Hypermethioninemia Encephalopathy due to Adenosine Kinase (ADK) Deficiency

Adenosine kinase (ADK) deficiency is a rare, inherited metabolic disease. A tiny change in both copies of the ADK gene makes the enzyme adenosine kinase work badly or not work. When this enzyme is weak, adenosine builds up. This also raises two closely linked chemicals, S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH). High SAH blocks many “methylation” steps in the body. This imbalance pushes methionine levels high in the blood (hypermethioninemia). The liver and brain are the most sensitive organs. Babies often show jaundice and liver problems first, and then they can have low muscle tone, slow development, seizures, and “encephalopathy” (brain dysfunction). The condition is autosomal recessive (both parents are carriers). There is no single “cure,” but early metabolic nutrition (methionine restriction under medical care) and good supportive care can improve outcomes in many children. PubMedPMCOrpha

Hypermethioninemia encephalopathy due to adenosine kinase (ADK) deficiency is a very rare, inherited metabolic disease. The ADK enzyme normally turns adenosine into AMP. When ADK does not work, adenosine builds up and disrupts the methionine (methylation) cycle. This causes high blood methionine (hypermethioninemia) and high S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH). Children usually present with a mix of brain symptoms (encephalopathy, seizures, developmental delay) and liver disease (jaundice, elevated liver tests, sometimes cholestasis), with homocysteine often normal. It is autosomal recessive (both gene copies affected). PMCPubMedOrphaMalaCards

Too much adenosine and disruption of the methionine cycle increase SAM and SAH. This “methylation traffic jam” can hurt developing brain cells and liver cells. That is why symptoms cluster in the brain (encephalopathy, seizures) and liver (hepatopathy). PMCPubMed

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Other names

This condition is also called: Adenosine kinase deficiency; Hypermethioninemia due to adenosine kinase deficiency; Hypermethioninemia encephalopathy due to ADK deficiency; ADK hypermethioninemia; Mental retardation, autosomal recessive 8 (historic term); OMIM #614300; MONDO:0100255. In rare-disease catalogs and genetic databases you may also see abbreviated labels like “ADK deficiency” or “HYE due to ADK deficiency.” These names all point to the same disease—loss of ADK enzyme activity leading to persistent hypermethioninemia with high SAM/SAH and a mixed neuro-hepatic picture. OrphaMalaCardsmonarchinitiative.org

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Types

Because case numbers are small, doctors describe patterns rather than strict subtypes. Think of a spectrum:

1. Early-onset neuro-hepatic type. Onset in infancy with developmental delay, hypotonia, seizures, feeding issues, jaundice or cholestasis, and high methionine/SAM/SAH. OrphaPubMed

2. Neurologic-predominant type. Developmental delay and epilepsy are prominent; liver involvement may be mild or intermittent. PubMed

3. Hepatic-predominant type. Liver disease (elevated transaminases, cholestasis) dominates; neurologic features vary. Some children improve when methionine intake is restricted. OrphaWiley Online Library

4. Multisystem type. Along with neuro-hepatic disease, some patients have dysmorphic facial features and occasional congenital heart defects (e.g., septal defects, pulmonary stenosis). Global Genes

These patterns reflect the same root cause (ADK gene variants) with variable severity. PMC

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Causes

Core cause: The disease itself is caused by pathogenic variants in the ADK gene leading to low or absent adenosine kinase activity. Everything else below either (a) explains why or how ADK becomes deficient, or (b) lists triggers that worsen the condition in affected patients. PMCPubMed

1. Biallelic ADK mutations (autosomal recessive). A child inherits one faulty ADK gene from each parent; enzyme activity falls and adenosine accumulates. PubMed

2. Missense variants that reduce enzyme function. Single amino-acid changes can severely cut ADK activity. PubMed

3. Nonsense or frameshift variants. Premature stop signals can abolish the enzyme. (General mechanism described in ADK cohort reports.) PubMed

4. Splice-site variants. Incorrect RNA splicing yields a nonfunctional enzyme. PubMed

5. Large deletions/structural variants in ADK. Rare but possible genetic losses that remove essential gene parts. (Mechanism inferred from monogenic IEM literature; confirmation requires molecular testing.) PubMed

6. Consanguinity (risk factor). Parents who are related are more likely to carry the same rare variant; this raises the chance of an affected child. (General autosomal-recessive risk factor.) PubMed

7. Founder effects in small populations. A rare variant can become more common in certain communities. (General rare-disease principle.) PubMed

8. High methionine intake in affected patients. Extra methionine adds substrate to the already impaired cycle and may worsen labs or symptoms. Wiley Online Library

9. Intercurrent infections/fever. Illness increases metabolic stress and can unmask or aggravate encephalopathy. (Reported across IEMs; case reports in ADK indicate decompensation with stress.) Frontiers

10. Fasting or poor intake. Catabolism pushes amino-acid flux and can raise ammonia/liver stress in vulnerable children. (General IEM management principle.) Wiley Online Library

11. Parenteral nutrition with high methionine. Some formulas are methionine-rich and may exacerbate hypermethioninemia. Wiley Online Library

12. Hepatotoxic drugs. Medicines that stress the liver (e.g., some anticonvulsants) may worsen transaminases in a liver-sensitive disorder. (General caution extrapolated for hepatopathy.) PubMed

13. Coexisting liver disease (any cause). Any extra liver injury reduces reserve and can worsen jaundice or coagulopathy. Orpha

14. Hypoxia/ischemia. Low oxygen harms sensitive brain and liver tissue already under metabolic strain. (General pathophysiology.) PMC

15. Dehydration. Worsens metabolic stability and can precipitate encephalopathy. (General IEM principle.) Wiley Online Library

16. Rapid weight loss or catabolic states. Increase amino-acid turnover and stress methylation balance. (General metabolic principle.) PMC

17. Concurrent methylation-cycle genetic variants (other genes). Rare digenic scenarios could theoretically modulate severity (e.g., GNMT/MAT1A/SAHH pathways), though ADK variants are primary. PMC

18. Prematurity. Immature liver function may amplify early presentations. (General hepatic-metabolic vulnerability.) Orpha

19. Delayed diagnosis. Without diet/monitoring, persistent metabolic imbalance worsens outcomes. (Case-series insights.) Frontiers

20. Inadequate protein-quality planning. Lack of guided methionine restriction in known cases can perpetuate high SAM/SAH. Wiley Online Library

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Symptoms

1. Developmental delay. The child reaches milestones late (sitting, walking, talking). This reflects brain involvement from the methylation imbalance. Orpha

2. Encephalopathy/lethargy. The child may be very sleepy or confused during illness or decompensation. PMC

3. Seizures/epilepsy. Fits can occur early and may repeat. They signal cortical irritability from metabolic stress. PubMed

4. Hypotonia (low muscle tone). Feels “floppy” when held; muscles lack normal resistance. Orpha

5. Feeding difficulty and poor weight gain. Babies may tire easily or vomit, leading to failure to thrive. Orpha

6. Irritability or abnormal cry. Brain stress can make babies difficult to soothe. Orpha

7. Jaundice and cholestasis. Yellow skin/eyes and pale stools can appear when bile flow is impaired. Orpha

8. Hepatomegaly and elevated liver enzymes. The liver may be enlarged and blood tests (ALT/AST) high. PMC

9. Coagulopathy or easy bruising (advanced cases). When the liver is very sick, clotting factors drop. Orpha

10. Dysmorphic facial features. Some children have frontal bossing, macrocephaly, hypertelorism, or a depressed nasal bridge. MalaCards

11. Hypoglycemia (sometimes). Low blood sugar can happen during illness or feeding problems. Global Genes

12. Cardiac defects in a minority. Reported defects include pulmonary stenosis and septal defects. Global Genes

13. Learning difficulties in older children. Even with treatment, school performance can be affected. PubMed

14. Vomiting and poor appetite during decompensation. Common with metabolic stress. Orpha

15. Head growth changes. Macrocephaly has been described in some cases. MalaCards

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Diagnostic tests

A) Physical examination

1. Growth and nutrition check. Measure weight, length/height, and head size to spot failure to thrive or macrocephaly. This sets a baseline and tracks response to therapy. Orpha

2. Neurologic exam. Look for low tone, brisk or reduced reflexes, seizures, and developmental level. Findings guide urgency of further tests. PubMed

3. Liver exam. Check for jaundice, enlarged liver, and signs of chronic liver disease. This correlates with blood test changes. PMC

4. Dysmorphology review and cardiac listen. Note facial features; listen for murmurs that may suggest structural heart disease. Global Genes

B) “Manual” bedside/developmental tests

5. Standardized developmental screening (e.g., Denver II). Simple tools help document delays and plan therapies. (General pediatric practice for neurodevelopmental disorders.) PubMed

6. Feeding/swallow assessment. Bedside evaluation for suck/swallow coordination and risk of aspiration; directs nutrition plans. (General pediatric hepatology/metabolic care.) Orpha

7. Clinical encephalopathy scoring. Serial mental-status checks during illness to detect worsening brain function. (General metabolic encephalopathy care.) PMC

8. Bedside coagulation risk review (bruising, petechiae). Physical signs that prompt urgent lab testing for coagulopathy. (General hepatopathy practice.) Orpha

C) Laboratory and pathological tests

9. Plasma amino-acid profile. Shows high methionine—a hallmark clue. Homocysteine is often normal, which helps distinguish ADK deficiency from other methylation disorders. MalaCards

10. Plasma SAM and SAH levels. Typically elevated, supporting methylation-cycle disruption. These biomarkers are very helpful. PMCmonarchinitiative.org

11. Urinary adenosine. May be increased and supports the enzyme defect. PubMed

12. Liver panel. ALT/AST, bilirubin (direct/total), GGT, albumin, and INR/PT help grade liver involvement. PMC

13. Ammonia and lactate. Check for metabolic decompensation or overlapping issues. (General IEM practice.) Orpha

14. Blood glucose. Screens for hypoglycemia during illness or feeding problems. Global Genes

15. ADK enzyme activity (research/specialized labs). Measuring activity in fibroblasts or lymphocytes can confirm the functional defect when available. PubMed

16. Molecular genetic testing (ADK gene). Definitive test—sequencing detects pathogenic variants; can add deletion/duplication analysis if needed. Guides family counseling. PubMed

17. Expanded metabolic panel to exclude look-alikes. Tests for MAT1A, GNMT, SAHH, and CBS-related disorders help rule out other causes of hypermethioninemia. PMC

18. Coagulation factors and vitamin levels (A, D, K). If cholestasis is present, fat-soluble vitamins and clotting can be impaired; this guides supplementation. (General cholestasis care.) Orpha

D) Electrodiagnostic tests

19. EEG. Evaluates seizures and background slowing expected in encephalopathy; helps choose anti-seizure therapy. PubMed

20. Evoked potentials (selected cases). If development is significantly delayed, these tests assess sensory pathway integrity. (General neuro-metabolic evaluation.) PubMed

E) Imaging tests

21. Brain MRI. May show non-specific white-matter changes or delayed myelination in metabolic encephalopathies; primarily used to assess extent and exclude other causes. PubMed

22. Liver ultrasound ± elastography. Non-invasive look at liver size, echotexture, and stiffness; tracks cholestasis or fibrosis. Orpha

23. Echocardiogram (if murmur or known risk). Screens for congenital heart defects reported in some patients. Global Genes

24. Abdominal Doppler (selected). Looks for portal hypertension or abnormal flow if liver disease is advanced. (General hepatology practice.) Orpha

Non-pharmacological treatments

Physiotherapy 

1. Early neuro-developmental therapy. Daily play-based exercises to build head control, rolling, sitting, and standing. Purpose: improve milestones. Mechanism: repeated practice strengthens neural pathways and muscles. Benefits: safer mobility and less caregiver strain.

2. Tone management and positioning. Use wedges, rolls, and proper seating to support low tone. Purpose: prevent collapse and fatigue. Mechanism: external support improves biomechanics. Benefits: better feeding and breathing.

3. Core and proximal strengthening. Short, frequent sessions (5–10 min) many times a day. Purpose: improve trunk stability. Mechanism: motor learning and muscle hypertrophy. Benefits: fewer falls.

4. Stretching program. Daily gentle stretches for ankles, hamstrings, hips, shoulders. Purpose: prevent contractures. Mechanism: maintains muscle-tendon length. Benefits: easier care and hygiene.

5. Balance and gait training. Supported standing, cruising between furniture, walker training. Purpose: safe mobility. Mechanism: vestibular/proprioceptive practice. Benefits: independence.

6. Oro-motor therapy. Suck-swallow-breath coordination, pacing feeds, nipple flow control. Purpose: safer feeding. Mechanism: task-specific training. Benefits: less aspiration, better growth.

7. Respiratory physiotherapy. Bubble PEP, assisted cough, chest mobility. Purpose: reduce infections. Mechanism: improves clearance and lung inflation. Benefits: fewer hospital visits.

8. Functional electrical stimulation (FES) (clinic-guided when appropriate). Purpose: activate weak muscles. Mechanism: external current triggers contraction. Benefits: better engagement in therapy.

9. Constraint-induced practice (for asymmetry). Purpose: increase use of weaker side. Mechanism: cortical re-organization. Benefits: improved bimanual skills.

10. Hydrotherapy. Water buoyancy allows practice with less gravity. Purpose: safe, longer sessions. Mechanism: unloads joints; sensory input. Benefits: confidence and endurance.

11. Orthotics and seating. AFOs, supportive chairs. Purpose: posture and foot alignment. Mechanism: external stabilization. Benefits: energy saving.

12. 24-hour positioning plan. Sleep wedges, prone time, frequent repositioning. Purpose: prevent pressure points and plagiocephaly. Mechanism: load distribution. Benefits: comfort, better sleep.

13. Serial casting or splinting (if spasticity later). Purpose: lengthen tight muscles. Mechanism: low-load prolonged stretch. Benefits: gait and hygiene.

14. Caregiver training. Teach safe transfers, handling, home exercise, seizure first-aid. Purpose: empower family. Mechanism: skill building. Benefits: fewer emergencies.

15. Adaptive equipment for play and school. Switches, supportive chairs, walkers. Purpose: access to learning. Mechanism: remove physical barriers. Benefits: inclusion and development.

Mind-Body / “Gene-informed” / Educational therapies 

1. Low-methionine nutrition plan with a metabolic dietitian (cornerstone). Purpose: lower methionine load. Mechanism: reduce substrate going into the faulty pathway. Benefits: liver improvement; may support neurodevelopment when started early. Wiley Online LibrarySpringerLink
2. Feeding therapy (SLT/OT): pacing, textures, safe swallow strategies. Purpose: safe calories to support growth.
3. Individualized education plan (IEP). Purpose: speech, occupational, and special education supports at school.
4. Sleep hygiene program. Fixed bedtime, quiet room, seizure safety. Purpose: protect brain health.
5. Behavioral therapy for attention and learning. Purpose: increase engagement.
6. Parent coaching and respite planning. Purpose: reduce burnout and maintain home program.
7. Infection prevention plan (vaccines up to date, hand hygiene). Purpose: reduce metabolic stress.
8. Genetic counseling. Purpose: explain inheritance, test siblings, family planning. Mechanism: identify carriers and options (prenatal / preimplantation).
9. Social work support for special low-protein foods and formula coverage.
10. Care coordination (metabolic specialist + neurologist + hepatologist + therapist + dietitian). Purpose: unify goals and timing of visits.

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Drug treatments

Important safety note: Doses below are typical pediatric starting ranges used by specialists for similar problems. Do not use this list for self-treatment. The exact drug, dose, timing, and interactions must be set by your child’s own clinicians—especially because liver function can change in ADK deficiency.

1. Levetiracetam (anti-seizure). Class: SV2A modulator. Dose: often 10–20 mg/kg twice daily, titrate (max varies by clinic). When: daily. Purpose: control seizures with minimal liver metabolism. Mechanism: reduces synaptic release. Side effects: irritability, somnolence.

2. Clobazam (adjunct for epilepsy). Class: benzodiazepine. Dose: ~0.25–0.5 mg/kg/day divided; slow titration. Purpose: add-on for refractory seizures. Mechanism: GABA-A enhancement. Side effects: sedation, tolerance, constipation.

3. Lamotrigine. Class: sodium-channel modulator. Dose: very slow titration beginning ~0.15–0.3 mg/kg/day; increase as guided. Purpose: broad-spectrum seizure control. Side effects: rash (report urgently), dizziness.

4. Topiramate. Class: multiple mechanisms. Dose: ~1–3 mg/kg twice daily, slowly titrate. Purpose: adjunct in generalized or focal seizures. Side effects: appetite loss, acidosis risk, stones.

5. Rescue benzodiazepine (intranasal midazolam or rectal diazepam). Purpose: stop prolonged seizures at home per plan. Dosing: weight-based per emergency plan. Side effects: sleepiness, respiratory depression—use only as prescribed.

6. Ursodeoxycholic acid (UDCA). Class: bile acid. Dose: ~10–30 mg/kg/day divided. When: daily if cholestasis. Purpose: support bile flow, reduce itch. Mechanism: cytoprotective, choleretic. Side effects: diarrhea, rare LFT changes.

7. Fat-soluble vitamins (A, D, E, K) (formulations for cholestasis). Dose: per deficiency and weight. Purpose: prevent bleeding (K), rickets (D), retinal/neurologic issues (A/E). Side effects: hypervitaminosis if overdosed.

8. Vitamin K (if INR high or for procedures). Dose: per protocol (e.g., 1–5 mg oral/IV as directed). Purpose: correct coagulopathy from cholestasis. Side effects: rare allergic reactions (IV).

9. Cholestyramine or rifampin (itch in cholestasis; specialist use). Purpose: pruritus control. Mechanism: bile acid binding (cholestyramine) or enzyme induction (rifampin). Side effects: drug interactions; monitor.

10. Proton-pump inhibitor (e.g., omeprazole) if severe reflux affects feeding. Dose: weight-based. Purpose: protect calories and reduce aspiration risk.

11. Polyethylene glycol for chronic constipation. Dose: per weight. Purpose: stool softening to reduce feeding pain and improve appetite.

12. Melatonin (sleep). Dose: small evening dose tailored to age. Purpose: improve sleep continuity (helps seizures and learning).

13. Acetaminophen (paracetamol) carefully dosed for fever/pain; avoid routine NSAIDs if liver labs are unstable. Purpose: comfort; reduce catabolic stress.

14. Antibiotics only for confirmed infections. Purpose: reduce metabolic stress and hospitalizations.

15. Avoid or use great caution: Valproate and other hepatotoxic drugs; review every new medication with the metabolic team. (Rationale: underlying liver vulnerability in many ADK patients.) PubMed

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Dietary “molecular” supplements

Key point: In ADK deficiency, methionine is high and SAM/SAH are high. “Methyl-donor” supplements (like betaine) can raise methionine further and are not routine here. Use only with a metabolic specialist.

1. Low-methionine medical formula (protein substitute with essential amino acids minus methionine). Dose: as dietitian prescribes. Function: lowers methionine load while giving needed protein for growth. Mechanism: substrate restriction. Wiley Online Library

2. Special low-protein foods (breads/pasta/rice). Function: allows calories without methionine excess.

3. MCT oil (if fat malabsorption). Function: easy energy; helps growth. Mechanism: direct portal absorption.

4. DHA/ARA (omega-3/6) for brain support. Function: neuronal membrane health.

5. Vitamin D (target normal level). Function: bone and immune support.

6. Vitamin E (in cholestasis). Function: antioxidant; neurologic protection.

7. Vitamin A (only if deficient; careful dosing). Function: vision/immune support.

8. Vitamin K (if INR high). Function: blood clotting.

9. Zinc (if low). Function: growth, immunity, taste.

10. Selenium (if low). Function: antioxidant enzyme systems.

*(These choices come from general cholestasis/neurodevelopment care; they are supportive. The main evidence-based intervention remains methionine restriction.) Wiley Online LibrarySpringerLink

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Immunity-booster / regenerative / stem-cell drugs”

There are no approved immunity-boosting, regenerative, or stem-cell drugs for ADK deficiency at this time. Experimental gene or cell therapies should be done only in clinical trials. Support growth, vaccines, sleep, and diet instead. (No dosages are given here because these therapies are not established for ADK deficiency.) PubMed

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Surgeries or procedures

1. Liver transplantation — rare, select cases with end-stage liver disease or liver failure. It may help liver function but does not correct all brain features; cases have been diagnosed even years after transplant. Why: life-saving when the liver fails. How: standard pediatric transplant pathway. PMC

2. Gastrostomy tube (G-tube) — for severe feeding difficulty or unsafe swallow. Why: secure calories and medicines. Procedure: endoscopic or surgical placement.

3. Vagus nerve stimulation (VNS) — for refractory epilepsy despite medicines. Why: reduce seizure burden. Procedure: implant a pulse generator under the skin.

4. Orthopedic procedures — for severe contractures or scoliosis if they develop with growth. Why: comfort, sitting, care.

5. Dental procedures under anesthesia with careful metabolic and airway planning. Why: prevent pain/infection that can worsen nutrition.

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Prevention strategies

1. Early, strict low-methionine diet per a metabolic dietitian. Wiley Online Library

2. Avoid hepatotoxic drugs unless a specialist approves.

3. Vaccines on time (including influenza).

4. Hand hygiene and quick infection care to reduce metabolic stress.

5. Regular growth and lab monitoring (methionine, SAM/SAH where available, liver panel, vitamins). Rare Diseases Info

6. Good sleep and seizure action plan.

7. Adequate calories (consider MCT or tube feeding if needed).

8. Annual therapy reviews (PT/OT/SLT/education).

9. Family genetic counseling; test siblings and plan future pregnancies.

10. Care coordinator or case manager to keep diet, drugs, and therapies aligned.

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When to see doctors urgently

• Long or repeated seizures; any seizure lasting >5 minutes.

• New or worsening jaundice, very pale stools, very dark urine.

• Bleeding, easy bruising, or very itchy child with cholestasis.

• Poor feeding, repeated vomiting, dehydration, or weight loss.

• Fever with lethargy, breathing problems, or unusual sleepiness.

• Any sudden skill loss (regression) or new weakness.

• If a new medication is suggested by anyone outside the metabolic team.

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What to eat and what to avoid

Core idea: lower the methionine load while meeting growth needs.

• Eat/Use more: special low-protein medical foods, low-methionine formula/protein substitute, fruits, many vegetables, measured portions of low-protein grains; plant oils; MCT oil if advised; adequate calories to support growth.

• Limit/Avoid: high-methionine foods such as meat, fish, eggs, hard cheese, many nuts and seeds, soy protein isolates, and large servings of standard grains/breads without counting toward the protein allowance.

• Always: follow the exact daily protein goal from your metabolic dietitian; spread protein across meals; keep a food and weight diary; bring labels to clinic. Wiley Online Library

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Frequently asked questions

1. Is ADK deficiency curable now? No. Care is diet + symptom control. Research continues. PubMed

2. What is the most important treatment? A low-methionine diet set by a metabolic dietitian. Wiley Online Library

3. Can early diet help the brain? Early cases show liver improvement and sometimes developmental gains, especially when diet starts early. Results vary. Wiley Online LibrarySpringerLink

4. What lab pattern is typical? High methionine with high SAM and high SAH; homocysteine often normal. Rare Diseases Info

5. How common is it? Extremely rare; only a few dozen patients reported worldwide. Frontiers

6. Will my child always have seizures? Not always; many do. Good seizure control and sleep help development.

7. Are there drugs to avoid? Avoid or use caution with hepatotoxic drugs (e.g., valproate). Always ask the metabolic team first. PubMed

8. Is liver transplant a cure? It can treat liver failure but is not a cure for the genetic problem; some children were diagnosed even after transplant. PMC

9. Can we use betaine or methyl donors? Not routinely in ADK deficiency; they can raise methionine more. Use only if a specialist advises. Wiley Online Library

10. What about SAM or SAH supplements? Not appropriate; these are already high in ADK deficiency. Rare Diseases Info

11. Should we count protein every day? Yes, to meet the prescribed allowance and avoid spikes.

12. What specialists do we need? Metabolic/genetics, neurology, hepatology, dietitian, PT/OT/SLT, social worker.

13. Will my other children have it? Each pregnancy has a 25% risk if both parents are carriers; testing is available.

14. Can adults have mild forms? Late recognition is possible; severity varies. ScienceDirect

15. Where can we read more? Orphanet/GARD summaries and peer-reviewed case series are helpful for families. OrphaRare Diseases Info

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.

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