Arthrogryposis due to Muscular Dystrophy

Arthrogryposis means a baby is born with more than one stiff joint (a “contracture”) that can’t move through a normal range. When the root cause of those contractures is a muscular dystrophy—a genetic condition that weakens muscles—doctors may describe it as arthrogryposis due to muscular dystrophy. In these cases, the baby’s muscles were too weak in the womb to move the joints normally. Less movement before birth leads to tight tendons and fixed joints at birth. This is one part of a broader group called arthrogryposis multiplex congenita (AMC). PM&R KnowledgeNow+2MSD Manuals+2

Muscular dystrophies that most often cause congenital contractures include the collagen VI–related dystrophies (Bethlem myopathy and Ullrich congenital muscular dystrophy), LAMA2-related (merosin-deficient) congenital muscular dystrophy, and Emery-Dreifuss muscular dystrophy. These disorders are genetic, affect muscle structure or its connection to surrounding tissues, and can present at birth or early infancy with joint stiffness in addition to weakness. NCBI+4PMC+4NCBI+4

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Other names

You may encounter these terms in reports or articles. They describe the same overall picture—multiple congenital contractures caused by a primary muscle disorder:

• Arthrogryposis multiplex congenita (AMC) due to neuromuscular disease (muscle cause). PM&R KnowledgeNow

• Congenital contractures associated with muscular dystrophy (general descriptive phrase). Cleveland Clinic

• Collagen VI–related dystrophy with contractures (Bethlem / Ullrich spectrum). PMC+1

• Merosin-deficient congenital muscular dystrophy (LAMA2-MD) with contractures. PMC+1

• Emery-Dreifuss muscular dystrophy with early contractures. NCBI

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Types

Doctors generally classify by the type of muscular dystrophy causing the contractures, because that guides prognosis, screening, and genetic counseling:

1. Collagen VI–related dystrophies (COL6A1/2/3 genes):
   These range from mild Bethlem myopathy to severe Ullrich congenital muscular dystrophy. Babies and children often have multiple flexion contractures (e.g., elbows, fingers, ankles) early in life, plus variable weakness. Skin findings (keratosis pilaris), distal hyperlaxity with proximal contractures, and later respiratory involvement can appear. NCBI+1

2. LAMA2-related congenital muscular dystrophy (merosin-deficient CMD):
   Newborns may show hypotonia (floppiness), feeding and breathing difficulties, hip dysplasia, and joint contractures/arthrogryposis. CK (a muscle enzyme) is often high, brain MRI may show white-matter changes, and weakness is prominent from infancy. PMC+2nmd-journal.com+2

3. Emery-Dreifuss muscular dystrophy (EDMD; LMNA, EMD and other genes):
   A hallmark is early, prominent contractures—especially of elbows, Achilles tendons, and spine—often in school-age years, sometimes earlier. There is also humero-peroneal muscle weakness and important cardiac conduction problems, so heart checks are essential. NCBI+1

4. Other congenital muscular dystrophy/dystrophy spectra with early contractures:
   Some “rigid-spine” or early-onset dystrophies display spine stiffness, distal weakness, and contractures; pattern-recognition with muscle MRI and genetics helps sort these conditions. American Academy of Neurology

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Causes

Below are causes or causal pathways that can lead to arthrogryposis when the underlying problem is muscular dystrophy. Each paragraph explains a distinct cause or mechanism within the muscular dystrophy spectrum.

1. Collagen VI gene defects (COL6A1, COL6A2, COL6A3):
   These genes help form the collagen VI network—part of the scaffolding around muscle fibers. Faults weaken the muscle–matrix connection. Movement in the womb drops, and contractures form. This is the core of the Bethlem–Ullrich spectrum. PMC

2. Ullrich congenital muscular dystrophy (severe collagen VI–related form):
   Severe early weakness plus proximal contractures with distal joint laxity can produce a striking arthrogryposis picture at or soon after birth. PMC

3. Bethlem myopathy (milder collagen VI–related form):
   Milder weakness but multiple flexion contractures over time—fingers, elbows, Achilles—sometimes noted at birth or early childhood. nmd-journal.com

4. LAMA2-related CMD (merosin-deficient CMD):
   Loss of laminin-211 (merosin) disrupts the muscle’s basement membrane. Reduced fetal movement leads to hip dysplasia and contractures, sometimes labeled arthrogryposis. PMC+1

5. Early-onset LAMA2-MD with arthrogryposis:
   New studies emphasize that arthrogryposis and joint contractures can be part of early LAMA2-MD, along with feeding and breathing issues. nmd-journal.com

6. Emery-Dreifuss muscular dystrophy (LMNA, EMD, others):
   Nuclear envelope protein defects cause early elbow/Achilles/spine contractures, sometimes before major weakness is seen. NCBI

7. Rigid-spine muscular dystrophy patterns:
   Some early-onset dystrophies show spinal rigidity with fixed joints because weak paraspinal and limb muscles can’t move normally in utero. American Academy of Neurology

8. Muscle–extracellular matrix interface failure:
   Across several dystrophies, disrupted links between muscle fibers and their surrounding support tissues limit fetal motion and promote contractures. Collagen VI disorders are the classic example. PMC

9. Basement membrane disruption:
   In LAMA2-MD, loss of laminin-211 undermines the basement membrane under muscle, producing profound weakness and contractures. PMC

10. Progressive tendon shortening secondary to weakness:
    Even after birth, chronic weakness means joints don’t cycle through full motion, so tendons and capsules tighten, sustaining or worsening contractures. (General mechanism noted across AMC from neuromuscular causes.) PM&R KnowledgeNow

11. Fetal akinesia sequence due to myopathic weakness:
    If muscles are weak very early in gestation, global reduction in fetal movement leads to multiple contractures (the “akinesia–contracture” pathway). PMC+1

12. Distal > proximal weakness patterns:
    Some dystrophies first weaken distal muscles of hands/feet. Less distal motion in utero can favor hand/foot contractures (e.g., clubfoot). nmd-journal.com

13. Spine extensor weakness:
    Weak spinal muscles can yield kyphosis or rigid spine with reduced trunk motion and secondary contractures. American Academy of Neurology

14. Respiratory muscle weakness (secondary effects):
    In severe CMDs, breathing muscle weakness can change chest wall motion and posture, stiffening shoulder and spine joints over time. PMC

15. Connective-tissue involvement beyond muscle:
    Collagen VI defects also affect connective tissues (e.g., skin), which can favor contractures because supporting tissues lack normal elasticity. PMC

16. Hip dysplasia co-occurrence:
    In early LAMA2-MD, hip dysplasia is common and can lock the hips in poor positions, compounding contractures. nmd-journal.com

17. Achilles tendon early shortening:
    In EDMD and collagen VI disorders, Achilles tightness is an early sign, leading to toe-walking or fixed equinus. NCBI

18. Elbow flexion contractures from reduced extension cycles:
    With weak triceps and shoulder girdle, the elbows may rest in a flexed position, slowly fixing in flexion. (Observed in EDMD and Bethlem.) NCBI+1

19. Capsular fibrosis:
    Prolonged immobility promotes fibrosis of joint capsules, a shared end-pathway across neuromuscular arthrogryposis. PM&R KnowledgeNow

20. Genetic spectrum breadth and overlap:
    Multiple genes and pathways lead to the same phenotype—multiple congenital contractures—so comprehensive genetic testing is often needed to pinpoint the exact cause. MSD Manuals

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Common symptoms and signs

1. Stiff joints at birth (more than one area), often wrists, elbows, hips, knees, or ankles. This is the core feature of arthrogryposis. Merck Manuals

2. Limited range of motion in affected joints; joints feel “stuck” or “frozen” without gentle stretching and therapy. Cleveland Clinic

3. Low muscle tone (hypotonia) and weakness, especially in congenital dystrophies like LAMA2-MD. Babies may be “floppy.” PMC

4. Delayed motor milestones (rolling, sitting, standing) because of both weakness and contractures. Cleveland Clinic

5. Clubfoot and hand deformities (e.g., clenched hands), which reflect reduced fetal movement. MSD Manuals

6. Hip dysplasia or dislocation, commonly paired with early CMDs. nmd-journal.com

7. Spine stiffness or abnormal curvature (rigid spine features in some dystrophies). American Academy of Neurology

8. Tight Achilles tendons with toe-walking or fixed equinus in EDMD and collagen VI disorders. NCBI

9. Elbow flexion contractures that limit reaching and dressing. NCBI

10. Breathing problems in severe LAMA2-MD and some collagen VI disorders; may require early respiratory support planning. PMC

11. Feeding difficulties in early LAMA2-MD (weak oromotor muscles, fatigue). PMC

12. Skin and soft-tissue clues in collagen VI disease (e.g., keratosis pilaris) alongside contractures. PMC

13. Fatigue and reduced endurance because weak muscles tire easily. nmd-journal.com

14. Cardiac rhythm problems (EDMD)—important because they can be silent early on. NCBI

15. Normal intelligence in many cases, though this depends on the exact genetic condition and associated brain findings. Merck Manuals

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Diagnostic tests

Doctors combine the story (history), the exam, imaging, electrical tests, blood tests, and genetics to confirm the muscular dystrophy cause of arthrogryposis and to guide care.

A) Physical examination

1. Global musculoskeletal exam:
   The clinician maps which joints are tight, how severe the stiffness is, and whether the pattern suggests a specific dystrophy (e.g., proximal flexion contractures with distal laxity in collagen VI disease). PMC

2. Range-of-motion (ROM) measurements:
   Goniometer measurements track contracture angles over time (e.g., elbows, knees, ankles) and help judge therapy response. (Standard practice within AMC workups.) PM&R KnowledgeNow

3. Neuromuscular strength and tone assessment:
   Graded manual muscle testing and tone checks (hypotonia vs spasticity) help distinguish primary muscle disease from nerve/brain causes. PM&R KnowledgeNow

4. Spine flexibility testing:
   Limited extension/rotation suggests rigid-spine patterns or early EDMD involvement. American Academy of Neurology

5. Cardiac and respiratory screening in clinic:
   In EDMD, heart rhythm evaluation is critical; in severe CMDs, early signs of breathing weakness prompt specialized testing. NCBI+1

B) Manual / bedside tests

6. Functional motor scales (age-appropriate):
   Clinicians may use standardized functional tests to capture day-to-day abilities and limitations linked to contractures and weakness. PM&R KnowledgeNow

7. Gowers’ maneuver observation:
   Rising from the floor using hands on thighs suggests proximal weakness typical of many dystrophies (supportive, not diagnostic alone). Merck Manuals

8. Contracture-focused stretching response:
   Careful trial of passive stretching during therapy helps distinguish fixed capsular tightness from dynamic stiffness. PM&R KnowledgeNow

9. Respiratory bedside measures (e.g., cough strength):
   Weak cough or shallow breathing in severe CMDs signals the need for formal respiratory testing. PMC

10. Screening for skin/soft-tissue clues:
    Findings such as keratosis pilaris in collagen VI disease can support the diagnostic impression. PMC

C) Lab and pathological tests

11. Serum creatine kinase (CK):
    Often elevated in dystrophies like LAMA2-MD; normal or mildly raised in some collagen VI conditions—helps triage next tests. PMC

12. Comprehensive genetic testing (panels/exome):
    Panels targeting COL6A1/2/3, LAMA2, LMNA/EMD, and other CMD genes are now standard; a precise genetic answer directs care and family counseling. MSD Manuals

13. Targeted single-gene testing:
    If the exam pattern screams one diagnosis (e.g., classic EDMD or collagen VI), clinicians may go directly to the likely gene(s). NCBI

14. Muscle biopsy (when genetics is unrevealing):
    Biopsy can show dystrophic changes and guide immunostaining (e.g., for collagen VI or laminin-211). It’s often reserved for unclear cases now that genetics is strong. PubMed

15. Protein immunohistochemistry / western blot (biopsy or skin fibroblasts):
    Loss or reduction of collagen VI or laminin-211 supports the diagnosis in the right clinical setting. American Academy of Neurology

D) Electrodiagnostic tests

16. Electromyography (EMG):
    Helps distinguish myopathic (muscle) from neurogenic (nerve/spinal) causes of arthrogryposis—key if the clinical picture is mixed. Washington University Orthopedics

17. Nerve conduction studies (NCS):
    Usually normal or near-normal in primary muscular dystrophy, which helps rule out peripheral neuropathy as the main driver. PubMed

18. Fetal movement surveillance (during pregnancy):
    When contractures are suspected prenatally, serial ultrasound and sometimes fetal MRI monitor akinesia and joint positions and prepare the care plan. PMC+1

E) Imaging tests

19. Muscle MRI (childhood):
    Pattern-recognition on muscle MRI can point toward specific dystrophies (e.g., typical signal patterns in collagen VI disease), supporting genetic results. PMC

20. Skeletal imaging (X-rays; targeted CT/MRI):
    Used to document hip dysplasia/dislocation, spine deformity, or complex foot/hand positions and to plan therapy or surgery if needed. MSD Manuals

Non-pharmacological treatments

Goal: keep joints as mobile as safely possible, support standing and hand use, delay or reduce surgeries, prevent pain and skin issues, and build participation in daily life.

1. Early, gentle range-of-motion (ROM) and stretching. Short, frequent, pain-free stretches taught to caregivers keep tissues supple and help positioning. Evidence is mostly expert consensus and small studies but is the cornerstone of care. BioMed Central+1

2. Positioning and splinting (day/night). Custom soft splints hold joints in a better position, help maintain gains after therapy or casting, and can reduce skin stress. jposna.com

3. Serial casting for feet/knees/elbows. Short runs of casts (often Ponseti-style for clubfoot) can increase passive motion and improve brace fit; effects on dynamic alignment are limited, so follow-up bracing is key. PubMed+1

4. Ankle-foot orthoses (AFOs) and custom shoes. Improve standing balance, knee control, and gait efficiency; also protect skin. Fit changes with growth, so regular reviews are needed. jposna.com

5. Task-oriented physiotherapy. Practice of real-life tasks (rolling, sitting, transfers, grasp-and-release) supports motor learning and independence; frequency is individualized. PMC+1

6. Occupational therapy and adaptive equipment. Splints for hands, built-up handles, and switch-based access can transform self-care and school tasks. BioMed Central

7. Aquatic therapy. Buoyancy allows safer joint movement and whole-body practice with less stress on stiff joints. Supportive evidence exists in pediatrics; AMC-specific data are limited. ERN ITHACA

8. Treadmill or body-weight–supported gait training. Improves endurance and stepping practice even with orthoses; evidence extrapolated from pediatric rehab. ERN ITHACA

9. Neuromuscular electrical stimulation (NMES). May help muscle activation in selected targets to support posture or hand use; use with caution and monitoring. ERN ITHACA

10. Hip surveillance and posture programs. Regular checks, supported sitting, and prone play reduce risk of hip dysplasia, contracture progression, and pressure issues. jposna.com

11. Pain management without medication first. Heat, gentle massage, pacing of activity, and sleep/position tweaks often reduce soreness linked to bracing or therapy. PMC

12. Respiratory support when needed (for certain CMDs). Airway clearance training, safe feeding positions, and early sleep-disordered breathing screening in LAMA2/COL6 phenotypes. NCBI+1

13. Feeding, speech, and swallow therapy. Addresses weak oral muscles, TMJ tightness, and reflux risks noted in some CMDs. NCBI

14. Education and caregiver training. Teaching home programs, safe handling, splint care, and skin checks improves outcomes and reduces complications. BioMed Central

15. Psychosocial and participation supports. School plans, mobility grants, and social inclusion improve quality of life as much as medical steps. PMC

Evidence note: High-quality trials in AMC are rare; consensus-based recommendations (2025) emphasize early, family-centered rehab and individualized goals. PMC+1

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Drug treatments

There is no medicine that “unlocks” a contracted joint. Drugs treat associated problems (pain, reflux, sleep-disordered breathing, infections) and, in some CMDs, the underlying muscle disease (e.g., steroids in Duchenne—not typically a cause of arthrogryposis—do not treat AMC). Any disease-modifying therapy is gene-specific and experimental for most CMDs. Always manage medications under a neuromuscular specialist.

1. Acetaminophen (paracetamol). For soreness after casting/therapy; gentle on stomach; dose by weight; avoid overdosing due to liver risk. Medscape

2. NSAIDs (e.g., ibuprofen) short courses. For inflammatory pain from irritation around braces or minor strains; watch gastric and renal cautions. Medscape

3. Proton-pump inhibitor or H2 blocker (if reflux). In LAMA2 CMD, reflux/aspiration risk is higher; treating reflux helps comfort and growth. NCBI

4. Vitamin D and calcium (if deficient). Protect bone health in low-mobility states; supplement only to correct deficiency or meet needs. NCBI

5. Bronchodilators/airway meds (when indicated). For reactive airway issues or secretions in weak cough; part of respiratory plans in some CMDs. NCBI

6. Antibiotics (promptly when needed). For chest infections in aspirators or those with weak cough; prevent decline and hospitalization. NCBI

7. Antispasmodics (limited role). Classic spasticity agents (baclofen, tizanidine) are usually not central in AMC from CMD, which is a low-movement, not high-tone, problem—use only if a clinician documents spasticity from another cause. Medscape

8. Botulinum toxin (select cases). Not a routine AMC therapy; may help if an antagonist muscle is clearly overactive and blocking progress, but evidence is sparse. PMC

9. Nutritional supplements as “medicines.” Avoid “muscle-building” claims without evidence; focus on diet quality and deficiency correction. Frontiers

10. Gene/biologic therapies (research stage for CMD). For LAMA2 and COL6 disorders, multiple approaches (gene replacement, exon skipping, cell therapy) are in preclinical/early clinical exploration; not standard of care yet. nmd-journal.com+1

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Dietary “molecular” supplements

Supplements do not loosen joints. The aim is to support growth, bone, and immune health in low-mobility states. Use dietitian guidance; check interactions.

1. Balanced protein intake (food-first). Supports growth and tissue repair; spread across the day; avoid mega-dosing that strains kidneys. NCBI

2. Vitamin D (if low). Essential for bone mineralization; lab-guided dosing prevents deficiency common in limited weight-bearing. NCBI

3. Calcium to dietary targets. Meet—not exceed—age targets for bone health. NCBI

4. Omega-3 fatty acids (food-first). May help general cardiometabolic health and inflammation balance; evidence in AMC is indirect. PMC

5. Fiber and fluids. Prevent constipation from low mobility; improves comfort and feeding tolerance. NCBI

6. Multivitamin (gap-filler). Low-dose, age-appropriate when intake is limited; avoid high-dose fat-soluble vitamins. NCBI

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Immunity booster / regenerative / stem-cell drugs

• There is no proven immune-booster pill for arthrogryposis or CMD; healthy sleep, vaccines, nutrition, and prompt infection care work best.

• Regenerative or stem-cell drugs for LAMA2/COL6 CMDs are investigational only and should be accessed, if at all, inside regulated clinical trials. nmd-journal.com+1

Four items to understand clearly:

1. Gene therapy concepts (investigational). Aim to restore missing proteins (laminin-α2 or collagen VI) or stabilize matrix; dosing and delivery remain challenges. nmd-journal.com

2. Cell-based therapy (preclinical/early). Tries to replace damaged muscle/support cells; safety and durable benefit are unproven. nmd-journal.com

3. Exon-skipping/editing (research). Sequence-specific; not available for clinical care in AMC-related CMDs. nmd-journal.com

4. Supportive vaccines & infection prevention (standard). “Boosts immunity” in the real-world sense by preventing avoidable illness. NCBI

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Surgeries

1. Clubfoot correction (Ponseti-based with modifications; possible tendon transfers). To achieve plantigrade, brace-tolerant feet for standing and walking. Repeat casting and staged releases are common. jposna.com

2. Knee flexion/extension contracture releases (with quadricepsplasty or hamstring lengthening as needed). To enable standing, transfers, and orthotic fit. jposna.com

3. Hip surgery (carefully selected). Address dislocation or severe contracture to improve sitting comfort, hygiene, and brace tolerance; decisions are individualized. jposna.com

4. Upper-limb tendon transfers/capsulotomies. To gain reach to mouth or perineum and functional grasp; therapy and splinting must follow. jposna.com

5. Spine surgery (if progressive deformity compromises function/skin). For balance, sitting, and skin protection; bracing and seating support remain essential. jposna.com

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Prevention tips

1. Start rehab immediately after birth; don’t wait. PMC

2. Learn and perform daily home ROM that is gentle and pain-free. BioMed Central

3. Protect skin under casts/splints; check pressure points daily. jposna.com

4. Keep braces fitting with regular reviews; kids grow fast. jposna.com

5. Vaccinate on schedule; treat infections promptly. NCBI

6. Ensure adequate nutrition, vitamin D and calcium if needed. NCBI

7. Maintain sleep hygiene and airway checks in CMDs. NCBI

8. Encourage safe physical play (including water) to build endurance. ERN ITHACA

9. Use adaptive tools early for independence and school success. BioMed Central

10. Join experienced care teams; this is a rare condition. PMC

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When to see doctors urgently or soon

• New redness, swelling, or skin breakdown under a cast/splint.

• Fever, cough, choking, or poor weight gain in infants with CMD (aspiration risk). NCBI

• Rapid loss of function, new pain, or deformity that blocks standing, transfers, or self-care. jposna.com

• Breathing pauses, snoring, morning headaches, or daytime sleepiness (possible sleep-disordered breathing). NCBI

• Feeding fatigue, reflux, or frequent chest infections. NCBI

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What to eat and what to avoid

• Eat: Regular meals with protein at each meal (fish, eggs, dairy, legumes), colorful fruits/vegetables, whole-grain fiber, and healthy fats; enough calcium and vitamin D for age; plenty of fluids to prevent constipation. NCBI

• Limit/Avoid: High-sugar drinks and ultra-processed snacks (empty calories), very high-dose supplements without labs, and any “muscle-building” products that promise cures. Focus on food-first, dietitian-guided plans. NCBI

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FAQs

1) Is arthrogryposis a single disease?
No. It’s a description of multiple joint contractures present at birth. Many different causes exist, including congenital muscular dystrophies. National Organization for Rare Disorders

2) Can therapy really change stiff joints?
Therapy can’t “cure” a contracture, but early, gentle stretching, positioning, and casting can improve motion, brace fit, and function—and reduce the number or extent of surgeries. PubMed+1

3) Why are clubfeet common?
Low fetal movement lets tendons and capsules tighten around the ankle and foot. Clubfoot treatment usually follows Ponseti principles with adaptations. jposna.com

4) Will medicines loosen joints?
No. Medicines treat pain, reflux, sleep/breathing, and infections. Contractures are managed with rehab, bracing, and sometimes surgery. Medscape

5) Are steroids helpful?
Steroids help some dystrophies like Duchenne, but they don’t treat arthrogryposis itself and are not standard for COL6 or LAMA2 CMDs. NCBI+1

6) Are there gene therapies?
Research is active for LAMA2 and collagen VI disorders, but these approaches are not standard care yet. Clinical trials may be available. nmd-journal.com

7) Does arthrogryposis get worse?
The contractures are typically non-progressive, but growth can unmask challenges, and the underlying muscle condition may have its own course—hence regular follow-up. PMC

8) What specialists should be on the team?
Pediatric rehab medicine, orthopedics, neuromuscular neurology, genetics, PT/OT, respiratory, nutrition/feeding, and social work/psychology. PMC

9) How often should braces be checked?
Every growth spurt or when redness, slipping, or new pain occurs—often every 3–6 months in early years. jposna.com

10) Can my child be active in sports?
Yes—adapted, safe activities (including swimming) are encouraged to build endurance, confidence, and social participation. ERN ITHACA

11) Is surgery always needed?
No. Many children do well with therapy, casting, and bracing; surgery is used to reach specific functional goals when conservative care isn’t enough. jposna.com

12) How common is arthrogryposis?
Estimates are roughly 1 in 3,000–5,000 live births across all causes. PMC

13) Can feeding and speech be affected?
Yes—in some CMDs due to jaw/tongue weakness and TMJ tightness; therapy and positioning help. NCBI

14) What about school accommodations?
Adaptive tools, extra time, seating plans, and assistive tech can support learning and independence. BioMed Central

15) Where can families find reliable information?
Rare Disease groups (NORD), GeneReviews for specific CMDs, and multidisciplinary AMC clinics provide credible, updated guidance. National Organization for Rare Disorders+2NCBI+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: September 23, 2025.

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