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Acute myeloid leukemia (acute myeloblastic leukemia)
Last reviewed: 07.07.2025
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[ Symptoms and diagnosis of acute myeloid leukemia
Symptoms include fatigue, pallor, fever, infections, bleeding, easy bruising; symptoms of leukemic infiltration are present in only 5% of patients (often as cutaneous manifestations). Diagnosis requires examination of peripheral blood smear and bone marrow. Treatment includes induction chemotherapy to achieve remission and post-remission therapy (with or without stem cell transplantation) to prevent relapse.
The incidence of acute myeloid leukemia increases with age and it is the most common leukemia in adults with a median age of onset of 50 years. Acute myeloid leukemia may develop as a secondary cancer after chemotherapy or radiation therapy for various types of cancer.
Acute myeloid leukemia includes a number of subtypes that differ from each other in morphology, immunophenotype, and cytochemistry. Based on the predominant cell type, 5 classes of acute myeloid leukemia have been described: myeloid, myeloid-monocytic, monocytic, erythroid, and megakaryocytic.
Acute promyelocytic leukemia is a particularly important subtype, accounting for 10-15% of all cases of acute myeloid leukemia. It occurs in the youngest group of patients (median age 31 years) and is predominantly found in a specific ethnic group (Hispanics). This variant often presents with bleeding disorders.
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Treatment of acute myeloid leukemia
The goal of initial therapy for acute myeloid leukemia is to achieve remission, and unlike acute lymphoblastic leukemia, response in acute myeloid leukemia is achieved with fewer drugs. The basic remission-induction regimen consists of continuous intravenous infusion of cytarabine or high-dose cytarabine for 5 to 7 days, during which time daunorubicin or idarubicin is given intravenously for 3 days. Some regimens include 6-thioguanine, etoposide, vincristine, and prednisolone, but the efficacy of these regimens is unclear. Treatment usually results in marked myelosuppression, infection, and bleeding; bone marrow recovery usually takes a long time. During this period, careful prophylactic and supportive therapy is vital.
In acute promyelocytic leukemia (APL) and some other variants of acute myeloid leukemia, disseminated intravascular coagulation (DIC) may be present at diagnosis, aggravated by the release of procoagulants by leukemic cells. In acute promyelocytic leukemia with the t(15;17) translocation, the use of AT-RA (trans-retinoic acid) promotes blast cell differentiation and correction of disseminated intravascular coagulation within 2-5 days; in combination with daunorubicin or idarubicin, this regimen can induce remission in 80-90% of patients, with long-term survival of 65-70%. Arsenic trioxide is also effective in acute promyelocytic leukemia.
Once remission is achieved, an intensification phase with these or other drugs is performed; high-dose cytarabine regimens may prolong remission, especially in patients under 60 years of age. Central nervous system prophylaxis is not usually performed, since central nervous system involvement is a rare complication with adequate systemic therapy. No benefit has been demonstrated from maintenance therapy in intensively treated patients, but it may be useful in other situations. Extramedullary involvement as an isolated relapse is rare.
Prognosis for acute myeloid leukemia
The remission induction rate ranges from 50 to 85%. Long-term disease-free survival is achieved in 20-40% of all patients and in 40-50% of young patients whose treatment included stem cell transplantation.
Prognostic factors help determine the treatment protocol and its intensity; patients with clearly unfavorable prognostic factors usually receive more intensive treatment because the potential benefit of such treatment presumably justifies the higher toxicity of the protocol. The most important prognostic factor is the karyotype of leukemic cells; unfavorable karyotypes are t(15;17), t(8;21), inv16(p13;q22). Other unfavorable prognostic factors are older age, history of myelodysplastic phase, secondary leukemia, high leukocytosis, absence of Auer rods. Using FAB or WHO classifications alone does not predict response to treatment.