Axial Spondylometaphyseal Dysplasia (SMDAX)

Axial spondylometaphyseal dysplasia is a very rare genetic bone growth disorder. “Axial” means the center line of the body (spine, ribs, pelvis, and nearby bones). “Spondylo-” refers to the spine. “Metaphyseal” refers to the ends of long bones where growth happens. Children with this condition are usually short. The chest can be narrow and the ribs short. The hips and top parts of the thigh bones (proximal femora) show changes on X-rays. Vision problems happen early because the retina slowly degenerates. Most reported families show autosomal recessive inheritance. Disease-causing variants have been found in two cilia-related genes, C21orf2 and NEK1, which help tiny cellular “antennae” (cilia) guide skeletal and retinal development. NCBI+4orpha.net+4PLOS+4

Axial spondylometaphyseal dysplasia (SMD-axial, OMIM 602271; ORPHA:168549) is a very rare genetic bone-growth disorder. It mainly affects the “axial” skeleton—spine, ribs, chest, pelvis—and nearby (“juxta-truncal”) long-bone ends (metaphyses), causing short stature (often rhizomelic in early childhood that later appears as a relatively short trunk), a narrow or flattened chest, hip changes, and platyspondyly (flattened vertebrae). A striking extra-skeletal feature is early, progressive retinal degeneration with vision loss. Pathogenic variants have been reported in cilia-related genes (C21orf2/CFAP410 and NEK1), supporting the view that SMD-axial is a skeletal ciliopathy with retinal involvement. PubMed+4NCBI+4orpha.net+4

Genetically, early descriptions suggested recessive inheritance; subsequently, disease-causing variants in C21orf2 (also called CFAP410) and NEK1 were found in families with SMD-axial and retinal dystrophy. This strengthens the biological link between primary cilia function, bone modeling, and photoreceptor survival. Even so, cases remain extremely few worldwide, and genetic heterogeneity likely exists. PLOS+2PubMed+2

At present there is no disease-specific approved drug for SMD-axial. Care is individualized: stabilize the spine and hips, preserve mobility and breathing, protect vision, and prevent complications. Genetic testing confirms the diagnosis and guides family counseling; low-vision rehabilitation is central for quality of life. BioMed Central+1

Other names

You may see these terms used in medical notes or papers:

• Spondylometaphyseal dysplasia, axial type; SMDAX; OMIM #602271. These all point to the same disorder. PubMed+1

• Axial SMD with retinal dystrophy. This emphasizes the eye involvement. PLOS

• Axial SMD due to C21orf2 or NEK1. These name the known genes. PLOS+1

Types

Because this is very rare, doctors often “type” it based on the gene or the main features rather than formal subtypes:

1. C21orf2-related axial SMD. Skeletal changes plus early retinal dystrophy; autosomal recessive. PLOS

2. NEK1-related axial SMD. Very similar clinical picture; confirms genetic heterogeneity (more than one gene can cause the same condition). Nature

3. Axial SMD—gene not identified. Some families meet clinical criteria, but the genetic cause is still unknown or not yet found by testing. rarediseases.info.nih.gov

Note: Other spondylometaphyseal dysplasias exist (for example, SPONASTRIME dysplasia), but they are different disorders with different genes and patterns, even though the names can look similar. PubMed

Causes

Each item explains a contributing mechanism or pathway. Together they describe why bones and eyes are affected.

1. Autosomal recessive inheritance. A child inherits two non-working copies of a gene (one from each parent). NCBI

2. Pathogenic variants in C21orf2. This gene helps cilia function; its failure disrupts skeletal growth plates and photoreceptors. PLOS

3. Pathogenic variants in NEK1. NEK1 is a cilia-associated kinase; variants disturb skeletal patterning and retinal health. Nature

4. Primary cilia dysfunction (a “ciliopathy”). Tiny cell projections guide growth plate signaling and retinal homeostasis; dysfunction causes bone and eye disease. hnl.com

5. Disrupted Hedgehog/WNT signaling at growth plates. Cilia help these signals; errors alter metaphyseal modeling of long bones. (Inference consistent with ciliopathy biology.) hnl.com

6. Abnormal chondrocyte maturation. Growth plate cartilage cells fail to mature normally, so metaphyses look irregular. orpha.net

7. Impaired endochondral ossification. The process of turning cartilage into bone at the metaphysis is inefficient or misdirected. orpha.net

8. Platyspondyly formation. Flattened vertebral bodies come from abnormal bone modeling in the spine. bredagenetics.com

9. Thoracic hypoplasia. Short, flared ribs create a small chest, sometimes leading to breathing issues. malacards.org

10. Lacy iliac crests. Characteristic pelvis X-ray pattern reflects altered bone microarchitecture. EMBL-EBI

11. Proximal femoral metaphyseal dysplasia. Short, broadened femoral necks disturb hip mechanics and gait. orpha.net

12. Retinal dystrophy (rod–cone or cone–rod). Progressive photoreceptor damage reduces vision over time. malacards.org

13. Rhizomelic growth pattern in early childhood. Upper arms and thighs grow slowly first; later, the trunk looks short. NCBI

14. Frequent airway infections secondarily. Narrow chest and small airways can increase infection risk. NCBI

15. Gene-negative families (unknown cause). Some patients have the phenotype without identified variants yet, indicating further genes remain to be discovered. rarediseases.info.nih.gov

16. Overlap with other cilia disorders. The same genes can also cause short-rib thoracic dysplasia, showing shared pathways. hnl.com

17. Postnatal growth failure. Growth slows after birth because growth plates are inefficient. NCBI

18. Metaphyseal cupping and flaring. The bone ends flare due to abnormal load and growth plate shape. EMBL-EBI

19. Skeletal patterning errors in utero. Early development sets the stage for axial and juxta-axial bone involvement. PubMed

20. Small case series and variable expressivity. With very few patients described, features vary even within the same gene. disorders.eyes.arizona.edu

Common signs and symptoms

1. Short stature. Children are shorter than peers because their bones grow more slowly and differently. NCBI

2. Short trunk (often after early rhizomelic pattern). The torso looks relatively short compared with limbs as the child grows. NCBI

3. Narrow, flattened chest. Short ribs and small thorax can be seen on exam and X-ray. disorders.eyes.arizona.edu

4. Breathing vulnerability. A small chest can mean mild breathing issues or more frequent respiratory infections. NCBI

5. Hip problems (abnormal proximal femur). Short, broad femoral necks can change gait and cause hip discomfort. orpha.net

6. Spinal changes (platyspondyly). Flattened vertebrae can lead to posture differences or mild back pain. bredagenetics.com

7. Metaphyseal irregularities. Doctors see flared or cupped bone ends at the hips and sometimes knees or shoulders. EMBL-EBI

8. Lacy iliac crests. A distinctive pelvis X-ray pattern that helps diagnosis. EMBL-EBI

9. Short ribs with cupped, flared ends. Characteristic rib shape supports the diagnosis. EMBL-EBI

10. Early vision problems. Poor night vision, peripheral vision loss, or trouble in dim light can start in childhood. malacards.org

11. Rapidly progressive visual decline. Retinal dystrophy often advances and needs early low-vision support. NCBI

12. Normal intelligence and development otherwise. Learning is usually age-appropriate. disorders.eyes.arizona.edu

13. Frontal bossing and facial features (some cases). Mild forehead prominence may be described. disorders.eyes.arizona.edu

14. Recurrent ear–nose–throat infections (secondary). Narrow chest and airway issues can contribute. NCBI

15. Gait differences. Hip morphology and short trunk can change walking pattern. orpha.net

How doctors diagnose it

A) Physical examination

1. Growth and body proportions check. The doctor measures height, sitting height, arm span, and leg segments to see short-trunk vs limb involvement. This pattern guides imaging. NCBI

2. Chest and breathing exam. The clinician looks for a narrow chest, listens to breath sounds, and checks for signs of reduced lung expansion. malacards.org

3. Spine and hip exam. Range of motion, posture, and gait are assessed to spot hip loading problems or scoliosis risk. bredagenetics.com

4. Ophthalmic symptom screen. Night vision, peripheral vision, and glare sensitivity are asked about because retinal dystrophy is common. malacards.org

B) Bedside/manual tests

5. Functional mobility tests (timed up-and-go / 6-minute walk). Simple timed tasks track endurance and hip/back comfort over time. orpha.net

6. Pulmonary function screening (peak flow in older children). A quick check for airflow limitation in those with small chests. malacards.org

7. Vision screening charts (age-appropriate). Early chart testing or LEA symbols can reveal reduced acuity before formal retinal testing. malacards.org

8. Postural assessment. Checking sagittal and coronal balance helps decide if formal spine imaging is needed. bredagenetics.com

C) Laboratory and pathological tests

9. Genetic testing panel. Targeted sequencing of C21orf2 and NEK1 confirms many cases; broader exome may be used if panel is negative. hnl.com

10. Parental carrier testing. Confirms autosomal recessive inheritance for family counseling. NCBI

11. Rule-out labs for other bone conditions. Calcium, phosphate, alkaline phosphatase, vitamin D, and inflammatory markers help exclude metabolic bone disease or inflammatory mimics. (General skeletal dysplasia work-up.) orpha.net

12. Research-level functional studies (rare). Some centers may study cilia function in fibroblasts to understand variant impact. (Inference from ciliopathy biology.) hnl.com

D) Electrodiagnostic and ophthalmic electrophysiology

13. Full-field electroretinography (ERG). Measures retina’s electrical response; reduced signals support retinal dystrophy even before fundus changes are obvious. malacards.org

14. Multifocal ERG. Maps central retinal function to quantify macular involvement that affects reading vision. malacards.org

15. Visual field testing. Finds peripheral field loss typical of rod–cone dystrophy patterns. malacards.org

16. Dark adaptometry (selected centers). Detects delayed dark adaptation in rod dysfunction; helpful in counseling about lighting. malacards.org

E) Imaging tests

17. Skeletal survey X-rays. Shows the hallmark pattern: short ribs with cupped anterior ends, mild platyspondyly, “lacy” iliac crests, and proximal femoral metaphyseal changes. This pattern points strongly to SMDAX. EMBL-EBI

18. Spine radiographs. Quantify vertebral flattening and check for alignment issues (e.g., early scoliosis). bredagenetics.com

19. Hip and pelvis radiographs. Define femoral neck shortening/broadening and acetabular coverage, guiding physio or orthopedic referrals. orpha.net

20. Ophthalmic imaging (OCT and fundus photos). Optical coherence tomography and fundus imaging monitor retinal layer thinning and pigmentary change over time. malacards.org

Non-pharmacological treatments (therapies & other supports)

1) Multidisciplinary care plan. Coordinate orthopedics, physiatry, pulmonology, ophthalmology/low-vision, genetics, physical/occupational therapy, and social work. A single written plan improves safety around anesthesia, surgery timing, spinal monitoring, and vision accommodations at school/work. BioMed Central

2) Activity-based physical therapy. Tailored PT focuses on core and paraspinal endurance, hip abductor strength, safe gait patterns, and fall prevention. It aims to maintain mobility and protect joints without overloading the spine and hips. BioMed Central

3) Assistive devices & orthoses. Intermittent bracing, canes, or walkers may reduce pain and energy cost of walking. For some, lightweight thoracolumbar support limits fatigue in prolonged sitting/standing; devices are fitted to avoid rib/chest compression. BioMed Central

4) Respiratory monitoring & airway care. Narrow chest and thoracic hypoplasia can reduce ventilatory reserve. Baseline and periodic pulmonary function tests, vaccination, airway clearance strategies during infections, and peri-anesthetic planning help reduce respiratory complications. NCBI

5) Spine surveillance with red-flag education. Regular clinical and imaging follow-up for progressive kyphoscoliosis or canal stenosis; teach families warning signs (new limb numbness/weakness, gait change, bladder/bowel symptoms) to prompt urgent review. BioMed Central

6) Hip preservation strategies. Early gait training, abductor strengthening, and avoidance of extreme impact loading may reduce symptoms from metaphyseal deformity; surgical opinions are sought when pain or function deteriorate. BioMed Central

7) Low-vision rehabilitation. Early referral for magnifiers, contrast enhancement, glare control, orientation & mobility training, and digital accessibility (screen readers, large-print interfaces) preserves independence as retinal disease progresses. American Academy of Ophthalmology

8) Genetic counseling & testing. Offer genetic confirmation (panels that include CFAP410/C21orf2 and NEK1) for diagnosis, recurrence risk, and access to research. Provide family planning support. Blueprint Genetics

9) School/work accommodations. Seating, larger fonts, extra time for reading, high-contrast materials, and ergonomic seating to support the spine can meaningfully improve participation and reduce fatigue. American Academy of Ophthalmology

10) Psychosocial support. Counseling and peer support address uncertainty and vision loss; social services help with disability benefits and transport. These interventions improve quality of life in inherited retinal disease and skeletal dysplasias. American Academy of Ophthalmology+1

---

Drug treatments

Important: None of the drugs below is approved specifically for SMD-axial. They are standard, FDA-labeled medicines clinicians may use to manage common symptoms (e.g., musculoskeletal pain or spasm), with careful risk–benefit review. Labels are cited to accessdata.fda.gov.

1) Acetaminophen (paracetamol). First-line analgesic for mild pain; spare use reduces GI/cardiovascular risks seen with NSAIDs. Usual adult max 3,000–4,000 mg/day (accounting for all combination products). Liver toxicity risk rises with overdose, alcohol use, or chronic high doses. FDA Access Data+1

2) Ibuprofen (NSAID). Helps inflammatory/mechanical pain and activity flare-ups; typical adult doses 200–800 mg per dose within label limits. Boxed warnings emphasize cardiovascular thrombotic events and GI bleeding/ulceration; use the lowest effective dose for the shortest time. FDA Access Data+1

3) Naproxen (NSAID). Longer-acting NSAID useful when twice-daily dosing aids adherence. Same boxed warnings as other NSAIDs; avoid around CABG surgery and assess GI risk (consider gastroprotection if needed). FDA Access Data+1

4) Celecoxib (COX-2 selective NSAID). May reduce GI ulcer risk vs. nonselective NSAIDs but still carries CV and GI warnings; consider in patients at higher GI risk who lack high CV risk. Dosing individualized; monitor for sulfonamide allergy. FDA Access Data+1

5) Topical diclofenac. For focal joint or soft-tissue pain when oral NSAIDs are undesirable; systemic exposure is lower than oral NSAIDs, but local skin reactions can occur. (Labeling principle reflected across topical NSAID monographs.) FDA Access Data

6) Gabapentin (neuropathic-type pain). If spinal stenosis or nerve irritation causes neuropathic features (burning, tingling), adjuvant agents like gabapentin are sometimes used; dosing titration and sedation risk are considered. (FDA labeling principles for gabapentin apply.) BioMed Central

7) Baclofen (antispasmodic). For painful muscle spasm around the spine/hips; sedation and dizziness can limit dosing—start low and go slow. (Use per labeled spasticity indications; extrapolated here for symptomatic spasm.) BioMed Central

8) Proton-pump inhibitor (e.g., omeprazole) for NSAID gastroprotection. In patients who require NSAIDs and have elevated GI risk, PPIs lower ulcer/bleed risk; clinicians select agent/dose per GI protection guidelines and labeling. FDA Access Data

9) Acetaminophen–ibuprofen fixed-dose combinations. When appropriate, fixed combinations improve adherence while limiting each component’s dose; watch cumulative acetaminophen to avoid hepatotoxicity. FDA Access Data

10) Peri-operative analgesia plans. If surgery is required, multimodal plans (acetaminophen ± short NSAID course ± regional techniques) minimize opioid exposure; dosing follows each product’s FDA label and anesthetic standards. FDA Access Data

Notes: Use opioids sparingly and short-term only when clearly indicated. Avoid routine corticosteroids for musculoskeletal pain in SMD-axial. All medication decisions must be individualized and supervised by clinicians who know the patient’s comorbidities. BioMed Central

---

Regenerative / immune-support / stem-cell–related” drugs

There are no approved immune boosters or stem-cell drugs for SMD-axial. The items below explain real, labeled medicines used for other conditions that clinicians may consider in specific off-label contexts (e.g., bone health) or not at all—listed here to clarify reality and discourage unproven “stem-cell” marketing.

1) Teriparatide (PTH 1-34). An anabolic osteoporosis drug that promotes bone formation and increases bone mineral density in adults at high fracture risk. It is not approved for skeletal dysplasias or for children; duration is limited (typically ≤2 years). Use here would be off-label and specialist-only. BioMed Central

2) Denosumab (anti-RANKL). An antiresorptive for osteoporosis that reduces fracture risk by suppressing osteoclast activity. Not a treatment for SMD-axial; discontinuation requires careful transition to avoid rebound effects. Off-label considerations demand specialist oversight. BioMed Central

3) Calcitriol (active vitamin D). A hormone for conditions with disordered calcium/phosphate balance; it supports bone mineralization in select scenarios but carries hypercalcemia risk. Use only when a true indication exists. BioMed Central

4) Growth hormone. GH does not correct most skeletal dysplasias and is not established for SMD-axial; outside of proven deficiency, it is not recommended. BioMed Central

5) Hematopoietic stem-cell therapy. Not indicated for SMD-axial; there is no evidence it improves skeletal or retinal features in this condition. Avoid commercial “stem-cell” clinics advertising cures. BioMed Central

6) Retinal gene or cell therapy (research context). For C21orf2/CFAP410-related retinopathy, management is currently supportive; no approved gene therapy exists as of October 15, 2025. Patients may be eligible for research registries or trials in inherited retinal degenerations. PMC+1

---

Dietary molecular supplements

There are no supplements proven to change SMD-axial biology. The items below reflect general bone/eye-health principles used only when indicated by clinical assessment (labs, diet review). Always avoid megadoses and drug–nutrient interactions.

1) Vitamin D3 (cholecalciferol). Corrects deficiency and supports calcium absorption and bone mineralization; dose is individualized to reach target serum 25-OH-D and avoid toxicity. BioMed Central

2) Calcium (dietary ± supplement). Aim for age-appropriate daily intake from food first; supplement only to fill a gap and avoid hypercalcemia or kidney stones. BioMed Central

3) Omega-3 fatty acids. May modestly aid dry-eye symptoms and general cardiometabolic health; choose purified products and disclose all supplements to clinicians. American Academy of Ophthalmology

4) Lutein/zeaxanthin. Dietary carotenoids that support macular pigment; in inherited retinal disease evidence is limited but risk is low at dietary doses—avoid high-dose vitamin A without specialist advice. American Academy of Ophthalmology

5) Protein adequacy. Adequate dietary protein supports muscle strength for spinal and hip stability; malnutrition worsens outcomes after surgery. BioMed Central

6) Balanced micronutrients (B-complex, magnesium, zinc). Correct documented deficits; there is no proof that supraphysiologic dosing helps skeletal dysplasia. BioMed Central

7) Hydration & fiber. Helpful for constipation from reduced mobility or medication side-effects (e.g., antispasmodics); tailor to GI tolerance. BioMed Central

8) Caffeine moderation. High caffeine can increase calcium losses and worsen sleep; moderate intake supports better rehabilitation participation. BioMed Central

---

Surgeries

1) Guided-growth or corrective osteotomies (lower limbs/hips). In selected patients with painful malalignment or progressive deformity limiting function, surgeons may realign bones to improve mechanics and reduce pain. Decisions hinge on growth stage, deformity pattern, and risks. BioMed Central

2) Spine deformity surgery (kyphoscoliosis). Considered for progressive curves that impair breathing, sitting balance, or cause neurologic compromise; meticulous planning is required due to small stature, rib deformity, and anesthetic risk. BioMed Central

3) Spinal canal decompression ± fusion. If stenosis causes neurologic deficits (gait change, weakness, bladder/bowel dysfunction), decompression relieves pressure; fusion may stabilize segments. Neuromonitoring is standard. BioMed Central

4) Hip reconstruction. Where femoral neck/acetabular morphology causes pain and instability, reconstruction can restore coverage and improve gait. BioMed Central

5) Ophthalmic procedures (select cases). While retinal dystrophy is not surgically reversible, cataract or macular complications—if present—are treatable; the ophthalmic team individualizes timing and low-vision integration. American Academy of Ophthalmology

---

Preventions

1. Keep immunizations up to date (influenza, pneumococcal, COVID-19 as recommended) to lower respiratory infection risk in those with small chests. NCBI

2. Avoid smoking and second-hand smoke to protect lung reserve. NCBI

3. Maintain healthy body weight to reduce mechanical load on hips/spine. BioMed Central

4. Fall-prevention at home (lighting, handrails, remove loose rugs). BioMed Central

5. Ergonomic seating and workstations that support the spine and reduce fatigue. BioMed Central

6. Sun protection and glare control to reduce retinal light stress and improve comfort. American Academy of Ophthalmology

7. Early treatment of respiratory infections and clear “when to call” plans. NCBI

8. Vision-safe environments (high-contrast labels, tactile markers, night lighting). American Academy of Ophthalmology

9. Pre-anesthesia planning in centers familiar with skeletal dysplasias. BioMed Central

10. Regular, moderate activity (walking, aquatic therapy) rather than high-impact sports. BioMed Central

---

When to see doctors (or go urgently)

See your care team promptly for: new back/leg pain with numbness or weakness; changes in walking or falls; new bladder/bowel difficulty; fast-worsening shortness of breath or chest infections; sudden vision changes (flashes, curtain, pain); medication side-effects such as GI bleeding (black stools, vomiting blood), persistent abdominal pain on NSAIDs, or signs of liver injury on acetaminophen (nausea, jaundice, dark urine). For routine care, schedule periodic reviews with orthopedics/spine, pulmonology, ophthalmology/low-vision, and PT/OT. BioMed Central+1

---

What to eat & what to avoid (simple, practical)

Eat a balanced, protein-adequate diet with calcium-rich foods (dairy or fortified alternatives, greens) and vitamin-D sources per local guidance; add colorful fruits/vegetables for lutein/zeaxanthin and general eye health; include whole grains and healthy fats (olive oil, nuts, fish). Limit ultra-processed foods, excess sugar, and high salt that can worsen blood pressure and bone health; moderate caffeine; avoid smoking and excess alcohol (bone and fall risk). Always clear supplements with your clinicians to avoid drug interactions. BioMed Central+1

---

FAQs

1) Is there a cure? No. Management focuses on spine/hip function, breathing, and vision support; research on cilia-related genes continues. PLOS

2) What gene is involved? Confirmed genes include C21orf2/CFAP410 and NEK1 in some families, but not all cases. Genetic testing helps confirm diagnosis. PLOS+1

3) How common is it? Extremely rare—only a handful of published cases; exact prevalence unknown. disorders.eyes.arizona.edu

4) Why does vision decline? The same cilia biology that shapes bone also supports photoreceptors; its failure can cause retinal dystrophy that progresses over time. Europe PMC

5) Can glasses fix the vision? Glasses correct refractive error but do not stop retinal degeneration; low-vision rehab provides practical tools and training. American Academy of Ophthalmology

6) Will growth hormone help height? Generally no—SMD-axial is a bone-modeling disorder; GH is not established for this condition outside documented deficiency. BioMed Central

7) What about stem-cell therapy? Not indicated for SMD-axial; avoid clinics selling unproven treatments. BioMed Central

8) Are there clinical trials? Trials for inherited retinal diseases or rare skeletal disorders may appear; eligibility depends on gene and phenotype—ask your genetics and ophthalmology teams. American Academy of Ophthalmology

9) Which pain reliever is safest? Many start with acetaminophen; NSAIDs can help flares but carry GI/CV risks—use the lowest effective dose for the shortest time, with clinician guidance. FDA Access Data+1

10) How often should the spine be checked? Typically yearly in growing children and as symptoms dictate in adults; sooner if new neurologic signs appear. BioMed Central

11) Can exercise make it worse? High-impact sports can worsen pain; guided, low-impact, core-focused activity is encouraged. BioMed Central

12) What about school/work? Accessibility tools (large print, high contrast, screen readers) and ergonomic supports can greatly help; ask for formal accommodations. American Academy of Ophthalmology

13) Should family members be tested? Genetic counseling can discuss carrier testing and reproductive options. Blueprint Genetics

14) Does it affect thinking or lifespan? Published cases report normal cognition; lifespan depends on complication control (respiratory, spinal). disorders.eyes.arizona.edu

15) Where can I read more? Orphanet and GARD overviews, PubMed case series, and recent CFAP410/NEK1 research are good starting points. orpha.net+2rarediseases.info.nih.gov+2

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 15, 2025.