SUMMARY Sixteen patients presented with B cell leukaemia (white cell count 26-269 x 109/1) which could not be classified as chronic lymphocytic (CLL), prolymphocytic leukaemia, or follicular lymphoma in leukaemic phase. Eleven patients (10 men, one woman) corresponded histologically to intermediate (INT) or mantle zone lymphoma, and five, with less well defined features, were designated small lymphocytic lymphoma with cleaved cells. The blood films showed a pleomorphic picture with lymphoid cells of predominantly medium size with nuclear irregularities and clefts. The membrane phenotype of the circulating cells showed strong immunoglobulin staining and reactivity with CD5 and FMC7 in all cases tested; CD1O was positive in six out of nine cases. The membrane phenotype of two of the five cases of small lymphocytic lymphoma was close to those of B-CLL and three resembled INT lymphoma. Bone marrow trephine biopsy specimens showed a diffuse pattern of infiltration in INT lymphoma. The median survival of these patients was less than two years, suggesting that a leukaemic presentation is associated with poor prognosis. By combining data from histology, membrane markers, and peripheral blood morphology, the leukaemic phase oftypical INT lymphoma can be defined in most cases.

BackgroundDespite bone marrow (BM) immunophenotyping by flow cytometry has progressively been recognized as an important tool for the diagnosis of myelodysplastic syndromes (MDS), the sparse knowledge about normal erythroid maturation and the lack of markers for erythroid characterization is a major shortcoming.MethodsHere, we analyzed the expression of CD43 and CD49d, two markers included in the diagnostic panel for B‐cell chronic lymphoproliferative disorders (B‐CLPD), in the CD34+ compartment of normal BM and along the normal and dysplastic erythroid maturation. For this, 13 normal BM aspirates and 18 BM aspirates from MDS patients were studied by flow cytometry.ResultsNormal BM presented a higher expression of CD43 and CD49d among CD34+ erythroid precursors, compared to CD34+ cells committed to the remaining hematopoietic cell lineages. CD43 expression progressively decreased along the normal erythroid maturation, whereas CD49d levels increased from Stage I to Stage II, were maintained in Stages II and III, and then decreased until the last stage of maturation. In MDS, the expression of CD43 and CD49d followed a similar pattern, but with decreased expression levels for both markers, observed in all erythroid maturation stages (P < 0.05).ConclusionsOur results point to the usefulness of CD43 and CD49d, two markers commonly present in B‐CLPD diagnosis panels, in the identification of dysplastic phenotypic features in the erythroid lineage. This allows a feasible and inexpensive way to identify patients who would benefit from a more extensive study to evaluate the presence of MDS, during the processing of suspected B‐CLPD samples. © 2019 International Clinical Cytometry Society

A 64-year-old woman is reported with Stage I (Rai) chronic lymphocytic leukaemia (CLL), in whom hypercalcemia developed when an increased proportion of prolymphocytic cells characterized a transformation of CLL in prolymphocytoid leukaemia (CLL/PL). Although hypercalcemia is more frequently found in T-cell leukaemia associated with human T lymphotropic lymphocyte type I, scattered reports indicate that patients with B-CLL can also be affected with this metabolic disturbance. The case described here, progressed with an indolent course of CLL for 26 months, when she was admitted with a very aggressive disease characterized by a high WBC count, splenomegaly and hypercalcemia. Despite an effort to achieve a clinical remission, she failed treatment and death was attributed to unresponsive hypercalcemia. The mechanism of hypercalcemia in such cases is unclear as no parathyroid adenoma or second malignant tumor was found ante mortem. This electrolytic disturbance would appear to be a direct consequence of the transforming leukaemia and a possible mechanism involving a secreted humoral factor that could lead to altered calcium metabolism.