Skin vascular disease

Summary

Skin vascular disease (MONDO:0019293) is a disease (an umbrella term covering 20 Mondo subtypes). A subtype of skin disorder — broader associated-gene and molecular evidence is on the parent page (see Disease family below).

At a glance

• Umbrella term: 20 Mondo subtypes

Clinical features

No curated clinical features (Orphanet) for this disease.

Identifiers

Disease identifiers

Field	Value
Canonical name	skin vascular disease
Mondo ID	MONDO:0019293
MeSH	D017445
Orphanet	79379
DOID	DOID:9540
NCIT	C35254
SNOMED CT	11263005
UMLS	C0162819
MedGen	102473
MedDRA	10062171
Anatomy (UBERON)	UBERON:0002049, UBERON:0035549
Is cancer (heuristic)	no

Also known as: skin vascular disorder · superficial vasculature disease · vascular disease of the skin · vascular skin disease · vasculature skin disease

Disease family

This is a subtype of skin 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 › integumentary system disorder › skin disorder › skin vascular disease

Related subtypes (71): dermatitis, cutaneous mucinosis, skin neoplasm, pyoderma, chronic ulcer of skin, systemic sclerosis, sunburn, severe cutaneous adverse reaction, paronychia, Achenbach syndrome, erythema multiforme, erythematosquamous dermatosis, exanthem, facial dermatosis, hand dermatosis, keratosis, leg dermatosis, lichen disease, lipodystrophy, mongolian spot, reactive cutaneous fibrous lesion, rosacea, scalp dermatosis, sebaceous gland disorder, skin atrophy, skin sarcoidosis, sweat gland disorder, vesiculobullous skin disease, hyperglobulinemic purpura, ainhum, cheilitis glandularis, erythema palmare hereditarium, multiple benign circumferential skin creases on limbs, actinic prurigo, congenital lethal erythroderma, Parana hard-skin syndrome, Bazex-Dupre-Christol syndrome, nephrogenic systemic fibrosis, erosive pustular dermatosis of the scalp, pseudoxanthoma elasticum-like papillary dermal elastolysis, toxic dermatosis, oral erosive lichen, chronic actinic dermatitis, Jessner lymphocytic infiltration of the skin, acquired kinky hair syndrome, primary cutaneous plasmacytosis, cutaneous pseudolymphoma, corticosteroid-sensitive aseptic abscess syndrome, interstitial granulomatous dermatitis with arthritis, epidermal disease, skin pigmentation disorder, Wells syndrome, solar urticaria, pellagra, hereditary epidermal appendage anomaly, keratosis pilaris, dermis disorder, aquagenic pruritus, Boudhina Yedes Khiari syndrome, non-neoplastic nevus, cutaneous sclerosis, pityriasis rotunda, hematohidrosis, skin disorder caused by infection, livedoid vasculopathy, prurigo nodularis, granuloma faciale, sclerema neonatorum, hereditary skin disorder, hand-foot syndrome, Nicolau syndrome

Subtypes (20): Behcet disease, blue rubber bleb nevus, familial multiple nevi flammei, Sneddon syndrome, generalized essential telangiectasia, cutis marmorata telangiectatica congenita, angioedema, malignant atrophic papulosis, familial cutaneous telangiectasia and oropharyngeal predisposition cancer syndrome, Maffucci syndrome, Bockenheimer syndrome, calciphylaxis cutis, cutaneous collagenous vasculopathy, Wyburn-Mason syndrome, Cobb syndrome, chilblain lupus, angioma serpiginosum, pityriasis lichenoides, livedo reticularis, atrophic papulosis

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.