 mg/day). Function: mitochondrial support/antioxidant; Evidence: exploratory. Discuss interactions. tfosdewsreport.org

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Immunity/regenerative/stem-cell-related therapies

These are systemic or biologic therapies reserved for moderate–severe, refractory disease, coordinated with your GVHD team.

1. Ruxolitinib (JAK1/2 inhibitor) — 10 mg orally twice daily (typical cGVHD dose; adjust per hematology). Purpose: treat steroid-refractory chronic GVHD; Mechanism: blocks JAK-STAT signaling; ocular signs/symptoms have improved in analyses and small series. Key risks: cytopenias, infections. IOVSPMC

2. Belumosudil (ROCK2 inhibitor) — 200 mg orally once daily. Purpose: refractory chronic GVHD after ≥1–2 prior lines; Mechanism: modulates Th17/Tfh pathways and fibrosis; response rates are meaningful in cGVHD and emerging reports suggest ocular benefit in some patients. Risks: GI upset, LFT elevations, interactions. PMCScienceDirectIOVS

3. Ibrutinib (BTK inhibitor) — 420 mg orally once daily in steroid-refractory cGVHD. Purpose: systemic control; Mechanism: B-cell signaling blockade; may secondarily help ocular involvement when overall GVHD improves. Risks: bleeding, atrial fibrillation, infections. PMCAstCT Journal

4. Cenegermin (recombinant human nerve growth factor) 20 µg/mL — 1 drop 6×/day for 8 weeks. Purpose: for neurotrophic keratitis on top of oGVHD, to heal persistent epithelial defects and improve corneal sensitivity. Mechanism: regenerates corneal nerves/epithelium. Caveat: indication is NK; used in selected oGVHD with neurotrophic changes. OXERVATE® (cenegermin-bkbj)NCBI

5. Autologous serum or platelet-rich plasma (PRP/platelet lysate) eye drops — commonly 20–100%, QID to hourly. Purpose: supply epithelium-friendly growth factors (EGF, fibronectin, vitamin A). Mechanism: biologic tear substitute that promotes healing on severely dry, inflamed surfaces. PubMedPMC

6. Umbilical-cord serum or allogeneic plasma drops — e.g., 20% QID (varies by protocol); in oGVHD cohorts, safety and symptomatic/epithelial improvements were reported. Mechanism: higher trophic factor content than autologous serum in some settings. (Prepared in regulated compounding setups.) PubMedSpringerLink

Note: Extracorporeal photopheresis and systemic calcineurin inhibitors or steroids are also part of whole-patient GVHD care; your hematology team directs these, and ocular outcomes often mirror systemic control. PMC

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Surgeries/procedures

1. Amniotic membrane therapy (e.g., PROKERA® ring or sutured graft) — Why: jump-start healing, reduce scarring/inflammation in severe surface disease or persistent epithelial defects. How: biologic bandage rich in anti-inflammatory/trophic factors for several days; studies show improved surface healing. aes.amegroups.orgASH Publications

2. Punctal cautery (permanent tear-drain closure) — Why: when plugs fall out or tears are extremely scant. How: heat seals the punctum to retain tears long term; improves symptoms/findings in oGVHD. PubMed

3. Tarsorrhaphy (partial lid sewing) — Why: protect the cornea in non-healing defects or exposure. How: narrows the opening to cut evaporation and friction; can be temporary or permanent. Wikipedia

4. Minor salivary gland transplantation — Why: in end-stage, refractory dry eye, transplanted glands secrete saliva to wet the surface. How: salivary tissue placed into the fornix provides continuous lubrication; case series/analyses show improved comfort and surface measures. PubMedLippincott Journals

5. Keratoprosthesis (artificial cornea) — Why: last resort for bilateral corneal blindness when standard grafts will fail. How: Boston KPro or similar devices can restore vision but carry high complication risk; only in highly selected oGVHD eyes. Lippincott Journals

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Prevention & self-care strategies

1. Start eye care before symptoms escalate;

2. Use preservative-free drops/meds when possible;

3. Keep a humidified home/office;

4. Wear wraparound eyewear outdoors;

5. Practice blink breaks on screens;

6. Do warm compress + lid hygiene daily;

7. Avoid smoke/wind/fans directly at your face;

8. Don’t sleep under strong airflow; use shields if lids don’t close fully;

9. Coordinate systemic GVHD control with your transplant team;

10. Follow-up regularly—catch erosions or pressure rises from steroids early. tfosdewsreport.orgAmerican Academy of Ophthalmology

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When to see a doctor

• Urgent (same day): sudden sharp pain, worsening light sensitivity, new blur that doesn’t clear with blinking, a white spot on the cornea, trauma, or discharge/fever (possible ulcer or perforation). PMC

• Soon (days): steady worsening dryness/redness, filaments, intolerance of light/screens, poor response to home care, or trouble keeping drops in due to stinging.

• Routine: after any transplant medication changes, or every 1–3 months during active oGVHD to adjust treatment and check eye pressure if using steroids. PMC

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What to eat & what to avoid

Eat more:

1. Oily fish (salmon, sardines) 2–3×/week for natural omega-3s;

2. Colorful veg/leafy greens (lutein/zeaxanthin, vitamin A precursors);

3. Citrus/berries (vitamin C);

4. Nuts/seeds (vitamin E);

5. Hydrating foods (soups, cucumbers) + regular water intake.

Limit/avoid when flaring:

1. Cigarette smoke exposure;
2. Very dry, spicy, or alcohol-heavy meals that worsen dehydration;
3. Highly processed foods rich in omega-6 oils (pro-inflammatory balance);
4. Excess caffeine late in the day if it worsens dryness;
5. Any supplement that interacts with your transplant meds—clear all supplements with your team first. (Nutrition is supportive; it doesn’t replace medical therapy.) tfosdewsreport.org

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Frequently asked questions (FAQs)

1) Is oGVHD “just dry eye”?
No. It’s immune-mediated damage to the ocular surface triggered by your transplant. Dryness is the leading symptom, but the disease involves inflammation, tissue remodeling, and risk to the cornea. PMC

2) How is it diagnosed?
By symptoms plus objective tests (staining, TBUT, Schirmer, meibography) and standardized scales (NIH eye score/ICCGVHD). Schirmer alone is not enough to follow disease activity. NatureAmerican Academy of Ophthalmology

3) Will steroid drops fix it?
Steroids calm flares quickly but are not a long-term solution because of side effects. Most people need steroid-sparing therapy (cyclosporine, tacrolimus, lifitegrast) to control inflammation safely. PMC

4) How long until cyclosporine/tacrolimus work?
Expect gradual improvement over 6–12 weeks; they remodel surface immunity. Stick with the plan unless side effects occur. PMC

5) Do scleral lenses really help?
Yes—by bathing the cornea in fluid all day and shielding it from air and friction. They can transform comfort and vision in severe disease. PubMed

6) Are punctal plugs safe?
Generally, yes. They can reduce symptoms and staining in oGVHD; some patients lose plugs and benefit from cautery for lasting effect. PMCPubMed

7) What about amniotic membrane (e.g., PROKERA)?
It’s a biologic bandage that accelerates healing and tames inflammation in severe surface disease or persistent defects. Often used for a few days. aes.amegroups.org

8) Do omega-3 supplements help?
Evidence is mixed: the large DREAM RCT didn’t show symptom benefit over placebo, though some analyses show improvements in signs or in specific groups. Food sources are reasonable; discuss supplements with your clinicians. New England Journal of MedicinePMC

9) What are “biologic” eye drops?
Autologous serum, platelet-rich plasma/lysate, and umbilical-cord serum provide growth factors and vitamins similar to natural tears—very useful in severe surface disease. They’re compounded under strict protocols. PubMedPMC

10) Can systemic GVHD medicines help my eyes?
Yes. Agents like ruxolitinib and belumosudil that control chronic GVHD can improve ocular involvement in some patients. Your hematology team decides timing and safety. IOVSPMC

11) Are moisture-chamber glasses worth it?
For many, yes. They trap humidity around the eyes and reduce evaporation; trials show benefits for signs/symptoms. PMC

12) Will I need surgery?
Most people improve without major surgery. In severe, non-healing cases, options like punctal cautery, tarsorrhaphy, amniotic membrane, or—rarely—keratoprosthesis are considered. PubMedaes.amegroups.orgLippincott Journals

13) How often should I follow up?
During active disease or treatment changes: every 1–3 months. Long-term stable patients: intervals individualized, with pressure checks if using steroids. PMC

14) Do preservatives matter?
Yes. Frequent preserved drops can aggravate the surface; preservative-free is strongly preferred in oGVHD. American Academy of Ophthalmology

15) What’s the big-picture plan?
Layer treatments: environment + scleral/eyewear + lid care + PF drops/ointments + immunomodulator drops, and escalate with biologic tears or systemic GVHD therapy as needed. Keep communication tight between your eye doctor and transplant team. PMC

 

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: August 16, 2025.