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Blood, Vol. 93 No. 10 (May 15), 1999:
pp. 3451-3456
Elevated Levels of Circulating Procoagulant Microparticles in
Patients With Paroxysmal Nocturnal Hemoglobinuria and Aplastic
Anemia
Bénédicte Hugel,
Gérard Socié,
Thi Vu,
Florence Toti,
Eliane Gluckman,
Jean-Marie Freyssinet, and
Marie-Lorraine Scrobohaci
From the Institut d'Hématologie et d'Immunologie,
Faculté de Médecine, Université Louis Pasteur,
Strasbourg, France; the Laboratoire Central d'Hématologie,
Hôpital Saint-Louis, Paris, France; and the Unité de
Recherche sur la Biologie des Cellules Souches et Service de Greffe de
Moëlle, Hôpital Saint-Louis, Paris, France.
Paroxysmal nocturnal hemoglobinuria (PNH), frequently occurring
during suppressed hematopoiesis including aplastic anemia (AA), is a
clonal disorder associated with an increased incidence of thrombotic
events. Complement-mediated hemolysis, impairment of the fibrinolytic
system, or platelet activation are thought to be responsible for the
associated thrombotic risk. We investigated here the elevation of
membrane-derived procoagulant microparticles in the blood flow of such
patients. Elevated levels of circulating microparticles were in fact
detected in both de novo PNH patients and AA subjects with a PNH clone,
but not in those with AA without a PNH clone. The cellular origin of
the microparticles was determined in PNH samples; most stemmed from
platelets. Glycophorin A+ particles were rarely detected.
Therefore, platelet activation, resulting in the dissemination of
procoagulant phospholipids in the blood flow, could be one of the main
causes for the elevated thrombotic risk associated with PNH. These
observations suggest that shed membrane particles can be considered a
valuable biological parameter for the assessment of possible thrombotic
complications in patients with PNH.
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