which require rapid therapeutic intervention, from benign hematologic disorders. This article provides a general overview of the acute leukemias and highlights the underlying pathophysiology, clinical prentation,chemicals and chemotherapeutic agents also increas the risk for the development of leukemia later in life. Potential agents include benzene, petroleum products, pesticides, hair dyes, tobacco smoking, and ionizing radi-
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The Acute Leukemias
Prabhas Mittal, MD
三顾茅庐教学设计Kenneth R. Meehan, MD
DIFFERENTIAL DIAGNOSIS
The differential diagnosis of acute leukemia in-cludes other conditions in which patients prent with
an elevated leukocyte count, anemia, and thrombocy-topenia. The include leukemoid reactions and deep-ated infections, which may be associated with an ele-vated leukocyte count and a left shift. Infection with Epstein-Barr virus may cau vere lymphocytosis with atypical lymphocytes prent on peripheral smear. The diagnosis can be made easily by the abnce of blasts in the conditions.竹笋鸡
Patients with acute leukemia may also prent with low leukocyte counts together with anemia and throm-bocytopenia. The differential diagnosis of this pren-tation includes the primary bone marrow dias of myelodysplastic syndrome and aplastic anemia. Infil-tration of the bone marrow by other neoplasms, in-cluding solid tumors and hematologic malignancies, may also prent with anemia and/or thrombocytope-nia. Immature forms of leukocytes rembling blasts may be en in vere megaloblastic anemia due to
folate and vitamin B
12deficiency. The work-up shown空想主义
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in Table 5 will assist in differentiating the dias from an acute leukemia.
TREATMENT OF ACUTE LEUKEMIAS
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Acute leukemia is a fatal dia if untreated, with a median survival of 3 months or less. The therapy for acute leukemias, both AML and ALL, is parated into 2 phas: the induction pha and the postremission pha. Induction therapy consists of multiple drugs ad-ministered over a period of days to weeks, with the intent of eradicating all blasts from the bone marrow and peripheral blood. Postremission therapy is initiat-ed approximately 4 to 8 weeks after induction chemo-therapy has ended, once the patient has recovered from the side effects of therapy and their blood counts have begun to normalize.
Although the majority of patients with AML or ALL will achieve remission following induction therapy, a high relap rate exists. As a result, postremission ther-apy is administered with the intention of preventing relap. The medications and durations of the postre-mission pha of therapy differ greatly between AML and ALL, as outlined below. The major caus of mor-bidity and mortality during induction and postremis-sion therapy are infection and hemorrhage. Cooper-ative group clinical trials are continuously trying to optimize the induction and postremission treatments of both AML and ALL with the hope of improving sur-vival rates.
Induction Therapy for AML
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Induction chemotherapy for AML consists of a com-bination of a cytosine analog (cytarabine, ara-C) and an anthracycline (idarubicin or daunorubicin). The stan-dard regimen includes 7 days of continuous infusion of cytarabine plus 3 daily infusions of idarubicin or daunorubicin, often called the “7 & 3” regimen. The complete respon (CR) rate is 50% to 70%.10,11Patients with aggressive types of AML, such as condary AML or
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Figure 1.Photomicrograph of a myeloblast showing 3 nucle-oli and an Auer rod within the cytoplasm.Figure 2. Photomicrograph of lymphoblasts with multiple nucleoli and prominent vacuoles within the cytoplasm.
