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IEMbase 0500: ALDOA-related aldolase A deficiency

Scope

Field Value
IEMbase ID 500
Nosology 3.3.08.01
Gene ALDOA
External IDs OMIM:611881; ORPHA:57
Generated mapping CANDIDATE; MEDIUM; Glycogen_Storage_Disease_Type_I.yaml
Candidate DisMech targets Glycogen_Storage_Disease_Type_I.yaml
Review date 2026-07-07

IEMbase phenotype signal

IEMbase represents autosomal recessive ALDOA-related aldolase A deficiency as glycogen storage disease type 12. No treatments are listed. Biochemical rows include decreased RBC aldolase A activity, normal-to-increased plasma creatine kinase, normal-to-increased liver and muscle glycogen, increased plasma bilirubin, and increased blood reticulocytes. Clinical rows include hemolytic anemia, optional rhabdomyolysis, muscle weakness, intellectual disability, short stature, dysmorphic features, low-set ears, thin lips, triangular face, and wide mouth.

DisMech phenotype coverage

Glycogen_Storage_Disease_Type_I.yaml is not the correct target. The local GSD I entry covers G6PC1/SLC37A4 glucose-6-phosphatase system deficiency and its hepatic/renal metabolic consequences. It does not model ALDOA, aldolase A enzyme deficiency, congenital nonspherocytic hemolytic anemia, or the dysmorphic/neurodevelopmental features described by IEMbase.

Glycogen_Storage_Disease_Type_VII.yaml has a partial phenotypic neighbor in the form of glycolytic myopathy plus hemolytic anemia, but that file is PFKM/Tarui disease and should not be used as exact ALDOA coverage.

Concordance and completeness

Judgement: false-positive candidate; true ALDOA/GSD XII local gap.

The generated candidate shares only "glycogen storage disease" vocabulary. IEMbase's source disease combines glycolytic enzyme deficiency, RBC hemolysis, muscle involvement, and developmental/dysmorphic features. The candidate DisMech file is a different carbohydrate-metabolism disorder centered on hepatic glucose release.

Curation actions

  • Do not map this record to Glycogen_Storage_Disease_Type_I.yaml.
  • Track ALDOA-related aldolase A deficiency / GSD XII as a local curation gap.
  • Preserve IEMbase prompts for RBC aldolase activity, hemolytic anemia, bilirubin/reticulocyte abnormalities, rhabdomyolysis, dysmorphic features, short stature, and intellectual disability for a future exact entry.