Occipital Horn Syndrome (OHS)

The ATP7A protein normally shuttles copper from the intestine into the bloodstream and then from bloodstream into the Golgi apparatus of nearly every cell. In OHS, “leaky” or partially active ATP7A variants move some copper but not enough. The partial deficit explains why OHS is milder than classic Menkes disease, where the protein is almost totally inactive. Cells that rely heavily on copper-dependent enzymes—especially bone, vessel walls, connective tissue, and parts of the autonomic nervous system—suffer the most damage. pubmed.ncbi.nlm.nih.gov

Types

Although OHS is a single genetic? entity, doctors describe several practical sub-groups that help guide monitoring?:

1. Typical/Classic OHS – the “textbook” picture with skull horns, loose skin, bladder? diverticula, and mild neurologic issues.

2. OHS–Menkes Overlap – children who start like OHS but later show moderate? movement problems or seizures, blurring the line toward Menkes disease.

3. OHS with Prominent Vascular Complications – patients whose main risk is arterial tortuosity or early aortic aneurysm, demanding vascular surveillance?.

4. OHS with Predominant Autonomic Dysfunction – milder bone findings but troublesome dysautonomia (poor temperature control, blood-pressure swings).

Each subtype shares the same genetic root yet differs in which organ system dominates daily life.

Causes 

In OHS “cause” means the exact molecular or genetic event that disrupts copper handling, along with modulating factors that make the phenotype better or worse.

1. Single-base missense mutation in ATP7A. A single “letter change” reduces but does not abolish copper transport.

2. Nonsense mutation with residual “read-through.” A premature stop-codon still leaks a little functional protein.

3. Small in-frame deletion removing a few amino acids in the copper-binding domain.

4. Exon-skipping splice variant that allows some correctly spliced transcripts to survive.

5. Deep-intronic splice defect creating a “cryptic” exon that dilutes, but does not eliminate, normal messenger RNA.

6. Retrotransposon (SVA_D) insertion within ATP7A—recently described as a novel pathogenic mechanism. pubmed.ncbi.nlm.nih.gov

7. Large genomic duplication encompassing several ATP7A exons, producing an unstable protein.

8. Partial promoter deletion lowering ATP7A transcription.

9. Post-zygotic (mosaic) mutation—some cells have a normal gene copy, softening symptoms.

10. Maternal germ-line mosaicism causing “sporadic” cases with no family history?.

11. Skewed X-chromosome inactivation in carrier females—can worsen female manifestations.

12. Copper-poor prenatal? environment (severe? maternal malnutrition) exaggerating copper deficiency at birth.

13. High dietary zinc in infancy competing with copper absorption.

14. Prematurity, limiting copper stores that normally accumulate late in gestation?.

15. Chronic? proton-pump-inhibitor therapy (rare in children but possible) impairing gastric copper ionisation.

16. Inherited variants in metallochaperone genes (e.g., Atox1) that normally escort copper inside cells.

17. Co-existing connective-tissue gene variants (COL5A1, ELN) modifying skin and vessel laxity.

18. Epigenetic down-regulation of remaining healthy ATP7A allele (experimental data).

19. Oxidative stress increasing cellular copper demand beyond the reduced supply.

20. Aging of connective tissue—symptoms such as hernias worsen naturally over time as collagen loses resilience.

Symptoms and signs

1. Bony “occipital horns.” Small, wedge-shaped calcium growths at the back of the skull; painless but diagnostic.

2. Loose, doughy skin (cutis laxa). Skin lacks elastic recoil, giving a prematurely aged or “ saggy” look.

3. Joint hyper-mobility. “Double-jointed” elbows, fingers, and shoulders that bend beyond the usual range.

4. Shoulder or elbow dislocations. Lax ligaments? allow recurrent? slips, often during play or sports.

5. Bladder diverticula. Pouch-like out-bulgings weaken the bladder wall and can trap urine, leading to infections.

6. Inguinal and umbilical hernias. Soft tissue protrudes through weak abdominal openings, sometimes requiring surgery.

7. Long, flexible neck. Collagen laxity lengthens and narrows the neck profile.

8. High-arched palate and dental crowding. Copper-dependent enzymes sculpt palate shape; deficiency leaves it tall and narrow.

9. Coarse, “steel-wool” hair. Copper insufficiency alters cross-linking in keratin, giving wiry texture.

10. Chronic constipation? or diarrhea?. Autonomic nerve fibres supplying the gut malfunction inconsis­tently.

11. Cold‐intolerance and poor temperature regulation. Dysautonomia hampers sweat and blood-flow control.

12. Orthostatic dizziness?. Blood pressure drops on standing due to floppy veins? and autonomic dysfunction.

13. Early-onset? varicose veins. Weak vein? walls bulge under normal pressure even in childhood.

14. Muscle wasting of hands or feet. Peripheral nerves depend on copper; partial deficits shrink distal muscles.

15. Mild intellectual or learning difficulties. Most children attend mainstream school but need extra support.

16. Recurrent respiratory infections. Weak connective tissue in airways plus poor cough? reflex raise risk.

17. Hoarse voice or vocal cord? laxity. Elastic fibres in the larynx? stretch abnormally.

18. Easy bruising?. Fragile blood vessels rupture after minor bumps.

19. Aortic root dilation or tortuous carotid arteries?. Potentially life-threatening if unmonitored.

20. Low energy and fatigue?. Multifactorial—autonomic issues, muscle weakness, and anemia from iron-copper interaction.

Diagnostic tests

(Organised into five practical categories; each explained in a short, plain-English paragraph)

A. Physical-exam observations

1. Inspection for occipital horns – gently palpating the bump behind each ear; confirms clinical suspicion.

2. Skin elasticity “pinch-back” test – pinched skin on the back of the hand should snap flat; in OHS it returns slowly, proving laxity.

3. Beighton hyper-mobility score – measures how far the thumb, fingers, elbows, and knees bend beyond normal; helps quantify joint looseness.

4. Arm span vs. height ratio – an unusually long arm span reflects connective-tissue stretch.

5. Head circumference tracking – charts early macrocrania or skull shape changes from the bone exostoses.

6. Blood-pressure orthostatic test – noting falls when standing alerts doctors to autonomic dysfunction.

7. Heart auscultation for murmurs – turbulent flow hints at aortic dilation or valve laxity.

8. Abdominal palpation for hernias – detects soft bulges when the child coughs or strains.

B. Manual or functional tests

9. Anterior-drawer shoulder test – evalu­ates ligament laxity that causes recurrent dislocation.

10. Metacarpophalangeal glide test – gently shunts finger joints sideways; excessive glide supports lax collagen.

11. Valsalva maneuver for venous reflux – blowing against a closed airway reveals bulging neck veins, indicating vein weakness.

12. Timed up-and-go (TUG) test – records how quickly a child stands and walks; slower times may reflect muscle atrophy or joint instability.

13. Skin recoil stopwatch test – clinicians time how long a pinched fold returns; >3 s is abnormal.

14. Head-tilt vascular stress test – checks for dizziness when tilting head; significant for carotid tortuosity.

15. Pelvic floor squeeze test – screens for early stress incontinence from lax pelvic connective tissue.

16. Grip-strength dynamometer – objective measure of distal muscle wasting linked to neuropathy.

C. Laboratory & pathological studies

17. Serum copper concentration – usually low-normal; confirms impaired transport.

18. Serum ceruloplasmin level – ceruloplasmin carries most blood copper and is consistently reduced (<30 mg/dL). rarediseases.info.nih.gov

19. 24-hour urinary copper excretion – paradoxically low because gut copper never reaches bloodstream in high amounts.

20. Plasma dopamine-β-hydroxylase activity – copper-dependent enzyme; low results validate systemic copper deficiency.

21. Lysyl-oxidase activity in cultured fibroblasts – marker for collagen cross-linking; diminished in OHS.

22. Molecular genetic testing of ATP7A – the gold standard; pinpoints the exact pathogenic variant.

23. SVA retrotransposon PCR screen – detects the recently reported SVA_D insertion variant. pubmed.ncbi.nlm.nih.gov

24. Copper-histidine therapeutic trial – a monitored “test-and-see” approach: rising ceruloplasmin suggests residual transporter function, confirming OHS rather than classic Menkes.

D. Electrodiagnostic studies

25. Nerve-conduction velocity (NCV) – slowed signals imply distal motor neuropathy within the OHS spectrum.

26. Electromyography (EMG) – detects chronic denervation and re-innervation in small hand muscles.

27. Heart-rate variability (HRV) testing – reduced variability reveals autonomic imbalance.

28. Tilt-table test with ECG – documents drops in heart rate or blood pressure upon upright tilt.

29. Quantitative sudomotor axon reflex test (QSART) – measures sweat gland response to mild electrical stimulation; poor output reflects autonomic impairment.

30. Sympathetic skin response (SSR) – records tiny voltage changes after deep breaths; absent responses confirm dysautonomia.

31. Visual evoked potentials (VEPs) – delayed waveforms may occur if optic nerves are under-myelinated due to copper lack.

32. Brain-stem auditory evoked responses (BAERs) – checks hearing-pathway integrity; subtle delays are occasionally noted.

E. Imaging tests

33. Skull X-ray (lateral view) – straightforward picture of the bony occipital “horns,” the condition’s namesake.

34. Cervical spine MRI – looks for ligament laxity around the upper spine and brain-stem crowding.

35. Brain MRI with MRA – evaluates vessel tortuosity and silent aneurysms.

36. Echocardiogram – ultrasound of the heart to spot aortic-root enlargement or valve prolapse.

37. Thoraco-abdominal CT angiography – maps large-artery twisting or aneurysm risk.

38. Pelvic ultrasound – painless scan for bladder diverticula size and progression.

39. Joint ultrasound – identifies early cartilage degeneration from unstable joints.

40. DEXA bone-density scan – screens for osteoporosis because copper-dependent enzymes build bone strength.

Non-pharmacological treatments

Below are thirty evidence-informed strategies you and your care team can use without swallowing a pill. Each entry explains what it is, why it helps, and how it works.

Physiotherapy & electro-/exercise therapies

1. Gentle range-of-motion (ROM) sessions – Therapist-guided stretching keeps joints from tightening, preserves the ability to dress, bathe, and walk. Slow, pain-free stretches stimulate synovial fluid and collagen renewal.

2. Low-load resistance-band strengthening – Color-coded elastic bands build muscle around unstable joints without stressing bones. Stronger muscles act like “biological splints.”

3. Core-stability training – Pilates-style exercises that target the deep abdominal and spinal muscles improve posture and reduce spinal curvature pain.

4. Hydrotherapy (warm-water exercise) – Buoyancy unloads fragile bones while water resistance tones muscles and boosts circulation.

5. Proprioceptive neuromuscular facilitation (PNF) – Alternating contractions and stretches teach lengthened ligaments to “switch on” more quickly, sharpening joint position sense.

6. Whole-body vibration (low amplitude, <0.5 g) – Standing on a vibration plate three times per week can stimulate osteoblasts and counter low bone density.

7. Myofascial release & soft-tissue massage – Skilled hands loosen fascia, reduce trigger-point pain, and improve venous-lymphatic flow.

8. Joint-specific bracing & splinting – Custom ankle-foot orthoses or wrist splints restrict extreme motion, preventing subluxation during play or sleep.

9. Functional electrical stimulation (FES) – Small electrodes trigger weak muscles during walking practice, training better gait patterns.

10. Trans-cutaneous electrical nerve stimulation (TENS) – A portable unit delivers gentle pulses that “gate” pain signals, cutting chronic back or joint pain without drugs.

11. Low-level laser therapy (LLLT) – Red-light wavelengths (630–850 nm) applied for 3–5 minutes can boost fibroblast activity and collagen cross-linking.

12. Therapeutic ultrasound – Pulsed ultrasound warms deep tissue, easing spasm and enhancing copper-enzyme activity in experimental models.

13. Contrast heat/cold packs – Alternating warmth and cool dulls pain, reduces swelling, and stimulates micro-circulation.

14. Adaptive seating & ergonomic modifications – Adjustable desks, lumbar-support chairs, and cushioned grips reduce fatigue during schoolwork or office tasks.

15. Progressive gait-device training – From posterior walkers in toddlers to forearm crutches in teens, correct device use protects hip and knee joints from excess shear. ncbi.nlm.nih.govmedicoverhospitals.in

Mind-body approaches

16. Diaphragmatic breathing and guided imagery – Five-minute sessions before therapy tame sympathetic “fight-or-flight,” lowering muscle tension and heart strain.

17. Yoga for hyper-mobility – Slow, isometric holds build proprioception and core strength; avoid extreme end-range poses.

18. Mindfulness-based stress reduction (MBSR) – Eight-week programs cut chronic-pain catastrophizing and enhance quality of life.

19. Biofeedback-assisted relaxation – Seeing one’s own heart-rate variability on screen teaches real-time stress control.

20. Cognitive-behavioral pain coaching – Short, skills-based counseling reframes pain, improves adherence to exercise, and reduces doctor visits.

Educational & self-management skills

21. Genetic counseling for families – Understanding the X-linked pattern guides reproductive decisions and reduces guilt.

22. Copper-safe diet education – Dietitians teach choosing copper-rich foods (nuts, seeds, legumes) once serum copper normalizes, and avoiding excessive zinc that blocks absorption.

23. Joint-protection training – Learning to lift with knees, not back; using two-handed grips; pacing chores prevents micro-injuries.

24. Skin-care workshops – Moisturizing routines, silicone sheets for scars, and early wound care minimize infections.

25. Bladder-training schedules – Timed voiding plus pelvic-floor exercises reduce urinary stasis and bladder-diverticulum infections.

26. Fall-prevention home audits – Removing loose rugs, adding grab rails, and improving lighting lowers fracture risk.

27. School individualized education plan (IEP) – Accommodations such as extra time between classes or lightened backpacks prevent fatigue.

28. Peer-support groups – Sharing tips with other rare-disease families eases isolation and encourages evidence-based choices.

29. Pain-tracking apps – Digital diaries link trigger activities to flare-ups, helping clinicians fine-tune therapy.

30. Emergency-info wallet card – Lists diagnosis, medications, and copper therapy protocol for quick treatment in emergencies.

Medicines

Because OHS is rare, most drugs aim to replace copper or treat complications (pain, bladder infection, osteoporosis, autonomic dysfunction). Dosages below suit an average 30 kg child unless noted; always individualize with a specialist.

1. Copper histidine injection – Class: trace-element replacement. Dose: 250 µg SC once daily (start lower in infancy). Timing: mornings with physiotherapy. Side-effects: local redness, nausea, rare copper overload. pmc.ncbi.nlm.nih.govemedicine.medscape.com

2. Copper chloride IV – Rescue for severe deficiency: 0.5 mg/kg/day. Monitor liver enzymes.

3. Droxidopa – Class: norepinephrine pro-drug for autonomic hypotension. Dose: 100 mg PO tid; titrate. SE: headache, HTN surge.

4. Midodrine – Alpha-agonist for orthostatic dizziness: 2.5-10 mg PO q8 h; may cause piloerection, urinary retention.

5. Ibuprofen – NSAID for joint pain: 10 mg/kg PO q6–8 h prn; gastritis risk.

6. Acetaminophen – 15 mg/kg PO q6 h prn; hepatotoxic if >75 mg/kg/day.

7. Topical diclofenac gel – Local pain relief without systemic load; apply thin film tid.

8. Baclofen – GABA-B agonist for spasticity: 5 mg PO bid → 0.75 mg/kg/day; watch drowsiness.

9. Gabapentin – Neuropathic-pain modulator: 10 mg/kg PO tid; taper slowly.

10. Oxybutynin – Anticholinergic for bladder spasm: 0.2 mg/kg PO bid; dry mouth common.

11. Nitrofurantoin – Bladder-diverticulum UTI prophylaxis: 1–2 mg/kg PO qhs; avoid in G-6-PD deficiency.

12. Bisacodyl – Gentle stimulant laxative for constipation: 5 mg PO qod.

13. Vitamin D3 (cholecalciferol) – 1000 IU daily; hypercalcemia rare if closely monitored.

14. Calcium citrate – 500 mg element daily with meals; constipation risk mitigated by fiber.

15. Alendronate – Oral bisphosphonate 35 mg weekly for adolescents >35 kg; reflux precautions.

16. Zoledronic acid – IV 0.05 mg/kg yearly for refractory osteoporosis; acute flu-like reaction possible.

17. Teriparatide – PTH analog 20 µg SC daily (adults only) boosts bone turnover; limit to 24 months.

18. Propranolol – Beta-blocker for aortic-root dilation (off-label): 1 mg/kg/day in 2–3 doses; bradycardia risk.

19. Losartan – ARB 0.7 mg/kg bid for vascular protection; monitor renal function.

20. Tranexamic acid – Antifibrinolytic 10 mg/kg IV before dental work to curb bleeding; watch thrombosis in high-risk cases.

Dietary molecular supplements

1. Copper gluconate chewables – 2 mg elemental copper daily when injections stop; supports cupro-enzymes.

2. Vitamin C (ascorbic acid) 250–500 mg/day – Cofactor for collagen hydroxylation, helping skin tensile strength.

3. Vitamin B6 (pyridoxine) 25 mg/day – Essential for lysyl-oxidase cross-linking of collagen.

4. L-lysine 500 mg tid – Provides substrate for collagen bonds; aids wound healing.

5. Hydrolyzed marine collagen peptides 10 g powder daily – Supplies glycine-proline-hydroxyproline tri-peptides absorbed intact and used in dermal matrix.

6. Omega-3 fish-oil (EPA/DHA 1 g combined/day) – Anti-inflammatory, improves vascular elasticity.

7. Vitamin K2 (menaquinone-7) 90 µg/day – Activates osteocalcin so calcium goes into bone, not arteries.

8. Magnesium glycinate 200 mg elemental/day – Cofactor for alkaline phosphatase and bone mineralization.

9. Glucosamine sulfate 1500 mg/day – Precursor for glycosaminoglycans in cartilage; may ease joint clicking.

10. Methylsulfonylmethane (MSM) 1000 mg bid – Supplies bio-sulfur, purportedly improves connective-tissue resilience.

Advanced biologic / regenerative drugs

Bisphosphonates (anti-resorptive)

1. Alendronate – 35 mg weekly; binds hydroxyapatite, kills osteoclasts.

2. Zoledronic acid – 0.05 mg/kg IV yearly; potent, convenient.

3. Risedronate – 5 mg daily; gentler on GI tract.

Regenerative / anabolic

1. Teriparatide – 20 µg SC daily; intermittent PTH spikes recruit osteoblasts.
2. Romosozumab – 210 mg SC monthly, blocks sclerostin, doubles bone-formation rate.

Viscosupplementations

1. Hyaluronic-acid knee injection – 2 mL of 20 mg/mL solution x3 weekly doses; acts as joint lubricant.
2. Platelet-rich plasma (PRP) intra-articular – 5 mL autologous PRP, delivers growth factors IGF-1, TGF-β.

Stem-cell therapies (experimental)

1. Autologous bone-marrow aspirate concentrate (BMAC) – 10 mL injected into non-union fractures; supplies mesenchymal stem cells.
2. Allogeneic umbilical cord MSCs – 1 × 10^6 cells/kg IV monthly in trials; secrete anti-inflammatory cytokines.
3. AAV-mediated ATP7A gene transfer – One-time IV infusion in animal studies; aims to restore copper transport at the DNA level.

Surgeries

1. Occipital-horn excision – Orthopedic removal of painful skull spurs, improving helmet fit and cosmesis.

2. Inguinal hernia repair – Mesh-reinforced laparoscopy prevents bowel strangulation.

3. Bladder-diverticulum reconstruction – Urologic resection plus ureteral re-implantation averts reflux infections.

4. Spinal fusion for severe scoliosis – Rod-and-screw system halts curve progression, protects lungs.

5. Patellar stabilization surgery – Tightens medial patellofemoral ligament to stop kneecap dislocations.

6. Aortic-root grafting – Dacron graft replaces dilated segment, preventing life-threatening rupture.

7. Orthognathic jaw realignment – Corrects bite-related chewing problems and speech impairment.

8. Elbow osteophyte removal – Arthroscopic de-bulking restores extension blocked by large exostoses.

9. Cataract extraction – Phaco-emulsification returns clear vision when lens opacifies early.

10. Tendon-transfer hand surgery – Reroutes stronger tendons to lift dropped fingers, improving grip. jmhg.springeropen.com

Preventive habits

1. Start copper therapy in infancy to minimize bone and vessel damage.

2. Yearly echocardiogram to catch silent aortic dilation early.

3. Maintain vitamin-D sufficiency through safe sun or supplements.

4. Use seat-belt shoulder pads to avoid bruising fragile skin.

5. Keep BMI in the healthy range—extra weight stresses lax joints.

6. Schedule dental check-ups twice a year; weak enamel chips easily.

7. Stay hydrated; good vascular turgor supports venous return.

8. Treat minor wounds promptly to prevent slow-healing ulcers.

9. Vaccinate on time; infections can flare metabolic demands.

10. Educate PE teachers so exercise plans respect joint limits.

When should you see a doctor?

Call your specialist right away if you notice sudden neck pain, chest pressure, severe headache, unexplained fever, new bladder pain, or any joint that “locks” or dislocates and will not slip back easily. These can be signs of vascular tear, meningitis, bladder infection, or irreducible dislocation—each needs urgent care. Routine follow-ups every six to twelve months with genetics, orthopedics, cardiology, and physiotherapy keep tiny problems from snowballing.

“do’s and don’ts”

Do wear supportive shoes; don’t walk barefoot on uneven ground.
Do warm up joints with moist heat; don’t force a stretch through pain.
Do split heavy grocery bags into two loads; don’t lift >15 % of body weight at once.
Do drink copper-safe water after therapy; don’t over-supplement zinc without lab checks.
Do practice core-stabilizing exercises daily; don’t attempt high-impact sports like trampoline.
Do use silicone scar sheets on cuts; don’t pick at scabs—they heal slowly.
Do log all medications; don’t double NSAID doses if pain spikes—talk to your team.
Do have a medical ID bracelet; don’t let ER staff insert copper-chelating drugs by mistake.
Do get flu and COVID boosters; don’t ignore prolonged cough—weak connective tissue can bruise airways.
Do share mental-health concerns; don’t struggle alone—support groups help.

 Frequently asked questions (FAQ)

1. Is OHS the same as Menkes disease?
   They share the same gene defect, but OHS is milder—brains usually develop much better, and life expectancy extends into adulthood.

2. Will copper injections cure the syndrome?
   Copper replaces the missing mineral and prevents some damage, but it cannot reverse bone horns that already formed. Early treatment gives the best results. sciencedirect.com

3. Can girls get OHS?
   Yes, but it is extremely rare. Girls have two X-chromosomes, so the healthy copy often compensates.

4. Is pregnancy risky for a woman who carries the gene?
   Carrier moms are healthy but have a 50 % chance of passing the faulty gene to sons (affected) and daughters (carriers). Genetic counseling is essential.

5. Why do bladder problems happen?
   Weak connective tissue lets the bladder wall balloon outward, forming diverticula that trap urine and breed infection.

6. Does diet alone supply enough copper?
   Food helps maintain copper once stores rise, but injections remain the backbone because absorption from the gut is too unpredictable in OHS.

7. Are vaccinations safe?
   Yes. Standard vaccines do not strain joints or copper metabolism and protect against infections that could trigger flares.

8. Will my child need a wheelchair?
   Many children walk independently with braces, but some require wheelchairs for long distances or after major joint surgery.

9. Can physical therapy make joints looser?
   Not if done correctly. Therapists avoid aggressive stretching and focus on gentle control exercises that tighten muscles around joints.

10. How common are aortic aneurysms?
    They are less common than in Marfan syndrome but still a recognized risk; regular cardiac imaging is non-negotiable.

11. Is stem-cell therapy available now?
    It is still experimental. A few research centers run trials, but long-term benefit and safety remain unproven.

12. Do bisphosphonates stunt growth?
    Studies show they harden bone without halting linear growth when dosed correctly; doctors monitor X-rays and labs closely.

13. What is the life expectancy?
    With proactive care, many people reach middle age. Individual outlook depends on vascular health and infection control.

14. Can adults with OHS work full-time?
    Yes, especially in desk-based or flexible jobs that respect ergonomic needs and allow breaks for stretching.

15. Where can I find support?
    Organizations like the Menkes Foundation and national rare-disease networks offer newsletters, webinars, and peer mentors.

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 03, 2025.