Medical expert of the article
New publications
Leukemia
Last reviewed: 23.04.2024
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
The cause and pathophysiology of leukemia
Malignant transformation, as a rule, occurs at the level of pluripotent stem cells, although sometimes transformation occurs in committed stem cells with a more limited ability to differentiate. Abnormal proliferation, clonal expansion and oppression of apoptosis (programmed cell death) leads to replacement of normal cellular elements of blood with malignant cells.
The risk of developing the majority of leukemias increases with the presence of an exposure to ionizing radiation in the anamnesis (for example, after the atomic bombardment in the cities of Nagasaki and Hiroshima), chemical compounds (for example, benzene); treatment with some antitumor drugs, in particular procarbazine, nitrosourea derivatives (cyclophosphamide, melphalan) and epipodophyllotoxins (etoposide, teniposide); infection with viruses (eg, human T-lymphotropic virus types 1 and 2, Epstein-Barr virus); chromosomal translocations; a number of diseases, such as immunodeficiency states, chronic myeloproliferative diseases, chromosomal diseases (eg, Fanconi anemia, Bloom's syndrome, ataxia-telangiectasia, Down's syndrome, infantile X-linked agammaglobulinemia).
Clinical manifestations of leukemia are caused by oppression of the mechanisms of formation of normal cellular elements and infiltration of organs by leukemia cells. Leukemia cells produce inhibitors and replace normal cell elements in the bone marrow, which leads to suppression of normal hematopoiesis with the development of anemia, thrombocytopenia and granulocytopenia. Infiltration of organs leads to an increase in the liver, spleen, lymph nodes, sometimes affects the kidneys and gonads. Infiltration of the meninges leads to clinical manifestations, which are caused by increased intracranial pressure (for example, paralysis of the cranial nerves).
Classification of leukemia
Initially, the terms "acute" and "chronic" leukemia were related to the life expectancy of patients, and at present leukemia is classified according to the degree of cell maturity. Acute leukemias consist mainly of immature, slightly differentiated cells (usually blast forms); Chronic leukemia is characterized by more mature cells. Acute leukemias are subdivided into lymphoblastic (ALL) and myeloblastic (AML) types, which according to the Franco-American-British (FAB) classification are divided into subtypes. Chronic leukemias are divided into lymphocytic (CLL) and myelocytic (CML).
Myelodysplastic syndromes include states with progressive bone marrow deficiency, but with an insufficient proportion of blast cells (<30%) to explicitly match the diagnosis of "acute myeloblastic leukemia"; from 40 to 60% of cases myelodysplastic syndrome is transformed into acute myeloblastic leukemia.
The leukemoid reaction is expressed granulocyte leukocytosis (ie, the number of white blood cells> 30 000 / μL) produced by normal bone marrow in response to a systemic infection or cancer. Although it is not a neoplastic disorder, a leukemoid reaction with very high leukocytosis may require differential diagnosis with chronic myelogenous leukemia.
The Franco-American-British classification of acute leukemia (FAB classification)
Acute lymphoblastic leukemia
L1 |
Monomorphic lymphoblasts with a rounded nuclei and a small cytoplasm |
L2 |
Polymorphic lymphoblasts with nuclei of various forms and large cytoplasm volume than with L1 |
L3 |
Lymphoblasts with small particles of chromatin in the nucleus and blue or dark blue cytoplasm with vacuolization |
Acute myeloblastic leukemia
M1 |
Undifferentiated myeloblastic leukemia; there are no granules in the cytoplasm |
M2 |
Myeloblastic leukemia with cell differentiation; poor granulation can be recorded both in individual cells and in a large number of them |
MH |
Promyelocytic leukemia; The granules are typical for promyelocytes |
M4 |
Myelomonoblastny leukemia; mixed myeloblastic and monocytic morphology |
M5 |
Monoblastic leukemia, mono-blast morphology |
MB |
Erythroleukemia; morphology of mostly immature erythroblasts, sometimes there are megaloblasts |
M7 |
Megacaroblastic leukemia; cells with processes, budding can be noted |
What do need to examine?
What tests are needed?
Who to contact?