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IEMbase 0597: HAO1-related hydroxyacid oxidase 1 deficiency

Scope

Field Value
IEMbase ID 597
Nosology 13.1.03.01
Gene HAO1
External IDs OMIM:605023
Generated mapping UNMAPPED; best candidate TACO1-Related_COX_Deficiency.yaml
Candidate DisMech targets HAO1-Related_Glycolate_Oxidase_Deficiency.yaml
Review date 2026-07-07

IEMbase phenotype signal

IEMbase represents HAO1-related hydroxyacid oxidase 1 deficiency, with alternate labels glycolate oxidase 1 deficiency, isolated glycolic aciduria, and GOX. The record is autosomal recessive, classified under disorders of glyoxylate and oxalate metabolism, has unknown treatability, and has no treatment rows.

Biochemical rows include normal urinary citric acid, normal-to-very-increased urinary oxalic acid, normal urinary glyceric acid, and very increased urinary glycolic acid. Clinical rows include achalasia, nephrolithiasis, psychomotor delay, alacrima, and anisocoria.

DisMech phenotype coverage

HAO1-Related_Glycolate_Oxidase_Deficiency.yaml is the correct local target. It models autosomal recessive HAO1/glycolate oxidase deficiency, impaired hepatic glyoxylate precursor metabolism, isolated hyperglycolic aciduria, normal oxalate/citrate/glycerate in the index family, and a cautious knowledge gap around whether hyperoxaluria is ever a direct HAO1 consequence.

TACO1-Related_COX_Deficiency.yaml is a false-positive generated candidate from mitochondrial/organic-acid neighborhood signals. It models TACO1-related Complex IV deficiency and Leigh syndrome, not HAO1/glyoxylate metabolism.

Concordance and completeness

Judgement: generated false negative; resolve to HAO1-Related_Glycolate_Oxidase_Deficiency.yaml.

IEMbase and DisMech agree on HAO1 identity, autosomal recessive inheritance, glycolate oxidase deficiency, isolated glycolic aciduria, very high urinary glycolic acid, and normal glycerate/citrate. IEMbase adds urinary oxalate and nephrolithiasis prompts that overlap with the local knowledge gap, but the local entry is more cautious: it treats hyperoxaluria as observed in one case and not yet proven as a general downstream consequence.

The IEMbase achalasia, alacrima, anisocoria, and psychomotor-delay rows are not obvious consequences of the local HAO1 mechanism and should be source-reviewed before import.

Curation actions

  • Promote this record to HAO1-Related_Glycolate_Oxidase_Deficiency.yaml.
  • Reject TACO1-Related_COX_Deficiency.yaml as an exact mapping.
  • Preserve urinary oxalate and nephrolithiasis as source-review prompts tied to the existing HAO1 hyperoxaluria knowledge gap.
  • Source-review achalasia, alacrima, anisocoria, and psychomotor-delay rows before adding them to DisMech.