Hypertrichosis of eyelid

Summary

Hypertrichosis of eyelid (MONDO:0001334) is a disease. A subtype of eyelid disorder — 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	hypertrichosis of eyelid
Mondo ID	MONDO:0001334
DOID	DOID:11669
ICD-10-CM	H02.86
ICD-11	1623148241
SNOMED CT	79830009
UMLS	C0155213
MedGen	509853
Anatomy (UBERON)	UBERON:0001711
Is cancer (heuristic)	no

Also known as: eyelid hypertrichosis (disease) · hypertrichosis (disease) of eyelid

Disease family

This is a subtype of eyelid disorder. 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 body system or component › disorder of orbital region › eye adnexa disorder › eyelid disorder › hypertrichosis of eyelid

Related subtypes (19): eyelid degenerative disorder, blepharophimosis, hypotrichosis of eyelid, entropion, lagophthalmos, stenosis of lacrimal punctum, stenosis of lacrimal passage, ectropion, eyelid neoplasm, blepharochalasis, blepharitis, eyelid hypopigmentation, telecanthus, cryptophthalmia, epiblepharon, congenital eyelid retraction, herpes zoster with dermatitis of eyelid, eyelid seborrheic keratosis, dermatosis of eyelid

Subtypes (1): Barber-Say syndrome

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.