Acute non-lymphoblastic leukemia due to therapy – diagnosis
Acute non-lymphoblastic leukemia and myelodysplastic syndrome can be caused by two types of therapy: either using alkylating agents and / or radiation therapy, or type II topoisomerase inhibitors. In the latter case, lymphoid leukemias can also be observed.
After therapy with alkylating agents and radiation, acute non-lymphoblastic leukemia occurs after 5 years or more. The risk of acute non-lymphoblastic leukemia depends on the total cumulative dose of the drugs, the age of the patient, and the combined use of the two methods of treatment. The onset of the disease is manifested in the form of myelodysplastic syndrome with cytopenia, multiline dysplasia.
Dysgranulo- and dyseritropoiesis are observed in the majority of patients, the number of basophils is increased. Often (up to 60% of cases) ring sideroblasts are found, in neutrophils, peroxidase deficiency is determined. As a rule, there is myeloblastic acute non-lymphoblastic leukemia, but there can also be myelomonoblastic, erythroblastic, megakaryoblastic and, less commonly, promyelocytic variants. The immunophenotype of blasts is characterized by heterogeneity.
They express myeloid antigens (CD13, CD33), early CD34, CD56 and / or lymphoid CD7. In the karyotype, unbalanced translocations or deletions of the 5th and / or 7th chromosome are often detected with the loss of all or part of the long arm of the chromosome. There are anomalies of other chromosomes: 1st, 12th, 14th, 18th, complex chromosomal aberrations.
Acute leukemia after therapy with topoisomerase II inhibitors occurs faster than after the use of alkylating agents. The latent period is on average 33-334 months. Among the drugs distinguish epipodophyllotoxins (etoposide and teniposide) and anthracyclines. Acute leukemias caused by these drugs, as a rule, belong to monoblastic or myelomonoblastic, although other variants of acute nonlymphoblastic leukemia, as well as acute lymphoblastic leukemia can occur. The most frequent violation of the karyotype is the presence of the llq23 abnormality as a result of translocations (9; 11), (11; 19), (6; 11).
In addition, translocations can be detected (8; 21), (3; 21), (6; 9). ALL is usually associated with t (4; ll) (q21; q23). In secondary acute leukemia, remission is less frequent and shorter than in primary.