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IEMbase 0159: DPYD-related dihydropyrimidine dehydrogenase deficiency

Scope

Field Value
IEMbase ID 159
Nosology 16.1.01.01
Gene DPYD
External IDs OMIM:274270; OMIM:612779; ORPHA:1675
Generated mapping UNMAPPED
Candidate DisMech targets None
Review date 2026-07-07

IEMbase phenotype signal

IEMbase represents this as DPYD-related dihydropyrimidine dehydrogenase deficiency, with alternate labels thymine-uraciluria and DPD. Treatability is marked unknown.

The biochemical rows show decreased WBC dihydropyrimidine dehydrogenase and increased 5-OH-methyluracil, plasma and urinary thymine, and plasma and urinary uracil. The clinical rows are variable and include cerebral atrophy, cerebellar white-matter MRI abnormalities, epilepsy/seizures, abnormal eye movements, nystagmus, optic atrophy, coloboma, microcephaly, feeding difficulties, hypotonia, hypertonia, hyperactivity, psychomotor retardation, intellectual disability, autism, and severe 5-fluorouracil toxicity in affected individuals and heterozygotes.

DisMech phenotype coverage

There is no local standalone DPYD/dihydropyrimidine dehydrogenase deficiency entry.

Chemotherapy_Induced_Diarrhea.yaml contains DPYD pharmacogenomic susceptibility to fluoropyrimidine toxicity and DPYD-guided dosing context. That is clinically relevant to the IEMbase 5-fluorouracil toxicity rows, but it is not the inherited DPYD deficiency disease target and does not model the thymine/uracil biochemical phenotype or neurodevelopmental presentation.

Concordance and completeness

Judgement: true local gap with pharmacogenetic overlap.

DisMech currently covers DPYD as a modifier of fluoropyrimidine toxicity, not as a monogenic inborn error of pyrimidine catabolism. The IEMbase disease has a distinct biochemical signature, clinical neurodevelopmental spectrum, and toxicity-risk implication that should not be collapsed into chemotherapy-induced diarrhea.

Curation actions

  • Leave IEMbase 159 unmapped for now.
  • Future curation should decide whether DPYD deficiency is represented as a metabolic disease entry, a pharmacogenetic/toxicity entry, or both with clear scope boundaries.
  • If curated, include WBC DPD activity, thymine/uracil accumulation, neurodevelopmental features, and severe fluoropyrimidine toxicity risk.