Red Cells with Paroxysmal Nocturnal Hemoglobinuria-phenotype in Patients with Acute Leukemia.

Autor: Meletis, John, Terpos, Evangelos, Samarkos, Michalis, Meletis, Christos, Apostolidou, Effie, Komninaka, Veroniki, Anargyrou, Konstantinos, Korovesis, Konstantinos, Mavrogianni, Despina, Variami, Eleni, Viniou, Nora, Konstantopoulos, Konstantinos
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Zdroj: Hematology; Mar2002, Vol. 7 Issue 2, p69-74, 6p
Abstrakt: CD55 and CD59 are complement regulatory proteins that are linked to the cell membrane via a glycosyl-phosphatidylinositol anchor. They are reduced mainly in paroxysmal nocturnal hemoglobinuria (PNH) and in other hematological disorders. However, there are very few reports in the literature concerning their expression in patients with acute leukemias (AL). We studied the CD55 and CD59 expression in 88 newly diagnosed patients with AL [65 with acute non-lymphoblastic leukemia (ANLL) and 23 with acute lymphoblastic leukemia (ALL)] using the sephacryl gel test, the Ham and sucrose lysis tests and we compared the results with patients' clinical data and disease course. Eight patients with PNH were also studied as controls. Red cell populations deficient in both CD55 and CD59 were detected in 23% of ANLL patients (especially of M 0 , M 2 and M 6 FAB subtypes), 13% of ALL and in all PNH patients. CD55-deficient erythrocytes were found in 6 ANLL patients while the expression of CD59 was decreased in only 3 patients with ANLL. No ALL patient had an isolated deficiency of these antigens. There was no correlation between the existence of CD55 and/or CD59 deficiency and the percentage of bone marrow infiltration, karyotype or response to treatment. However no patient with M 3 , M 5 , M 7 subtype of ANLL and mature B- or T-cell ALL showed a reduced expression of both antigens. The deficient populations showed no alteration after chemotherapy treatment or during disease course. This study provides evidence about the lower expression of CD55 and CD59 in some AL patients and the correlation with their clinical data. The possible mechanisms and the significance of this phenotype are discussed. [ABSTRACT FROM AUTHOR]
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