ABSTRACT
Recent studies of acute erythroleukemias have reaffirmed DiGuglielmo's syndrome (M6a, myeloblast-predominant) and disease (M6b, pronormoblast-predominant). M6c (mixed myeloblast/pronormoblast) has also been described. However, MDS is still defined according to the percentage of myeloblasts (% myeloblasts) without including the pronormoblast count. A 20-year retrospective study was performed to identify cases demonstrating >or=50% erythrocytic component and <30% calculated blasts (FAB exclusion criteria) without underlying cause (96 cases). Pronormoblast and myeloblast counts and other variables were analyzed as possible explanatory variables of the variations in survival. Considered alone, increasing % myeloblasts and/or percentage of pronormoblasts (% pronormoblasts) were significant predictors of decreasing survival. When all variables were considered as a multivariate group, the best fitting statistical model for predicting survival was a function of age, % pronormoblasts, IPSS cytopenias, platelet count, and percentage erythrocytic component. Of these, % pronormoblasts was by far the most significant. Nonappearance of % myeloblasts in this model is indicative of high correlations of this count with other variables.
Subject(s)
Erythroblasts , Leukemia, Erythroblastic, Acute/pathology , Models, Statistical , Myelodysplastic Syndromes/pathology , Age Factors , Disease-Free Survival , Erythroblasts/pathology , Erythrocyte Count , Erythrocytes/pathology , Granulocyte Precursor Cells/pathology , Humans , Leukemia, Erythroblastic, Acute/mortality , Male , Middle Aged , Multivariate Analysis , Myelodysplastic Syndromes/mortality , Platelet Count , Predictive Value of Tests , Prognosis , Retrospective StudiesABSTRACT
This article provides a review of the acute leukemias with updated basic and practical information. The main emphasis is on techniques used to arrive at the correct diagnosis. Although morphology and cytochemistry were the mainstays of diagnosis in the past, new developments in immunophenotyping, cytogenetics, molecular biology, and in vitro assays have improved the understanding of this disease dramatically and enable the identification of new entities with distinct clinicobiologic features.
