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IEMbase 0110: ALAS2-related erythroid 5-aminolevulinate synthase deficiency

Scope

Field Value
IEMbase ID 110
Nosology 17.1.01.01
Gene ALAS2
External IDs OMIM:300751; ORPHA:75563
Generated mapping UNMAPPED
Candidate DisMech targets None for a disease entry; contextual mention in Myopathy_Lactic_Acidosis_and_Sideroblastic_Anemia.yaml differential diagnosis
Review date 2026-07-07

IEMbase phenotype signal

IEMbase represents this as ALAS2-related erythroid 5-aminolevulinate synthase deficiency, with alternate labels X-linked recessive sideroblastic anemia type 1 and XLSA. Treatability is marked unknown, though the treatment table lists hemin with low-level evidence.

The cached JSON has no characteristic biochemical rows. The non-characteristic clinical rows are dysmorphic erythrocytes, liver dysfunction, and increased bone-marrow sideroblasts, with adolescent/adult onset patterning.

DisMech phenotype coverage

There is no curated DisMech disease entry for ALAS2-related sideroblastic anemia. Inherited_Porphyria.yaml contains ALAS2-related X-linked protoporphyria, but that is the opposite ALAS2 direction: erythroid ALAS2 superactivity/gain of function with protoporphyrin accumulation and photosensitivity. It should not be reused for ALAS2 deficiency.

Myopathy_Lactic_Acidosis_and_Sideroblastic_Anemia.yaml mentions X-linked sideroblastic anemia only as a differential diagnosis for ALAS2-related pure sideroblastic anemia without mitochondrial myopathy. That is useful context, but it is not phenotype coverage for a standalone XLSA disease model.

Concordance and completeness

Judgement: true unmapped disease gap.

The IEMbase record is sparse but points to a distinct hematologic heme-synthesis disorder centered on ring sideroblasts and erythroid morphology, not a porphyria. DisMech currently has related heme and sideroblastic-anemia context, but no ALAS2-deficiency entry that could be assessed for concordant phenotypes.

Curation actions

  • Do not map this to ALAS2-related X-linked protoporphyria.
  • Consider a future standalone X-linked sideroblastic anemia / ALAS2 deficiency entry if sideroblastic anemia scope is expanded.
  • Reuse the MLASA differential-diagnosis note only as context, not as a canonical target.