Calcific Discitis

Calcific discitis is a distinct form of intervertebral disc pathology characterized by the deposition of calcium salts—most often in the nucleus pulposus—that can extend through the cartilaginous endplates and provoke an inflammatory reaction in adjacent vertebral bodies. Although idiopathic pediatric cases have been recognized since the mid-20th century, adult presentations—particularly in the thoracic spine—have only recently gained wider attention as both incidental and symptomatic findings. Clinically, calcific discitis may mimic infectious spondylodiscitis, vertebral neoplasm, or acute degenerative disc disease, leading to potential misdiagnosis and unnecessary invasive procedures. Imaging modalities such as plain radiography, computed tomography (CT), and magnetic resonance imaging (MRI) are central to its recognition, revealing characteristic round or oval intradiscal calcifications with associated marrow edema but without aggressive bone destruction PubMed CentralAJNR.

Calcific discitis is a rare condition characterized by calcium crystal deposits within the intervertebral disc, leading to inflammation, pain, and reduced mobility. These deposits—often composed of hydroxyapatite—can trigger the body’s immune response, causing acute flare-ups of back or neck pain. Although it most commonly affects older adults, anyone with disc degeneration may develop this condition.

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Anatomy of the Intervertebral Disc in Calcific Discitis

Understanding calcific discitis demands a firm grasp of normal disc anatomy. The intervertebral disc is not a simple cushion but rather a sophisticated fibrocartilaginous organ engineered for load distribution, mobility, and spinal stability.

A. Structure

The intervertebral disc comprises three principal components:

1. Annulus fibrosus

2. Nucleus pulposus

3. Cartilaginous endplates

Annulus fibrosus is an outer ring of 15–25 concentric lamellae of fibrocartilage. Its collagen fibers alternate orientation by approximately ±60° to the vertical, conferring resistance to torsional and tensile forces. Type I collagen predominates in the outer layers, providing tensile strength, while type II predominates nearer the nucleus, granting compressive resilience WikipediaKenhub.

Nucleus pulposus is a hydrated gel, rich in proteoglycans (aggrecan) and type II collagen, with up to 90 % water content in youth. It behaves hydraulically under load, distributing compressive forces evenly in all directions (Pascal’s law). This hydrostatic function is crucial for shock absorption and even load transmission to the vertebral endplates WikipediaRadiology Key.

Cartilaginous endplates are thin layers of hyaline cartilage sandwiched between the disc and adjacent vertebral bodies. They anchor the annulus and nucleus to bone, allow nutrient diffusion into the avascular disc proper, and serve as a semipermeable barrier regulating fluid exchange Radiology Key.

B. Location

Intervertebral discs occupy the spaces between vertebral bodies from C2–3 through L5–S1, numbering 23 in total (6 cervical, 12 thoracic, 5 lumbar) RadiopaediaWikipedia. They constitute approximately one-third of the spinal column’s height, with greatest thickness (7–10 mm) in the lumbar region to accommodate higher loads Kenhub. Discs at C0–1 and C1–2 are specialized and lack a typical nucleus pulposus; thus, discitis does not occur at these segments.

C. Origin and Insertion

Unlike muscles, the disc’s collagenous fibers “originate” and “insert” by anchoring into the ring apophyses—thickened cortical rims of the vertebral bodies—via Sharpey’s fibers. The outer annular lamellae insert into the periosteum of the vertebral ring apophysis, while inner lamellae interdigitate with the cartilaginous endplates. This architectural integration secures the disc against compressive and shear forces Radiology Key.

D. Blood Supply

In adults, the intervertebral disc is essentially avascular. Vessels supply only the outer one-third of the annulus fibrosus via branches of the spinal segmental arteries. Cartilaginous endplates retain microcirculation in early life but lose most vessels by adolescence. Nutrient delivery to the inner annulus and nucleus depends entirely on diffusion through the endplates (imbibition), a process that diminishes with degeneration and aging Radiology Key.

E. Nerve Supply

Sensory innervation is confined to the outer annulus fibrosus. The sinuvertebral (recurrent meningeal) nerve provides pain fibers, augmented by branches from the ventral rami and gray rami communicantes of spinal nerves. Deeper layers and the nucleus pulposus lack innervation under normal conditions. Inflammatory or degenerative states, however, may permit deeper nociceptive ingrowth PubMed Central.

F. Functions

1. Shock absorption: The nucleus pulposus, by virtue of its high water content, dissipates axial loads, protecting vertebral bodies and facet joints.

2. Load transmission: Uniform pressure distribution across the disc prevents focal stress risers that could damage endplates or bone.

3. Flexibility and motion: Annular lamellae permit controlled flexion, extension, lateral bending, and rotation of the spinal segment.

4. Spinal stability: The disc, together with ligaments and facets, restricts excessive movement, preserving alignment.

5. Height maintenance: Disc thickness maintains intervertebral foraminal height, ensuring space for exiting nerve roots.

6. Barrier function: The intact annulus fibrosus prevents nucleus extrusion, and the endplates regulate biochemical exchange. RadiopaediaRadiology Key.

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Types of Calcific Discitis

Although calcific discitis can manifest in varied clinical contexts, it is broadly categorized by patient age, symptomatology, chronicity, and anatomic distribution:

1. Pediatric Idiopathic Calcific Discitis

   • Typically occurs between ages 5–10 without clear precipitating factors.

   • Presents with acute neck or back pain, often after minor viral illness.

   • Self-limiting, with spontaneous radiographic resolution over weeks to months Radiopaedia.

2. Adult-Onset Acute Calcific Discitis

   • Most frequently affects middle-aged adults (mean age 40–60) in the thoracic spine (T8–T12).

   • Acute severe spinal pain ± mild fever and elevated inflammatory markers.

   • Imaging: central intradiscal calcification with endplate edema on MRI; CT most sensitive for calcification JRheumAJNR.

3. Chronic Persistent Calcific Discitis

   • Demonstrates calcification that may persist for years.

   • Pain is often milder but can flare with mechanical stress.

   • Radiographs and CT show stable dense calcific foci; MRI variable edema PubMed Central.

4. Asymptomatic Incidental Calcification

   • Identified incidentally on imaging for unrelated indications.

   • No associated pain or clinical signs; often in elderly patients.

   • Requires no intervention; follow-up imaging may show stability or resorption PubMed Central.

5. Symptomatic Calcific Discitis Mimicking Infection

   • May present with fever, leukocytosis, raised ESR/CRP, and severe pain, closely simulating discitis-osteomyelitis.

   • Critical to differentiate by absence of frank bone destruction, paravertebral abscess, and positive cultures Wiley Online Library.

6. Location-Based Subtypes

   • Cervical: More common in children; may cause torticollis or dysphagia if C2–3 involved.

   • Thoracic: Predominant in adults; mid-back pain.

   • Lumbar: Rare; can mimic degenerative disc disease or herniation AJNR.

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Causes of Calcific Discitis

1. Physiologic Age-Related Degeneration

   • Disc aging leads to alterations in proteoglycan content and hydration, promoting dystrophic calcification Nature.

2. Repetitive Microtrauma

   • Chronic mechanical loading and microtears in annulus fibers create niduses for calcium deposition Radiology Key.

3. Acute Direct Trauma

   • Single high-energy injury can disrupt endplates and incite intradiscal calcification.

4. Crystal Arthropathies (CPPD, Gout)

   • Calcium pyrophosphate dihydrate (CPPD) or monosodium urate crystals may deposit in disc matrix.

5. Metabolic Disorders (Hyperparathyroidism)

   • Elevated PTH causes hypercalcemia and ectopic soft-tissue calcifications, including in discs.

6. Chronic Kidney Disease

   • Uremic milieu and secondary hyperparathyroidism predispose to calcific deposition.

7. Endocrine Disorders (Hypothyroidism)

   • Altered thyroid hormone levels can influence cartilage matrix turnover and mineralization.

8. Genetic Predisposition

   • Polymorphisms in ANK or ENPP1 genes affect inorganic phosphate/pyrophosphate balance, promoting calcification Nature.

9. Post-Surgical Changes

   • Instrumentation or fusion alters biomechanics and may accelerate disc calcification.

10. Radiation Therapy

    • Ionizing radiation can induce cartilage matrix damage and dystrophic calcification.

11. Infection (Low-Grade or Subclinical)

    • Chronic low-virulence infection may trigger inflammatory calcification without overt spondylodiscitis signs.

12. Inflammatory Spondyloarthropathies (e.g., Ankylosing Spondylitis)

    • Chronic inflammation of the spine can extend into disc spaces, leading to calcification.

13. Ischemia of Cartilaginous Endplates

    • Vascular compromise impairs nutrient diffusion, causing cell death and calcium precipitation.

14. Vitamin D Excess or Deficiency

    • Both hypervitaminosis D (promoting hypercalcemia) and deficiency (altering bone-cartilage interface) can contribute.

15. Smoking

    • Nicotine-induced vasoconstriction impairs disc nutrition, fostering degeneration and calcification.

16. Obesity

    • Increased axial loading accelerates degenerative and dystrophic calcific changes.

17. Autoimmune Disorders (e.g., Rheumatoid Arthritis)

    • Systemic inflammatory cytokines can affect disc matrix integrity and calcific propensity.

18. Nutritional Deficiencies (Magnesium, Zinc)

    • Micronutrient imbalances disrupt chondrocyte function and extracellular matrix homeostasis.

19. Drug-Induced (e.g., Chronic Steroids)

    • Long-term glucocorticoid therapy promotes bone and cartilage catabolism, leading to calcification.

20. Idiopathic

    • In many pediatric and adult cases, no clear cause is identified, implying multifactorial or yet-undiscovered mechanisms.

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Symptoms of Calcific Discitis

1. Localized Axial Pain

   • Sharp or aching pain in the region of the affected disc, often aggravated by movement PubMed Central.

2. Fever

   • Low-grade fever in acute inflammatory presentations, potentially misleading toward infection Wiley Online Library.

3. Elevated ESR/CRP

   • Mild to moderate rise in inflammatory markers, reflecting marrow edema and adjacent vertebral inflammation Wiley Online Library.

4. Limited Range of Motion

   • Stiffness in flexion/extension or lateral bending due to pain and inflammation.

5. Paraspinal Muscle Spasm

   • Reactive guarding and tightness of muscles adjacent to the lesion.

6. Radiating (Radicular) Pain

   • Extension of discomfort along nerve dermatomes when annular or neural structures are irritated.

7. Tenderness to Palpation

   • Focal tenderness over spinous process or paraspinal region on exam.

8. Night Pain

   • Pain exacerbated at rest or when supine, due to fluid shifts in disc.

9. Positional Relief

   • Some patients feel better leaning forward, offloading the disc.

10. Dysphagia or Odynophagia

    • Rare in high cervical involvement causing prevertebral swelling.

11. Headache

    • Occipital headache if upper cervical discs (C2–3) are affected.

12. Weight Loss/Malaise

    • Mild systemic symptoms in prolonged or severe cases.

13. Night Sweats

    • Occasional diaphoresis, again mimicking infection.

14. Neurologic Deficit

    • Rare; significant mass effect or extension into neural foramina can cause radiculopathy.

15. Gait Disturbance

    • In extreme cases with thoracic or high lumbar involvement impacting spinal stability.

16. Sensory Changes

    • Paresthesias in a dermatomal distribution when nerve roots are inflamed.

17. Hyperreflexia

    • Upper motor neuron signs if calcification extends into spinal canal.

18. Myelopathic Signs

    • Spasticity or bladder/bowel dysfunction in very advanced or misdiagnosed cases.

19. Mechanical Crepitus

    • Uncommon grinding sensation during movement in chronic cases.

20. Asymptomatic

    • Many incidental cases remain completely without clinical signs PubMed Central.

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Diagnostic Tests for Calcific Discitis

1. Plain Radiography

   • First-line; reveals dense, round or oval calcific deposits within disc space. Sensitivity ~50 % PubMed Central.

2. Computed Tomography (CT)

   • Highest sensitivity for detecting intradiscal calcification and delineating its morphology PubMed Central.

3. Magnetic Resonance Imaging (MRI)

   • T2-weighted images show high-signal marrow edema; gadolinium enhancement of adjacent endplates; nucleus may enlarge PubMed Central.

4. Bone Scintigraphy

   • Increased uptake at affected disc due to acute inflammation; nonspecific but sensitive to active disease.

5. Positron Emission Tomography (PET/CT)

   • Focal FDG uptake in acute cases; differentiates from neoplasm when equivocal Radiopaedia.

6. Ultrasound

   • Limited utility; may detect prevertebral soft-tissue swelling in cervical cases.

7. Dual-Energy CT

   • Differentiates calcium from urate or CPPD crystals by material decomposition algorithms.

8. Serum C-Reactive Protein (CRP)

   • Mild to moderate elevation correlates with inflammatory activity Wiley Online Library.

9. Erythrocyte Sedimentation Rate (ESR)

   • Often raised, but typically <100 mm/hr, lower than infectious spondylodiscitis.

10. Complete Blood Count (CBC)

    • Leukocytosis may be present in acute symptomatic cases; mild compared to infection.

11. Serum Calcium and Phosphate

    • Assesses metabolic contributors (e.g., hyperparathyroidism).

12. Parathyroid Hormone (PTH)

    • Investigates endocrine causes when hypercalcemia detected.

13. Vitamin D Levels

    • Evaluates for deficiency or excess impacting mineral homeostasis.

14. Renal Function Tests

    • Chronic kidney disease as a risk factor for soft-tissue calcification.

15. Serum Uric Acid

    • Screens for gouty crystal deposition in disc.

16. Rheumatoid Factor (RF) & ANA

    • Excludes systemic autoimmune arthritides.

17. HLA-B27 Testing

    • Assesses for spondyloarthropathies that may involve disc inflammation.

18. CT-Guided Disc Aspiration/Biopsy

    • Rarely indicated; differentiates infection or neoplasm from sterile calcific process.

19. Histopathology & Polarized Light Microscopy

    • Identifies CPPD or other crystals; confirms dystrophic calcification.

20. Discography

    • Functional injection test; no longer routinely used but can localize pain generator.

Non-Pharmacological Treatments

Below are 30 evidence-based, drug-free approaches for managing pain and improving function in calcific discitis. Each includes a brief description, its purpose, and how it works.

1. Heat Therapy

   • Description: Applying warm packs to the affected region.

   • Purpose: Relieve muscle tension and pain.

   • Mechanism: Increases blood flow, promoting healing and relaxation.

2. Cold Therapy

   • Description: Ice packs applied intermittently.

   • Purpose: Reduce inflammation and numb pain.

   • Mechanism: Constricts blood vessels, minimizing swelling.

3. Physical Therapy (PT)

   • Description: Guided exercises with a licensed therapist.

   • Purpose: Restore flexibility and strength.

   • Mechanism: Targets stabilizing muscles and corrects movement patterns.

4. Transcutaneous Electrical Nerve Stimulation (TENS)

   • Description: Low-voltage electrical currents via skin electrodes.

   • Purpose: Distract the nervous system from pain signals.

   • Mechanism: Stimulates non-pain fibers, inhibiting pain pathways.

5. Cervical/Lumbar Traction

   • Description: Gentle pulling of the spine segments.

   • Purpose: Reduce disc pressure and nerve compression.

   • Mechanism: Creates negative pressure within the disc space.

6. Chiropractic Manipulation

   • Description: Controlled spinal adjustments by a chiropractor.

   • Purpose: Improve joint mobility and reduce pain.

   • Mechanism: Realigns vertebrae, relieving mechanical stress.

7. Massage Therapy

   • Description: Manual soft-tissue techniques.

   • Purpose: Decrease muscle tension and improve circulation.

   • Mechanism: Enhances lymphatic drainage and relaxes muscles.

8. Acupuncture

   • Description: Insertion of fine needles at specific points.

   • Purpose: Modulate pain and promote healing.

   • Mechanism: Stimulates endorphin release and alters pain signaling.

9. Acupressure

   • Description: Finger pressure on acupuncture points.

   • Purpose: Relieve pain without needles.

   • Mechanism: Similar neural modulation as acupuncture.

10. Ultrasound Therapy

    • Description: Sound-wave application via a wand.

    • Purpose: Deep tissue warming and healing.

    • Mechanism: Increases cell metabolism and blood flow.

11. Low-Level Laser Therapy (LLLT)

    • Description: Non-invasive light at specific wavelengths.

    • Purpose: Accelerate tissue repair.

    • Mechanism: Photobiomodulation enhances cellular energy.

12. Hydrotherapy

    • Description: Exercises in warm water pools.

    • Purpose: Reduce weight-bearing stress.

    • Mechanism: Buoyancy supports the body, easing movements.

13. Yoga

    • Description: Gentle stretching and postural exercises.

    • Purpose: Improve flexibility and core strength.

    • Mechanism: Promotes spinal alignment and muscle balance.

14. Pilates

    • Description: Core-focused strengthening routines.

    • Purpose: Enhance trunk stability.

    • Mechanism: Targets deep abdominal and back muscles.

15. Ergonomic Assessment

    • Description: Workplace/posture evaluation.

    • Purpose: Minimize injury risk.

    • Mechanism: Adjusts seating, desk height, and posture to reduce strain.

16. Posture Correction

    • Description: Training to maintain neutral spine.

    • Purpose: Prevent abnormal loading.

    • Mechanism: Realigns spinal curves, reducing disc pressure.

17. Bracing

    • Description: Wearing a corset or brace.

    • Purpose: Limit painful movements.

    • Mechanism: Provides external support and immobilization.

18. Weight Management

    • Description: Diet and exercise plan.

    • Purpose: Decrease spinal load.

    • Mechanism: Reduces axial pressure on discs.

19. Core Strengthening

    • Description: Abdominal and back muscle exercises.

    • Purpose: Stabilize spine.

    • Mechanism: Creates a muscular “corset” around the spine.

20. Walking Programs

    • Description: Daily low-impact walking routines.

    • Purpose: Maintain mobility and circulation.

    • Mechanism: Stimulates nutrient diffusion into discs.

21. Mindfulness & Relaxation

    • Description: Breathing, meditation exercises.

    • Purpose: Lower pain perception.

    • Mechanism: Reduces stress hormones that exacerbate inflammation.

22. Cognitive Behavioral Therapy (CBT)

    • Description: Psychological counseling sessions.

    • Purpose: Manage pain-related anxiety.

    • Mechanism: Reframes negative pain thoughts, lowering stress.

23. Biofeedback

    • Description: Electronic monitoring of muscle activity.

    • Purpose: Teach relaxation of tense muscles.

    • Mechanism: Provides visual/auditory feedback to control muscle tension.

24. Ergonomic Footwear

    • Description: Shoes with proper arch support.

    • Purpose: Improve posture and gait.

    • Mechanism: Aligns lower limbs, reducing spinal compensation.

25. Activity Modification

    • Description: Avoiding aggravating tasks (e.g., heavy lifting).

    • Purpose: Prevent flare-ups.

    • Mechanism: Limits mechanical stress on discs.

26. Education & Self-Care Training

    • Description: Instruction on body mechanics.

    • Purpose: Empower patients to manage pain.

    • Mechanism: Teaches safe movement patterns.

27. Neuromuscular Re-education

    • Description: Balanced muscle activation drills.

    • Purpose: Restore correct movement.

    • Mechanism: Retrains muscle firing patterns.

28. Prolotherapy (Dextrose Injections)

    • Description: Small sugar-water injections near ligaments.

    • Purpose: Strengthen spinal ligaments.

    • Mechanism: Induces a mild inflammatory response for tissue repair.

29. Ozone Therapy

    • Description: Oxygen/ozone gas injected around the disc.

    • Purpose: Reduce inflammation.

    • Mechanism: Oxidizes inflammatory mediators, shrinking deposits.

30. Ultrasound-Guided Barbotage

    • Description: Needle irrigation of calcifications under imaging.

    • Purpose: Physically remove calcium crystals.

    • Mechanism: Flushes out deposits, relieving inflammation.

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Pharmacological Treatments

These 20 medications can help manage pain and inflammation in calcific discitis. For each, see dosage, drug class, timing, and common side effects.

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Dietary Molecular Supplements

Supplementation can support disc health and reduce inflammation.

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Advanced Drug Therapies

Targeted agents for modifying disease processes in calcific discitis:

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Surgical Options

When conservative measures fail, these procedures may be considered:

1. Ultrasound-Guided Barbotage: Needle-based irrigation and removal of calcium crystals.

2. Percutaneous Discectomy: Minimally invasive removal of disc material under imaging.

3. Endoscopic Discectomy: Small-tube endoscopic excision of disc fragments.

4. Microdiscectomy: Microscope-assisted removal of offending disc tissue.

5. Open Laminectomy: Removal of lamina to decompress nerve roots.

6. Spinal Fusion: Securing adjacent vertebrae with bone grafts or hardware.

7. Artificial Disc Replacement: Implanting a prosthetic disc to preserve motion.

8. Chemonucleolysis: Injection of enzymes (e.g., chymopapain) to dissolve disc material.

9. Laser Nucleoplasty: Laser ablation of disc tissue to reduce pressure.

10. Arthroscopic Debridement: Limited removal of calcific deposits via joint scope.

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Prevention Strategies

Simple lifestyle tips can lower the risk of developing disc calcification:

1. Regular Low-Impact Exercise (e.g., swimming, walking)

2. Maintain Healthy Body Weight

3. Ergonomic Workstation Setup

4. Proper Lifting Techniques

5. Core Strengthening Routines

6. Stay Hydrated (≥8 cups water/day)

7. Balanced Diet (rich in anti-inflammatory foods)

8. Adequate Vitamin D & Calcium Intake

9. Avoid Smoking & Excessive Alcohol

10. Periodic Posture Checks

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When to See a Doctor

Seek prompt medical attention if you experience:

• Severe, Unrelenting Pain persisting >4 weeks

• Neurological Signs (numbness, weakness, tingling)

• Systemic Symptoms (fever, unexplained weight loss)

• Night Pain disrupting sleep

• Bowel or Bladder Dysfunction

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Frequently Asked Questions (FAQs)

1. What causes calcific discitis?
   Calcific discitis arises when calcium crystals deposit in the intervertebral disc, often linked to age-related degeneration, minor trauma, or metabolic factors. The crystals irritate the disc, triggering inflammation and pain.

2. What are the main symptoms?
   Common symptoms include localized back or neck pain, stiffness, muscle spasms, and sometimes nerve compression symptoms like radiating pain or numbness in an arm or leg.

3. How is it diagnosed?
   Diagnosis relies on imaging—X-rays show disc calcification, while MRI or CT scans assess inflammation and rule out infection. A careful clinical history and exam confirm the diagnosis.

4. Can calcific discitis resolve on its own?
   Yes. Many cases, especially asymptomatic ones, can resolve as the body gradually reabsorbs calcium deposits, often within weeks to months.

5. What exercises help?
   Gentle stretching, core stabilization, and low-impact aerobic exercises (walking, swimming) improve blood flow, reduce stiffness, and support spinal health.

6. Which over-the-counter drugs work best?
   NSAIDs like ibuprofen or naproxen can alleviate pain and inflammation; acetaminophen helps reduce pain but lacks anti-inflammatory action.

7. Are dietary supplements effective?
   Supplements such as omega-3 fatty acids, vitamin D, and collagen may support disc health and reduce inflammation, but you should discuss dosages with a healthcare provider.

8. When is surgery needed?
   Surgery is considered if severe pain persists despite 6–12 weeks of conservative care, or if significant nerve compression leads to weakness or loss of function.

9. What are the risks of surgery?
   Possible risks include infection, nerve injury, adjacent segment disease, and the need for future procedures.

10. Can physical therapy cure calcific discitis?
    While PT cannot remove calcium deposits, it can strengthen supporting muscles, improve mobility, and reduce pain during the body’s natural healing process.

11. Is calcific discitis the same as herniated disc?
    No. A herniated disc involves nucleus pulposus protrusion, whereas calcific discitis involves calcium crystal deposition within the disc space.

12. How long does recovery take?
    Recovery varies: mild cases may improve within weeks, while severe cases could take several months of combined treatments.

13. Are alternative therapies helpful?
    Acupuncture, massage, and yoga can complement standard care by reducing pain and promoting relaxation, but they should not replace medical treatments.

14. Will calcific discitis recur?
    Recurrence is possible, especially if underlying risk factors—like poor posture or disc degeneration—aren’t addressed through prevention strategies.

15. How can I prevent complications?
    Adopting a spine-friendly lifestyle—regular exercise, good posture, weight control, and ergonomic setups—helps prevent flare-ups and promotes long-term disc health.

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: May 10, 2025.

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