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Related Experiment Video

Updated: Jun 2, 2026

Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets

Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets

Published on: November 29, 2024

Quebec platelet disorder.

Catherine P M Hayward¹, Georges E Rivard

¹Departments of Pathology and Molecular Medicine, Michael G DeGroote Centre for Learning, McMaster University, 1280 Main Street West, Hamilton, Ontario, Canada. haywrdc@mcmaster.ca

Expert Review of Hematology

|April 19, 2011

Summary

This summary is machine-generated.

Quebec platelet disorder (QPD) is a bleeding disorder caused by a PLAU gene mutation. This defect leads to overactive platelets, impacting fibrinolysis and causing bleeding issues.

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Last Updated: Jun 2, 2026

Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets

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Published on: November 29, 2024

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Published on: January 31, 2018

Area of Science:

Hematology
Genetics
Molecular Biology

Background:

Quebec platelet disorder (QPD) is an autosomal dominant bleeding disorder.
It is characterized by a gain-of-function defect in fibrinolysis.
Recent advances have elucidated its genetic cause and pathogenesis.

Purpose of the Study:

To summarize expert opinions on QPD features.
To review recent advances in understanding QPD pathogenesis.
To highlight the genetic cause of QPD.

Main Methods:

Review of recent scientific literature.
Expert opinion synthesis.
Analysis of genetic and molecular mechanisms.

Main Results:

QPD is caused by a copy number variation mutation in the PLAU gene.
This mutation leads to urokinase plasminogen activator (uPA) overexpression during megakaryopoiesis.
Results in profibrinolytic platelets with active uPA in α-granules.

Conclusions:

QPD is the first bleeding disorder linked to a PLAU mutation.
It is also the first identified bleeding disorder resulting from a gene copy number mutation.
Understanding the molecular defect provides insights into fibrinolysis regulation.