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IEMbase 0029: SUOX-related isolated sulfite oxidase deficiency

Scope

Field Value
IEMbase ID 29
Nosology 1.5.09.01
Gene SUOX
External IDs OMIM:272300
Generated mapping UNMAPPED; best fuzzy candidate SCO1-Related_COX_Deficiency.yaml
Candidate DisMech targets none currently valid
Review date 2026-07-07

IEMbase phenotype signal

IEMbase represents isolated sulfite oxidase deficiency. Characteristic clinical features are psychomotor delay and pharmacoresistant seizures. Additional clinical findings include neonatal seizures, axial hypotonia, peripheral hypertonia, movement abnormality, feeding difficulties, microcephaly, hemiplegia, ectopia lentis, cerebral and cerebellar atrophy, cystic white-matter changes, and ventriculomegaly.

The biochemical profile is distinctive for sulfite metabolism: high S-sulfocysteine in plasma and urine, high taurine, high thiosulfate, high sulfite, low total homocysteine, normal methionine, normal plasma/urine uric acid, and secondary alpha-aminoadipic semialdehyde, pipecolic acid, and low CSF PLP signals. No treatments are listed.

DisMech phenotype coverage

There is no current DisMech entry for isolated SUOX deficiency. The fuzzy candidate SCO1-Related_COX_Deficiency.yaml is a false positive. SCO1-related COX deficiency is a mitochondrial complex IV assembly disorder with copper delivery/COX dysfunction, hepatic failure, encephalopathy, seizures, hypopituitarism, and lactic acidosis. It does not model sulfite/sulfocysteine accumulation, ectopia lentis, or the SUOX-specific biochemical pattern.

Concordance and completeness

Judgement: generated status is correctly unmapped; the SCO1 candidate is not a valid disease target.

IEMbase gives enough phenotype and laboratory structure for a future isolated sulfite oxidase deficiency entry. A future curation should also distinguish isolated SUOX deficiency from molybdenum cofactor deficiency, where uric acid patterns and broader cofactor biology differ.

Curation actions

  • Do not map this record to SCO1-Related_COX_Deficiency.yaml.
  • Consider a future isolated sulfite oxidase deficiency entry if sulfur amino-acid disorders are being expanded.
  • Preserve the discriminating labs: high sulfite/S-sulfocysteine with normal uric acid and normal methionine.