Leukemias

The leukocytes or white blood cells are the cells that participate in the defense of the organism. Within the leukocytes we find different types, such as polymorphonuclear cells, lymphocytes or monocytes, each of them with a specific function within the immune system.

Leukocytes originate in the bone marrow, from immature cells called blasts that differentiate to create the various types of leukocytes. When it occurs, for different reasons, a loss of the control mechanisms of the proliferation of these white blood cells speaks of leukemia, that is, a cancer of leukocytes and their precursor blasts.

Types of leukemias

Depending on the type of blasts involved in leukemia are distinguished lymphatic leukemias, if the lymphoblasts, the precursors of lymphocytes, or of myeloid leukemias, if the cells that cause cancer are the precursors of red blood cells, platelets and the rest of the leukocytes. Likewise, depending on its establishment and the proportion of mature and immature cells involved in leukemia, it can be sharp, with a predominance of immature forms and a rapid evolution, or chronicle, with a greater number of mature cells and a slower progression.

Therefore, when a patient suffers from hematological cell cancer where there is a predominance of mature leukocytes (with the exception of lymphocytes), said pathology will be classified as chronic myeloid leukemia.

How is it produced?

Chronic myeloid leukemia essentially affects middle-aged people and it is known that it is related to a specific genetic alteration, however the cause or causes that may trigger said alteration are unknown. Chromosomes consist of two large regions that differ in size, the so-called short arms and long arms. When the short arms of chromosome number 22 break off from the rest of the chromosome and join chromosome 9, a new structure is formed called Philadelphia chromosome. This alteration has been seen to appear in 95% of cases in the cells of patients with chronic myeloid leukemia. When this alteration occurs, two oncogenes come into contact, that is, two genes that, if altered, can trigger oncological processes. Together they give rise to a protein that stimulates the cell proliferation of myeloblasts, the precursors of mainly non-lymphocyte leukocytes, although this protein can also act on the precursors of red blood cells and megakaryocytes. Likewise, this chromosome can also occur in up to 20% of B lymphocytes. When this protein activates the cell proliferation of myeloblasts, the cells begin to reproduce and occupy space in the bone marrow, displacing the rest of healthy cell lines, which have less space to proliferate. The cancerous leukocytes pass into the blood and from there they can colonize other organs, especially lymph nodes, liver and spleen.

Symptoms

Initially, most patients usually do not present any type of symptoms and it is as the disease progresses that a toxic syndrome is established, characterized by tiredness, weakness, weight loss, and anorexia. When leukocytes enter the blood, they tend to invade the lymph nodes, which is why it is common for patients to present lymphadenopathy. Likewise, in most cases there is hepatomegaly and splenomegaly by the same invasion of leukocytes. As the disease progresses, the proliferation of leukocytes accelerates and immature forms begin to appear in the blood: this is what is called the accelerated phase of chronic myeloid leukemia. 80% of patients go to this phase, in which both hepatomegaly and splenomegaly increase and malignant cells can infiltrate other tissues giving peripheral tumors. Later, once the transformation phase is established, as the immature cells invade the bone marrow and occupy more than 50% of the tissue or their presence in the blood exceeds 30%, what is called blast crisis is entered. because at that time the immature cells, the blasts, are the predominant ones. Up to 60% of patients with chronic myeloid leukemia progress rapidly to the blast phase without going through the transformation phase. In this phase there is a deterioration of the general state, as weight loss accelerates, appetite is lost more and fatigue increases. The anemia worsens, which contributes to the worsening of the patient's condition. It also tends to increase the size of the liver and spleen, fever appears, there is bone pain and sometimes fractures may occur. Most blast phases lead to acute myeloid leukemia, but acute lymphocytic leukemia can occur in up to 25% of cases. In addition to anemia, due to the alteration of leukocytes and the decrease in platelet levels, severe infections and hemorrhagic processes appear. Exceptionally, the transformation from chronic leukemia to the acute phase, that is, the proliferation of immature forms, can take place in leukocytes that are colonizing other organs and not in the bone marrow. If that happens, the tumors formed by myeloblasts that occur in these organs are called chloromas.

Diagnosis

The diagnosis of chronic myeloid leukemia will be based on and on the bone marrow biopsy. In a large number of cases, the diagnosis will be made by a chance finding of high levels of leukocytes when performing a blood test. In the same analysis, a decrease in both platelets and red blood cells can be detected in advanced stages. Chronic myeloid leukemia should be suspected in elderly patients with fatigue, weakness and weight loss, and anorexia with no other apparent cause. Likewise, it should be taken into account as a diagnosis in patients in whom an increase in the size of the liver, spleen or both is explored or referred. A blood test will show an increase in total leukocyte counts, as well as a normochromic normocytic anemia (with normal-sized red blood cells and a normal amount of hemoglobin) and without elevated reticulocytes in the blood, the precursor forms of red blood cells. , a fact that indicates that the bone marrow cannot respond to anemia because it is affected. Platelets can be both decreased and elevated. In the blast phase, more than 30% of myeloblasts will be observed in the blood.

The confirmatory diagnosis will be provided by the bone marrow biopsy, which will show an increase in cellularity, especially at the expense of myeloid cells. In the transformation and blast phases, the number of myeloblasts will be significantly increased, being greater than 50%. There are genetic methods to determine the presence of the Philadelphia chromosome in malignant cells.

Imaging tests such as computerized axial tomography (TAC) and ultrasound They will make it possible to assess the presence or absence of lymph node, liver, splenic involvement or other locations.

Treatment

The only curative treatment that exists is the bone marrow transplant. The rest of the treatments are palliative. If the transplant cannot be performed, treatment with interferon will be chosen. In case of severe anemia, the patient should be transfused.

Poor prognostic factors are advanced age, severe anemia, giant splenomegaly, a higher number of leukocytes and platelets in the blood, a high percentage of blasts, and the absence of the Philadelphia chromosome.

Precautionary measures

Given the unknown origin of chronic myeloid leukemia, despite the proven association with the Philadelphia chromosome mutation, there are no preventive measures against it.