Combined oxidative phosphorylation defect type 27

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ORPHA:477774OMIM:616672E88.8
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Overview

Combined oxidative phosphorylation defect type 27 (also written as COXPD27) is a rare inherited disorder that affects the way cells produce energy. Every cell in the body relies on tiny structures called mitochondria to convert food into usable energy. In COXPD27, a fault in the MTFMT gene disrupts this energy-making process, causing the mitochondria to work poorly. This is sometimes called a mitochondrial translation defect because the gene normally helps mitochondria build the proteins they need to function. Because energy production is essential for every organ, COXPD27 can affect many parts of the body at once. The brain and muscles are especially vulnerable because they need large amounts of energy to work properly. Children with this condition often show signs of Leigh syndrome or a Leigh-like illness, which involves progressive damage to specific areas of the brain. Common symptoms include developmental delays, muscle weakness, poor coordination, breathing difficulties, and problems with vision or eye movement. There is currently no cure for COXPD27. Treatment focuses on managing symptoms, supporting nutrition, and using certain vitamins or supplements that may help mitochondria work a little better. A team of specialists is usually needed to provide the best care. Early diagnosis is important so that supportive therapies can begin as soon as possible.

Also known as:

Key symptoms:

Developmental delay or regression (losing skills already learned)Muscle weakness or low muscle tone (feeling floppy)Poor coordination and balance problemsDifficulty breathing or episodes of rapid breathingProblems with eye movement or drooping eyelidsVision problemsFeeding difficulties in infancyFailure to thrive or poor weight gainSeizuresFatigue and very low energyBrain abnormalities visible on MRI (Leigh syndrome pattern)Elevated lactic acid in the bloodSpeech and language delays

Clinical phenotype terms (29)— hover any for plain English
TetraparesisHP:0002273Diffuse cerebral atrophyHP:0002506Decreased activity of mitochondrial complex IVHP:0008347Decreased activity of mitochondrial complex IHP:0011923Decreased activity of mitochondrial complex IIIHP:0011924Multifocal seizuresHP:0031165Epileptic encephalopathyHP:0200134Nonimmune hydrops fetalisHP:0001790
Inheritance

Autosomal recessive

Passed on when both parents carry the same gene change; often skips generations

Age of Onset

Infantile

Begins in infancy, roughly 1 month to 2 years old

Orphanet ↗OMIM ↗NORD ↗

Treatments

No FDA-approved treatments are currently listed for Combined oxidative phosphorylation defect type 27.

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No actively recruiting trials found for Combined oxidative phosphorylation defect type 27 at this time.

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No specialists are currently listed for Combined oxidative phosphorylation defect type 27.

View NORD Rare Disease Centers ↗Undiagnosed Disease Network ↗

Treatment Centers

8 centers
🏥 NORD

Baylor College of Medicine Rare Disease Center

Baylor College of Medicine

📍 Houston, TX

🏥 NORD

Stanford Medicine Rare Disease Center

Stanford Medicine

📍 Stanford, CA

🔬 UDN

NIH Clinical Center Undiagnosed Diseases Program

National Institutes of Health

📍 Bethesda, MD

🔬 UDN

UCLA UDN Clinical Site

UCLA Health

📍 Los Angeles, CA

🔬 UDN

Baylor College of Medicine UDN Clinical Site

Baylor College of Medicine

📍 Houston, TX

🔬 UDN

Harvard/MGH UDN Clinical Site

Massachusetts General Hospital

📍 Boston, MA

🏥 NORD

Mayo Clinic Center for Individualized Medicine

Mayo Clinic

📍 Rochester, MN

👤 Mayo Clinic Center for Individualized Medicine

🏥 NORD

UCLA Rare Disease Day Program

UCLA Health

📍 Los Angeles, CA

Travel Grants

No travel grants are currently matched to Combined oxidative phosphorylation defect type 27.

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Community

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Caregiver Resources

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Questions for your doctor

Bring these to your next appointment

  • Q1.What specific changes were found in the MTFMT gene, and what do they mean for my child's health?,Which specialists should be part of my child's care team, and how often should we see each one?,Are there any supplements or vitamins that might help, and what is the evidence for them?,What are the warning signs of a metabolic crisis, and what should I do if one happens?,How will this condition affect my child's development and learning, and what therapies are recommended?,Are there any clinical trials or research studies we should consider joining?,What is the risk that future children in our family could be affected, and should other family members be tested?

Common questions about Combined oxidative phosphorylation defect type 27

What is Combined oxidative phosphorylation defect type 27?

Combined oxidative phosphorylation defect type 27 (also written as COXPD27) is a rare inherited disorder that affects the way cells produce energy. Every cell in the body relies on tiny structures called mitochondria to convert food into usable energy. In COXPD27, a fault in the MTFMT gene disrupts this energy-making process, causing the mitochondria to work poorly. This is sometimes called a mitochondrial translation defect because the gene normally helps mitochondria build the proteins they need to function. Because energy production is essential for every organ, COXPD27 can affect many par

How is Combined oxidative phosphorylation defect type 27 inherited?

Combined oxidative phosphorylation defect type 27 follows a autosomal recessive inheritance pattern. Genetic counseling can help families understand recurrence risk and testing options.

At what age does Combined oxidative phosphorylation defect type 27 typically begin?

Typical onset of Combined oxidative phosphorylation defect type 27 is infantile. Age of onset can vary across affected individuals.