Aplastic anaemia and paroxysmal nocturnal haemoglobinuria: a study of the GPI-anchored proteins on human platelets.
Twenty-six consecutive patients with acquired aplastic anaemia (AA) and nine patients with de novo paroxysmal nocturnal haemoglobinuria (PNH) were included in this study. In these 35 patients a GPI-anchored molecule defect at the platelet surface was investigated by flow-cytometry. Platelets from eight out of the nine patients with de novo PNH were found to be deficient for the GPI-anchored molecule CD55, CD58 and CD59. We also detected a GPI-anchored molecule defect on monocytes, granulocytes, and erythrocytes in all patients with de novo PNH. Among the 26 AA patients, a GPI defect was detected on platelets in five patients. Interestingly, these five patients were also found to have a GPI-anchored molecule defect on erythrocytes, whereas in 10 patients the GPI-anchored molecule defect was only detected on monocyte and polymorphonuclear (PMN) cells.
Vu
T
T
Laboratoire Central d'Hématologie, Hôpital Saint-Louis, Paris, France.
Griscelli-Bennaceur
A
A
Gluckman
E
E
Sigaux
F
F
Carosella
E D
ED
Menier
C
C
Scrobohaci
M L
ML
Socié
G
G
D000741:Anemia, Aplastic / Q000097:blood*; D001792:Blood Platelets / Q000378:metabolism*; D004912:Erythrocytes / Q000378:metabolism; D005434:Flow Cytometry; D017261:Glycosylphosphatidylinositols / Q000378:metabolism*; D006457:Hemoglobinuria, Paroxysmal / Q000097:blood*; D006801:Humans; D009000:Monocytes / Q000378:metabolism; D009504:Neutrophils / Q000378:metabolism
D017261:Glycosylphosphatidylinositols