Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired clonal disorder 
characterized by a decrease or absence of glycosylphosphatidylinositol 
(GPI)-anchored molecules such as CD55 and CD59 from the surface of affected 
cells, resulting in intravascular hemolysis, cytopenia, and venous thrombosis. A 
PNH-like phenotype has been detected in various hematological disorders, mainly 
in aplastic anemia and myelodysplastic syndromes, but also in 
lymphoproliferative syndromes (LPSs). To the best of our knowledge, CD55- or 
CD59-deficient red cells have not been detected in plasma cell dyscrasias 
(PCDs). The aim of this study was the detection of CD55- and/or CD59-deficient 
red cell populations in patients with PCD. Seventy-seven patients were 
evaluated; 62 with multiple myeloma (MM), 7 with Waldenstrom macroglobulinemia 
(WM), 6 with monoclonal gammopathy of undetermined significance (MGUS), and 2 
with heavy chain disease (HCD). The sephacryl gel microtyping system was 
applied; Ham and sucrose lysis tests were also performed on all samples with 
CD55- or CD59-negative populations. Red cells deficient in both molecules were 
detected in 10 (12.9%) of 77 patients with PCD: 2 (28.6%) of 7 with WM, 1 
(16.6%) of 6 with MGUS, 6 (9.6%) of 62 with MM, and 1 of 2 patients with HCD. 
Isolated CD55 deficiency was found in 28.5% of all PCD patients, whereas 
isolated CD59 deficiency was not observed in any patients. These findings 
illustrate the existence of the PNH phenotype in the red cells of patients with 
PCD; further investigation is needed into the mechanisms and significance of 
this phenotype.