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IEMbase 0063: ACADSB-related 2-methylbutyryl-CoA dehydrogenase deficiency

Scope

Field Value
IEMbase ID 63
Nosology 1.2.09.01
Gene ACADSB
External IDs OMIM:610006
Generated mapping MAPPED by alias_exact:2 methylbutyryl coa dehydrogenase deficiency
Candidate DisMech targets 2-Methylbutyryl-CoA_Dehydrogenase_Deficiency.yaml
Review date 2026-07-07

IEMbase phenotype signal

IEMbase represents this as autosomal recessive ACADSB-related 2-methylbutyryl-CoA dehydrogenase deficiency, with alternate labels short/branched-chain acyl-CoA dehydrogenase deficiency, 2-methylbutyrylglycinuria, and MBCD. Treatability is marked unknown.

The biochemical signal includes high urinary 2-methylbutyrylglycine, normal-high isobutyrylglycine, high blood or plasma C5 2-methylbutyrylcarnitine, high C5/C2 ratio, low fibroblast 2-methylbutyryl-CoA dehydrogenase activity, normal-high 2-ethylhydracrylic acid, high urinary 2-methylbutyric acid, possible anion-gap abnormality, and low-normal glucose.

IEMbase does not list characteristic clinical features. Additional features include autism spectrum disorder, decreased cortical sulci, hypoglycemia, axial hypotonia, asymptomatic individuals, and psychomotor delay. No treatment rows are present in the cached record.

DisMech phenotype coverage

The generated mapping to 2-Methylbutyryl-CoA_Dehydrogenase_Deficiency.yaml is correct. DisMech models SBCADD as an autosomal recessive isoleucine-metabolism disorder caused by ACADSB variants, with accumulation of C5 acylcarnitine 2-methylbutyrylcarnitine, urinary 2-methylbutyrylglycine, and 2-ethylhydracrylic acid through R-pathway rerouting.

DisMech covers the largely asymptomatic newborn-screening phenotype, the minority symptomatic phenotype with developmental delay, seizures, hypotonia, failure to thrive, microcephaly, autism, dyskinetic cerebral palsy, and muscle atrophy, plus stress-sensitive decompensation, C5-isomer ambiguity, ACAD substrate promiscuity, carnitine supplementation, catabolic-stress avoidance, emergency protocols, controversial diet management, valproate avoidance, newborn screening, and longitudinal monitoring.

Concordance and completeness

Judgement: correct mapping and high concordance.

IEMbase adds useful compact diagnostic details, especially the C5/C2 ratio, fibroblast enzyme activity, urinary 2-methylbutyric acid, decreased cortical sulci, hypoglycemia, and axial hypotonia. DisMech is stronger for the mechanistic distinction from IVA, the R-pathway/2-ethylhydracrylic acid branch, the mostly asymptomatic course, and management uncertainty.

Curation actions

  • Keep the generated mapping to 2-Methylbutyryl-CoA_Dehydrogenase_Deficiency.yaml.
  • Preserve explicit distinction from IVA because both can produce elevated C5.
  • Consider IEMbase C5/C2 and fibroblast enzyme rows as future diagnostic enrichment candidates.