Cicatricial Conjunctivitis

“Cicatricial” is another word for “caused by a scar.” “Conjunctivitis” means inflammation of the conjunctiva―the thin, clear membrane that covers the white of your eye and lines the inside of your eyelids. Put them together and cicatricial conjunctivitis is long-lasting inflammation that leaves permanent scar tissue on the conjunctiva. Those scars gradually shrink (a process doctors call contracture), tugging on surrounding structures—eyelids, tear-gland openings, and even the cornea. The scarring can seal the normal pocket between the lid and the eyeball (the fornix), make the eyelids turn inward (entropion), and misdirect lashes so they scratch the cornea (trichiasis). Vision-threatening dryness, infection, or corneal ulcer can follow. Unlike the everyday “pink eye” that clears in days, cicatricial conjunctivitis is a chronic, progressive disorder that demands detective-level diagnosis and active, often lifelong care.

Cicatricial conjunctivitis is a long-term inflammatory disease in which the thin, moist membrane that lines the white of the eye and the inner eyelids (the conjunctiva) becomes chronically inflamed and gradually replaced by fibrous scar tissue. “Cicatricial” literally means “scarring.” Over months or years the scar tissue can shrink, tighten, and pull on surrounding structures. This leads to red, dry, gritty eyes, distorted eyelids, eyelashes that rub the cornea (trichiasis), and progressive loss of vision if left uncontrolled. Unlike ordinary pink-eye, cicatricial conjunctivitis almost never resolves on its own—early, sustained treatment is essential.

Healthy conjunctiva is soft, moist, and elastic. In cicatricial disease the supporting layer (the substantia propria) is invaded by immune cells that release enzymes and pro-fibrotic chemicals such as transforming growth factor-β. These messengers order fibroblasts—the tissue’s “repair crew”—to lay down thick, disorganized sheets of collagen. Over time those sheets behave like shrink-wrap, shortening the conjunctiva and fixing it to the deeper tissues. The same inflammatory tide can destroy goblet cells that normally secrete the mucin layer of tears and can wipe out accessory lacrimal glands that produce the watery layer. The end result is a dry, fragile ocular surface that cannot heal efficiently.

The main types doctors recognise

Although every case shares the core feature of progressive scarring, clinicians break cicatricial conjunctivitis into several practical categories based on what is driving the scarring. Understanding the type helps guide treatment and tells the eye-care team how closely to watch for damage elsewhere in the body.

1. Auto-immune mucous-membrane pemphigoid (ocular cicatricial pemphigoid) – the conjunctiva is the chief target of an autoimmune attack on proteins that glue the surface layer to the deeper tissue.

2. Stevens-Johnson syndrome / toxic epidermal necrolysis – a sudden, drug-triggered immune storm that peels skin and mucous membranes; months later the healed conjunctiva contracts.

3. Trachoma-related scarring – recurrent infection by Chlamydia trachomatis causes decades-long scarring, still common in parts of Africa and Asia.

4. Chemical or thermal burns – alkali splash, acid injury, or uncontrolled radio-frequency heat in cosmetic procedures can destroy conjunctival stem cells and spark scarring.

5. Chronic mechanical trauma – long-standing entropion, poorly fitted contact lenses, or prosthetic eyes can set up low-grade inflammation that eventually scars.

6. Post-surgical fibrosis – aggressive healing after pterygium or strabismus surgery can tighten the conjunctiva.

7. Graft-versus-host disease – donor immune cells after bone-marrow transplant attack the patient’s conjunctiva, teeth, skin, and lungs, leading to dryness and scarring.

8. Atopic or vernal kerato-conjunctivitis – severe, unrelenting allergy in childhood can remodel the conjunctiva into a tough, milky sheet.

9. Rosacea-related ocular surface disease – inflammatory mediators in facial rosacea can spill over onto the conjunctiva, tipping it toward fibrosis.

Remember that one person can belong to more than one category—for example, a burn victim who later receives a bone-marrow transplant may develop additive scarring from both causes.

Causes

1. Ocular cicatricial pemphigoid (OCP) – a mis-timed immune response makes antibodies against hemidesmosome proteins (BP180, BP230). The antibodies unlock complement proteins, setting off chronic inflammation.

2. Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) – sulfonamide antibiotics, anticonvulsants, or cold medicines can push T-cells to kill skin and mucus cells; the healing phase lays down scar tissue.

3. Trachoma – repeated C. trachomatis infections trigger follicles, then papillary hypertrophy, then scarring. Each infection layer is like adding a thin coat of glue.

4. Sulfur mustard gas exposure – veterans of chemical warfare can develop delayed-onset limbal stem-cell deficiency and conjunctival fibrosis.

5. Alkali burns (e.g., lye) – alkali penetrates deep, saponifying cell membranes within seconds; stem-cell loss means the epithelium heals as contractile scar.

6. Long-term glaucoma drops (benzalkonium chloride toxicity) – preservatives strip lipid membranes, inducing sub-epithelial fibrosis over years.

7. Prolonged soft-contact-lens overwear – micro-trauma plus bacterial exotoxins maintain low-grade inflammation.

8. Radiation therapy to orbit/nasal sinuses – ionizing radiation kills basal cells and microvasculature, nudging tissue to scar rather than regenerate.

9. Atopic keratoconjunctivitis – interleukin-4 and -5 keep eosinophils active; their granule proteins erode conjunctiva and invite fibroblasts.

10. Graft-versus-host disease – donor T-cells perceive conjunctival antigens as “foreign,” launching a lichen-planus-like fibrosing reaction.

11. Severe vitamin A deficiency – dryness and metaplasia weaken tissue; secondary infections and healing drive scars.

12. Chronic papillary conjunctivitis from ocular prosthesis – the rough front surface rubs each blink, stirring scarring cytokines.

13. Rosacea – meibomian gland inflammation spills onto conjunctiva; cathelicidin peptides activate fibroblasts.

14. Long-standing entropion or trichiasis – in-turned lashes scrape epithelium; each micro-ulcer heals with a filament of scar.

15. Rare inherited syndromes (EEC, aniridia with PAX6 mutation) – abnormal limbal stem cells fail to preserve conjunctival architecture, promoting fibrosis from early life.

Symptoms

1. Persistent redness – dilated blood vessels remain even on “good” days because scarring prevents proper vascular regulation.

2. Dry-gritty sensation – goblet-cell loss means fewer mucins to lubricate the eye; each blink feels like sandpaper.

3. Foreign-body feeling – strands of scar tissue (“symblepharon”) tether lid to globe; every eye movement tugs painfully.

4. Burning or stinging – exposed nerve endings from a thin tear film fire continuously.

5. Photophobia (light sensitivity) – dry, eroded corneal nerves become hypersensitive, and an irregular surface scatters light.

6. Stringy or mucous discharge – poor tear circulation allows proteins to condense into ropy strands.

7. Blurred or fluctuating vision – an uneven tear film acts like a warped lens, especially after blinking.

8. Eyelid malposition (entropion or ectropion) – scarring shortens the posterior (inner) lamella, flipping the lid inward or, rarely, outward.

9. Pain on eye movement – symblepharon restrict motion, so the globe tugs on scarred tissue each time you look sideways.

10. Loss of eyelashes or mis-directed lashes – follicles are destroyed or rotated by contracting tissue.

Diagnostic tests

A. Physical-exam-based investigations

1. Comprehensive history and visual-acuity check
   The doctor documents drug exposures, autoimmune disease, or travel to trachoma-endemic areas. Visual acuity serves as a baseline to measure future damage and guides urgency of treatment.

2. External inspection and lid-position analysis
   Good lighting reveals entropion, lagophthalmos, or lash loss. Skin scarring, mouth ulcers, or genital lesions hint at systemic mucous-membrane pemphigoid or SJS.

3. Slit-lamp biomicroscopy
   This microscope magnifies 10–40× and projects a thin light beam to map conjunctival scarring, measure fornix depth, and spot keratinized plaques on the cornea.

4. Ocular-surface staining with fluorescein and lissamine-green
   Dyes pool in damaged epithelium. A pattern of scattered punctate spots suggests early dryness; large confluent patches warn of stem-cell failure.

5. Tear-film break-up time (TBUT)
   After a fluorescein drop the examiner times how many seconds elapse before black “dry spots” appear. Under 10 seconds signals unstable tears, common in scarring disease.

B. Manual or bedside functional tests

6. Eyelid eversion and fornix-depth measurement
   The examiner flips the upper lid and inserts a sterile ruler inside the fornix. A normal upper fornix is 13‒15 mm deep; less than 8 mm suggests moderate scarring.

7. Forced-duction test
   Under topical anesthetic, fine forceps grasp the eye at the limbus to check passive rotation. Restriction implies scarring bands anchoring the globe.

8. Schirmer I test
   A filter-paper strip placed in the lower lid measures basic tear output over five minutes. Less than 5 mm wetting confirms severe aqueous deficiency.

9. Eyelash epilation and regrowth observation
   Lashes are gently removed; in active cicatricial disease they often grow back misdirected within weeks, whereas in a quiet eye they take months.

C. Laboratory and pathological studies

10. Conjunctival biopsy for haematoxylin–eosin histology
    A 3 × 2 mm sample from the inferior fornix is fixed and stained. Thickened collagen bundles, loss of epithelial goblet cells, and subepithelial fibrosis clinch the diagnosis.

11. Direct immunofluorescence (DIF)
    A fresh biopsy is snap-frozen and labeled with fluorescent anti-human IgG, IgA, and C3. Linear basement-membrane staining proves ocular cicatricial pemphigoid.

12. Indirect immunofluorescence (IIF)
    Patient serum is applied to monkey oesophagus substrate. Circulating anti-basement-membrane antibodies, when present, glow under UV light, supporting systemic involvement.

13. ELISA for BP180/BP230 antibodies
    A quantitative blood test detects these specific pemphigoid antibodies and helps monitor response to systemic immunosuppressants.

14. Microbiological culture/PCR for Chlamydia trachomatis
    Conjunctival swabs go to an NAAT lab. A positive result earns extra antibiotics and signals community screening is needed.

D. Electrodiagnostic or sensor-based assessments

15. Blink-reflex electromyography
    Surface electrodes over orbicularis oculi record impulse latency after corneal air-puff. Delayed reflex may follow fibrosis of the lid margin sensory nerves.

16. Tear-osmolarity testing (electrical impedance)
    A disposable microchip touches the tear meniscus; elevated salt concentration (> 308 mOsm/L) indicates evaporative or aqueous-deficient dryness caused by scarring.

17. Infra-red meibography with dynamic thermal imaging
    High-resolution IR cameras map oil-gland dropout and surface temperature. Heat loss points to gland atrophy common in long-standing cicatricial disease.

E. Imaging-based evaluations

18. Anterior-segment optical coherence tomography (AS-OCT)
    Like an “optical ultrasound,” AS-OCT captures 5-µm cross-sections. It quantifies conjunctival thickness, locates fibro-vascular plaques, and measures symblepharon depth without touching the eye.

19. In vivo confocal microscopy
    A handheld lens scans living tissue cell-by-cell. Loss of limbal stem-cell palisades and activated keratocyte patterns warn of impending corneal melt.

20. Orbital CT or MRI
    Ordered when scarring seems deeper than visible or when double vision hints at extra-ocular-muscle fibrosis. Imaging also rules out a masquerading tumor or retained foreign body.

Non-Pharmacological Treatments

(Grouped as Exercise Therapies, Mind-Body Approaches, and Educational Self-Management)

Medications suppress inflammation, but scarring still accelerates when the ocular surface is dry, contaminated, or mechanically irritated. Lifestyle and rehabilitative tactics give drugs a chance to work and empower patients to protect their vision long-term.

Exercise Therapies

1. Blink Training
   Description – Conscious, full eyelid closes every 5 seconds for 5 minutes, 4 times a day.
   Purpose – Redistributes tear film and prevents eyelid adhesions.
   Mechanism – Mechanical sweeping of inflammatory debris and activation of meibomian glands to release protective oils.

2. Lid-Margin Massage
   Gentle rolling of both lids with a clean fingertip for 30 seconds after warm compresses. Improves oil flow, easing dryness.

3. Warm Compress Routines
   42 °C moist heat packs applied for 10 minutes twice daily liquefy meibomian secretions, reducing friction on the scarred conjunctiva.

4. Ocular Surface Stretching
   Guided outward “yawning” of the eyelids with sterile cotton-tipped applicators (performed by a clinician) keeps shrinking conjunctiva from tethering lids to the globe.

5. Facial Yoga for Orbicularis Strength
   Repetitive gentle squints and releases strengthen the blinking muscle so each blink becomes more complete.

6. Protected Tear Break-Up Time (pTBUT) Drills
   Using non-preserved artificial tears, patients note how long tears last before blur appears; then train to blink just before that moment, minimizing dry exposure.

7. Micro-scleral Lens Insertion Practice
   Daily rehearsal of applying and removing large-diameter fluid-filled lenses improves confidence and reduces handling trauma.

Mind-Body Approaches

8. Mindfulness-Based Stress Reduction (MBSR)
   Guided meditation 20 minutes daily lowers systemic cortisol and inflammatory cytokines linked to auto-immune flares.

9. Biofeedback-Assisted Relaxation
   Heart-rate variability devices teach patients to enter parasympathetic “rest-and-digest” mode, which dampens immune overactivity.

10. Guided Imagery for Symptom Control
    Visualizing cool, soothing tears reduces perceived dryness and pain, breaking the itch–rub–scar cycle.

11. Progressive Muscle Relaxation
    Systematically tensing and releasing facial muscles lessens reflex blepharospasm (painful forced eyelid closure) common in severe cases.

12. Cognitive-Behavioral Therapy (CBT)
    Short-term CBT helps reframe catastrophic thoughts (“I’m going blind”) into proactive coping plans, boosting adherence to complex regimens.

13. Yoga-Nidra (Yogic Sleep)
    A 30-minute guided session promotes deep relaxation; small trials show reduced tear film osmolarity (saltiness) afterward—an anti-dryness effect.

Educational Self-Management

14. Disease Literacy Workshops
    Small-group sessions where ophthalmologists explain disease stages and treatment goals; knowledge predicts better follow-up and lower scar progression.

15. Environmental Trigger Identification
    Patients learn to keep symptom diaries, correlating flares with pollen, smoke, makeup, or screen time, then minimize causative exposures.

16. Protective Eyewear Training
    Wrap-around glasses and moisture chambers retain humidity and shield from windborne irritants.

17. Digital-Device Hygiene
    The 20-20-20 rule (look 20 ft away for 20 sec every 20 min) plus blue-light filters cut blinking deficits and oxidative stress.

18. Contact Lens Safety Modules
    Emphasize strict hand-washing, daily disposable lenses, and no overnight wear to avoid secondary infections that accelerate scarring.

19. Tear-Friendly Home Modifications
    Using humidifiers (>45 % RH), avoiding ceiling fans over beds, and switching to preservative-free household cleaners reduces ocular dryness.

20. Shared-Decision-Making Checklists
    Printable checklists empower patients to ask about drug alternatives, side-effect warning signs, and surgery timelines, fostering collaboration.

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Evidence-Based Drugs

(Class, Typical Adult Dose, Timing, Key Side Effects—always confirm with your ophthalmologist)

1. Prednisolone Acetate 1 % Eye Drops – Topical corticosteroid; 1 drop every 2 hours acute, taper to 2–4×/day; watch for cataract, glaucoma.

2. Topical Cyclosporine A 0.05–0.1 % – Calcineurin inhibitor; 1 drop twice daily; may sting, rare burning or infection risk.

3. Tacrolimus 0.03 % Ointment – Off-label peri-ocular immunomodulator; apply thin layer at bedtime; local redness or herpes reactivation possible.

4. Dapsone 100 mg tablets – Sulfone antibiotic-immunomodulator; once daily; screen for G6PD deficiency, monitor blood counts/methemoglobinemia.

5. Azathioprine 1–2 mg/kg/day – Purine-synthesis blocker; take with food morning and night; monitor liver enzymes, WBC.

6. Mycophenolate Mofetil 1 g twice daily – Lymphocyte DNA blocker; GI upset, teratogenic—use contraception.

7. Cyclophosphamide 2 mg/kg/day – Alkylating agent for severe OCP; take early morning, drink plenty of water; risk of bladder toxicity, infections.

8. Methotrexate 15–25 mg once weekly – Anti-folate; folic-acid rescue 1 mg/day; beware liver fibrosis, lung inflammation.

9. Rituximab 375 mg/m² IV weekly ×4 – Anti-CD20 monoclonal; given in hospital; infusion reactions, hepatitis B reactivation.

10. Doxycycline 100 mg twice daily (or 40 mg once AM sub-antimicrobial) – Tetracycline anti-collagenase; photosensitivity, reflux esophagitis.

Note: Choices depend on severity, comorbidities, and pregnancy status. Combination therapy is common; dosing can vary.

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Dietary Molecular Supplements

Safety first: Tell your physician about every supplement—some interact with immunosuppressants.

1. Omega-3 Fatty Acids (DHA/EPA) – 2 g/day; lowers ocular surface inflammation by shifting prostaglandin balance.

2. Vitamin A (Retinyl Palmitate) – 5,000 IU/day oral or 0.01 % eye ointment nightly; supports conjunctival goblet-cell mucus production.

3. Vitamin D3 (Cholecalciferol) – 2,000 IU/day; modulates T-helper cell activity.

4. Vitamin C (Ascorbic Acid) – 500 mg twice daily; co-factor for collagen remodeling and antioxidant defense.

5. Zinc Gluconate – 20 mg/day; needed for epithelial repair enzymes.

6. N-Acetylcysteine (NAC) – 600 mg twice daily or 5 % eye drops 3×/day; breaks down mucous filaments and replenishes glutathione.

7. Curcumin (Turmeric Extract with Piperine) – 500 mg three times daily; suppresses NF-κB inflammatory signaling.

8. Lutein & Zeaxanthin – 10 mg lutein + 2 mg zeaxanthin daily; concentrates in ocular tissues, protecting against oxidative stress.

9. Selenium (as Selenomethionine) – 200 µg/day; complements glutathione peroxidase.

10. Multi-strain Probiotics (≥10 billion CFU/day) – Improve gut barrier, indirectly calming systemic auto-immunity.

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Regenerative / Stem-Cell-Based “Drugs”

1. Autologous Serum Eye Drops (20 %)
   Dose – 1 drop 6–10×/day from patient’s own blood.
   Function – Delivers epidermal growth factor, fibronectin, and vitamin A.
   Mechanism – Mimics natural tears, promoting epithelial healing and inhibiting scar enzymes.

2. Platelet-Rich Plasma (PRP) Eye Drops
   Similar schedule; high platelet-derived growth factor accelerates repair.

3. Cord Blood Serum Drops
   Allogeneic but highly anti-inflammatory; used every 2–4 hours for severe epithelial defects.

4. Amniotic Membrane Extract Drops
   Freeze-dried amnion lysate instilled 4×/day; rich in anti-fibrotic cytokines.

5. Cultivated Limbal Epithelial Stem-Cell Suspension
   Topical application after debridement; 1 mL bolus under bandage lens once; repopulates limbal stem cell niche.

6. Mesenchymal Stem-Cell-Conditioned Media
   Experimental; 1 drop hourly first week, then taper; exosomes transfer anti-scarring micro-RNAs.

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Surgeries

1. Mucous-Membrane Grafting
   Procedure – Oral buccal mucosa harvested and sutured to scarred conjunctiva.
   Benefits – Restores smooth, moist surface and prevents lid-globe fusion.

2. Amniotic Membrane Transplantation
   Biological patch from donor placenta placed on ocular surface; supplies anti-inflammatory proteins and acts as scaffold.

3. Limbal Stem-Cell Transplantation (Simple Limbal Epithelial)
   Healthy limbal tissue from patient’s other eye or a donor replaces destroyed stem cells; can halt progressive corneal opacity.

4. Eyelid Entropion / Trichiasis Repair
   Rotational sutures or tarsal wedge resection rotates lashes outward, preventing corneal scratches.

5. Boston Keratoprosthesis (Artificial Cornea)
   For end-stage corneal scarring; acrylic cylinder fixed into cornea restores a clear optical pathway, rapidly improving sight when other grafts fail.

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Preventive Strategies

1. Treat any episode of conjunctivitis early.

2. Never use preserved eye drops long-term unless essential; prefer preservative-free.

3. Wear wrap-around sunglasses in dusty or windy places.

4. Keep ambient humidity above 45 %.

5. Avoid rubbing your eyes—use chilled lubricants instead.

6. Manage systemic autoimmune diseases aggressively in partnership with a rheumatologist.

7. Quit smoking to reduce oxidative stress on the ocular surface.

8. Get yearly eye exams even if stable—scarring can restart silently.

9. Vaccinate against infections (e.g., measles) that can trigger SJS.

10. Educate family members: prompt referral if they notice red, stuck-together lids.

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When to See an Eye Doctor Immediately

• Sudden increase in pain, redness, or light sensitivity.

• New mucus threads attaching lids to eyeball (early symblepharon).

• Vision drop or fog that doesn’t clear after blinking.

• Blood-tinged tears or blistering skin lesions (possible Stevens-Johnson onset).

• Any infection symptoms if you’re on immunosuppressants: fever, chills, mouth sores.

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Things to Do—And to Avoid

Do:

1. Use preservative-free artificial tears hourly if advised.

2. Follow your blink drill schedule faithfully.

3. Apply warm compresses before bedtime.

4. Log daily symptoms in a smartphone diary.

5. Keep medication and supplement lists updated for every clinician.

Avoid:

1. Sleeping in contact lenses.

2. Over-the-counter “get-the-red-out” vasoconstrictor drops.

3. Smoking or second-hand smoke exposure.

4. Rubbing or tapping the eyes, even when itchy.

5. Skipping follow-up appointments because “they look okay.”

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Frequently Asked Questions (FAQs)

1. Is cicatricial conjunctivitis contagious?
   No—the underlying auto-immune or scarring process itself cannot spread from person to person, although trachoma infection can.

2. Can the scarring be reversed?
   Early inflammation can be suppressed; established dense scars rarely disappear but surgery or regenerative drops can restore function.

3. Will I need medication forever?
   Many patients taper to low-dose maintenance once scarring is quiet. The schedule is individualized.

4. Are topical steroids dangerous?
   Long courses can cause glaucoma or cataracts, but benefits outweigh risks when monitored carefully.

5. Is it safe to drive?
   If vision meets legal standards and glare is controlled with moisture chambers, yes—ask your ophthalmologist for a formal assessment.

6. Can diet really help my eyes?
   Anti-inflammatory nutrients support tear quality; they do not replace immunosuppressive drugs but can reduce flare frequency.

7. Do blue-light-blocking glasses treat the disease?
   They reduce digital eye strain and dryness triggers but do not affect the immune component directly.

8. What’s the difference between serum drops and artificial tears?
   Serum drops contain natural growth factors and vitamins absent in synthetic lubricants, promoting healing.

9. Will insurance cover stem-cell therapy?
   Coverage varies; many regenerative treatments remain experimental outside tertiary centers.

10. How long does mucous-membrane graft surgery take to heal?
    Comfort returns in 1–2 weeks; full surface maturation can take 3 months.

11. Can children develop cicatricial conjunctivitis?
    Yes, especially in genetic blistering disorders or severe Stevens-Johnson syndrome; prognosis improves with early immunotherapy.

12. Is laser eye surgery (LASIK) contraindicated?
    Strongly discouraged—pre-existing tear film instability and immune activation raise complication risk.

13. Are over-the-counter antihistamine drops helpful?
    They may ease itching but often contain preservatives; use preservative-free versions only under advice.

14. Could my dry mouth and skin rash be related?
    Possibly—auto-immune diseases such as mucous membrane pemphigoid often involve multiple mucosal sites. Report all symptoms.

15. Do I need to stop contact sports?
    Protective goggles make most sports feasible; avoid dusty fields or chlorine pools during active flares.

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: July 17, 2025.

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