Skip to content

IEMbase 0163: GCDH-related glutaric acidemia type 1

Scope

Field Value
IEMbase ID 163
Nosology 1.2.05.01
Gene GCDH
External IDs OMIM:231670; ORPHA:25
Generated mapping MAPPED to Glutaryl-CoA_Dehydrogenase_Deficiency.yaml
Candidate DisMech targets Glutaryl-CoA_Dehydrogenase_Deficiency.yaml
Review date 2026-07-07

IEMbase phenotype signal

IEMbase represents this as GCDH-related glutaryl-CoA dehydrogenase deficiency, with alternate labels glutaric acidemia type 1 and GA-I. Treatability is marked yes.

The biochemical rows include blood and plasma C5-DC glutarylcarnitine reported as normal to increased, urinary 3-hydroxyglutaric acid normal to increased, glutaric acid in dried blood spot, plasma, and urine normal to increased, urinary glutaconic acid normal to increased, increased ASAT/ALAT and creatine kinase, and plasma glucose decreased to normal. The clinical rows include macrocephaly, temporal hypoplasia/dilated external CSF spaces, striatal atrophy, periventricular white-matter abnormalities, acute encephalopathic crises, dystonia, dyskinesia, chorea, parkinsonism, hypokinesia, movement disorder, axial hypotonia, ataxia, dysarthria, feeding/swallowing difficulties, vomiting, pneumonia, acrodermatitis, peripheral neuropathy, headache, vertigo, and gliomas. IEMbase treatment rows include carnitine, lysine restriction, protein-defined diet, and sick-day management.

DisMech phenotype coverage

Glutaryl-CoA_Dehydrogenase_Deficiency.yaml is the correct target. It models biallelic GCDH loss of function, impaired lysine, hydroxylysine, and tryptophan catabolism, accumulation of glutaric acid, 3-hydroxyglutaric acid, and glutarylcarnitine, brain exposure to toxic catabolites, striatal vulnerability, acute encephalopathic crises, dystonia, macrocephaly, frontotemporal atrophy, white-matter changes, newborn screening, lysine-restricted diet, carnitine, emergency illness management, and investigational gene therapy, chaperone, and bezafibrate approaches.

Concordance and completeness

Judgement: correct mapping with high concordance.

The IEMbase and DisMech profiles agree on GCDH, GA1 identity, C5DC, glutaric/3-hydroxyglutaric acid biomarkers, macrocephaly, striatal injury, white-matter imaging, encephalopathic crises, dystonia/movement disorder, and standard metabolic treatment. DisMech is stronger for mechanistic causality, module-level treatment rationale, newborn screening, and investigational treatments. IEMbase adds or foregrounds glutaconic acid, ASAT/ALAT, creatine kinase, glucose, acrodermatitis, peripheral neuropathy, pneumonia, vertigo, abasia/astasia, and gliomas as review targets.

Curation actions

  • Keep the mapping to Glutaryl-CoA_Dehydrogenase_Deficiency.yaml.
  • Consider future biomarker refinement for glutaconic acid, ASAT/ALAT, creatine kinase, glucose, and the "normal to increased" low-excreter wording.
  • Review the rarer IEMbase phenotype rows, especially gliomas, acrodermatitis, peripheral neuropathy, pneumonia, vertigo, abasia, and astasia.