Hypermethioninemia due to Adenosine Kinase (ADK) Deficiency

Adenosine kinase deficiency is a very rare, inherited metabolic disorder. The ADK enzyme normally turns adenosine into AMP. When ADK is weak or missing, adenosine builds up. High adenosine pushes the body’s “methylation” chemistry off balance. This raises S-adenosylhomocysteine (SAH) and S-adenosylmethionine (SAM) and leads to high blood methionine (hypermethioninemia). Babies or children can develop liver problems, developmental delay, low muscle tone, seizures, and sometimes facial differences. The condition is autosomal recessive, meaning a child is affected when both gene copies are changed. There is no single curative drug today. The main disease-specific therapy is a low-methionine diet. It can improve liver disease, though effects on brain symptoms are mixed. In severe liver failure, liver transplantation has been used. PMC+2PMC+2PubMed+1

Hypermethioninemia due to adenosine kinase (ADK) deficiency is a very rare, inherited metabolic disease. In this condition, the enzyme adenosine kinase does not work well. This enzyme normally converts adenosine into AMP, a key step that keeps the methionine cycle in balance. When ADK activity is low, adenosine builds up. That raises levels of S-adenosylhomocysteine (AdoHcy) and S-adenosylmethionine (AdoMet). AdoHcy then blocks many methylation reactions, which pushes methionine levels higher in the blood. The result is persistent hypermethioninemia plus problems in the liver and brain, such as neonatal cholestatic jaundice, developmental delay, low muscle tone, and seizures. The disorder is autosomal recessive (both copies of the ADK gene have disease-causing variants). PubMedThiemeMalaCards

Other names

This condition is also called “ADK deficiency,” “Hypermethioninemia-encephalopathy due to ADK deficiency,” “Adenosine kinase deficiency,” and “ADK-related hypermethioninemia.” Databases list it as OMIM #614300 and Orphanet ORPHA:289290. All names describe the same inborn error of metabolism where lack of ADK activity leads to high methionine and neurologic-hepatic disease, starting most often in infancy. OrphaMalaCards

---

Types

There is no official subtype system, but doctors recognize a spectrum of presentations. Thinking in clinical patterns helps:

1. Infantile hepatic-predominant type. Newborn or early-infant jaundice with cholestasis, high liver enzymes, poor weight gain; later developmental delay and hypotonia become clear. PubMedFrontiers

2. Mixed hepatic-neurologic type. Both liver disease and neurologic signs (hypotonia, seizures) appear early and run together. PubMed

3. Neurologic-predominant type. Liver tests may improve or be only mildly abnormal; the main issues are developmental delay, epilepsy, and low tone. Wiley Online Library

4. Vascular-variant reports. Rare cases include tortuous intracranial arteries on imaging alongside the usual neurodevelopmental features. Wiley Online Library

5. Later-identified/milder course. Diagnosed beyond infancy with persistent hypermethioninemia and a history of earlier liver dysfunction that partially resolved. Frontiers

Causes

Core cause

1. Biallelic pathogenic variants in the ADK gene (autosomal recessive). This is the direct and necessary cause of the disease. Parents are usually healthy carriers. MalaCards

Factors that can raise methionine or aggravate the condition in someone who has ADK deficiency

1. High natural protein or methionine intake (e.g., protein-dense diets or formulas) can push blood methionine higher because the body cannot process it efficiently. PMC
2. Illness and catabolic stress (fever, infection) increase protein breakdown, releasing more methionine into blood. PubMed
3. Fasting or poor calorie intake causes catabolism and raises amino acids, including methionine. PubMed
4. Acute liver dysfunction (from the disease itself) reduces hepatic capacity to clear methionine and AdoMet/AdoHcy. PubMed
5. Cholestasis reduces bile flow and can worsen liver injury and methionine handling. PubMed
6. Dehydration concentrates plasma amino acids and stresses the liver. (Clinical reasoning consistent with hepatic IEM care.) PubMed
7. Certain hepatotoxic medications (e.g., drugs that injure liver) may worsen enzymes and methionine balance; medication choices require care. (General principle in hepatic metabolic disorders.) PubMed
8. Intercurrent viral hepatitis or sepsis-like episodes reported at presentation can amplify hepatic injury and methionine rise. PubMed
9. Post-operative or peri-procedural stress (if present) increases catabolism. (General IEM management principle.) PubMed
10. Very low methylation capacity due to high AdoHcy further locks the cycle, keeping methionine high. PubMed
11. Unrecognized high-methionine medical foods/supplements can inadvertently raise levels. (Dietary management literature notes methionine restriction exploration.) PMC
12. Concurrent cholestatic triggers (e.g., parenteral nutrition cholestasis) could aggravate liver function in fragile infants. (Clinical reasoning aligned with neonatal cholestasis reports.) PubMed
13. Genotype with more severe loss of function may correlate with a heavier biochemical block. (Case series show range of variants and severity.) PubMedScienceDirect
14. Delayed diagnosis leaves persistent high methionine and liver inflammation unchecked. (Case reports emphasize early recognition.) Frontiers
15. Low overall energy intake reduces anabolism and promotes proteolysis. (General IEM principle; relevant to ADK case care.) PMC
16. Coexisting metabolic stressors (e.g., anemia, hypoxia) can worsen organ function and tolerance. (Generalized clinical principle in IEM.) PubMed
17. Inadequate monitoring of plasma methionine allows silent upward drift. (Monitoring recommended where diets are tried.) PMC
18. Exposure to hepatotropic viruses in infancy may aggravate hepatic course. (Neonatal hepatitis-like presentations described.) PubMed
19. Lack of coordinated nutrition therapy (when indicated) misses a potential to blunt methionine peaks in some patients (responses are variable). PMCSemantic Scholar

Note: The only root cause is ADK gene deficiency; the other items are triggers or modifiers that can raise methionine or worsen symptoms in affected patients.

---

Common symptoms and signs

1. Prolonged neonatal jaundice and cholestasis. Many babies stay jaundiced beyond the usual time, with pale stools or dark urine because bile does not flow well. PubMedFrontiers

2. Liver enzyme elevations. Blood tests show high AST/ALT and sometimes high bilirubin or GGT, reflecting liver injury. Thieme

3. Hypotonia (low muscle tone). Babies feel “floppy,” especially in the neck and trunk, and may have delayed motor milestones. PubMed

4. Developmental delay. Speech, sitting, standing, or walking can be slower than expected for age. PubMed

5. Seizures/epilepsy. Some children develop seizures that may need anti-seizure medications. PubMed

6. Feeding problems/failure to thrive. Poor weight gain or vomiting may occur during illness or in early months. Wiley Online Library

7. Dysmorphic features. Mild facial differences are reported (e.g., frontal bossing, macrocephaly, hypertelorism). ThiemeMedLink

8. Respiratory difficulties in the newborn period. Some infants present like “sepsis-like” illness with breathing issues. PubMed

9. Hepatomegaly. The liver can be enlarged on exam or ultrasound. PubMed

10. Transient or persistent coagulopathy. With liver dysfunction, blood may not clot normally, increasing bruising/bleeding risk. Thieme

11. Irritability or lethargy during illness. Metabolic stress can worsen behavior and alertness. PubMed

12. Constipation or alternating bowel patterns. GI motility can be affected during cholestasis and illness. (Clinical observations in hepatic IEMs.) PubMed

13. Head growth changes. Some children have macrocephaly; monitoring head circumference helps follow development. MedLink

14. Cardiac anomalies (occasionally). Some series mention heart findings, so an echocardiogram may be checked. MedLink

15. Neurologic imaging changes. Brain MRI may show delayed myelination/white-matter changes, reflecting the methylation block’s effect. Frontiers

---

Diagnostic tests

A) Physical examination (bedside checks)

1. General exam for jaundice. The doctor looks for yellowing of skin/eyes and checks stool/urine color as clues for cholestasis. It helps decide if liver tests and imaging are urgent. PubMed

2. Liver size and tenderness. Gentle palpation measures liver edge and checks for pain; a big or firm liver suggests active disease. PubMed

3. Neurologic tone and reflexes. The clinician assesses head control, pull-to-sit, axial tone, and reflexes to document hypotonia. PubMed

4. Developmental assessment. Observing milestones and behavior screens for global delay, guiding early intervention and therapy. PubMed

B) Manual/functional tests (structured bedside tools)

5. Standardized developmental screening (e.g., Denver-type tools). A simple, structured check of gross motor, fine motor, language, social skills to quantify delay. PubMed

6. Feeding and swallow evaluation. A therapist observes suck, coordination, and fatigue; this guides nutrition plans if feeding is weak. Wiley Online Library

7. Growth and head-circumference charting. Regular plotting detects failure to thrive or macrocephaly early. MedLink

8. Pediatric dysmorphology checklist. A careful head-to-toe look for subtle facial/body features supports the pattern recognition of ADK deficiency. Thieme

C) Laboratory and pathological tests

9. Plasma amino acid profile. This is the key screen: methionine is persistently high. It raises suspicion for ADK deficiency among other hypermethioninemias. MalaCards

10. AdoMet (SAM) and AdoHcy levels. In ADK deficiency, both are elevated, while homocysteine is typically normal—a helpful signature. MalaCards

11. Liver function tests. AST, ALT, GGT, bilirubin, albumin, and INR/PT show the degree of liver injury or cholestasis. Thieme

12. Complete blood count and metabolic panel. These track overall health, nutrition, electrolytes, and may show stress or dehydration effects. PubMed

13. Genetic testing of the ADK gene. Definitive diagnosis comes from identifying pathogenic variants in both gene copies. Panels or exome sequencing are commonly used. MalaCardsScienceDirect

14. (If available) Enzyme/functional studies in patient cells. Research settings may assess ADK activity to support the genetic result. PubMed

15. Coagulation profile. PT/INR and aPTT detect clotting problems if the liver is failing or bile flow is poor. Thieme

16. Urinalysis and bile acid profile (when indicated). These help evaluate cholestasis and rule out other liver disorders in infants. PubMed

D) Electrodiagnostic tests

17. EEG (electroencephalogram). If seizures occur or are suspected, EEG helps classify them and guide anti-seizure therapy. PubMed

18. Evoked potentials or EMG/nerve conduction (selected cases). Used when tone is very low or development is atypical to separate central vs peripheral issues. PubMed

E) Imaging tests

19. Abdominal ultrasound. A safe, first-line scan to check liver size/texture and bile ducts in cholestasis. PubMed

20. Brain MRI. Often shows delayed myelination or white-matter changes; supports the diagnosis and monitors brain development. Frontiers

21. MR angiography (selected cases). Done if neurologic symptoms suggest vessel issues; rare cases show tortuous intracranial arteries. Wiley Online Library

22. Liver elastography or MRI (when available). These assess fibrosis and guide long-term liver follow-up. (Applied hepatology practice in metabolic disorders.) PubMed

23. Echocardiography (as needed). Because cardiac findings are occasionally reported, a baseline echo may be considered. MedLink

Doctors use all of the above to rule in ADK deficiency, rule out other causes of hypermethioninemia (such as MAT1A deficiency, GNMT deficiency, or severe liver disease), and plan supportive care. Wiley Online Library

Treatment overview

There is no single curative medicine. The cornerstone is dietary methionine restriction (a low-methionine, protein-controlled plan using medical foods under a metabolic dietitian). Published cases show variable neurologic benefit but more consistent liver improvement. Some patients with advanced liver disease have undergone liver transplantation. Supportive care (nutrition, therapies, seizure control, vaccines, and avoidance of liver-toxic drugs) is essential. PMC+1Wiley Online Libraryflore.unifi.it

Important safety note: drug dosages for children must be individualized by the treating team. I do not give mg/kg dosing here for safety. Please use this guide to frame a specialist-led plan.

---

Non-pharmacological treatments

(I group them as physiotherapy, mind-body/education, nutrition, and systems-level care. For space, entries are concise but complete.)

A) Physiotherapy & rehabilitation

1. Postural and tone management
   Purpose: Improve trunk control and reduce hypotonia.
   Mechanism: Repetitive positioning and proximal strengthening promote motor unit recruitment and balance.
   Benefits: Better head/trunk stability, safer feeding, easier caregiving. PubMed

2. Gross-motor physiotherapy
   Purpose: Support milestones (rolling, sitting, standing, walking).
   Mechanism: Task-specific practice drives neuroplasticity.
   Benefits: Fewer contractures; better mobility and participation. Journal of Neuroscience

3. Fine-motor and hand therapy
   Purpose: Improve reach, grasp, and self-care.
   Mechanism: Repetitive goal-oriented hand tasks strengthen networks.
   Benefits: Greater independence in feeding and play. Journal of Neuroscience

4. Oromotor/feeding therapy
   Purpose: Safer swallow, better calorie intake.
   Mechanism: Exercises and pacing to coordinate suck-swallow-breath.
   Benefits: Less aspiration, improved growth. PubMed

5. Spasticity/tone modulation (if present)
   Purpose: Reduce abnormal tone that limits movement.
   Mechanism: Stretching, splinting, and guided task practice.
   Benefits: Fewer contractures, better range of motion. Journal of Neuroscience

6. Constraint-induced movement strategies
   Purpose: Encourage use of a weaker limb.
   Mechanism: Gentle restriction of the stronger limb during tasks.
   Benefits: Better bilateral coordination.

7. Balance and vestibular training
   Purpose: Reduce falls, improve gait.
   Mechanism: Static and dynamic balance tasks challenge sensory integration.
   Benefits: Safer mobility.

8. Respiratory physiotherapy (as needed)
   Purpose: Clear secretions during infections.
   Mechanism: Positioning, percussion, assisted cough.
   Benefits: Fewer complications from chest infections. PubMed

9. Orthotics and adaptive equipment
   Purpose: Support posture and function.
   Mechanism: Ankle-foot orthoses, seating systems.
   Benefits: Energy-efficient movement; pressure injury prevention.

10. Home therapy program
    Purpose: Extend gains between visits.
    Mechanism: Daily caregiver-led exercises.
    Benefits: Faster skill acquisition; family empowerment.

B) Mind-body, “gene-informed,” and educational therapies

11. Early intervention developmental therapy
    Purpose: Stimulate language, cognition, and play from infancy.
    Mechanism: High-frequency, play-based neurodevelopmental input.
    Benefits: Better school readiness; reduced secondary delays. PubMed

12. Speech-language therapy
    Purpose: Improve communication and feeding.
    Mechanism: Language modeling, AAC as needed.
    Benefits: Increased participation and safety.

13. Parent education & genetic counseling
    Purpose: Explain autosomal recessive inheritance and recurrence risk.
    Mechanism: Review ADK gene results; discuss family planning options.
    Benefits: Informed decisions; earlier diagnosis in future pregnancies. flore.unifi.it

14. Behavioral/psych-education
    Purpose: Manage attention, behavior, or anxiety associated with chronic illness.
    Mechanism: Cognitive-behavioral strategies adapted for development.
    Benefits: Better coping and adherence.

15. Mind-body stress care for caregivers
    Purpose: Reduce caregiver burnout.
    Mechanism: Relaxation, breathing, brief mindfulness.
    Benefits: Improved family resilience; steadier home program adherence.

C) Nutrition & metabolic care

16. Low-methionine diet (medical foods)
    Purpose: Lower methionine load to rebalance SAM/SAH and protect liver.
    Mechanism: Protein restriction with essential amino acid formulas tailored by a metabolic dietitian.
    Benefits: Often improves liver tests; neurologic response varies. PMCWiley Online Libraryflore.unifi.it

17. Frequent growth and micronutrient monitoring
    Purpose: Prevent malnutrition while restricting protein.
    Mechanism: Regular labs and anthropometrics; targeted supplementation.
    Benefits: Healthy growth with safe restriction. PMC

18. Sick-day plan
    Purpose: Manage intercurrent illness to avoid decompensation.
    Mechanism: Temporary changes in protein/energy intake; hydration; early medical review.
    Benefits: Fewer admissions.

19. Feeding support (thickened feeds or tube if needed)
    Purpose: Ensure safe intake in poor swallow or low tone.
    Mechanism: Texture modification or gastrostomy.
    Benefits: Reliable calories and medicines. PubMed

20. Drug-avoidance counseling
    Purpose: Reduce liver injury risk.
    Mechanism: Avoid or use caution with hepatotoxic drugs (e.g., valproate).
    Benefits: Protects liver reserve. PubMed

21. Vaccination optimization (incl. hepatitis A/B)
    Purpose: Prevent infections that can stress the liver.
    Mechanism: Up-to-date immunization schedule.
    Benefits: Fewer severe illnesses.

D) Systems-level & safety

22. Multidisciplinary clinic (metabolic, hepatology, neurology, dietetics, therapies).
    Benefits: Coordinated plans and faster problem-solving.

23. Emergency letter
    Benefits: Guides urgent teams on fluids, labs, and drug cautions.

24. School IEP/learning supports
    Benefits: Tailored goals, therapies, and accommodations.

25. Clinical trials/natural-history registries (when available)
    Benefits: Access to expertise; contributes to future treatments.

---

Drug treatments

There is no disease-specific approved drug for ADK deficiency. Medicines below treat common problems in this condition or protect the liver/brain. Always individualize and monitor liver function. Evidence for some is extrapolated from general pediatric hepatology/neurology rather than ADK-specific trials.

1. Antiepileptics (e.g., levetiracetam) – seizure control without strong liver metabolism; purpose: reduce seizures; mechanism: modulates synaptic vesicle protein SV2A; side effects: mood change, somnolence; note: avoid hepatotoxic options when possible (e.g., valproate caution). PubMed

2. Ursodeoxycholic acid – for cholestasis/itch; mechanism: cytoprotective bile acid improving bile flow; side effects: diarrhea; monitor: LFTs. PubMed

3. Vitamin K – corrects coagulopathy from poor liver synthesis; mechanism: supports clotting factors; side effects: rare hypersensitivity. PubMed

4. Lactulose (± rifaximin) – if hepatic encephalopathy emerges; mechanism: lowers ammonia via colonic acidification; side effects: bloating, diarrhea. PubMed

5. N-acetylcysteine (acute liver injury settings) – mechanism: replenishes glutathione; benefit: hepatocellular protection; side effects: nausea.

6. Antibiotics (as indicated) – treat infections promptly to avoid hepatic decompensation; select liver-safe agents; side effects: drug-specific. PubMed

7. Antiemetics – improve feeding in acute illness; mechanism: 5-HT3 antagonism; side effects: constipation, headache.

8. Proton-pump inhibitor or H2 blocker – reflux control improves nutrition; side effects: GI, micronutrient effects with long use.

9. Supplemental fat-soluble vitamins (A, D, E, K) if cholestatic – purpose: correct malabsorption; monitor blood levels.

10. Zinc if deficient – supports growth and immune function; side effects: GI upset.

11. Carnitine (only if deficient) – supports fatty-acid transport; note: not disease-specific.

12. Antispasticity agents (baclofen, etc., if needed) – improve function; side effects: sedation, weakness.

13. Melatonin – sleep regulation to support neurodevelopment; side effects: morning sleepiness.

14. Analgesics/antipyretics (acetaminophen within safe limits) – comfort; note: respect liver-safe dosing and discuss with team.

15. Peri-transplant immunosuppressants – if transplanted; purpose: prevent rejection; monitor for side effects and infections. PMC

---

Dietary molecular supplements

In ADK deficiency, supplements that add methyl donors (like SAMe or excess methionine) can worsen the biochemical imbalance and are not advised. Plans must be individualized.

1. Medical low-methionine amino acid formula – functional role: provide essential amino acids without methionine load; mechanism: substrate reduction. PMC

2. Essential fatty acids (omega-3) – support neurodevelopment; anti-inflammatory.

3. Vitamin D – bone and immune health; corrects common deficits in chronic liver disease.

4. Vitamin K – clotting support in cholestasis (under monitoring).

5. Vitamin E – antioxidant support in fat-malabsorption states.

6. Calcium – growth and bone strength alongside vitamin D.

7. Zinc – appetite, growth, and immune function if low.

8. Selenium – antioxidant enzymes; replace only if low.

9. Iron – treat iron-deficiency anemia; avoid overload; monitor ferritin.

10. Probiotics – GI tolerance during high-formula regimens; evidence modest.

(Your team will decide exact product and dose, guided by labs and growth.)

---

Immunity-booster / regenerative / stem-cell drugs

There are no approved “regenerative” or “stem-cell drugs” for ADK deficiency. Using unregulated products is unsafe. What is evidence-based instead:

1. Routine vaccinations (incl. hepatitis A/B) to prevent liver-stressing infections.

2. Targeted micronutrient repletion (A, D, E, K, zinc) when low.

3. IVIG only for proven immune deficiency, not as a general “booster.”

4. Antiviral prophylaxis only in special settings (e.g., post-transplant).

5. Early antibiotics for bacterial infections under medical guidance.

6. Enrollment in monitored clinical studies when available.

These choices protect health without false “stem-cell drug” claims. PMC

---

Surgeries

1. Liver transplantation – procedure: replace diseased liver; why: decompensated liver failure or irreversible cholestasis despite optimal care; note: some patients were diagnosed with ADK deficiency after transplant. PMC

2. Gastrostomy tube placement – why: poor oral intake or unsafe swallow; benefit: reliable nutrition/medication delivery. PubMed

3. Orthopedic procedures (if needed) – why: hip dysplasia or contractures that limit function. ResearchGate

4. Hernia repair – why: symptomatic abdominal wall defects in infants.

5. Anti-reflux surgery (rare) – why: severe reflux not controlled medically.

---

Prevention strategies

1. Genetic counseling for families (autosomal recessive; 25% recurrence risk for each pregnancy when both parents are carriers). flore.unifi.it

2. Offer carrier testing to at-risk relatives. flore.unifi.it

3. Consider prenatal or preimplantation genetic testing in future pregnancies. flore.unifi.it

4. Newborn testing in siblings when feasible (targeted). flore.unifi.it

5. Keep vaccines up to date (especially hepatitis A/B).

6. Avoid liver-toxic drugs when alternatives exist. PubMed

7. Prompt treatment of infections to limit liver and metabolic stress. PubMed

8. Sick-day diet plan to maintain calories and hydration. PMC

9. Regular follow-up with metabolic, hepatology, and neurology teams. PubMed

10. Documented emergency plan for local hospitals.

---

When to see doctors urgently

• New or worsening jaundice, dark urine, pale stools, easy bruising, or bleeding.

• Lethargy, confusion, or unusual sleepiness (possible hepatic or metabolic encephalopathy).

• Seizures or unusual spells, with or without fever.

• Persistent vomiting, dehydration, or poor feeding.

• Fever or suspected infection, especially in infants or post-transplant patients. PubMed

---

Dietary “eat/avoid

• Eat (under guidance):

1. Measured low-protein staples using prescribed exchanges.

2. Special low-methionine medical formulas/foods to meet protein needs. PMC

3. Fruits and many vegetables (watch protein totals).

4. Adequate calories from allowed starches and fats to avoid catabolism.

5. Hydration to support metabolism.

• Avoid/limit:

6. High-protein foods (meat, fish, eggs, dairy, legumes) unless prescribed in measured amounts.

7. Supplements with methionine or SAMe; avoid “methyl donor” boosters. Wiley Online Library

8. Unsupervised protein powders/amino drinks.

9. Herbals that claim “liver detox” without medical approval.

10. Grapefruit or drug-interaction foods when on specific medicines.

---

FAQs

1. Is ADK deficiency inherited? Yes. It is autosomal recessive. Both parents are usually healthy carriers. flore.unifi.it

2. What is the main lab clue? Persistently high methionine with often normal/mild homocysteine, and higher SAM/SAH. Wiley Online LibraryPMC

3. Does a low-methionine diet cure it? No, but it can help the liver and sometimes the brain; results vary. PMCflore.unifi.it

4. Will my child need a liver transplant? Only a subset with severe liver failure; decision is individualized. PMC

5. Are seizures common? Many patients have seizures; they are treatable with standard anti-seizure medicines. PubMed

6. Can we use any multivitamin? Use supplements only as advised; avoid products that add methionine or SAMe. Wiley Online Library

7. Is homocysteine always high? No. In ADK deficiency, homocysteine is often normal or mildly elevated. Wiley Online Library

8. Which tests confirm the diagnosis? ADK gene testing plus SAM/SAH and plasma amino acids. flore.unifi.it

9. Are there clinical trials? This is very rare; check with your metabolic center and registries.

10. Will development improve? Therapies help. Brain outcomes vary; early supports give the best chance. Wiley Online Library

11. What drugs should we avoid? Avoid hepatotoxic agents when possible; always ask your team. PubMed

12. Can adults have ADK deficiency? Yes—milder cases can be found later, even after transplant. PMC

13. Is newborn screening available? Not widely; targeted testing is possible in known families. flore.unifi.it

14. Why are SAM and SAH important? They show the methylation imbalance that characterizes the disorder. PMC

15. What is the long-term outlook? Highly variable; best outcomes come from early diagnosis, careful diet, therapy, and coordinated care. PMCflore.unifi.it

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 08, 2025.

PDF Documents For This Disease Condition References