Corneal Keloid

A corneal keloid is an uncommon, benign but potentially sight-threatening over-growth of fibrous scar tissue that sits on, or invades into, the normally crystal-clear cornea. Under the microscope the lesion is packed with dense, disorganised collagen fibres, activated fibroblasts and excess glycoproteins; Bow­man’s membrane is usually ruptured, and the surface epithelium becomes hyper-plastic and uneven. Clinically the keloid appears as a pearly-white or gray, elevated mound, often vascularised, that can enlarge for months or even years after the inciting event. Because the cornea supplies two-thirds of the eye’s focusing power, even a small opaque mound can scatter incoming light and blur vision, while larger plaques may distort the corneal curvature enough to trigger irregular astigmatism or amblyopia. EyeWiki

Keloidogenesis represents an exaggerated wound-healing response. After any corneal injury the body releases cytokines (e.g., TGF-β, PDGF, IL-6) that normally switch keratocytes into repair mode. In susceptible individuals—probably those with a genetic predilection and a persistently inflamed ocular surface—this cascade never switches off. Fibroblasts keep laying down collagen, angiogenic signals sprout new vessels, and myofibroblasts contract, pulling adjacent stroma into a thick lump. The process is analogous to cutaneous keloids seen on earlobes and sternum, but the optical consequences are far more serious because the cornea must remain transparent to work. NCBI

A corneal keloid is an uncommon, pearly-white, elevated nodule that forms on the front layer of the eye after the normal corneal-wound-healing cascade goes awry. Fibroblasts proliferate, Bow-man’s layer splinters, and disorganised collagen accumulates, creating a bulging “scar-tumour” that can blur vision, cause glare, and cosmetically disfigure the eye. Although many cases follow obvious triggers—penetrating trauma, chemical burns, herpetic keratitis, surgery, or chronic atopic blepharitis—up to one-third are idiopathic or congenital. Fewer than 100 well-documented cases have been published since 1865, underscoring the disease’s rarity. EyeWikiPubMed

Pathophysiology

Any deep epithelial or stromal injury releases transforming-growth-factor-β (TGF-β) and platelet-derived growth factors that recruit fibroblasts. In susceptible corneas those fibroblasts over-express collagen types I & III, while matrix metalloproteinases underperform, so collagen turnover slows. Disrupted Bow-man’s layer fails to act as a “speed-bump,” letting scar tissue mushroom anteriorly. Chronic inflammation, eye-rubbing, eyelid malposition, and oxidative stress worsen the cycle, explaining why atopic eye disease or neurotrophic keratopathy predispose patients. PMC

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Types of corneal keloid

1. Primary (congenital or idiopathic) – lesions arise without any documented trauma, infection or surgery. They are thought to begin in utero or early infancy when corneal stromal development is dysregulated. These keloids may remain small for years before suddenly enlarging during adolescence or after minor eye rubbing. PMC

2. Secondary (acquired) post-traumatic – the classic scenario. Any penetrating or blunt corneal insult—abrasion, foreign body, alkali burn, penetrating keratoplasty suture track—can kick-start keloid formation months or even decades later. The long lag helps clinicians distinguish keloids from simple hypertrophic scars, which plateau once the epithelium closes. PubMed

3. Secondary to chronic surface disease – persistent epithelial breakdown in severe atopic keratoconjunctivitis, neurotrophic keratopathy, Stevens–Johnson syndrome, ocular cicatricial pemphigoid or chronic herpetic keratitis can produce a “never-ending” wound-healing milieu that favors keloidogenesis. PMC

4. Radiation-related or post-orbital tumour therapy – ionising radiation alters keratocyte DNA and vascular supply, sometimes leading to delayed exuberant scarring many years after treatment. PMC

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Main causes

1. Penetrating corneal trauma – a laceration that slices through Bow­man’s membrane triggers maximal fibroblast activation, setting the stage for bulky collagen deposition long after the wound closes.

2. Severe mechanical abrasion – even “simple” scratches that denude large epithelial areas leave Bow­man’s layer patchy, and the repair can overshoot into keloid. AAFP

3. Retained or deeply embedded foreign body – metals or vegetative matter create persistent irritation and stromal inflammation, fuelling fibroplasia. NCBI

4. Thermal or chemical burns (alkali > acid) – these rapidly dissolve stromal proteoglycans and unleash intense cytokine storms.

5. Infectious keratitis (bacterial, fungal, viral) – ulceration plus immune infiltration damages the collagen lattice, predisposing to scar over-growth.

6. Repeated corneal surgeries – multiple PKPs, PRKs or LASIK enhancements continuously disrupt wound stability.

7. Tight or broken corneal sutures – friction and micro-movement prolong inflammation at the wound edge.

8. Chronic contact-lens–induced hypoxia – epithelial micro-breaks and neovascularisation supply scaffolding for fibrosis.

9. Neurotrophic keratopathy – loss of trigeminal sensation prevents normal blink-induced epithelial turnover; stagnant ulcers persist.

10. Atopic eye disease – constant rubbing, tear film cytokines and eosinophil products amplify fibroblast activity. PMC

11. Ocular cicatricial pemphigoid – auto-antibodies attack basement membrane, leading to relentless surface breakdown.

12. Stevens–Johnson syndrome / toxic epidermal necrolysis – severe mucocutaneous inflammation melts corneal epithelium; subsequent healing is chaotic.

13. Radiation therapy to orbit – endothelial loss and fibroblast DNA changes promote excessive stromal repair.

14. Excessive ultraviolet light exposure – UV induces ROS-mediated collagen cross-linking and keratocyte apoptosis that may distort wound modulation.

15. Genetic keloid diathesis – individuals who develop skin keloids on ears or shoulders frequently form corneal keloids after minor ocular trauma.

16. Uncontrolled diabetes mellitus – hyperglycaemia hampers orderly collagen remodelling and heightens AGE-related stiffness.

17. Chronic topical steroid abuse – paradoxically, prolonged steroids thin epithelium and may mask slow stromal injury that later fibroses.

18. Severe keratoconjunctivitis sicca (dry eye) – desiccation cracks epithelium, opening “micro-wound” portals for fibroblast migration.

19. Exposure keratopathy from lagophthalmos – inadequate lid closure leaves cornea constantly desiccated and inflamed, breeding scar tissue.

20. Congenital corneal dermoid resection – removal of limbal dermoids can leave bare, limbal stroma that proliferates into keloid if healing is unbalanced.

Each cause feeds one or more components of keloid pathophysiology—persistent inflammation, disrupted Bow­man’s layer, ongoing neovascular supply, or excessive myofibroblast activity—so preventing recurrence hinges on minimising these triggers.

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Common symptoms and signs

1. Blurred or foggy vision – the opaque mound scatters light, lowering visual acuity, especially in bright sunlight.

2. Glare and halos at night – irregular surface curvature spreads on-coming headlights into rings.

3. Photophobia (light sensitivity) – inflamed corneal nerve endings and stray light both make looking at light painful. uvahealth.com

4. Foreign-body sensation – the elevated plaque disturbs lid glide, making patients feel as though grit is in the eye.

5. Chronic redness – superficial blood vessels grow into the lesion, injecting the surrounding conjunctiva with visible redness.

6. Tearing (epiphora) – reflex lacrimation tries to flush debris but instead blurs sight further.

7. Bland or throbbing ocular ache – deeper stromal nerves become stretched by the rigid scar.

8. Astigmatic headaches – asymmetrical corneal curvature forces ciliary muscles to strain, causing brow ache.

9. Diminished contrast sensitivity – scattering reduces the eye’s ability to discriminate subtle shading.

10. Monocular diplopia (double vision in one eye) – refracted rays hit two retinal points because the surface contour is highly irregular.

11. Reduced corneal sensitivity – paradoxically, chronic keloid may desensitise nerves as fibrosis strangulates terminals.

12. Peripheral corneal thinning adjacent to lesion – differential biomechanical stress may “pull” on nearby tissue.

13. Progressive enlargement of the white mass – patients notice the spot growing toward the pupil over months.

14. Visible superficial vessels crossing limbus – angiogenic factors create feeder vessels that are easily seen in a bright mirror. Cleveland Clinic

15. Psychological distress or cosmetic concern – the striking appearance can lead to anxiety and reduced social confidence, especially in children.

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Further diagnostic tests

A. Physical-exam based

1. Torch-light external inspection – with room lights off, a simple pen-torch shows the pearly mound, its size, vascularity and whether it encroaches on the pupil. It also reveals lid closure quality and gross conjunctival inflammation.

2. Visual-acuity testing with Snellen or logMAR chart – quantifies the functional impact; unequal acuities hint at keloid-induced optical distortion rather than neurological disease.

3. Slit-lamp biomicroscopy – the ophthalmologist focuses a thin beam across the cornea to map depth, edges, colour, vessel presence and over-lying epithelial health in real-time high magnification. The slit beam can detect any stromal infiltrate suggesting infection.

4. Pupillary light reflex evaluation – although mainly neurological, an afferent pupillary defect would urge clinicians to rule out optic-nerve or macular disease before attributing vision loss solely to the keloid.

B. Manual / bedside tests

5. Fluorescein staining and cobalt-blue illumination – liquid dye pools in epithelial defects, showing whether the keloid’s surface is intact, leaking or at risk for infection.

6. Cotton-wisp or Cochet–Bonnet esthesiometry – gently touching the cornea checks corneal nerve integrity; hypo-aesthesia suggests neurotrophic component that worsens prognosis.

7. Non-contact or Goldmann applanation tonometry – measures intra-ocular pressure; raised IOP plus large keloid could tip diagnosis toward co-existing glaucoma risk.

8. Schirmer tear test – a small filter paper strip in the lower lid measures tear production over five minutes, screening for dry-eye contribution to ongoing surface damage.

C. Laboratory / pathological tests

9. Histopathology of excised tissue – definitive diagnosis. Pathologists look for thick, haphazard collagen bundles, claw-shaped epithelium and disrupted Bow­man’s membrane, confirming keloid rather than dermoid, granuloma or malignancy. PubMed

10. Periodic-acid–Schiff (PAS) stain and Masson trichrome – special stains highlight basement-membrane fragments and collagen turnover, helping stage maturation.

11. Microbial culture and sensitivity – any ulcerated surface is swabbed to rule out secondary bacterial or fungal infection that might masquerade as rapid keloid growth.

12. Polymerase-chain-reaction (PCR) for herpes simplex virus (HSV) – chronic HSV keratitis causes recurrent epithelial loss and scarring that can lead to keloid; positive PCR alters long-term anti-viral management.

D. Electrodiagnostic / biomechanical tests

13. Ocular response analyser (ORA) corneal-hysteresis measurement – a rapid air-puff and infra-red detector calculate visco-elastic damping; low hysteresis implies stroma stiffened by scar, guiding surgical planning.

14. Corneal pachymetry with ultrasound probe – not imaging per se; it gives a tactile sound-wave-based map of thickness, showing whether the keloid invades full thickness or remains superficial.

15. Visual-evoked potential (VEP) – electrodes on the scalp record cortical responses to flashing light; normal VEP with poor acuity confirms the problem lies in the front (cornea) not the back (optic nerve).

16. Electro-retinogram (ERG) – while rarely needed, a normal ERG reassures that retinal photoreceptors are intact when vision is disproportionately poor, ruling out masquerading retinal dystrophies.

E. Imaging tests

17. Anterior-segment optical coherence tomography (AS-OCT) – light-wave interferometry creates cross-sectional images at micron-level resolution, revealing precise depth, stromal disorganisation, and epithelial thickness. It also shows cleavage planes that help surgeons plan lamellar resection.

18. Ultrasound biomicroscopy (UBM, 50 MHz) – high-frequency sound shows deeper extension into Descemet’s membrane or anterior chamber; useful when the keloid is opaque to light-based OCT.

19. Corneal topography / tomography (Scheimpflug or Placido-disc) – maps curvature and elevation. Localised steepening or flattening patterns quantify irregular astigmatism and track post-operative regression.

20. High-resolution orbital CT or MRI – ordered when the lesion appears unusually bulky or when concomitant scleral, orbital or eyelid pathology is suspected, ensuring no hidden mass or calcification.

Collectively, these twenty tools let clinicians: (a) confirm the diagnosis, (b) stage the lesion’s invasiveness, (c) identify active inflammation or infection, (d) calculate the optical burden, and (e) strategise whether medical quietening or surgical excision plus grafting will give the best visual rehabilitation.

Non-Pharmacological Treatments

(Each entry is a stand-alone paragraph describing the therapy, its purpose, and its mechanism.)

1. Observation & Lubrication – Frequent preservative-free artificial tears keep the epithelial surface wet, reduce microtrauma during blinking, and dilute inflammatory cytokines; early, tiny lesions sometimes plateau without invasive care.

2. Protective Eyewear – Poly-carbonate safety glasses guard against repeat trauma, the most consistent external driver of keloid growth, breaking the injury-inflammation cycle.

3. Therapeutic Soft Contact Lenses – Bandage lenses shield regenerating epithelium, stabilise the tear film, and lessen pain, allowing quieter stromal remodelling.

4. PROSE / Scleral Lenses – Fluid-filled vaults bathe the cornea in saline all day, minimising shear forces and optical distortion for larger or central nodules.

5. Pressure Patching & Silicone Eye Pads – Gentle, sustained pressure is thought to down-regulate fibroblast activity (paralleling silicone-sheet therapy used for cutaneous keloids).

6. Digital Corneal Massage – Carefully taught, low-amplitude lid massage may thin pliable collagen in early lesions, though evidence is anecdotal.

7. Cryotherapy – Cold-probe application induces vascular shutdown and fibroblast apoptosis, shrinking select superficial keloids.

8. Pulsed Dye Laser (PDL) – 585-nm pulses target haemoglobin in new vessels, starving hyper-vascular lesions and dampening TGF-β signalling.

9. Nd:YAG Disruption – Low-energy shots into the keloid’s apex create cavitation bubbles, fragmenting collagen bundles in slim lesions.

10. Intense Pulsed Light (IPL) – Used mainly for ocular-rosacea–related dry eye; IPL’s anti-inflammatory effect can indirectly calm keloid progression.

11. Ultraviolet-A Corneal Cross-Linking – Riboflavin-activated UVA light stiffens stromal collagen, hampering further bulge and adding biomechanical stability.

12. Low-Dose Superficial Radiotherapy – Borrowed from cutaneous keloid care, it inhibits fibroblast mitosis when surgery is contraindicated.

13. Amniotic Membrane Transplantation (AMT) – The membrane delivers anti-scarring cytokines, acts as a biologic bandage, and has shown success as an adjunct in three published cases. PubMed

14. Autologous Serum Eye Drops (20 %) – Contain epidermal-growth-factor and fibronectin, speeding healthy epithelial resurfacing, which in turn limits aberrant fibroplasia.

15. Platelet-Rich Plasma Drops – High platelet-derived-growth-factor levels foster orderly stromal remodelling and quell inflammation.

16. Topical Growth-Factor Antagonist Therapy – Experimental heparin-binding peptides compete with TGF-β, aiming to normalise collagen turnover.

17. Phototherapeutic Keratectomy (PTK) – Excimer-laser ablation “shaves” microns of abnormal collagen with sub-micron precision, smoothing the surface and often halting regrowth when paired with adjuvant drugs. EyeWiki

18. Micropulse Diode Laser Therapy – Sub-threshold pulses lower fibroblast viability without overt tissue destruction; early studies mirror benefits seen in skin.

19. Patient Education & Behavioural Change – Teaching patients to avoid eye-rubbing, adhere to treatment, and attend follow-ups directly affects outcomes.

20. Psychologic Support – Visible ocular lesions can cause anxiety; counselling improves adherence and overall quality of life, indirectly improving healing dynamics.

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Key Drug Treatments

(Dose ranges are adult averages; paediatric use requires specialist adjustment.)

1. Prednisolone Acetate 1 % Ophthalmic Suspension – Class: Corticosteroid. Dose: 1 drop every 2 h for 1 week, taper over 6 weeks. Timing: Start at first sign of lesion activity. Side-effects: Raised IOP, cataract, infection risk. PMC

2. Fluorometholone 0.1 % – Softer steroid for long-term maintenance; similar schedule, lower IOP risk.

3. Triamcinolone Acetonide (40 mg/mL) Intralesional Injection – 0.1–0.2 mL into keloid once monthly × 3. Potently arrests fibroblast proliferation; may cause transient ocular hypertension.

4. Mitomycin C 0.02 % Drop – Class: Alkylating antimetabolite. Dose: 1 drop qid for 14 days post-keratectomy or 2 minutes intra-op soak. Suppresses DNA synthesis in residual fibroblasts. Side-effects: Delayed epithelial healing, scleral melt if overdosed. PubMedLiebert Publisher

5. 5-Fluorouracil 1 % Topical – 1 drop qid for 2-4 weeks or 0.1 mL 50 mg/mL intrastromal injection; inhibits thymidylate synthase, reducing collagen production.

6. Tranilast 300 mg orally daily – Class: Anti-allergic/keloid modulator; blocks mast-cell histamine release and TGF-β signalling; small case series show adjunct benefit post-keratoplasty. PubMed

7. Cyclosporine A 0.05 % Eye Drops – Calcineurin inhibitor dosed bid; decreases IL-2 and downstream fibroblast activation.

8. Tacrolimus 0.03 % Ointment – Similar pathway; thin smear bid on closed lids to limit perilesional inflammation.

9. Interferon-α2b 1 MIU/mL – Off-label topical qid; promotes collagenase activity, softening lesions; flu-like systemic symptoms rare at ocular doses.

10. Bevacizumab 1.25 mg subconjunctival – Anti-VEGF monoclonal antibody; regresses neovascular tents that feed the keloid, indirectly starving fibroblasts; retreat every 6–8 weeks as needed.

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Dietary Molecular Supplements for Ocular Surface Healing

1. Omega-3 Fatty Acids (1000 mg EPA + DHA daily) – Anti-inflammatory eicosanoid shift aids epithelial recovery, proven in dry-eye trials. PMC

2. Vitamin A (900 µg retinol equivalents) – Essential for mucin gene expression and epithelial integrity.

3. Vitamin C (500 mg) – Collagen-synthesis co-factor; scavenges reactive oxygen species in healing corneas.

4. Vitamin E (400 IU mixed tocopherols) – Lipid-phase antioxidant that stabilises cell membranes during oxidative stress.

5. Vitamin D₃ (1000 IU) – Modulates innate immunity, reducing chronic ocular surface inflammation.

6. Lutein 10 mg + Zeaxanthin 2 mg – Concentrate in macula but also protect anterior segment against blue-light oxidative damage; observational links to faster epithelial closure.

7. Zinc (10 mg) – Cofactor for superoxide-dismutase and collagenase enzymes, balancing scar turnover.

8. Selenium (55 µg) – Integral for glutathione-peroxidase, boosting antioxidant defences.

9. Curcumin (500 mg with piperine bid) – Down-regulates NF-κB; topical nano-curcumin gels are under study for corneal scarring.

10. Green-Tea Catechins (EGCG 300 mg) – Polyphenols cut IL-1β and TNF-α release, easing inflammatory drive. Prevention

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Regenerative / Stem-Cell–Based Pharmaceutical Approaches

1. CALEC (Cultivated Autologous Limbal Epithelial Cells) – One-time bio-engineered sheet transplanted onto a denuded cornea; restores native epithelium and halted keloid regrowth in a recent phase I trial (0.5–1 cm² graft). Mass General Brigham

2. Holoclar® – EMA-approved limbal-stem-cell therapy; single 2×3 mm autologous graft; mechanism mirrors CALEC.

3. Umbilical-Cord-Blood Serum (30 %) Drops, q2h – Rich in growth factors; accelerates re-epithelialisation and modulates fibrosis genes.

4. Platelet-Rich Plasma-Derived Exosome Eye Drops (0.5 mL qid) – Nanovesicles carry anti-fibrotic miRNAs; early compassionate-use cases report flattening of immature keloids.

5. Adipose-Derived Mesenchymal Stem Cell Suspension (2×10⁶ cells subconjunctival) – Secretes hepatocyte-growth-factor and stromal-derived-factor-1, tipping balance toward regenerative healing.

6. 20 % Autologous Serum Drops (already listed under non-pharmacological but pharmacologic composition warrants mention) – Dosage q2h during waking hours for 4–8 weeks; supplies fibronectin and epithelial-growth-factor for orderly lamina restoration.

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Surgical Procedures & Why They Are Performed

1. Superficial (Manual) Keratectomy – Surgeon excises the keloid lump plus a 0.5-mm margin, restoring a smooth optical surface and allowing re-epithelialisation over healthier stroma.

2. Phototherapeutic Keratectomy (Excimer Laser) – Computer-guided laser vapourises 50-150 µm of anterior stroma; done when lesion is shallow and centrally located. UPMC | Life Changing Medicine

3. Lamellar Keratoplasty – Diseased anterior layers are removed and replaced by donor lamella, sparing endothelium; ideal for mid-stromal involvement with clear posterior cornea. PubMed

4. Penetrating Keratoplasty (Full-Thickness Graft) – Entire cornea swapped when keloid penetrates deep stroma or recurs after lamellar graft, aiming to restore clarity and globe shape. PMC

5. Amniotic Membrane Transplant (with or without keratectomy) – Provides a biologic scaffold rich in anti-fibrotic factors; especially useful for recurrent or inflammatory lesions. PubMed

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Practical Preventions

1. Wear certified eye protection during sports, manual work, or windy, sandy environments.

2. Treat any corneal infection promptly to avert intense stromal inflammation.

3. Control allergic eye disease; reduce itching that provokes rubbing.

4. Follow post-operative eye-drop schedules strictly after any ocular surgery.

5. Keep contact lenses clean and change on schedule to avoid microtrauma.

6. Maintain good eyelid hygiene to prevent blepharitis-related inflammation.

7. Hydrate adequately; a stable tear film resists epithelial breakdown.

8. Avoid smoking; tobacco smoke doubles oxidative stress on corneal tissue.

9. Eat an antioxidant-rich diet (see below).

10. Schedule yearly comprehensive eye exams, or sooner if symptoms evolve.

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When to See an Eye-Care Professional

Seek urgent ophthalmic review if you notice a new pearly or white bump on the cornea, any sudden drop in vision, pain, photophobia, eye redness that persists > 48 hours, or after any eye trauma—even if minor. Early therapy curbs lesion size and improves surgical outcomes.

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What to Eat – and What to Avoid

Eat more: leafy greens (spinach, kale), oily fish (salmon, sardine), citrus fruits, colourful peppers, carrots/sweet-potatoes, nuts & seeds, eggs, turmeric-spiced dishes, berries, and green-tea.
Limit or avoid: ultra-processed sugary snacks, trans-fat fried foods, very salty packaged meals, binge alcohol, smoking (yes, not a food but crucial), high-glycaemic soft drinks, energy drinks high in caffeine, cured meats, artificial food dyes, and chronic excessive red-meat intake.

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Frequently Asked Questions

1. Is a corneal keloid cancer? – No, it is benign scar tissue without malignant potential.

2. Can it make me blind? – Large central lesions can block or distort vision, but timely therapy usually preserves sight.

3. Will over-the-counter eye drops cure it? – Lubricants ease symptoms but do not reverse established keloids; medical or surgical care is required.

4. Is it contagious? – Absolutely not; you cannot “catch” a keloid from someone else.

5. Who is at highest risk? – People with prior corneal trauma, surgery, or chronic inflammatory eye disease; darker skin phenotypes may scar more aggressively.

6. Can children develop corneal keloids? – Yes, congenital cases exist; paediatric ophthalmology referral is vital.

7. What are the earliest signs? – A tiny, glistening white spot on the cornea, mild haze, or increased glare at night.

8. Does surgery guarantee it won’t come back? – Recurrence rates vary (10-40 %); adjuvant drugs like Mitomycin C and steroids cut the risk.

9. How long is recovery after keratectomy? – Epithelial healing takes 1-2 weeks; visual stabilisation may need several months.

10. Can I wear contact lenses afterward? – Often yes, but only under medical guidance to avoid repeat trauma.

11. What eye-drop side effects should I watch for? – Steroids can raise eye pressure—report headaches, haloes, or nausea promptly.

12. Is LASIK safe if I had a corneal keloid? – No; corneal lasers for refractive correction are contraindicated until the ocular surface is stable post-treatment.

13. Are corneal keloids hereditary? – Very rarely; most cases are acquired.

14. Will insurance cover treatment? – Medically necessary excision or transplantation is usually covered; cosmetic procedures may not be.

15. What can I do at home right now? – Stop rubbing your eyes, use preservative-free artificial tears, and book an eye exam.

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 01, 2025.