Glaucoma with elevated episcleral venous pressure

Summary

Glaucoma with elevated episcleral venous pressure (MONDO:0007663) is a disease. A subtype of hereditary glaucoma — 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	glaucoma with elevated episcleral venous pressure
Mondo ID	MONDO:0007663
MeSH	C564235
OMIM	137700
UMLS	C1842030
MedGen	333975
GARD	0024569
Is cancer (heuristic)	no

Also known as: glaucoma with elevated episcleral venous pressure

Disease family

This is a subtype of hereditary glaucoma. 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: disease › human disease › disease by etiologic mechanism › disease of genetic or genomic mechanism › hereditary disease › hereditary glaucoma › glaucoma with elevated episcleral venous pressure

Related subtypes (11): exfoliation syndrome, glaucoma 1, open angle, P, iris hypoplasia with glaucoma, glaucoma 1, open angle, O, glaucoma secondary to spherophakia/ectopia lentis and megalocornea, congenital glaucoma, juvenile open angle glaucoma, anterior segment dysgenesis 3, hereditary glaucoma, primary closed-angle, OPTN-related open angle glaucoma, TEK-related primary glaucoma

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.