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IEMbase 0440: TUFM-related mitochondrial elongation factor Tu deficiency

Scope

Field Value
IEMbase ID 440
Nosology 10.3.05.01
Gene TUFM
External IDs OMIM:610678; ORPHA:254925
Generated mapping UNMAPPED; low candidate Mitochondrial_Trifunctional_Protein_Deficiency.yaml
Candidate DisMech targets No exact local target
Review date 2026-07-07

IEMbase phenotype signal

IEMbase represents TUFM-related mitochondrial elongation factor Tu deficiency, also called combined oxidative phosphorylation defect 4 (COXPD4). It records autosomal recessive inheritance. Biochemical rows include decreased respiratory chain activity in fibroblasts and markedly increased plasma lactate. Clinical rows include neonatal, infantile, or childhood encephalopathy, leukodystrophy, and death. There are no treatment rows.

DisMech phenotype coverage

There is no exact local DisMech target for TUFM/COXPD4. No local TUFM- or COXPD4-specific disease file was identified.

The generated Mitochondrial_Trifunctional_Protein_Deficiency.yaml candidate is a false positive. Local mitochondrial trifunctional protein deficiency is a HADHA/HADHB long-chain fatty-acid oxidation disorder with long-chain hydroxyacylcarnitines, hypoketotic hypoglycemia, cardiomyopathy, rhabdomyolysis, liver disease, and neuropathy. It does not represent TUFM mitochondrial translation dysfunction or COXPD4.

Concordance and completeness

Judgement: true TUFM/COXPD4 local gap; reject mitochondrial trifunctional protein deficiency as an exact mapping.

The generated candidate shares mitochondrial wording but differs in gene, proximal mechanism, pathway, and expected biomarker profile.

Curation actions

  • Keep this record unmapped until a TUFM mitochondrial elongation factor Tu deficiency or COXPD4 target exists.
  • Do not map to Mitochondrial_Trifunctional_Protein_Deficiency.yaml.
  • If curated, include TUFM, autosomal recessive inheritance, mitochondrial translation elongation-factor dysfunction, combined OXPHOS deficiency, decreased fibroblast respiratory-chain activity, severe lactic acidosis, encephalopathy, leukodystrophy, and early death.