Trichoodontoonychodysplasia

Tricho-odonto-onychodysplasia is a genetic condition in which the outer body tissues that come from the ectoderm (hair, teeth, nails, skin, sweat glands) do not form normally. People often have very sparse or dry hair, nail changes (thin, brittle, split, or oddly shaped nails), and tooth problems like missing teeth or very thin/weak enamel. Some have dry skin, thick skin on palms/soles (palmoplantar keratoderma), and sweating problems (either too little or too much). A well-described related form (OODD) has many of these features and is linked to WNT10A gene changes; other tricho-odonto-onycho disorders may have different inheritance patterns and extra features such as syndactyly. PMC+2PubMed+2

Trichoodontoonychodysplasia is a very rare genetic ectodermal dysplasia. “Tricho-odonto-onycho-dermal” simply means it mainly involves hair (tricho), teeth (odonto), nails (onycho), and skin (dermal). People typically have dry or sparse hair, missing or small teeth with thin enamel, brittle or ridged nails, and thick or sweaty skin on the palms and soles. Most reported families show autosomal recessive inheritance caused by pathogenic variants in the WNT10A gene, which guides early development of hair follicles, tooth buds, nails, and skin appendages. PMC+2Nature+2

Other names

Tricho-odonto-onycho-dermal dysplasia (TOOD/TOODD), odonto-onycho-dermal dysplasia (OODD), a WNT10A-related ectodermal dysplasia, and the historical label tricho-odonto-onycho-dermal syndrome. These names refer to the same core clinicogenetic entity; many modern reports use OODD because WNT10A variants are the major cause. PubMed+2Cell+2

Types

Because this condition is rare, “types” are based on pattern and severity rather than strict subtypes:

1. Classic OODD – the full pattern: severe tooth agenesis and enamel defects, nail dystrophy, dry hair, smooth tongue (papillae loss), palmoplantar hyperkeratosis, and variable sweating problems (too little or too much). Most have biallelic WNT10A variants. PMC+1

2. OODD with eyelid/sweat-gland features (WNT10A spectrum) – some families show overlap with other WNT10A phenotypes (e.g., apocrine hidrocystomas in Schöpf-Schulz-Passarge syndrome). This is best viewed as a phenotypic spectrum of WNT10A-related ectodermal dysplasias. Wiley Online Library+1

3. Milder/heterozygous WNT10A presentations – carriers can have isolated tooth number or enamel changes or subtle nail or hair signs, illustrating variable expressivity. Nature

Take-home: clinicians use genotype (WNT10A) + feature pattern to label the “type,” because the spectrum overlaps with other ectodermal dysplasias. NCBI

Causes

1. Pathogenic variants in WNT10A disrupt a signaling protein crucial for tooth, hair, nail, and skin appendage formation—the main proven cause. Nature

2. Autosomal recessive inheritance—most affected individuals inherit one altered WNT10A copy from each parent. PMC

3. Loss-of-function WNT10A mutations (nonsense, splice-site, frameshift) reduce or abolish protein function, producing the full OODD phenotype. PMC

4. Missense WNT10A mutations can alter structure or receptor interaction, sometimes yielding complete OODD in homozygotes. Nature

5. Compound heterozygosity (two different WNT10A variants) can cause classic disease with variable severity. Wiley Online Library

6. Genetic background/modifiers—other developmental genes likely modify hair/teeth/nail severity, explaining differences within families. (Inference consistent with variability in WNT10A disorders.) Nature+1

7. Consanguinity increases the chance both parents carry the same rare WNT10A variant, raising autosomal-recessive risk. PMC

8. Embryonic ectodermal pathway disturbance—broad disruption of ectodermal organogenesis underlies the shared hair/teeth/nail/skin features (the ectodermal dysplasia concept). NCBI

9. Defective enamel formation (amelogenesis) driven by WNT10A loss explains thin/soft enamel. PMC

10. Abnormal tooth bud initiation leads to hypodontia/oligodontia. Nature

11. Impaired hair-follicle morphogenesis causes dry/sparse hair. PMC

12. Nail matrix dysplasia disrupts nail plate growth, causing ridging and brittleness. PMC

13. Altered sweat gland development/function yields hyperhidrosis or hypohidrosis of palms/soles in some patients. PMC

14. Papillae loss on the tongue (smooth tongue) reflects reduced development/maintenance of lingual papillae. PubMed

15. Skin barrier changes promote palmoplantar keratoderma and generalized dry skin. PMC

16. Phenotypic overlap within WNT10A spectrum can add features (e.g., eyelid cysts) in some families. Wiley Online Library

17. Heterozygous state can “cause” mild isolated dental anomalies, a partial expression of the same pathway defect. Nature

18. Diagnostic delay is common because findings span multiple specialties (dentistry, dermatology), which can worsen dental wear and nail damage if untreated. BioMed Central

19. Misclassification as other “tooth-nail” syndromes (e.g., Witkop) can occur if skin and tongue signs are missed. PMC

20. Environmental wear on thin enamel (dietary acids, bruxism) does not cause the disorder but worsens dental damage in affected individuals. (Clinical management principle in EDs.) NCBI

Symptoms and signs

1. Missing or small teeth (hypodontia/oligodontia)—often many permanent teeth never form. PMC

2. Thin, weak enamel—teeth look yellow-brown, wear quickly, and are cavity-prone. PMC

3. Dry, sparse hair—hair may feel rough and be hard to style. PMC

4. Brittle, ridged nails (onychodysplasia)—nails can split, peel, or grow slowly. PMC

5. Smooth tongue—the tiny bumps (papillae) are reduced, giving a flat, smooth look. PubMed

6. Thick skin on palms/soles (palmoplantar keratoderma)—may crack or feel tender. PMC

7. Sweating problems—hands/feet may sweat too much or too little. PMC

8. Very dry skin (xerosis)—needs frequent moisturizing. PMC

9. Mouth dryness or burning in some patients with smooth tongue. PubMed

10. Cosmetic concerns and self-esteem impact due to hair/teeth/nail appearance—common in ectodermal dysplasias. NCBI

11. Tooth sensitivity and pain from enamel thinning and rapid wear. PMC

12. Chewing difficulty because of missing teeth and enamel defects. PMC

13. Speech clarity issues when many teeth are missing, especially front teeth. (Dental consequence noted across EDs.) NCBI

14. Recurrent nail infections due to nail plate fragility and splits. (Dermatologic consequence of onychodysplasia.) PMC

15. Family clustering—others in the family may have similar findings, often with consanguinity in classic cases. PMC

Diagnostic tests

A) Physical examination

1. Full skin–hair–nail exam to document dryness, palmoplantar keratoderma, hair sparseness, and nail ridging. This bedside step guides which labs/genetics to order. PMC

2. Oral exam by a dentist to count missing teeth, assess enamel thickness, and note wear or cavities. Dental patterns are a major diagnostic clue. PMC

3. Tongue inspection for smooth surface and papillae loss, which is highly characteristic in OODD. PubMed

4. Sweat pattern check of palms/soles (history and inspection) to note hyperhidrosis/hypohidrosis. PMC

5. Family history and pedigree (including consanguinity), because most classic cases are autosomal recessive. PMC

B) “Manual” clinical tests

6. Dental charting with study models to map tooth absence/shape and plan prosthetic rehabilitation. (Core in ED dental care.) NCBI

7. Hair-shaft light microscopy on plucked hairs to look for structural changes consistent with ectodermal dysplasia. NCBI

8. Dermoscopy of nails and skin to visualize nail plate ridging/splitting and palmoplantar keratosis patterns non-invasively. NCBI

9. Salivary flow assessment (sialometry) if mouth dryness or caries risk is high to tailor preventive care. NCBI

10. Dietary/bruxism assessment to quantify enamel wear contributors; helpful in management though not diagnostic per se. NCBI

C) Laboratory and pathological tests

11. Targeted WNT10A gene sequencing (Sanger or NGS) is the definitive test to confirm the clinical diagnosis. Nature

12. Ectodermal dysplasia gene panel if the phenotype is atypical or if WNT10A is negative, to survey overlapping ED genes. NCBI

13. Copy-number analysis (exome CNV or chromosomal microarray) when single-gene testing is unrevealing but suspicion remains. (General ED genetics workflow.) NCBI

14. Segregation testing in parents/siblings to document autosomal-recessive inheritance and carrier status. PMC

15. Skin biopsy (optional)—histology may show nonspecific hyperkeratosis; used mainly to exclude other disorders. PMC

16. Enamel micro-hardness/mineral density assays (research/advanced dental care) to quantify enamel weakness and monitor restorations. (ED dental literature principle.) NCBI

17. Microbiology for nail infections if recurrent paronychia is present, to guide treatment (secondary issue in onychodysplasia). PMC

D) Electrodiagnostic and physiologic tests

18. QSART (quantitative sudomotor axon reflex test) or electrodermal activity testing to objectively measure sweat gland function in patients with hyper-/hypohidrosis of the palms/soles. (Useful in EDs with sweat dysfunction.) NCBI

19. Thermoregulatory sweat testing (whole-body mapping) when heat-intolerance or anhidrosis is suspected, to quantify risk and guide lifestyle counseling. NCBI

20. Audiology is sometimes added when families report hearing issues, mainly to exclude other EDs in the differential; classic OODD does not typically cause hearing loss. NCBI+1

E) Imaging tests

21. Panoramic dental X-ray (OPG) to count missing teeth and view root/crown shapes—standard in evaluation. PMC

22. Cone-beam CT of jaws (if planning implants) to map bone volume and anchor positions safely. (Dental implant planning in EDs.) NCBI

23. Intraoral radiographs to assess enamel thickness, caries, and restorative needs tooth by tooth. PMC

24. High-frequency ultrasound or clinical photography to document palmoplantar keratoderma and track response to keratolytics. (Derm follow-up technique.) NCBI

25. Nailfold capillaroscopy/dermoscopy images to characterize nail plate/matrix changes over time (noninvasive monitoring). NCBI

Non-pharmacological treatments (therapies & others)

1. Gentle scalp care and breakage prevention—use mild shampoos, avoid heat/traction; reduces hair shaft stress; works by lowering mechanical and chemical damage to fragile hair. MalaCards

2. Daily barrier moisturizers (ceramide-rich emollients) for dry skin and keratoderma; aim to soften skin and reduce cracks; restore stratum-corneum lipids and water retention. PMC+1

3. Urea/lactic acid keratolysis (OTC products) to thin thick palms/soles; goal is comfort and fewer fissures; breaks hydrogen bonds in keratin to soften plaques. ScienceDirect

4. Callus debridement & protective padding by podiatry; reduces pain and splits; mechanical removal lowers pressure and water loss. PMC

5. Antiperspirant routines & absorbent fabrics for hyperhidrosis; improve comfort and infection prevention; blocks eccrine duct output and improves microclimate. PMC

6. Behavioral sweat triggers control (heat, spicy foods, stress plans); reduces flares; lowers sympathetic sweating stimuli. FDA Access Data

7. Dermoscopy-guided nail care (short trimming, avoid harsh manicures); prevents splits; reduces lever forces on thin plates. PMC

8. Dental fluoride varnish & sealants on existing enamel; prevent decay; fluoride promotes remineralization and sealants block acids. PMC

9. Removable partial dentures in childhood for missing teeth; restores chewing and speech; replaces lost tooth units to share bite forces. PMC

10. Orthodontic planning for spacing/bite; improves function and aesthetics; redistributes tooth positions and prepares for implants later. PMC

11. Prosthodontic crowns/onlays for weak enamel; protects surfaces; adds hard cover to reduce wear. PMC

12. Mouthguards/nightguards when enamel is soft; protects against bruxism; buffers tooth-to-tooth forces. PMC

13. Sun and friction protection for keratoderma areas; prevents cracks; reduces microtrauma and UV-driven dryness. PMC

14. Silicone sheets/pressure therapy for keloids (AD variant); flatten scars; modulates collagen and hydration under occlusion. MalaCards

15. Dandruff/follicular keratosis routines (gentle exfoliation); smoother texture; reduces follicular plugging mechanically. MalaCards

16. Paronychia prevention (dry hands, avoid cuticle cutting); lowers infections; preserves cuticle barrier. FDA Access Data

17. Footwear/insoles to off-load thick plantar areas; less pain; redistributes pressure and friction. PMC

18. Speech and feeding support if tooth loss affects articulation/chewing; improves function; compensates for missing dentition. PMC

19. Genetic counseling for family planning; explains inheritance/risks; clarifies recurrence risk and testing options. PMC

20. Psychosocial support for appearance-related stress; improves coping; structured counseling reduces anxiety and stigma. PMC

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Drug treatments

Important: No medicine is FDA-approved specifically for tricho-odonto-onychodysplasia. Drugs below are used for symptoms (off-label where noted). FDA label links come from accessdata.fda.gov and show approved uses/safety for each drug; your clinician decides off-label use based on symptoms.

1. Acitretin (oral retinoid) for severe palmoplantar keratoderma: reduces thickening; class: retinoid; dose/time: individualized low-to-moderate daily dosing; purpose: soften keratoderma; mechanism: normalizes epidermal differentiation; key risks: teratogenicity, lipid/liver monitoring. (FDA label: Soriatane). FDA Access Data+1

2. Tazarotene (topical retinoid 0.05–0.1%) for localized keratoderma/follicular plugs; class: topical retinoid; purpose/mechanism: RAR-mediated normalization of keratinization; risks: irritation, avoid in pregnancy. (FDA label: Tazorac). FDA Access Data

3. Isotretinoin (oral) for very refractory follicular keratosis or severe acne in affected areas; class: retinoid; mechanism: reduces sebaceous activity/keratinization; risks: strict pregnancy prevention, lipid/liver monitoring. (FDA labels: Accutane/Absorica). FDA Access Data+1

4. High-potency topical corticosteroids (e.g., clobetasol) short courses for inflamed keratoderma fissures or keloid itch; class: corticosteroid; purpose: anti-inflammatory; risks: skin atrophy, HPA suppression if overused. (FDA labels: Clobetasol products). FDA Access Data+1

5. Glycopyrronium cloth 2.4% (Qbrexza) for axillary hyperhidrosis; class: anticholinergic; dose: once daily; purpose: reduce sweating; mechanism: blocks muscarinic receptors; risks: dry mouth, blurred vision. (FDA label). FDA Access Data+1

6. OnabotulinumtoxinA (Botox) injections for severe axillary hyperhidrosis not controlled by topicals; class: neuromuscular blocker; purpose: reduce sweat; mechanism: blocks acetylcholine release; risks: injection site pain, weakness (area specific). (FDA label). FDA Access Data+1

7. Topical antifungals (e.g., ciclopirox) for mild nail fungus superinfection; purpose: clear fungus; mechanism: antifungal cell-membrane effects; used per label in onychomycosis—off-label if dystrophy is non-fungal. (FDA labels exist; illustration via terbinafine systemic below). FDA Access Data

8. Oral terbinafine only if true onychomycosis proven (KOH/culture), since nails in this disorder are fragile; class: allylamine antifungal; dose: standard onychomycosis courses; risks: hepatotoxicity; confirm diagnosis before use. (FDA labels: Lamisil). FDA Access Data+1

9. Topical antibiotics (short course) for secondary paronychia; purpose: treat bacterial overgrowth; mechanism: local antimicrobial; risk: resistance/dermatitis; use only when needed under clinician guidance. (General practice consistent with infection care; not disease-specific). FDA Access Data

10. Oral antibiotics for acute bacterial skin infections from fissures; purpose: resolve infection; risk: GI effects/resistance; culture-guided when possible. (General infection care guidance). FDA Access Data

11. Topical retinoid rotation (adapalene/tazarotene) to maintain follicular opening with fewer side effects; mechanism: normalize keratinization; risk: irritation/photodermatitis—sun protection needed. (Tazarotene FDA label representative). FDA Access Data

12. Keratolytic topicals (high-strength urea/salicylic acid) for plaques and fissures; mechanism: break keratin; risk: irritation—avoid deep fissures. (OTC monograph level; supportive barrier evidence). ScienceDirect

13. Short steroid/antibiotic combination for inflamed nail folds; purpose: reduce inflammation + infection; risk: atrophy/yeast if prolonged—keep brief. (General dermatology practice). FDA Access Data

14. Topical calcineurin inhibitors (pimecrolimus/tacrolimus) for steroid-sensitive areas (e.g., groin, folds) with dermatitis; mechanism: T-cell modulation; risk: burning, black-box warning counseling. (Non-FDA-specific to this disease). PMC

15. Aluminum chloride antiperspirants as first-line for hyperhidrosis before prescription agents; mechanism: obstructs sweat ducts; risk: irritation; use nightly then taper. (Standard hyperhidrosis approach; Botox/Qbrexza labels support stepped care). FDA Access Data

16. Topical anesthetics (for fissure pain) limited use before debridement; purpose: comfort; risk: sensitization with overuse. (General practice). PMC

17. Silicone gel for keloids with or without steroid injections; purpose: flatten/pruritus relief; mechanism hydrating occlusion; combine with intralesional therapy if needed. (Keloid supportive care). MalaCards

18. Anticholinergic or botulinum toxin for palmar/plantar hyperhidrosis (specialist care); purpose: sweat control; risks: weakness (palms), pain; selection individualized. (Botox label limitations note). FDA Access Data

19. Fluoride toothpaste and high-fluoride gels for enamel defects; purpose: caries prevention; mechanism: remineralization. PMC

20. Antiseptic mouthrinses to lower caries/infection risk around fragile enamel and restorations. PMC

Safety note: Retinoids (acitretin, isotretinoin, tazarotene) are teratogenic—strict pregnancy avoidance and FDA iPLEDGE-type precautions apply; decisions are specialist-led with informed consent. FDA Access Data+1

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Dietary molecular supplements

1. Biotin—may help brittle nails/hair when deficiency exists; supports keratin production; small studies/case series suggest improved nail thickness/firmness; large RCTs are lacking. Typical supplemental doses vary widely (e.g., 1–3 mg/day in nail reports). PubMed+1

2. Vitamin D—supports hair-follicle cycling and immune balance; deficiency can worsen hair and skin health; dose individualized to blood levels. PMC

3. Zinc—key for keratin, immunity, and wound healing; deficiency causes nail and hair changes; dose guided by labs to avoid copper imbalance. NCBI

4. Omega-3 fatty acids—may improve skin-barrier function and dryness; typical EPA+DHA 1–2 g/day with meals if no contraindications. PMC

5. Ceramide-supporting lipids (oral/topical)—aim to strengthen barrier lipids; evidence growing; doses vary by product. PMC+1

6. Iron (if deficient)—low iron worsens hair fragility; replacement per ferritin/hemoglobin targets only when deficiency proven. NCBI

7. Protein/essential amino acids—adequate dietary protein supports keratin synthesis; aim for consistent intake across meals. PMC

8. B-complex (if low)—supports cellular turnover; correct only documented deficiencies. PMC

9. Vitamin A (avoid excess)—retinoid biology affects keratinization, but overdosing harms hair/skin and is teratogenic—use only if deficient under supervision. FDA Access Data

10. Selenium (if low)—antioxidant support; excessive doses risk toxicity; test-and-treat approach. ScienceDirect

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Immunity-booster / regenerative / stem-cell” drug concepts

There are no FDA-approved “stem cell” drugs for this condition. Below are clinician-directed options sometimes discussed for symptoms or tissue healing—they are not disease-modifying therapies for TOO.

1. OnabotulinumtoxinA—reduces axillary sweating to prevent maceration/infections; dose per FDA label for hyperhidrosis; mechanism: acetylcholine blockade at neuroglandular junction. FDA Access Data

2. Glycopyrronium cloth—topical anticholinergic for hyperhidrosis; daily application; mechanism: muscarinic receptor antagonism. FDA Access Data

3. Topical calcineurin inhibitors—local immune modulation for dermatitis around fissures; thin layers; mechanism: inhibits T-cell activation. (Not FDA-approved for this disease; general dermatology use). PMC

4. Acitretin—epidermal “normalizer” in severe keratoderma; carefully selected adults only; teratogenic; requires labs/contraception. FDA Access Data

5. Tazarotene—topical normalization of keratinization on plaques; thin application at night; monitor irritation. FDA Access Data

6. Isotretinoin—rare escalation for severe follicular keratosis/acne; strict pregnancy prevention; mechanism: decreases sebaceous activity/keratinization. FDA Access Data

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Surgeries

1. Syndactyly release (AD variant) to separate fused digits; improves function and hygiene. MalaCards

2. Excision + adjuvant therapy for scalp keloids (pressure, steroid, silicone, or laser); reduces bulk and itch; recurrence prevention is key. MalaCards

3. Dental implants in late adolescence/adulthood when growth stabilizes; replaces missing teeth for chewing and speech. PMC

4. Orthognathic surgery if severe bite discrepancies persist after orthodontics; improves chewing and facial balance. PMC

5. Partial nail procedures (matrixectomy) for painful, repeatedly infected nails with severe dystrophy; relieves pain and improves shoe-wear. FDA Access Data

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Preventions

1. Daily ceramide moisturizer after bathing. PMC

2. Foot care: urea cream + gradual callus filing; avoid abrupt peeling. ScienceDirect

3. Sun and heat management (hats, breathable fabrics) to reduce sweat triggers and dryness. FDA Access Data

4. High-fluoride toothpaste/varnish and dental sealants. PMC

5. Regular dental follow-up for early caries repair. PMC

6. Nail protection: keep nails short, avoid aggressive manicures. PMC

7. Prompt care of fissures to prevent infections. FDA Access Data

8. Keloid control: early silicone/pressure therapy after trauma. MalaCards

9. Sweat control plan: antiperspirants first; escalate to Rx if needed. FDA Access Data

10. Genetic counseling before family planning. PMC

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When to see doctors

See a dermatologist and dentist/orthodontist early if your child (or you) has very sparse hair, unusual nails, missing/weak teeth, thick palms/soles, or unusual sweating. Early care improves comfort, chewing, speech, and self-confidence. If palms/soles crack, or nails become painful or infected, seek care promptly. Ask about genetic testing and family counseling to understand inheritance and plan future care. PMC+1

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What to eat / what to avoid

Eat a balanced diet rich in protein, zinc-containing foods (seafood, meats, legumes), omega-3 sources (fish, flax), and vitamin D (dietary sources and adequate safe sun or prescribed supplements if low). These support skin barrier and keratin structures when deficiencies are present. Avoid very low-protein fad diets, minimize alcohol/smoking (delay healing), and limit irritant spicy/very hot foods if they trigger sweating flares. Supplements should be lab-guided, especially zinc and vitamin D. NCBI+2PMC+2

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FAQs

1) Is this condition contagious?
No. It is genetic, not an infection. Family patterns can exist due to inheritance. PMC

2) What gene is most often involved?
In OODD, WNT10A variants are common; other tricho-odonto-onycho disorders may vary. PMC

3) Will hair grow normally later?
Hair usually remains sparse or fragile; gentle care reduces breakage. Some AD families report “corkscrew hair.” MalaCards

4) Are teeth always missing?
Many have hypodontia or weak enamel; dentists can restore function with sealants, prostheses, or implants. PMC

5) Are nails curable?
Nails are genetically thin/fragile. Protection, careful trimming, and treating infections help, but do not “cure” the base problem. FDA Access Data

6) Is there a single approved medicine?
No. Treatment is symptom-based (e.g., keratoderma, hyperhidrosis) using approved drugs off-label when appropriate. FDA Access Data+2FDA Access Data+2

7) Are retinoids safe?
They can help keratinization but have major risks (especially pregnancy with oral retinoids). Use only under specialist care with strict precautions. FDA Access Data+1

8) Can biotin fix my nails/hair?
It may help if you’re deficient; evidence is limited. Discuss testing and dosing with your clinician. PubMed

9) Why is my tongue smooth?
Loss of papillae is part of the ectodermal change in some forms like OODD. PMC

10) What about sweating issues?
Start with antiperspirants and fabrics; consider glycopyrronium cloth or Botox if severe. FDA Access Data+1

11) Do I need genetic testing?
It helps confirm the type and guide family planning and research eligibility. PMC

12) Are implants possible if many teeth are missing?
Yes, usually after growth is complete; a prosthodontist plans timing and graft needs. PMC

13) Can nails get fungus more easily?
Distorted nails can trap moisture and get secondary fungus; test before oral antifungals. FDA Access Data

14) Will thick soles go away?
They can be improved with regular keratolysis, emollients, and protective care; severe cases may need retinoids. FDA Access Data

15) Is research ongoing?
Yes—especially around WNT signaling and hair/skin regeneration biology. 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: October 04, 2025.

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