Aplastic anaemia and paroxysmal nocturnal haemoglobinuria: a study of the GPI-anchored proteins on human platelets
| Autor: | A Griscelli-Bennaceur, F Sigaux, Eliane Gluckman, C. Menier, E D Carosella, Thi Thanh Vu, M L Scrobohaci, Gérard Socié |
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| Rok vydání: | 1996 |
| Předmět: |
Blood Platelets
Erythrocytes Glycosylphosphatidylinositols Neutrophils Anemia CD58 Hemoglobinuria Paroxysmal CD59 Biology Monocytes Antigen hemic and lymphatic diseases medicine Humans Platelet Aplastic anemia Monocyte Anemia Aplastic Hematology Flow Cytometry medicine.disease carbohydrates (lipids) medicine.anatomical_structure Immunology lipids (amino acids peptides and proteins) Hemoglobinuria |
| Zdroj: | British Journal of Haematology. 93:586-589 |
| ISSN: | 1365-2141 0007-1048 |
| DOI: | 10.1046/j.1365-2141.1996.d01-1684.x |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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