Nomenclature principles and basic criteria
The key factor determining whether a hemoblastosis belongs to one group or another is the degree of maturity of the cells that make up the basis of the tumor.
- Acute hemoblastoses develop from a pool of immature cells. In medical terminology, such forms are traditionally referred to as "blastic".
- Chronic hemoblastoses have a fundamentally different morphological picture. They are represented by more mature cellular elements. The root "-cytic" is used in the diagnosis to designate them.
It is important to understand that the terms "acute" and "chronic" in this context reflect not so much the rate of symptom development as the morphological substrate and the degree of differentiation of the tumor cells.
Acute forms of hemoblastoses
The morphological substrate of acute leukemias is always blast tumor cells. These are extremely aggressive conditions. If the patient is left without specialized treatment, the disease inevitably leads to a fatal outcome within a few weeks or months. However, given proper and timely initiated therapy, the prognosis changes drastically and can be quite favorable.
Based on the cellular composition, the following variants of acute hemoblastoses are distinguished:
- Acute lymphoblastic leukemia.
- Acute myeloblastic leukemia.
- Acute myelomonoblastic leukemia.
- Acute erythromyeloblastic hemoblastosis.
- Acute megakaryoblastic leukemia.
These diseases are of particular concern in pediatric practice. Acute leukemias account for about 30% of all malignant tumors diagnosed in children. The absolute leader in frequency is acute lymphoblastic leukemia, accounting for approximately 24% of cases, making it the most common childhood malignancy. The peak incidence of this form is recorded in toddlers aged 2–3 years. Acute myeloblastic leukemia accounts for a significantly smaller share in children—about 6%.
Modern medicine demonstrates high treatment effectiveness: in recent years, with acute lymphoblastic leukemia, doctors have managed to achieve stable and long-term remission in almost 90% of clinical cases.
Chronic forms and their transformation
Unlike acute processes, the cellular substrate of chronic hemoblastoses consists of relatively differentiated cells of the hematopoietic tissue.
The classification of chronic forms is also based on the type of predominant cells. There are five main variants:
- Chronic lymphocytic leukemia (lymphocytic leukemia). Hairy cell leukemia is traditionally included in this same group.
- Chronic myelocytic leukemia (myelogenous leukemia).
- Chronic myelomonocytic leukemia.
- Erythrocytic hemoblastosis. In clinical practice, this condition often appears under the names polycythemia vera or Vaquez disease.
- Megakaryocytic hemoblastosis.
A critically important aspect of the pathophysiology of chronic hemoblastoses is their ability to progress with changes in cellular composition. Chronic forms frequently transform into their acute counterparts. This formidable process, accompanied by a sharp deterioration in the patient's condition, is designated by the term exacerbation of chronic hemoblastosis or blast crisis.
Briefly: answers to topical questions
What are the characteristic peripheral blood (hemogram) changes in acute leukemias?
Characteristic peripheral blood changes in acute leukemias include the appearance of blast cells, suppression of normal hematopoiesis, and specific phenomena. Key changes include:
- Leukemic hiatus (hiatus leukaemicus) — the presence of blast and mature forms in the blood with a complete absence of intermediate maturing cells, which is pathognomonic for acute myeloblastic leukemia.
- Leukemization — the release of immature and blast tumor cells into the bloodstream.
- Cytopenia — the development of anemia, thrombocytopenia, and neutropenia due to the displacement of normal hematopoietic lineages by the tumor clone of blast cells.
What specific cytogenetic markers are characteristic of chronic myelogenous leukemia?
The key cytogenetic marker of chronic myelogenous leukemia is the Philadelphia chromosome.
- Philadelphia chromosome (Ph chromosome) — an abnormal 22nd chromosome, the presence of which is the main diagnostic sign of this pathology.
- Chimeric gene (BCR-ABL) — the gene associated with this mutation, which encodes a specific protein.
The consequence of this anomaly is an increase in tyrosine kinase enzyme activity, which leads to the stimulation of cell proliferation and the slowing of terminal differentiation.
To easily remember the terminology: if a disease name has the root "-blastic" (e.g., myeloblastic), it is always an acute hemoblastosis. If it sounds like "-cytic" (myelocytic), you are dealing with a chronic form.
Class and exam questions
What is the main criterion for dividing hemoblastoses into acute and chronic?
The main criterion is the cellular substrate of the tumor. Acute hemoblastoses consist of immature blast cells, whereas chronic forms are represented by relatively differentiated, more mature cells of the hematopoietic tissue.
What is the prognosis for a patient with acute hemoblastosis?
Without medical intervention, the prognosis is extremely unfavorable—a fatal outcome occurs within a few weeks or months. However, with correct and timely therapy, the prognosis can become favorable. For example, in acute lymphoblastic leukemia, long-term remission is achieved today in almost 90% of cases.
How often do hemoblastoses occur in childhood?
Acute leukemias account for about 30% of all malignant tumors in children. The most common is acute lymphoblastic leukemia (about 24%), with the peak incidence occurring at the age of 2–3 years. Acute myeloblastic leukemia is less common—in approximately 6% of cases.
What does the term "blast crisis" mean?
A blast crisis is a process of exacerbation of chronic hemoblastosis, in which the disease transforms into an acute form. During this period, the pool of immature blast cells begins to rapidly increase in the hematopoietic tissue.
What else to study on this topic
- Morphological differences between blast and cytic cells
- Mechanisms of blast crisis development
- Features of the course of polycythemia vera (Vaquez disease)
- Specifics of hairy cell leukemia
- Principles of therapy for acute lymphoblastic leukemias
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