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IEMbase 0280: ABCD1-related X-linked adrenoleukodystrophy and adrenomyeloneuropathy

Scope

Field Value
IEMbase ID 280
Nosology 14.2.01.01
Gene ABCD1
External IDs OMIM:300100; ORPHA:369942
Generated mapping UNMAPPED; weak candidate adrenoleukodystrophy.yaml
Candidate DisMech targets adrenoleukodystrophy.yaml
Review date 2026-07-07

IEMbase phenotype signal

IEMbase represents ABCD1-related X-linked adrenoleukodystrophy and adrenomyeloneuropathy. Prevalence is listed as 1:17,000. Treatability is marked yes.

The characteristic clinical row is hyperpigmentation. Additional rows include adrenal insufficiency, Addison crisis, electrolyte changes, gonadal failure, sexual dysfunction, leukodystrophy, spastic paresis, peripheral nerve involvement, sphincter-control problems, behavioral disorder, dementia, epilepsy, abnormal EEG, abnormal brain evoked response audiometry, abnormal VEP, perceptive hearing loss, vision loss or optic atrophy, and alopecia. The biochemical hallmark is increased plasma very-long-chain fatty acids.

Treatment rows include hematopoietic stem-cell transplant, marked as lowering VLCFA and targeting neurologic features, and lentiviral gene therapy for cerebral adrenoleukodystrophy.

DisMech phenotype coverage

adrenoleukodystrophy.yaml is the correct local target despite the generated UNMAPPED status. The local entry models ABCD1-mediated peroxisomal fatty-acid transport failure, VLCFA accumulation, oxidative stress, astrocyte and microglial dysfunction, blood-brain-barrier disruption, inflammatory cerebral demyelination, adrenomyeloneuropathy spinal-cord axonopathy, adrenocortical dysfunction, and gonadal dysfunction. It includes childhood cerebral ALD, AMN, and Addison-only subtypes.

The local phenotype coverage includes progressive spastic paraplegia, bladder and bowel dysfunction, adrenal insufficiency, hyperpigmentation, weight loss, anorexia, CNS demyelination, cerebral white-matter lesions, hypogonadism, leukoencephalopathy, behavioral abnormality, cognitive impairment, visual loss, progressive myelopathy, and peripheral neuropathy. Local treatments include lentiviral gene therapy, hematopoietic stem-cell transplantation, glucocorticoid replacement, VLCFA testing, molecular testing, and brain MRI.

Concordance and completeness

Judgement: false negative mapping; resolve to adrenoleukodystrophy.yaml.

IEMbase and DisMech agree on ABCD1 identity, X-linked inheritance, elevated plasma VLCFA, adrenal disease with hyperpigmentation, cerebral leukodystrophy, AMN/spastic myelopathy, peripheral nerve involvement, sphincter dysfunction, gonadal/sexual dysfunction, behavioral and cognitive disease, visual involvement, HSCT, and lentiviral gene therapy. DisMech is richer for mechanistic chain, subtype structure, adrenal steroid replacement, diagnostics, and current trial context.

IEMbase adds review prompts for perceptive hearing loss, abnormal BAEP/VEP, EEG abnormality, alopecia, and Addison-crisis wording.

Curation actions

  • Resolve this record to adrenoleukodystrophy.yaml.
  • Treat the generated weak candidate as a true target; the low score appears to be a matching/naming artifact rather than a biology issue.
  • Use IEMbase's hearing-test, VEP/EEG, alopecia, and Addison-crisis rows as enrichment prompts.