Foix-Alajouanine syndrome

Summary

Foix-Alajouanine syndrome (MONDO:0019196) is a disease. A subtype of arteriovenous hemangioma/malformation — broader associated-gene and molecular evidence is on the parent page (see Disease family below).

Clinical features

No curated clinical features (Orphanet) for this disease.

Identifiers

Disease identifiers

Field	Value
Canonical name	Foix-Alajouanine syndrome
Mondo ID	MONDO:0019196
Orphanet	79093
ICD-11	937824238
SNOMED CT	230379007
UMLS	C0472347
MedGen	141629
GARD	0004163
Is cancer (heuristic)	no

Also known as: angiodysgenetic necrotizing myelopathy · familial osteosclerosis with abnormalities of the nervous system and meninges · Subacute angiohypertrophic myelomalacia · Subacute ascending necrotizing myelitis · Subacute necrotizing myelitis

Disease family

This is a subtype of arteriovenous hemangioma/malformation. Genetic, therapeutic, and trial evidence is largely curated at the broader-term level — see the parent page for the associated-gene cohort and molecular evidence.

Classification path: human disease › disease by etiologic mechanism › cancer or benign tumor › neoplastic disease or syndrome › neoplasm › benign neoplasm › cardiovascular organ benign neoplasm › benign blood vessel neoplasm › hemangioma › arteriovenous hemangioma/malformation › Foix-Alajouanine syndrome

Related subtypes (6): arteriovenous malformations of the brain, vein of Galen aneurysm, cerebrofacial arteriovenous metameric syndrome, facial arteriovenous malformation, Cobb syndrome, dural sinus malformation

Genetics & variants

GWAS landscape

No GWAS associations recorded — common-variant (GWAS) studies don’t cover this disease (typical for Mendelian / rare diseases). See the curated gene cohort and Mendelian overlap below.

Variant details and genetic-evidence tiers

No tiered GWAS variants or ClinVar records for this disease.

Genes & proteins

No associated-gene cohort resolved for this disease. Atlas builds the molecular and therapeutic sections — associated genes, protein families, druggability, pathways, interactions, and drug associations — by aggregating over a disease’s associated genes (resolved via GWAS / GenCC / ClinVar / CIViC), and none resolved here. This is expected for antibody-mediated, autoimmune, or otherwise non-gene-defined conditions; the curated evidence for this disease is its clinical features, GWAS susceptibility, and clinical trials (above).

Function

No pathway enrichment — requires an associated-gene cohort.

Therapeutics

No druggable-target or therapeutic data for this disease’s cohort.

Clinical trials & evidence

Clinical trials

Clinical trials: 0.