Combined oxidative phosphorylation defect type 13

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ORPHA:319514OMIM:614932E88.8
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Overview

Combined oxidative phosphorylation defect type 13 (COXPD13) is an extremely rare genetic disorder that affects how cells produce energy. Inside nearly every cell in your body, there are tiny structures called mitochondria that act like power plants, converting food into usable energy through a process called oxidative phosphorylation. In COXPD13, a genetic change in the PNPT1 gene disrupts this energy-making process, leading to problems in multiple organs that need a lot of energy to function properly. This condition typically appears in infancy or early childhood. Children with COXPD13 may experience hearing loss (often sensorineural, meaning it involves the inner ear or nerve pathways), developmental delays, movement problems, muscle weakness, and brain abnormalities that can be seen on MRI scans. Some children also develop vision problems and may have episodes of worsening symptoms during illness or stress. The severity can vary between affected individuals, but the condition generally has a significant impact on development and daily functioning. There is currently no cure for COXPD13. Treatment focuses on managing symptoms and supporting the child's development. This may include hearing aids or cochlear implants for hearing loss, physical and occupational therapy, and careful monitoring by a team of specialists. Some doctors may try mitochondrial supplements such as coenzyme Q10 or riboflavin, though their effectiveness has not been proven in clinical trials for this specific condition.

Also known as:

Key symptoms:

Hearing loss (sensorineural)Developmental delayMuscle weaknessMovement difficulties or poor coordinationVision problemsBrain abnormalities on MRIDelayed speech developmentIntellectual disabilityPoor growth or failure to thriveLow muscle tone (floppiness)Fatigue and low energyEpisodes of worsening symptoms during illnessDifficulty with balance and walking

Clinical phenotype terms (33)— hover any for plain English
Abnormal basal ganglia morphologyHP:0002134Orofacial dyskinesiaHP:0002310Hip contractureHP:0003273Subsarcolemmal accumulations of abnormally shaped mitochondriaHP:0003548Type 2 muscle fiber atrophyHP:0003554Type 1 muscle fiber predominanceHP:0003803Ankle flexion contractureHP:0006466Lower limb hypertoniaHP:0006895Gastrostomy tube feeding in infancyHP:0011471Elevated CSF neopterin levelHP:0040204Mitochondrial respiratory chain defectsHP:0200125
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 13.

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No actively recruiting trials found for Combined oxidative phosphorylation defect type 13 at this time.

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No specialists are currently listed for Combined oxidative phosphorylation defect type 13.

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 13.

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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.How severe is my child's condition based on the specific genetic mutations found?,What therapies should we start right away to support development?,Should my child take any mitochondrial supplements like coenzyme Q10 or carnitine?,What should we do if my child gets sick — is there a sick-day emergency plan?,How often should hearing and vision be checked?,Are there any clinical trials or research studies we could participate in?,Should other family members be tested to see if they are carriers?

Common questions about Combined oxidative phosphorylation defect type 13

What is Combined oxidative phosphorylation defect type 13?

Combined oxidative phosphorylation defect type 13 (COXPD13) is an extremely rare genetic disorder that affects how cells produce energy. Inside nearly every cell in your body, there are tiny structures called mitochondria that act like power plants, converting food into usable energy through a process called oxidative phosphorylation. In COXPD13, a genetic change in the PNPT1 gene disrupts this energy-making process, leading to problems in multiple organs that need a lot of energy to function properly. This condition typically appears in infancy or early childhood. Children with COXPD13 may e

How is Combined oxidative phosphorylation defect type 13 inherited?

Combined oxidative phosphorylation defect type 13 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 13 typically begin?

Typical onset of Combined oxidative phosphorylation defect type 13 is infantile. Age of onset can vary across affected individuals.