Piedra

Summary

Piedra (MONDO:0000253) is a disease. A subtype of disorder of pilosebaceous unit — 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	piedra
Mondo ID	MONDO:0000253
MeSH	D010854
SNOMED CT	402135006
UMLS	C0031898
MedGen	45923
Anatomy (UBERON)	UBERON:0002074
Is cancer (heuristic)	no

Also known as: black piedra · black Piedras · hair shaft fungal infectious disease · piedra, black · piedra, White · Piedras · Piedras, black · Piedras, White · steroid-modified tinea infection · White piedra · White Piedras

Disease family

This is a subtype of disorder of pilosebaceous unit. 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 › disorder of pilosebaceous unit › piedra

Related subtypes (8): hypotrichosis, hair follicle neoplasm, folliculitis, sebaceous gland disorder, hair anomaly, hypertrichosis, Katsantoni-Papadakou-Lagoyanni syndrome, trichostasis spinulosa

Subtypes (3): endothrix infectious disease, white piedra, black piedra

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.