Factor 5 excess with spontaneous thrombosis

Summary

Factor 5 excess with spontaneous thrombosis (MONDO:0007594) is a disease. A subtype of inherited thrombophilia — 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	factor 5 excess with spontaneous thrombosis
Mondo ID	MONDO:0007594
MeSH	C565026
OMIM	134400
UMLS	C1851378
MedGen	341996
GARD	0024564
Is cancer (heuristic)	no

Also known as: Proaccelerin Excess

Disease family

This is a subtype of inherited thrombophilia. 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 › hematologic disorder › blood coagulation disease › thrombophilia › inherited thrombophilia › factor 5 excess with spontaneous thrombosis

Related subtypes (11): thrombophilia due to thrombin defect, thrombophilia due to activated protein C resistance, thrombophilia, X-linked, due to factor 9 defect, thrombophilia, familial, due to decreased release of tissue plasminogen activator, heparin cofactor 2 deficiency, hereditary thrombophilia due to congenital histidine-rich (poly-L) glycoprotein deficiency, hereditary antithrombin deficiency, thrombomodulin-related bleeding disorder, hereditary thrombophilia due to congenital protein S deficiency, hereditary thrombophilia due to congenital protein C deficiency, thrombophilia, X-linked, due to factor 8 defect

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.