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IEMbase 0662: NR1H4-related progressive familial intrahepatic cholestasis 5

Scope

Field Value
IEMbase ID 662
Nosology 14.8.07.02
Nosology code IEM0808
Gene NR1H4
External IDs OMIM:617049; ORPHA:69665
Generated mapping UNMAPPED; best candidate Progressive_Familial_Heart_Block.yaml
Candidate DisMech targets Broad cholestasis and bile-acid context only; no exact NR1H4/PFIC5 target
Review date 2026-07-07

IEMbase phenotype signal

IEMbase represents autosomal recessive NR1H4-related progressive familial intrahepatic cholestasis 5, also labeled nuclear bile-acid receptor deficiency or farnesoid X receptor deficiency.

The clinical signal is neonatal or infantile intrahepatic cholestasis, jaundice, and liver failure. Biochemical rows include increased bilirubin, increased transaminases/ASAT/ALAT, normal GGT, and variable ammonia and glucose. Hypoglycemia is represented as a possible infancy/childhood clinical feature.

DisMech phenotype coverage

No exact NR1H4, FXR, nuclear bile-acid receptor deficiency, or PFIC5 local target was identified.

Inborn_Disorder_of_Bile_Acid_Synthesis.yaml gives broad bile-acid metabolism context for inherited cholestatic disorders, but it is built around bile-acid synthesis and conjugation enzyme/transporter defects such as HSD3B7, AKR1D1, CYP7B1, AMACR, CYP27A1, BAAT, and SLC27A5. It does not model NR1H4/FXR signaling deficiency or progressive familial intrahepatic cholestasis type 5.

The generated Progressive_Familial_Heart_Block.yaml candidate is a lexical false positive and should not be used.

Concordance and completeness

Judgement: true local gap. Existing bile-acid and cholestasis context can help orient a curator, but it is not disease-level coverage for NR1H4-related PFIC5.

The most important phenotype package to preserve is normal-GGT neonatal cholestasis with jaundice, liver failure, increased bilirubin and transaminases, and possible hypoglycemia/hyperammonemia.

Curation actions

  • Add a dedicated NR1H4/PFIC5 target if this record is curated into DisMech.
  • Do not accept the progressive familial heart block candidate.
  • Preserve normal GGT as a discriminating biochemical prompt.
  • Use the bile-acid synthesis umbrella only as broad context, not as exact coverage.