RESUMEN
We present the clinical and laboratory features of 2 patients with B prolymphocytic leukemia. Both are females of the fifth and seventh decade of life. One had the classical clinical picture of massive splenomegaly and a high white cell count, with characteristic prolymphocytes, and the other was asymptomatic, with a low white cell count. The cells were positive to B cell lineage reagents with strong surface immunoglobuline (Ig) and unreactive to T cell antibodies. Analysis of Ig genes at the DNA level demonstrated that both cases had heavy-chain gene rearrangements, confirming the B-cell origin. These are the first patients of prolymphocytic leukemia described in Chile.
Asunto(s)
Leucemia Prolinfocítica , Anciano , Sondas de ADN , Femenino , Marcadores Genéticos , Humanos , Inmunofenotipificación , Leucemia Prolinfocítica/sangre , Leucemia Prolinfocítica/genética , Leucemia Prolinfocítica/inmunología , Persona de Mediana EdadRESUMEN
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.