Abstract
Intracellular lysozyme (muramidase) activity was measured in leukemic blasts and mature neutrophilic granulocytes from 20 patients with acute myeloblastic and myelomonocytic leukemia and in 11 patients with acute lymphoblastic leukemia after differential centrifugation of cells in Ficoll and extraction of lysozyme with n-butanol. Considerable abnormalities in cellular lysozyme activity were found both in qualitative and quantitative terms. In contrast to normal myeloblasts, leukemic blasts of the myeloid series contained lysozyme in a considerable number of cases. Although no clear-cut distinction was seen, those patients with positive blast lysozyme reactivity tended to have the highest plasma lysozyme levels, whereas no good correlation was found between morphologic differentiation along myeloblastic or monocytoblastic lines of blasts and lysozyme reactivity. Calculations of the magnitude of lysozyme production in acute leukemias with high plasma lysozyme concentration was compatible with the hypothesis that in these cases lysozyme must be secreted by intact blasts and that, consequently, plasma lysozyme activity reflects the total leukemic cell mass. In mature neutrophilic granulocytes from patients with acute myeloblastic and myelomonocytic leukemia in relapse, the mean lysozyme activity was significantly decreased, although a great deal of variation was found. In remission, neutrophil lysozyme activity seemed to increase; among several possibilities this might be a reflection of different clones being operative in relapse and remission. In acute lymphoblastic leukemia, lysozyme activity in neutrophils was constantly low in relapse and increased to normal following induction of remission, which may be the main explanation of the low plasma lysozyme activity found in this type of acute leukemia. It is unexplained and puzzling why intraneutrophil lysozyme activity is low in a leukemic type where the myeloid cells are not believed to be primarily leukemic; one possible reason might be an effect of cell-to-cell interaction with the leukemic cell population.
