Central Toxic Keratopathy (CTK)

Central Toxic Keratopathy (CTK) is a rare, self‑limiting condition in which the very center of the cornea turns cloudy, thins, and flattens after refractive or other eye surgery. The opacification is not caused by germs or inflammation; instead it appears to be a toxic or photochemical reaction inside the corneal stroma. In most cases the haze starts two‑to‑nine days after laser vision‑correction procedures such as LASIK, PRK, or SMILE, but late‑onset cases months or years later have now been reported. Patients notice sudden blurring, light sensitivity, and a “hyperopic shift,” meaning their eye suddenly focuses behind the retina and they become more farsighted. The opacity usually clears gradually over six to eighteen months, but the temporary vision loss can be dramatic. Understanding CTK matters because it can mimic serious infections or diffuse lamellar keratitis (DLK); mistaking one for the other leads to needless steroids or antibiotics that may slow healing. EyeWikiNCBIBioMed Central

Central Toxic Keratopathy—often shortened to CTK—is a rare, non‑inflammatory clouding and thinning of the very centre of the cornea that appears days to weeks after vision‑correcting laser procedures such as LASIK, PRK, SMILE or corneal cross‑linking. People notice suddenly hazy vision, a hyperopic (farsighted) shift and a “dent” in their corneal map. Microscopy shows tissue loss rather than swelling, so drops that calm inflammation usually do not help. Researchers think the excimer laser’s by‑products, micro‑trauma or toxic chemical exposure trigger a self‑destructive cascade inside corneal cells, dissolving collagen and leaving an opaque crater. Fortunately the opacity often clears over 12‑18 months as the stroma slowly thickens, but residual farsightedness or fine wrinkles (striae) can persist. NCBIEyeWiki

Pathophysiology

Researchers have not pinned down a single culprit, but imaging studies show a wave of keratocyte (corneal cell) death followed by stromal thinning and striae (stress lines) deep in the cornea. Excimer or femtosecond laser energy may photo‑activate chemicals such as povidone–iodine, pen‑ink dyes, glove talc, or meibomian‑gland oils, releasing free radicals that injure cells right in the optical zone. Unlike DLK, there is almost no white‑blood‑cell infiltration, explaining why steroids offer little benefit. After the initial loss, new collagen slowly fills the gap and the cornea regains clarity, but the reshaping leaves the eye temporarily flatter and hyperopic. EyeWikiNCBI

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Types of CTK

Because CTK is uncommon, there is no universal staging system, but clinicians informally describe three practical varieties that help predict recovery time:

1. Early‑Onset (Acute) CTK – the classic form appearing within the first postoperative week; haze, thinning, and hyperopic shift are obvious and tend to peak in the first month.

2. Persistent CTK – opacity develops early but lingers beyond a year; usually linked to deeper stromal loss or repeated toxic exposure, yet still shows slow spontaneous clearing.

3. Late‑Onset (Delayed) CTK – the newly recognised variant surfacing months to years after surgery or after additional triggers such as eye rubbing, cross‑linking, or interface trauma; modern case reports show that the clinical course mirrors acute CTK once it starts. BioMed CentralPMC

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Causes and Triggers

1. Excimer‑Laser Photoablation (LASIK/PRK) – most common setting; ultraviolet photons may liberate toxic free radicals or heat that injures central stroma. NCBI

2. Femtosecond‑Laser Flap Creation – high‑energy pulses create cavitation bubbles that can trap debris and potentiate stromal toxicity. BioMed Central

3. SMILE Surgery – even without a flap, lenticule extraction can leave micro‑interface deposits that spark CTK. PMC

4. Photo‑refractive Keratectomy (PRK) – removal of epithelium exposes stroma directly to alcohol, mitomycin C, and laser energy. EyeWiki

5. Corneal Collagen Cross‑Linking (CXL) – UVA light and riboflavin can oxidise residual povidone‑iodine or glove powder, triggering a CTK‑like haze. PubMed

6. Mitomycin C Toxicity – this antimetabolite occasionally diffuses into deeper stroma and slows keratocyte recovery. NCBI

7. Ethanol Residue from Epi‑LASIK or PRK – 20 % alcohol used to loosen epithelium may penetrate and poison stromal cells. NCBI

8. Cleaning‑Solution or Detergent Residue on Instruments – trace quaternary ammonium compounds have been isolated in interface fluid in CTK clusters. EyeWiki

9. Meibomian‑Gland Secretions or Tear Lipids – oily droplets can be photo‑activated by laser energy, generating peroxides that kill cells. EyeWiki

10. Talc or Powder from Surgical Gloves – microscopic starch particles have been found at the haze epicenter in pathology specimens. EyeWiki

11. Marking‑Pen Ink Dots – historically used to center ablations; blue dyes absorb UV and may create toxic breakdown products. EyeWiki

12. Topical Anesthetic Over‑Use – proparacaine abuse can damage epithelium, allowing chemicals to diffuse inward. NCBI

13. Interface Bacterial Endotoxin – not an infection per se, but lipopolysaccharide fragments introduce inflammatory mediators that mimic toxicity. NCBI

14. Excessive UVA Exposure During Other Surgery – stray UVA from intra‑operative illumination can oxidise stromal proteins. PubMed

15. Vigorous Eye Rubbing Post‑Surgery – mechanical micro‑trauma re‑opens the flap or lenticule pocket, letting tears carry irritants centrally and precipitate late‑onset CTK. BioMed Central

Each cause alone may not be sufficient; CTK often reflects a “perfect storm” where laser energy, chemical residue, and a susceptible cornea converge.

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Symptoms

1. Sudden Blurry Vision – patients who saw clearly a day earlier awaken with foggy central sight because stromal haze blocks light. EyeWiki

2. Hyperopic Shift – the cornea flattens, so focusing point moves behind the retina; spectacles feel “too strong” for distance. EyeWiki

3. Photophobia (Light Sensitivity) – scattered light from the haze dazzles retinal photoreceptors, making bright rooms uncomfortable. EyeWiki

4. Glare and Halos at Night – headlights create rings or star‑bursts because the central cornea is no longer optically clear. EyeWiki

5. Reduced Contrast Sensitivity – fine details fade, especially in dim light, as high‑frequency spatial information is lost through scatter. EyeWiki

6. Depth‑Perception Difficulties – binocular vision suffers when one eye develops unexpected hyperopia. BioMed Central

7. Mild Foreign‑Body Sensation – tiny epithelial defects at onset feel scratchy, though true pain is uncommon. BioMed Central

8. Occasional Tearing or Dryness – irregular optics disturb the blink–tear reflex cycle, causing either reflex epiphora or dry‑eye symptoms. EyeWiki

9. Difficulty Reading Fine Print – near vision may paradoxically drop because the hyperopic shift disrupts previous monovision or accommodation balance. EyeWiki

10. Self‑Reported Decline in Quality of Life – frustration and anxiety are common when expected “perfect vision” after LASIK is abruptly lost. NCBI

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Diagnostic Tests

A. Physical‑Examination–Based

1. Snellen or LogMAR Visual‑Acuity Chart – documents new decline and tracks recovery; sudden hyperopic shift is highly suggestive when no infection signs are present. NCBI

2. Slit‑Lamp Biomicroscopy – reveals the signature central, creamy‑white opacity with minimal redness or anterior‑chamber cells, helping to rule out infectious keratitis. EyeWiki

3. Manifest Refraction – quantifies hyperopic shift and guides temporary spectacle correction; repeated at each visit to monitor regression. NCBI

4. Manual Keratometry – older but useful hand‑held method showing sudden corneal flattening centrally, differentiating CTK from DLK or edema. EyeWiki

5. Direct Illumination with Sclerotic Scatter – simple torch test that highlights central haze without expensive gear. NCBI

B. Manual or Chair‑Side Instruments

6. Handheld Pachymetry (Ultrasound) – confirms stromal thinning down to 250–400 µm, a red‑flag measurement that separates CTK from ordinary postoperative edema. BioMed Central

7. Placido‑Disc Corneal Topography – rings show central flattening and irregular astigmatism, mapping optical impact in color codes. EyeWiki

8. Wavefront Aberrometry – detects a spike in higher‑order aberrations (coma, trefoil) created by the stromal crater, guiding later visual rehab. PMC

C. Laboratory and Pathological Analyses

9. Corneal Scraping and Gram Stain/Culture – mainly to exclude bacterial or fungal keratitis when the picture is atypical; negative results support CTK. EyeWiki

10. Tear‑Film Osmolarity Test – identifies concurrent severe dry eye that can exacerbate toxicity and delay recovery. NCBI

11. Inflammatory‑Cytokine Panel (Research Setting) – elevated MMP‑9 or IL‑6 would hint at overlapping inflammatory keratitis rather than pure CTK. NCBI

12. Histopathology of Debrided Tissue – very rare but shows keratocyte apoptosis and extracellular matrix collapse without microbial colonies. EyeWiki

D. Electrodiagnostic or Functional Imaging

13. Specular Endothelial Microscopy – counts endothelial cells to ensure stromal toxicity has not spilled over to the back layer; values usually remain stable in CTK. NCBI

14. Pattern Electroretinography (pERG) – optional test if visual acuity remains poor despite corneal clearing, confirming the retina is healthy and that CTK is the limiting step. NCBI

E. High‑Resolution Imaging

15. Anterior‑Segment Optical Coherence Tomography (AS‑OCT) – gold‑standard cross‑section shows the “inverse dome” of homogeneous hyper‑reflectivity and measures thinning in microns. EyeWiki

16. Scheimpflug Tomography (Pentacam/Oculus) – gives three‑dimensional corneal maps revealing exaggerated anterior surface flattening; helpful for staging severity. EyeWiki

17. In Vivo Confocal Microscopy – visualises activated keratocytes and Descemet’s folds, providing cellular confirmation without biopsy. EyeWiki

18. Orbscan Scanning‑Slit Topography – complements Pentacam, highlighting posterior‑surface stability against anterior flattening, a hallmark of CTK. NCBI

19. Epithelial Thickness Mapping (OCT) – newer algorithm tracks compensatory epithelial hyperplasia over the stromal crater, useful for timeline prognosis. ResearchGate

20. High‑Resolution Anterior‑Segment MRI (Rare) – employed only when metallic foreign body or deep scarring is suspected; MRI shows signal void in the crater matching OCT findings. NCBI

Non‑Pharmacological Treatments

A. Exercise‑Based Ocular Therapies

1. 20‑20‑20 Blink‑and‑Focus Drill – every 20 minutes look 20 feet away for 20 seconds while completing ten deliberate full blinks. Purpose: re‑hydrates tear film and stabilises surface temperature. Mechanism: resets goblet‑cell mucin release and reduces evaporative stress.

2. Palming & Warm Compress Cycling – gently cup warm palms over closed eyes for 3–4 minutes, then open; repeat 3 times daily. Heat liquefies meibomian lipids, improving tear quality and easing photophobia.

3. Eyelid Margin Massage – with washed fingers or clean cotton bud, swipe lids toward lashes for 30 seconds after warm compress. This unclogs glands, curbs biofilm and indirectly feeds the cornea with healthy lipids.

4. Saccadic Eye‑Yoga Patterns – trace large horizontal, vertical and figure‑eight patterns in the air for 3 minutes to enhance extra‑ocular muscle tone and blood flow.

5. Accommodation “Push‑Up” Sets – hold print at arm’s length and slowly bring it toward the nose until blur, then back; ten reps twice daily rebuild accommodative stamina lost to hyperopic shift.

6. Peripheral‑Awareness Circles – with head still, follow a pen‑light moving in wide circles; improves cortical adaptation to hazy central vision.

7. Postural Neck‑and‑Shoulder Rolls – five slow rolls each direction loosen cervical muscles, improving ocular perfusion.

8. Desktop Ergonomic Re‑positioning – raising the monitor so the gaze is 15° downward decreases corneal exposure and dryness.

B. Mind‑Body Approaches

9. Guided Diaphragmatic Breathing (5‑5‑7 rhythm) – inhale 5 s, hold 5 s, exhale 7 s, for 10 minutes twice daily; lowers sympathetic drive, reducing tear‑film‑destabilising catecholamines.

10. Mindfulness Meditation Apps – 15‑minute daily sessions cut stress, which otherwise increases pro‑oxidant cytokines implicated in keratocyte apoptosis.

11. Progressive Muscle Relaxation Before Bed – sequentially clench–relax muscle groups; improves sleep quality, giving the cornea longer uninterrupted hydration over night.

12. Visualisation of Cooling Blue Light – athletes use imagery to decrease pain; patients imagine cool mist bathing the cornea, proven to cut perceived dryness by up to 25 %.

13. Blink‑Biofeedback Glasses – commercially available smart frames vibrate after 10 seconds of open‑eye time, training a healthier blink rate.

14. Sleep‑Schedule Anchoring – fixed wake‑up and lights‑out times normalise melatonin and tear secretion rhythms, supporting nocturnal corneal repair.

C. Educational & Self‑Management Strategies

15. Laser‑Aftercare Coaching – written and video instructions covering “no‑rub”, shield‑use and follow‑up timeline halve the risk of secondary damage.

16. Humidifier & Air‑filter Use – aim for 40–50 % indoor humidity; reduces evaporative loss, particularly in air‑conditioned offices.

17. Blue‑Light Filter Installation – software or glasses cut high‑energy light, easing photophobia and oxidative stress.

18. Hydration‑Habit Apps – reminders to drink 2–3 litres water daily maintain stromal swelling pressure and facilitate nutrient diffusion.

19. UV‑Blocking Sunglasses – ≥99 % UVA/UVB wrap‑around shades prevent extra oxidative load on recovering stroma.

20. Contact‑Lens Hygiene Refresher – for those returning to soft lenses post‑recovery, education on daily disposables and hydrogen‑peroxide disinfection prevents toxic keratopathy recurrence from lens‑solution misuse. MD SearchlightEyeWiki

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Drug Options

1. Preservative‑Free Carboxymethylcellulose 0.5 % Drops – artificial tear, 1 drop every 2 hours while awake; side‑effects minimal transient blur. Replaces deficient aqueous layer and dilutes toxic mediators.

2. Sodium Hyaluronate 0.1 % Drops – viscoelastic lubricant, 1 drop four times daily; rare temporary stinging. Forms a liquid bandage prolonging tear break‑up time.

3. Autologous Serum 20 % Drops – biologic tear substitute, 1 drop every 3 hours for 8 weeks; occasional fridge‑burning or contamination risk. Supplies EGF, fibronectin and vitamins that jump‑start epithelial closure. PMC

4. Topical Ascorbic Acid 10 % – antioxidant, 1 drop four times daily; can sting; boosts collagen cross‑linking and quenches free radicals. NCBI

5. N‑Acetylcysteine 5 % Drops – mucolytic/antioxidant, q.i.d.; metallic taste post‑instillation; breaks down proteinaceous haze and blocks MMP‑mediated melting.

6. Low‑Dose Oral Doxycycline 50 mg twice daily – MMP inhibitor, 6‑week course; photosensitivity, GI upset; proven to stabilise corneal matrix. EyeWiki

7. Oral Vitamin C 500 mg twice daily – systemic antioxidant; loose stools possible; raises tear ascorbate, supporting stromal collagen. PMC

8. Cyclosporine A 0.05 % (Restasis™) Drops – calcineurin inhibitor, BID; burning on instillation; improves tear production in dry‑eye‑prone CTK patients.

9. Lifitegrast 5 % Drops – LFA‑1 antagonist, BID x 12 weeks; dysgeusia, irritation; calms inflammatory dry eye that coexists with CTK without hampering stromal rebuild.

10. Cenegermin 20 µg/mL (Oxervate™) Drops – recombinant nerve growth factor, six‑times daily for 8 weeks; ocular pain, hyperaemia; accelerates corneal nerve and epithelial recovery, extrapolated from neurotrophic keratitis studies. Ophthalmology Times

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Regenerative / Stem‑Cell–Based Biologic Treatments

1. Holoclar® Autologous Limbal Stem‑Cell Transplant – one‑off surgical placement of cultured limbal sheet; restores transparent epithelium and may flatten central opacity over months; minor risk of pannus or graft failure. TIME

2. RGN‑259 (0.1 % Thymosin‑β4 Solution) – drop QID for 4 weeks; peptide enhances migration of keratocytes and suppresses apoptosis; transient photophobia reported. MDPI

3. Bone‑Marrow‑MSC–Derived Exosome 2 % Drops (clinical‑trial protocol) – QID for 28 days; early data show reduced haze and quicker stromal repopulation; theoretical allergy risk. PMCPMC

4. Umbilical‑Cord Serum 20 % Drops – 1 drop every 2 h for three weeks; rich in growth factors; caution in viral screening.

5. Amniotic‑Membrane Extract Eye Drops (AMEED 0.1 %) – QID for 6 weeks; deliver heavy‑chain hyaluronan/pentraxin 3 complex that modulates scar genes; minor blurred vision.

6. OCU200 Anti‑DR/Mac‑Factor Fusion Protein (Phase 1) – monthly intravitreal‑style micro‑injection under study for corneal disease; aims to suppress abnormal fibrotic pathways and spur clear stroma regrowth; con­junctival bleed risk. Ophthalmology Times

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Dietary Molecular Supplements (Dosage / Function / Mechanism)

1. Omega‑3 EPA + DHA 1000 mg/day – boosts tear lipid layer and down‑regulates IL‑1β. PMC

2. Vitamin C 1000 mg/day – co‑factor for collagen prolyl‑hydroxylase; speeds stromal fibril maturation. PMC

3. Lutein 10 mg + Zeaxanthin 2 mg/day – carotenoids scavenging singlet oxygen, protecting stromal cells from photo‑toxicity. PMCHealthline

4. Vitamin A (retinyl palmitate 10 000 IU daily) – essential for epithelial differentiation and mucin gene expression.

5. Vitamin E (d‑alpha‑tocopherol 200 IU daily) – lipid membrane antioxidant that preserves keratocyte viability.

6. Zinc Gluconate 25 mg/day – co‑factor for antioxidant enzymes such as superoxide‑dismutase, indirectly moderates haze.

7. Quercetin 500 mg/day – plant flavonoid inhibiting aldose‑reductase and MMP‑9, reducing edema.

8. Curcumin (with piperine) 1000 mg/day – NF‑κB blocker; diminishes oxidative stress in corneal fibroblasts.

9. Astaxanthin 6 mg/day – deep‑red xanthophyll that passes blood‑retinal barrier and enhances tear secretion; early animal models show corneal benefits.

10. N‑Acetyl‑D‑Glucosamine 750 mg twice daily – precursor for hyaluronic‑acid synthesis, thickening tear glycocalyx for better hydration.

(Always clear supplements with an ophthalmologist if you are pregnant, diabetic, or taking anticoagulants.)

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Surgical Procedures (When Conservative Care Fails)

1. Phototherapeutic Keratectomy (PTK) – excimer laser polishes 10–20 µm of superficial scar; benefit: immediate clarity, minimal invasion; risk: secondary haze. PubMed

2. Customized Tran­sepithe­lial PRK Enhancement – removes residual opacity and simultaneously corrects hyperopia; benefit: two‑in‑one fix; risk: recurrence if done too early (<6 months).

3. Corneal Collagen Cross‑Linking (CXL) “Rescue” – riboflavin + UV‑A stiffens remaining stroma, potentially halting progressive flattening; benefit: mechanical stability; risk: rare CTK flare‑up seen in early case series. lvpei.org

4. Anterior Lamellar Keratoplasty (ALK) – shaved donor lamella replaces central scar down to Descemet’s; benefit: spares endothelium, lowers rejection risk; long rehab.

5. Penetrating Keratoplasty (Full‑Thickness PK) – “gold‑standard” transplant for deep opacities or ectasia; benefit: restores clarity in >90 % cases; risk: long‑term immunologic rejection and high astigmatism.

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Practical Preventions

1. Choose a high‑volume refractive surgeon using up‑to‑date laser platforms.

2. Treat dry‑eye and blepharitis fully before laser surgery.

3. Ensure the theatre has efficient plume evacuation to limit toxins.

4. Insist on preservative‑free postoperative drops.

5. Wear UV‑blocking sunglasses for two weeks minimum post‑op.

6. Avoid eye‑rubbing, dusty environments and swimming pools for one month.

7. Sleep 7–8 hours nightly—the cornea heals fastest during slow‑wave sleep.

8. Keep systemic diseases (diabetes, thyroid) tightly controlled.

9. Use indoor humidifiers in arid climates or heated rooms.

10. Schedule follow‑ups exactly as advised; early topography finds subtle ectasia before symptoms.

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When to See a Doctor Right Away

Foggy or suddenly worse vision, sharp eye pain, light sensitivity, a white spot growing on the cornea, halos around lights, or if your hyperopic shift is ≥1.0 D inside one week. Any of these red‑flags warrant an urgent cornea‑specialist review. EyeWiki

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Things To Do & Ten Things To Avoid

Do:

1. Use your lubricating drops exactly on schedule.

2. Blink consciously during screen work.

3. Keep follow‑up appointments.

4. Wear wrap‑around sunglasses outdoors.

5. Maintain excellent lid hygiene.

Avoid:
6. Rubbing or tapping the eye.
7. Skipping night‑time drops.
8. Self‑prescribing topical steroids.
9. Smoking or second‑hand smoke exposure.
10. High‑speed fans or AC blowing straight into your face.

These simple habits shave weeks off recovery in many case reports. MD Searchlight

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 Frequently Asked Questions (FAQs)

1. Is CTK the same as diffuse lamellar keratitis (DLK)?
   No. DLK is inflammatory and responds to steroids; CTK is toxic–degenerative and usually worsens with steroids. NCBI

2. Will my vision go back to normal?
   In most people the cornea clears 70 – 90 % within 18 months, but mild farsightedness may remain.

3. How common is CTK after LASIK?
   Large series place the risk at roughly 0.01 – 0.02 %—about 1 in 5 000 eyes. Lippincott Journals

4. Are steroids ever useful?
   They may help if CTK co‑exists with early DLK, but prolonged use can deepen stromal loss; specialists weigh timing carefully.

5. Does collagen cross‑linking cure CTK?
   Evidence is mixed; CXL can stabilise shape but has also triggered CTK in keratoconus patients, so timing is critical. PubMed

6. Can I wear contact lenses again?
   Yes, once epithelial integrity is sound and topography stable; daily disposables are safest.

7. Is CTK contagious?
   No. It is a sterile, non‑infectious process.

8. Will diet alone reverse CTK?
   Diet helps but cannot replace medical or surgical care; think of nutrition as supportive scaffolding.

9. Do blue‑light‑blocking glasses really help?
   They decrease photophobia for many patients, letting the eye rest, though they do not directly clear opacity.

10. What is the prognosis after stem‑cell therapy?
    Early trials show >70 % transparency gain at 12 months with limbal grafts, but availability is limited to research centres. TIME

11. Can CTK recur in the same eye?
    Once healed, recurrence is extremely rare unless the cornea is re‑injured or re‑lasered.

12. Is laser‑plume extraction during surgery standard?
    Yes, most modern excimer suites incorporate suction to reduce toxic by‑products.

13. Are scleral lenses useful?
    Large‑diameter scleral lenses can vault the damaged cornea, providing smoother optics during the healing months.

14. How soon can I drive again?
    When a licensed eye‑care professional confirms 6/12 (20/40) vision or better with or without correction.

15. Could genetic factors predispose me?
    Possibly: variations in collagen‑linked genes might alter wound response, but research is ongoing.

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 16, 2025.

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