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Acute myeloid leukemia (acute myeloblastic leukemia)

 
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Last reviewed: 24.06.2018
 
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In acute myelogenous leukemia, malignant transformation and uncontrolled proliferation of anomalously differentiated, long-lived precursor cells of the myeloid series causes the appearance of blast cells in circulating blood, replacement of normal bone marrow with malignant cells.

trusted-source[1], [2], [3], [4], [5], [6], [7], [8], [9], [10], [11]

Symptoms and Diagnosis of Acute Myeloblastic Leukemia

Symptoms include fatigue, pallor, fever, infection, bleeding, easily formed subcutaneous hemorrhage; the symptoms of leukemic infiltration are present only in 5% of patients (often as skin manifestations). To establish the diagnosis, it is necessary to study the smear of peripheral blood 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 myelogenous leukemia increases with age, this is the most common leukemia in adults with a median age of development of the disease, equal to 50 years. Acute myeloblastic leukemia can develop as a secondary cancer after chemotherapy or radiation therapy for various types of cancer.

Acute myeloblastic leukemia includes a number of subtypes that differ in morphology, immunophenotype, and cytochemistry. Based on the prevailing cell type, 5 classes of acute myeloblastic leukemia are described: myeloid, myeloid monocytic, monocytic, erythroid and megakaryocytic.

Acute promyelocytic leukemia is a particularly important subtype and accounts for 10-15% of all cases of acute myeloblastic leukemia. It occurs in the youngest group of patients (median age 31 years) and predominantly in a particular ethnic group (Hispanics). This variant often debuts with blood clotting disorders.

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Treatment of acute myeloblastic leukemia

The goal of initial therapy for acute myeloblastic leukemia is to achieve remission, and, in contrast to acute lymphoblastic leukemia, in acute myelogenous leukemia the response is achieved with fewer drugs. The baseline remission induction mode includes a prolonged intravenous infusion of cytarabine or cytarabine in high doses for 5-7 days; during this time for 3 days intravenously injected daunorubicin or idarubicin. Some regimens include 6-thioguanine, etoposide, vincristine and prednisolone, but the effectiveness of these treatment regimens is unclear. Treatment usually leads to severe myelosuppression, infectious complications and bleeding; until the restoration of bone marrow usually takes a long time. During this period, careful preventive and maintenance therapy is vital.

With acute promyelocytic leukemia (APL) and some other variants of acute myelogenous leukemia, disseminated intravascular coagulation (DVS) may be present at the time of diagnosis, aggravated by the release of procoagulants by leukemia cells. In acute promyelocytic leukemia with translocation t (15; 17), the use of AT-PA (transretinic acid) promotes the differentiation of blast cells 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 a long-term survival rate of 65-70%. Arsenic trioxide is also effective in acute promyelocytic leukemia.

After reaching remission, the phase of intensification with these or other drugs is carried out; regimes using cytarabine in high doses can increase the duration of remission, especially in patients under 60 years of age. Prevention of central nervous system damage is usually not carried out, since with sufficient systemic therapy, central nervous system damage is a rare complication. Patients receiving intensive treatment did not demonstrate the benefits of maintenance therapy, but in other situations it can be useful. Extramedullary lesions as an isolated relapse are rare.

Forecast for acute myelogenous leukemia

The frequency of induction of remission ranges from 50 to 85%. Long-term survival without disease 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 protocol of treatment and its intensity; patients with manifestly unfavorable prognostic factors usually receive more intensive treatment, because the potential advantage of such treatment presumably justifies the higher toxicity of the protocol. The most important prognostic factor is the karyotype of leukemia cells; Adverse karyotypes are t (15; 17), t (8; 21), inv16 (p13; q22). Other adverse prognostic factors are the older age, the myelodysplastic phase in history, secondary leukemia, high leukocytosis, the absence of Auer sticks. The use of only the classifications of the FAB or WHO does not allow one to predict the response to treatment.

trusted-source[12], [13], [14], [15], [16], [17], [18], [19], [20], [21], [22], [23], [24]

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