The mechanisms of hemorrhage in acute leukemias (AL) are related to the direct effect of leukemic cells infiltrating the vascular walls and affecting the blood coagulation, causing damage to the megakaryo cyte system, changes in liver function, and subsequent decrease in the synthesis of some blood coagulation factors, increase in blood fibrinolytic activity, and the disseminated intravascular coagulation 1-4 (DIC). The effects of antileukemic agents on the blood coagula tion system in patients with leukemia represent sepa rate problems. Hemorrhagic diathesis is one of the most severe complications of AL and is often the direct cause of death. The basic difference between the particular forms lies in the cytologic type of leu kocytes undergoing the leukemic proliferation. There are, moreover, some differences in the clinical evolu tion and the response to therapy between AL of the myeloblastic and the lymphoblastic types. The mor phologic classification of AL is still a subject of dis cussion and in that regard the French-AmericanBritish (FAB) and World Health Organization (WHO) classifications should be mentioned. The FAB classi fication divides AL into six types of acute nonlymphocytic leukemias, that is, acute myeloblastic leukemias (AML), designed as M 1 to M 6 , and three types of acute lymphoblastic leukemia (ALL) corresponding to L 1 to L 3 . 5 However, currently several other AL classifications have been proposed and difficulties of reproducing the morphologic classification at dif ferent centers and the uncertainty about the impor tance of such classifications for prognosis is still un resolved. 6

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