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IEMbase 0438: ACAD9-related Acyl-CoA dehydrogenase 9 deficiency

Scope

Field Value
IEMbase ID 438
Nosology 7.1.09.01
Gene ACAD9
External IDs OMIM:611126; ORPHA:99901
Generated mapping UNMAPPED; low candidate Glutaryl-CoA_Dehydrogenase_Deficiency.yaml
Candidate DisMech targets ACAD9_Deficiency.yaml
Review date 2026-07-07

IEMbase phenotype signal

IEMbase represents autosomal recessive ACAD9 deficiency as a complex I assembly disorder with hypoglycemia and lactic acidosis. Biochemical rows include increased plasma and urine lactate, increased lactate/pyruvate ratio, increased alanine, decreased free carnitine, increased long-chain acylcarnitines, increased creatine kinase, transaminase elevation, ketosis-related organic acids, hyperammonemia, and hypoglycemia. Clinical rows include dilated cardiomyopathy, encephalopathy, exercise intolerance, failure to thrive, hearing loss, axial hypotonia, liver dysfunction or failure including Reye-like liver failure, neurologic dysfunction, rhabdomyolysis, and skeletal myopathy. IEMbase records riboflavin as a treatment row.

DisMech phenotype coverage

ACAD9_Deficiency.yaml is the correct local target. It describes biallelic ACAD9 disease as a mitochondrial complex I assembly-factor disorder, not as a primary fatty-acid beta-oxidation defect, and covers complex I deficiency, oxidative phosphorylation failure, cardiomyopathy, exercise intolerance, lactic acidosis, muscular weakness, and riboflavin responsiveness.

The generated Glutaryl-CoA_Dehydrogenase_Deficiency.yaml candidate is a false positive. Local GCDH deficiency is glutaric acidemia type 1, with lysine, hydroxylysine, and tryptophan catabolism, glutaric acid and 3-hydroxyglutaric acid biomarkers, and encephalopathic crises. It does not represent ACAD9 complex I assembly disease.

Concordance and completeness

Judgement: false negative; resolve IEMbase 438 to ACAD9_Deficiency.yaml.

The local target has high mechanism and treatment concordance for the core complex I/riboflavin-responsive disorder. IEMbase adds useful phenotypic prompts for long-chain acylcarnitines, hypoglycemia, liver dysfunction, Reye-like liver failure, rhabdomyolysis, and hearing loss that should be checked against primary evidence before import.

Curation actions

  • Map IEMbase 438 to ACAD9_Deficiency.yaml.
  • Do not map to Glutaryl-CoA_Dehydrogenase_Deficiency.yaml.
  • If importing IEMbase-derived prompts, prioritize ACAD9 complex I assembly, lactic acidosis, cardiomyopathy, skeletal myopathy, exercise intolerance, riboflavin responsiveness, and verify the liver, hearing, rhabdomyolysis, hypoglycemia, and acylcarnitine rows against source evidence.