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N/A N=187

PCORI Urea Cycle Disorder Study

Urea Cycle Disorders

Enrolled (actual)
187
Serious AEs
0.0%
Results posted
Jan 2021
Primary outcome: Primary: Mortality — 18.4; 20.7 participant per 1000 person-years

Study Design & Population

Study type
Observational
Phase
N/A
Interventions
No Intervention Given (Other)
Age
Pediatric, Adult
Sex
All
Sponsor
Children's National Research Institute
Primary completion
Jun 2019

Outcome Measures

OutcomeResultp-value
PRIMARY
Mortality
18.4; 20.7
PRIMARY
Neurocognitive Function: Full-Scale IQ
80.1; 82
PRIMARY
Total Quality of Life
69.8; 55.6

Summary

Urea cycle disorders (UCD) are genetic disorders caused by the liver's inability to break down ammonia from proteins; ammonia then accumulates and is toxic to the brain. UCD cause brain damage and intellectual and developmental disabilities and even death. Treatment for UCD is either conservative management which involves a low-in-protein diet, drugs, and amino acid supplements or liver transplantation; each carries their own risks. This study aims to help patients to make the decision about different management alternatives by providing them with scientific information that is currently lacking. Aim 1 of this study will compare survival, neurocognitive function, and patient-reported quality of life.

Eligibility Criteria

Inclusion Criteria

Aim 1 (UCD patients):

  • Age 18 and under
  • Diagnosed with the following Neonatal-type urea cycle disorders:
  • CPSD, OTCD, ASD or ALD, as defined as follows:
  • Diagnosis of CPS I deficiency, defined as decreased (less than 20 % of control) CPS I enzyme activity in liver, and/or an identified pathogenic mutation, and/or hyperammonemia and first-degree relative meets at least one of the criteria for CPS I deficiency
  • Diagnosis of OTC deficiency, defined as the identification of a pathogenic mutation, and/or less than 20% of control of OTC activity in the liver, and/or elevated urinary orotate (greater than 20 uM/mM) in a random urine sample or after allopurinol challenge test, and/or hyperammonemia and first degree relative meets at least one of the criteria for OTC deficiency
  • Diagnosis of AS deficiency (Citrullinemia), defined as a greater than or equal to 10-fold elevation of citrulline in plasma, and/or decreased (less than 20% of control) AS enzyme activity in cultured skin fibroblasts or other appropriate tissue, and/or identification of a pathogenic mutation in the AS gene, and/or hyperammonemia and first degree relative meets at least one of the criteria for AS Deficiency
  • Diagnosis of AL deficiency (Argininosuccinic Aciduria, ASA), defined as the presence of argininosuccinic acid in the blood or urine, and/or decreased (less than 20% of control) AL enzyme activity in cultured skin fibroblasts or other appropriate tissue, and/or identification of a pathogenic mutation in the AL gene, and/or hyperammonemia and first degree relative meets at least one of the criteria for AL Deficiency
  • Willing to participate in at least 1 neurocognitive assessment and 1 quality of life assessment
  • Permit access to medical records and medical providers

Exclusion Criteria

Aim 1:

  • Rare and unrelated comorbidities (e.g., Down's syndrome, intraventricular hemorrhage in the newborn period, and extreme prematurity)
View full record on ClinicalTrials.gov →

Data sourced from ClinicalTrials.gov (NCT02740153). Outcome figures and adverse-event rates are extracted automatically from the registry's posted results and are provided for clinician reference, not as a substitute for the primary publication.

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