BACKGROUND: Paroxysmal nocturnal hemoglobinuria (PNH) results due to decrease or absence of glycosylphosphatidylinositol-anchored (GPI) molecules, such as CD55 and CD59, from the surface of the affected cells. PNH-phenotype has been described in various hematological disorders, mainly aplastic anemia and myelodysplastic syndromes; recently it has been reported in patients with lymphoproliferative syndromes and multiple myeloma (MM). MATERIALS AND METHODS: We evaluated the presence of CD55 negative and/or CD59 negative red blood cell (RBC) populations in newly diagnosed treatment naive-54 chronic lymphocytic leukemia (CLL) and 29 MM patients by flow cytometry. RESULTS: PNH-phenotype was not reported in any patient; however, RBC populations deficient in CD55 were detected in 16.66% (9/54) CLL and 6.89% (2/29) MM patients. Clinical presentation or the hematological parameters did not show any relationship with the presence of CD55 deficient RBC population. CONCLUSION: Our study showed absence of PNH-phenotype in patients with CLL and MM; however, isolated CD55 deficient RBC were identified in both CLL and MM. Larger prospective studies by other centers, including simultaneous analysis of granulocytes for the presence of PNH-phenotype, are needed to corroborate these findings and to work out the mechanisms and the significance of the existence of this phenotype in these patients.
BACKGROUND:Paroxysmal nocturnal hemoglobinuria (PNH) results due to decrease or absence of glycosylphosphatidylinositol-anchored (GPI) molecules, such as CD55 and CD59, from the surface of the affected cells. PNH-phenotype has been described in various hematological disorders, mainly aplastic anemia and myelodysplastic syndromes; recently it has been reported in patients with lymphoproliferative syndromes and multiple myeloma (MM). MATERIALS AND METHODS: We evaluated the presence of CD55 negative and/or CD59 negative red blood cell (RBC) populations in newly diagnosed treatment naive-54 chronic lymphocytic leukemia (CLL) and 29 MM patients by flow cytometry. RESULTS: PNH-phenotype was not reported in any patient; however, RBC populations deficient in CD55 were detected in 16.66% (9/54) CLL and 6.89% (2/29) MM patients. Clinical presentation or the hematological parameters did not show any relationship with the presence of CD55 deficient RBC population. CONCLUSION: Our study showed absence of PNH-phenotype in patients with CLL and MM; however, isolated CD55 deficient RBC were identified in both CLL and MM. Larger prospective studies by other centers, including simultaneous analysis of granulocytes for the presence of PNH-phenotype, are needed to corroborate these findings and to work out the mechanisms and the significance of the existence of this phenotype in these patients.