Cap myopathy (also called cap disease or congenital myopathy with caps) is a rare inherited muscle condition. In this disorder, skeletal muscles (the muscles we use for movement) are weak and have low tone from birth or early life. Under the microscope, doctors see special “cap-like” areas at the edges of many muscle fibers; these “caps” are made of disorganized thin filaments in the contractile machinery. The weakness often affects the face, neck, shoulders, and hips first; some people also have chest wall shape changes and breathing weakness. Severity varies widely—from mild lifelong weakness to serious breathing problems in infancy. MedlinePlus+2Orpha+2
Cap myopathy is a disorder that primarily affects skeletal muscles, the muscles that the body uses for movement. People with Cap myopathy have muscle weakness (myopathy) and poor muscle tone (hypotonia) throughout the body, but they are most severely affected in the muscles of the face, neck, and limbs. The name Cap myopathy comes from characteristic abnormal cap-like structures that can be seen in muscle cells when muscle tissue is viewed under a microscope. Individuals in whom 70 to 75 percent of muscle cells have caps typically have severe breathing problems and may not survive childhood, while those in whom 10 to 30 percent of muscle cells have caps have milder symptoms and can live into adulthood. Cap myopathy can be caused by genetic changes in the in the ACTA1, TPM2, or TPM3 genes. This condition follows an autosomal dominant manner of inheritance, however, most cases are not inherited; they result from new genetic changes in the gene and occur in people with no history of the disorder in their family.
Cap myopathy is most often caused by changes (pathogenic variants) in one of three genes that help muscles contract: ACTA1 (skeletal muscle α-actin), TPM2 (β-tropomyosin), or TPM3 (γ-tropomyosin). These proteins form or regulate the thin filaments that slide to make muscles shorten. When the gene is altered, thin filaments assemble or interact abnormally, and cap-like disorganized areas appear in muscle fibers. MedlinePlus+2ScienceDirect+2 Most reported cases follow autosomal dominant inheritance, which means one changed copy of the gene can cause disease. However, many people with cap myopathy are the first in their family due to a new (de novo) genetic change. Genetic counseling is recommended for families because severity and features can vary even within a family. MedlinePlus
Muscle biopsy shows “caps”—zones just beneath the cell membrane where thin filaments and Z-disk material are abnormally clumped and enzyme activity is reduced; electron microscopy confirms disorganized thin filaments and thickened/expanded Z-material. Sometimes nemaline rods (another thin-filament abnormality) appear together with caps. These features help pathologists distinguish cap myopathy from other congenital myopathies. JAMA Network+2SciSpace+2
Cap myopathy is a rare, inherited muscle disease that mainly affects the skeletal muscles we use for movement. Under the microscope, the patient’s muscle fibers show special “cap-like” areas near the outer edge of the fiber. These caps are made of disorganized thin filaments (actin–tropomyosin parts of the sarcomere). The abnormal thin filaments make muscle contraction weak. Symptoms usually begin at birth or in early childhood and progress slowly. Many people have low muscle tone (hypotonia), delayed motor milestones, facial and neck weakness, and sometimes breathing problems because the respiratory muscles are weak. The condition is most often autosomal dominant, and many cases arise from a new (de novo) mutation with no prior family history. Known genes include ACTA1, TPM2, and TPM3. MedlinePlus+2GARD Information Center+2
Pathologists named the disease “cap” myopathy because stains such as NADH-TR and trichrome highlight sharply demarcated, cap-like rims at the fiber edges. These correlate with disorganized Z-line material and thin filaments under electron microscopy. neuromuscular.wustl.edu+1
Other names
You might also see: Cap disease, or Congenital myopathy with caps. All refer to the same disorder and the same key biopsy finding. MedlinePlus
Types
- By age and severity. Doctors often describe a severe neonatal form (symptoms at birth, feeding/breathing support often needed) and a childhood-onset, milder form with slow progression. Severity can relate to how many fibers show caps; about 70–75% cap-positive fibers often predicts severe respiratory problems and poor survival, while 10–30% cap-positive fibers is usually milder. GARD Information Center
- By gene. Subtypes relate to mutations in ACTA1 (skeletal α-actin), TPM2 (β-tropomyosin), and TPM3 (α-tropomyosin-slow). Cap-type structures have also been reported (less commonly) in patients with variants in NEB (nebulin), DES (desmin), and MYPN (myopalladin), showing overlap among congenital myopathies. MedlinePlus+1
- By distribution. Some people have more axial and neck weakness (head control, posture), while others notice proximal limb weakness (hips/shoulders) or mixed patterns; facial weakness is common. Progression is usually slow. Orpha+1
Causes
In hereditary myopathies, “cause” usually means the gene change/mechanism that disrupts muscle contraction. Here are 20 clearly worded causes linked to cap myopathy or cap-like pathology.
ACTA1 mutations (α-actin). Pathogenic changes in ACTA1 disturb thin-filament assembly, making the cap structures and weakening contraction. Often de novo and autosomal dominant. MedlinePlus
TPM2 mutations (β-tropomyosin). Tropomyosin helps regulate actin–myosin binding; TPM2 variants can impair regulation and lead to caps and weakness. MedlinePlus
TPM3 mutations (α-tropomyosin-slow). Similar mechanism to TPM2; abnormal thin-filament control gives poor force and cap morphology. MedlinePlus
De novo dominant variants. Many patients have a new pathogenic variant not present in parents, explaining sporadic cases. MedlinePlus+1
Dominant inheritance in families. When inherited, one altered copy is enough to cause disease in each generation. MedlinePlus
Thin-filament disorganization. The central common pathway is mis-built or mis-regulated thin filaments forming cap-like rims. ScienceDirect
Z-line material abnormalities. Z-disk proteins become disorganized at fiber edges, visible on histology and EM. neuromuscular.wustl.edu
NEB (nebulin) variants with cap-type structures (rare). Some patients with nebulin changes show cap-type rims, underlining mechanistic overlap with other congenital myopathies. Arkana Laboratories
DES (desmin) variants with cap-type pathology. Intermediate filament defects can also produce cap-like regions. Arkana Laboratories
MYPN (myopalladin) variants with cap-type pathology. Z-disc scaffolding problems can lead to cap-like rims. Arkana Laboratories
Impaired actin–tropomyosin interaction. Tropomyosin mutations can block normal on–off control of myosin binding along actin. MedlinePlus
Sarcomere assembly defects. Faulty assembly of sarcomere parts during development yields structurally weak fibers. ScienceDirect
Cofilin-2 pathway disturbance (overlap biology). CFL2 is actin-severing; its deficiency disturbs actin turnover, demonstrating thin-filament vulnerability in congenital myopathies (reported mainly in nemaline/myofibrillar myopathy, but mechanistically relevant). PubMed+2Cell+2
Myosin pathway overlap (MYH7). Some myosin heavy chain (MYH7) disorders show skeletal myopathy with possible cardiac involvement; while not classic cap myopathy, they illustrate neighboring sarcomeric mechanisms that can produce mixed patterns. PubMed+1
Cap percentage within fibers. Greater proportion of cap-positive fibers (e.g., 70–75%) links to more severe disease and respiratory failure risk. GARD Information Center
Modifier genes. Background variants may alter severity (inference from congenital myopathy literature and variable expressivity). PMC
Protein mislocalization at costameres/Z-disks. Misplaced structural proteins worsen contractile coupling. PMC
Secondary myofibrillar disarray. Once structure is unstable, fibers develop broader myofibrillar disorganization that sustains weakness. neuromuscular.wustl.edu
Respiratory muscle susceptibility. Some congenital myopathies show disproportionate respiratory muscle involvement, magnifying symptoms. Wiley Online Library
Random (stochastic) fiber involvement. Uneven cap formation among fibers produces patchy weakness patterns within the same muscle. (Synthesis from histopathology sources.) neuromuscular.wustl.edu
Common symptoms
Low muscle tone (hypotonia). Babies may feel “floppy,” with delayed head control and slow motor milestones like sitting or walking. Orpha
General muscle weakness. Weakness can involve face, neck, trunk, and limbs; getting up from the floor or lifting the head can be hard. Orpha
Facial weakness. A flat facial expression, poor eye closure, or weak mouth muscles may be noticed. Orpha
Neck and axial weakness. Trouble holding the head up and maintaining posture is common. BioMed Central
Proximal limb weakness. Hips and shoulders are often more affected than hands and feet; climbing stairs or lifting arms overhead is difficult. Orpha
Distal involvement (variable). Some patients notice hand or ankle weakness or foot drop, depending on pattern. Orpha
Scapular winging and thin shoulder girdle. Weak shoulder stabilizers make shoulder blades stick out. Orpha
Scoliosis or chest wall shape changes. Weak trunk muscles can allow spinal curves or a small, stiff chest. Orpha
Feeding difficulties in infancy. Poor sucking or swallowing can occur in severe neonatal cases. ResearchGate
Breathing problems. Weak breathing muscles can cause rapid breathing, frequent infections, or need for non-invasive ventilation, especially in severe phenotypes. GARD Information Center
Sleep-related breathing issues. Hypoventilation or sleep apnea may appear because the diaphragm and chest muscles are weak. PMC
Fatigue and poor endurance. Muscles tire quickly, and activity tolerance is low. BioMed Central
Joint contractures. Tight joints develop over time when weak muscles cannot move the joint fully. Medscape
Delayed motor milestones. Late sitting, standing, and walking reflect early hypotonia and weakness. Orpha
Variable long-term course. Many have slow progression; severity differs widely between individuals and even within families. BioMed Central
Diagnostic tests
A) Physical Exam
Neuromuscular exam. The clinician looks for hypotonia, patterns of weakness (face, neck, trunk, proximal limbs), and reflex changes. The pattern—plus family history—raises suspicion for a congenital myopathy. Medscape+1
Craniofacial and bulbar evaluation. Examination of facial movement, jaw strength, palate, and swallowing can reveal facial/bulbar weakness that fits the cap myopathy profile. Orpha
Respiratory assessment. Rate, chest movement, cough strength, and signs of shallow breathing are checked, because respiratory muscle weakness is a major risk. PMC
Spine and posture inspection. The clinician looks for scoliosis, lumbar lordosis, or rigid spine, which often accompanies congenital myopathies. posna.org
B) Manual/Bedside Functional Tests
Manual Muscle Testing (MMT). Strength is graded by resistance testing (e.g., the Oxford scale). It maps which muscle groups are weaker and establishes a baseline to track over time. Medscape
Range-of-motion and goniometry. Measuring joint motion detects early contractures so therapy and bracing can start promptly. Medscape
Adam’s forward bend test (scoliosis screen). A simple bend-forward test helps detect trunk asymmetry that suggests scoliosis from axial weakness. BioMed Central
Timed functional tests (e.g., 10-meter walk, rise-from-chair). Quick bedside measures of endurance and function show day-to-day impact and are easy to repeat. Medscape
C) Laboratory & Pathology
Serum creatine kinase (CK). CK is often normal or only mildly raised in congenital myopathies, helping separate them from muscular dystrophies that show high CK. PMC
Genetic testing (panel or exome). Next-generation sequencing looks for pathogenic variants in ACTA1, TPM2, TPM3 and related genes. Finding a causative variant can confirm diagnosis without biopsy. MedlinePlus
Muscle biopsy—light microscopy. Special stains (e.g., Gomori trichrome, NADH-TR) show the classic cap-like rims at fiber edges. This is the morphologic hallmark when genetics is inconclusive or to understand pathology. neuromuscular.wustl.edu
Immunohistochemistry. Antibodies to proteins like desmin, α-actinin, tropomyosin, actin, nebulin, myotilin help characterize the cap regions and rule in/out overlaps. neuromuscular.wustl.edu
Electron microscopy (EM). EM reveals disorganized Z-line material and thin-filament abnormalities that match cap formation on light microscopy. neuromuscular.wustl.edu
Targeted family testing. Once a mutation is found, relatives can be tested to clarify inheritance and offer genetic counseling. MedlinePlus
D) Electrodiagnostic & Physiologic Monitoring
Electromyography (EMG). EMG often shows a myopathic pattern (small, short-duration motor unit potentials), supporting a primary muscle process rather than nerve disease. Medscape
Nerve conduction studies (NCS). Typically near-normal, which helps rule out neuropathy; this supports a myopathy diagnosis. Medscape
Overnight sleep study (polysomnography) or nocturnal CO₂/oximetry. Detects hypoventilation or sleep apnea due to weak breathing muscles so that non-invasive ventilation can be started early. PMC
E) Imaging
Muscle MRI. MRI maps selective muscle involvement and can guide which genes to test and where to biopsy; it also helps follow disease over time. nmd-journal.com+1
Spine radiographs. Simple X-rays quantify scoliosis, guide bracing, and help plan surgery if curves progress. BioMed Central
Echocardiogram (when indicated). Most cap myopathy cases do not have heart disease, but if gene/phenotype suggests overlap (e.g., myosinopathies), echo screens for structural or functional problems. PubMed
Non-pharmacological treatments (therapies and other supports)
Notes for readers: These measures are the backbone of care. They are tailored by a neuromuscular team and adjusted over time.
Physiotherapy for flexibility and posture. Gentle daily stretching prevents joint contractures and maintains posture and comfortable movement. Programs add low-load, regular activity without over-fatiguing weak muscles. PMC
Targeted strengthening at sub-maximal intensity. Carefully dosed, non-fatiguing strengthening (e.g., gravity-reduced movements, water-based therapy) supports function without injuring fragile fibers. PMC
Occupational therapy (energy conservation + adaptive techniques). OT teaches joint-protection, pacing, and equipment use (pens, grips, utensils) to improve independence at school and work. PMC
Orthoses and positioning. Night splints, AFOs, wrist splints, or scapular supports help alignment, reduce strain, and delay contractures or foot deformity. Medscape
Respiratory surveillance. Regular checks (spirometry, cough peak flow, sleep studies) catch early hypoventilation; treatment is introduced before complications occur. nmd-journal.com
Airway clearance training. Cough-assist techniques (manual or device-assisted), breath-stacking, and postural drainage reduce infections and atelectasis in weak cough. nmd-journal.com
Non-invasive ventilation (NIV) at night when indicated. CPAP/BiPAP supports weak breathing muscles during sleep, improving daytime energy and preventing complications of chronic hypoventilation. nmd-journal.com
Nutrition and growth support. A dietitian helps maintain healthy weight, adequate protein, calcium, and vitamin D for bone health; this reduces fracture risk and supports rehabilitation. PMC
Swallowing assessment. Speech-language therapy evaluates chewing/swallow safety; strategies and textures reduce aspiration. Feeding tubes are considered when aspiration or poor growth persists. PMC
Scoliosis monitoring. Regular spine assessment, early bracing if helpful, and timely surgical referral when curves progress. Curve control aids breathing mechanics. PMC
Pain and fatigue management (non-drug). Heat, gentle massage, activity pacing, sleep hygiene, and mindfulness help chronic myofascial discomfort without sedatives. PMC
Safe anesthesia planning. Anesthesia teams avoid depolarizing muscle relaxants and volatile triggers in neuromuscular disease when possible and prepare for difficult ventilation and postoperative respiratory support. Frontiers+1
Vaccination planning. Up-to-date flu and pneumococcal vaccines lower respiratory infection risk in people with weak cough. PMC
Assistive mobility devices. Strollers, walkers, or wheelchairs (manual or power) maintain participation and reduce falls as distances increase. PMC
School and workplace accommodations. Rest breaks, elevator access, extra time for fine-motor tasks, and ergonomic seating keep performance and attendance stable. PMC
Psychosocial support. Counseling and peer-support reduce stress and improve adherence to long-term care plans for families and adults. PMC
Sleep optimization. Routine, positional therapy, and sleep-study guided interventions prevent compounding fatigue from sleep-disordered breathing. nmd-journal.com
Bone health program. Weight-bearing as able, sunlight exposure, and vitamin D/calcium intake minimize osteopenia risks from reduced mobility. PMC
Genetic counseling. Families learn inheritance, recurrence risk, and options for future pregnancies. MedlinePlus
Emergency care plan. A written plan flags respiratory baseline, anesthesia cautions, and contact details, reducing risk during intercurrent illness or surgery. PMC
Medicine and cap myopathy — important safety note
There is no FDA-approved medicine that treats cap myopathy itself. Care is supportive and focuses on lungs, nutrition, bones, and preventing complications. Medicines below are used for symptoms or risks that often accompany congenital myopathies (for example, weak cough, reflux, spasticity in atypical cases, or anesthesia emergencies). Where I cite the FDA label, it is to describe the drug’s approved use and safety, not to imply FDA approval for cap myopathy. Off-label decisions must be individualized by the treating clinician. PMC+1
Drug options used symptomatically or peri-operatively
Albuterol (inhaled, short-acting bronchodilator). Helps relieve bronchospasm in people with co-existing asthma or reactive airways and can assist pre-airway-clearance sessions. Label describes dosing and cautions for asthma; not disease-modifying for myopathy. FDA Access Data+1
Budesonide/albuterol (as-needed combo for asthma in adults). May be relevant if a cap-myopathy patient also has asthma, reducing exacerbations; not a myopathy therapy. FDA Access Data
Guaifenesin (expectorant, OTC monograph). Sometimes used to thin secretions during infections; clinicians weigh benefits vs. limited evidence in neuromuscular disease. (No specific FDA label PDF; OTC monograph governs.) PMC
Dantrolene (IV) for malignant hyperthermia crisis. In the rare event of an anesthesia-triggered MH episode in a neuromuscular patient, IV dantrolene is life-saving; labels specify dosing and preparation. Preventive stocking is standard in ORs. FDA Access Data+1
Glycopyrrolate (pre-op antisialagogue, reversal adjunct). Reduces secretions and helps manage vagal effects during anesthesia; label details dosing and cautions. FDA Access Data+1
Acetaminophen (analgesic/antipyretic). For postoperative or musculoskeletal pain, chosen to avoid respiratory-depressant opioids when possible. (OTC monograph; use per clinician judgment.) PMC
Ibuprofen (NSAID). For pain and inflammation from contractures or orthopedic issues; use carefully with GI and renal precautions. (OTC/Rx labeling applies.) PMC
Omeprazole (PPI). For reflux symptoms that raise aspiration risk; label covers GERD/ulcer dosing and safety. FDA Access Data+1
Intranasal influenza vaccine / pneumococcal vaccines (per schedule). Reduce respiratory infections that can be severe when cough is weak. (Vaccines are FDA-licensed biologics; follow national schedules.) PMC
Saline nebulization. Moisturizes airways before assisted cough (device/OTC solution; not a disease-specific drug). nmd-journal.com
Short steroid bursts for co-existing reactive airway exacerbations. Used for asthma flares per standard guidelines—not for myopathy. (Class labeling and guidelines apply.) PMC
Baclofen (oral). Not routinely required in cap myopathy (which is not a spasticity disorder), but may help if a person has secondary spasticity from other causes; multiple baclofen formulations are FDA-labeled for spasticity. FDA Access Data+2FDA Access Data+2
Antibiotics (as indicated) for bacterial chest infections. Standard-of-care when pneumonia/bronchitis is suspected to prevent decompensation; selections follow local guidelines. PMC
Vitamin D and calcium (supplements). Not drugs for myopathy; used to maintain bone health if intake or mobility is low, under clinician supervision. PMC
Mucolytics (e.g., hypertonic saline). Sometimes used with airway clearance devices to aid mucus mobilization when infections increase secretions. nmd-journal.com
Antireflux alginate preparations. Adjunct for reflux symptoms when PPIs are insufficient; may reduce micro-aspiration risk. PMC
Topical anesthetics and regional techniques (peri-procedural). Allow procedures while minimizing systemic anesthetic exposure in patients with respiratory weakness. PMC
Sugammadex (where available) to reverse certain neuromuscular blockers. Helps reduce postoperative residual weakness if rocuronium/vecuronium had to be used. (Label details vary by region.) Frontiers
Laxatives/softeners for constipation in low-mobility patients. Prevent strain and discomfort that worsen breathing mechanics; used per general GI guidance. PMC
Antiemetics (peri-operative). Reduce aspiration risk after procedures; choice individualized to cardiac/respiratory status. Frontiers
Dietary molecular supplements (what they do)
Evidence in congenital myopathies is limited; supplements should only be used with a clinician/dietitian to avoid interactions and false expectations. Guidance emphasizes good overall nutrition and vitamin D. PMC
Vitamin D3. Supports bone mineralization when mobility is reduced; levels are checked and doses individualized. PMC
Calcium. Complements vitamin D to maintain bone strength; total daily intake is tailored to age and diet. PMC
Protein adequacy (whey/casein if needed). Adequate protein helps preserve lean mass when activity is limited; excess is not helpful. PMC
Omega-3 fatty acids. May support general cardiometabolic health and low-grade inflammation; not disease-modifying for cap myopathy. PMC
Creatine monohydrate (trial-based). Some neuromuscular conditions report small improvements in short-term muscle performance; discuss risks/benefits first. PMC
Coenzyme Q10. Sometimes tried empirically in myopathies for mitochondrial support; evidence remains limited. PMC
Carnitine. Considered if documented deficiency or long-term tube feeds; not routine otherwise. PMC
Multivitamin (age-appropriate). Covers micronutrient gaps in picky eaters or those with feeding fatigue. PMC
Fiber supplementation. Helps constipation related to decreased mobility. PMC
Electrolyte rehydration solutions during illness. Support hydration when respiratory infections reduce intake. PMC
Immunity-booster / regenerative / stem-cell” drugs
There are no approved regenerative or stem-cell drugs for cap myopathy. Research in related congenital myopathies is ongoing, but clinical use is experimental. Safe, proven “immune boosters” do not exist; instead, clinicians prioritize vaccination, nutrition, sleep, and early infection treatment. (Below lists evidence-based medical principles, not disease-specific “boosters.”) PMC
Seasonal influenza vaccination. Reduces severe respiratory infections in people with weak cough. PMC
Pneumococcal vaccination (per age/risk). Prevents pneumonia that can be dangerous in neuromuscular weakness. PMC
Nutrition optimization (protein + vitamin D/calcium). Supports general immunity and bone health; not a drug. PMC
Sleep and NIV when indicated. Restorative sleep improves daytime immunity and function. nmd-journal.com
Early antibiotics for bacterial chest infections. Evidence-based treatment to prevent decline, not an “immune booster.” PMC
Dantrolene availability for ORs. Safety measure for anesthesia emergencies; not regenerative. FDA Access Data
Surgical/procedural options (when and why)
Posterior spinal fusion for progressive scoliosis. Considered when curves progress despite bracing to improve sitting balance and lung mechanics. PMC
Achilles tendon lengthening or foot surgery for severe contracture. Improves foot position, orthotic fit, and walking safety when conservative care fails. PMC
Tracheostomy (selected cases). For patients with severe, persistent ventilatory failure or airway clearance problems not controlled by non-invasive methods. nmd-journal.com
Gastrostomy (feeding tube). Protects nutrition and reduces aspiration when oral feeding is unsafe or too tiring. PMC
Orthopedic releases for upper-limb contractures. Selected tendon releases improve hygiene or function when splints/therapy cannot. PMC
Practical prevention tips
Keep vaccines current (flu, pneumococcal) to avoid severe chest infections. PMC
Do daily gentle stretches to prevent contractures. PMC
Maintain healthy weight and vitamin D/calcium intake for bones. PMC
Sleep on a regular schedule; seek a sleep study if snoring, morning headaches, or daytime sleepiness appear. nmd-journal.com
Use airway-clearance strategies at the first sign of a cold. nmd-journal.com
Carry an anesthesia alert letter outlining peri-operative precautions. Frontiers
Pace physical activity; avoid over-fatigue. PMC
Plan regular dental care (weak facial muscles can increase oral pooling). PMC
Monitor spine and chest wall shape during growth. PMC
Arrange early referrals (respiratory, dietetics, genetics) instead of “watchful waiting.” PMC
When to see a doctor urgently
Signs of night-time hypoventilation: morning headaches, poor sleep, daytime sleepiness, or frequent wakes. nmd-journal.com
Chest infection not improving within 24–48 hours, rising work of breathing, or weak cough. nmd-journal.com
Rapidly worsening scoliosis pain or new posture change. PMC
Feeding difficulties, choking, or weight loss. PMC
Any planned procedure with anesthesia—share your myopathy plan in advance. Frontiers
What to eat / avoid
Eat more of: balanced protein (fish, eggs, legumes), calcium-rich foods (dairy/fortified alternatives), vitamin-D sources (fatty fish, fortified milk), fruits/vegetables for fiber, and adequate fluids. These support bone health, regularity, and energy. PMC
Limit: heavily processed foods, very salty meals (fluid retention, blood pressure), deep-fried foods (reflux), large late-night meals (sleep quality), and excess caffeine (sleep disruption). Tailor textures if chewing/swallowing is tiring. 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: November 10, 2025.
