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IEMbase 0180: AKR1D1-related BASD type 2

Scope

Field Value
IEMbase ID 180
Nosology 14.8.02.01
Gene AKR1D1
External IDs OMIM:604741; ORPHA:79303
Generated mapping CANDIDATE; Inborn_Disorder_of_Bile_Acid_Synthesis.yaml#BASD Type 2
Candidate DisMech targets Inborn_Disorder_of_Bile_Acid_Synthesis.yaml#BASD Type 2
Review date 2026-07-07

IEMbase phenotype signal

IEMbase represents this as AKR1D1-related Delta4-3-oxosteroid-5beta-reductase deficiency, with alternate labels 5beta-reductase deficiency and SRD5B1. Treatability is marked yes.

The biochemical rows emphasize increased urinary 7-alpha-hydroxy-3-oxo- cholenoic acids and 7alpha,12alpha-dihydroxy-3-oxo-4-cholenoic acids, increased plasma allochenodeoxycholic acid and allocholic acid, positive AKR1D1 sequencing, increased ASAT/ALAT, normal-to-increased alkaline phosphatase and gamma-GT, increased or normal-to-increased prothrombin ratio, low-to-normal albumin, increased or normal-to-increased conjugated bilirubin, and low-to-normal cholesterol. Clinical rows include neonatal or infantile cholestasis, giant-cell hepatitis, lobular and periportal inflammation, pseudoacinar transformation, abnormal canaliculi and microvilli, ascites, edema, hepatosplenomegaly, and jaundice. Treatment rows list chenodeoxycholic acid and ursodeoxycholic acid.

DisMech phenotype coverage

Inborn_Disorder_of_Bile_Acid_Synthesis.yaml#BASD Type 2 is the correct target. The local subtype covers AKR1D1/SRD5B1, defective Delta4-3-oxosteroid 5beta-reductase activity, accumulation of 3-oxo-Delta4 bile acids and allocholic bile acids, severe neonatal cholestasis, fat-soluble vitamin deficiency, bleeding risk, progressive liver injury, and bile acid replacement therapy.

Concordance and completeness

Judgement: accept the generated candidate as the correct subtype mapping.

IEMbase and DisMech agree on the gene, enzyme defect, toxic atypical bile acid intermediates, normal or low gamma-GT cholestasis pattern, neonatal or infantile liver disease, bleeding risk, and bile acid treatment. IEMbase adds more granular analytes, particularly specific 3-oxo-Delta4 and allocholic bile acid species, and separates chenodeoxycholic acid from ursodeoxycholic acid treatment rows. DisMech is stronger for mechanism and group-level treatment rationale.

Curation actions

  • Resolve this record to Inborn_Disorder_of_Bile_Acid_Synthesis.yaml#BASD Type 2.
  • Consider adding the specific urinary and plasma allocholic/3-oxo bile acid species if the BASD type 2 subtype is enriched.
  • Review whether ursodeoxycholic acid should be represented separately from primary bile acid replacement in the local treatment model.