Letter to editor.
Aida Habib1,
Corinne Kunzelmann2,
Wael Shamseddeen3,
Fatiha Zobairi2,
Jean-Marie Freyssinet2,
Ali Taher3
1 Department of Biochemistry
3 Internal Medicine, American University of Beirut, Lebanon; The Chronic Care Center, Hazmieh, Lebanon;
2 INSERM, U770, Université Paris-Sud, Le Kremlin-Bicêtre,
France; Université Louis Pasteur, Faculté de Médecine, Institut
d’Hématologie et d’Immunologie, Strasbourg, France
Correspondence: Aida Habib, Department of
Biochemistry, American University of Beirut, PO Box 11-236 Beirut,
Lebanon. Phone: international +961.135000 ext. 4882. Fax: international
+961.1370814. E-mail:ah31@aub.edu.lb
Patients with β-thalassemia intermedia (β TI) are completely asymptomatic until adult life, experiencing only mild anemia, maintaining hemoglobin levels between 7 and 10 g/dL, and require only occasional blood transfusions, if any. MPs are shed submicrometric plasma membrane fragments (~0.1–1 µm) harboring negatively-charged procoagulant phosphatidylserine (PS) in their extracellular membrane leaflet. They mainly derive from apoptotic or activated cells, and generally present a procoagulant potential.1 Increased levels of circulating MPs were described in many disorders with major vascular and thrombotic symptoms.2