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IEMbase 0125: CYP17A1-related 17,20-Lyase deficiency

Scope

Field Value
IEMbase ID 125
Nosology 24.2.05.02
Gene CYP17A1
External IDs OMIM:202110; ORPHA:90796
Generated mapping UNMAPPED
Candidate DisMech targets Partial mechanistic neighbor Congenital_Adrenal_Hyperplasia.yaml#17A-OHD; no standalone isolated 17,20-lyase deficiency target
Review date 2026-07-07

IEMbase phenotype signal

IEMbase represents this as CYP17A1-related 17,20-lyase deficiency, with alternate label P450c17 deficiency. Treatability is marked unknown.

The IEMbase signal is sparse. Characteristic biochemical rows include mildly increased or normal-to-high 17-OH-progesterone. The only extracted clinical row is cryptorchidism. No treatment rows are listed.

DisMech phenotype coverage

Congenital_Adrenal_Hyperplasia.yaml includes a 17A-OHD subtype and a CYP17A1 17-hydroxylase/17,20-lyase deficiency mechanism. That local subtype is appropriate for combined CYP17A1 deficiency with cortisol and sex-steroid deficiency plus relative mineralocorticoid precursor excess.

The local CAH entry does not currently separate isolated 17,20-lyase deficiency from 17-alpha-hydroxylase deficiency. Its CYP17A1 coverage is broader and more mineralocorticoid/cortisol oriented than this IEMbase record.

Concordance and completeness

Judgement: generated unmapped result is a partial false negative, but the local target is only an umbrella/neighbor.

The best available local context is the CAH 17A-OHD subtype, because it is the only local CYP17A1 disease branch. However, IEMbase 0125 appears to be the isolated 17,20-lyase branch rather than the full 17-alpha-hydroxylase/17,20-lyase deficiency profile. The IEMbase signal of cryptorchidism and mild 17-OH-progesterone elevation does not match the fuller local CAH mineralocorticoid-excess profile closely enough to call it complete coverage.

Curation actions

  • Do not create a hard standalone mapping to CAH without preserving the isolated 17,20-lyase nuance.
  • Record Congenital_Adrenal_Hyperplasia.yaml#17A-OHD as partial local context until a CYP17A1 isolated 17,20-lyase subtype or entry exists.
  • Consider future subtype splitting if DisMech needs to distinguish isolated 17,20-lyase deficiency from combined CYP17A1 CAH.