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Eosinophilic leukemia - symptoms and signs, treatment and life prognosis. Eosinophilic leukemia Treatment of chronic leukemia

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In medical practice under eosinophilia understand the condition of the blood in which there is an increase in the level of special blood cells - eosinophils. In this case, infiltration (impregnation) of other tissues with eosinophils is also observed. For example, with an allergic rhinitis, eosinophils can be found in nasal secretions, with bronchial asthma with bronchitis - in sputum, with accumulation of blood in the lungs or pleural tumors - in pulmonary fluid.

In an adult, the number of eosinophils in the blood is considered normal from 0.02 x 10 9 / l to 0.3 x 10 9 / l.

The following degrees of eosinophilia are distinguished:
1. Small - up to 10% of the total number of leukocytes.
2. Moderate – 10-20%.
3. High – over 20%.

Persistent eosinophilia is most often a sign of helminthic infections, allergic reactions, and some leukemias.

Eosinophilia - a symptom or a disease?

Eosinophilia is not an independent disease, but a sign (symptom) of many infectious, autoimmune, allergic and other diseases. Their list is quite wide.

4. Symptoms of gastrointestinal diseases.
Since many diseases of the digestive system lead to disruption of the intestinal microflora, the process of cleansing the body of toxins slows down, which leads to an increased content of eosinophils. With such dysbiosis, the patient may be bothered by vomiting and nausea after eating, pain in the umbilical region, diarrhea, cramps, signs of hepatitis (jaundice, liver enlargement and pain).
5. Blood diseases.
Systemic histiocytosis against the background of eosinophilia is characterized by frequent infectious diseases, enlarged liver and spleen, damage to the lymph nodes, cough, cyanosis of the skin (blue discoloration), dyspnea (difficulty breathing).
Along with eosinophilia, with lymphogranulomatosis there is fever, pain in the bones and joints, weakness, itching over most of the skin surface, lymphadenopathy, enlargement of the liver and spleen, and there may be a cough.
Eosinophilia in non-Hodgkin's lymphoma is also accompanied by fever, weakness, loss of body weight and motor activity, as well as symptoms characteristic of damage to certain areas. Thus, when a tumor appears in the abdominal area, symptoms such as thirst, abdominal enlargement, and intestinal obstruction are noted. From the central nervous system - headaches, paralysis and paresis, decreased vision and hearing. Chest pain, cough, facial swelling, and difficulty swallowing may occur.

Pulmonary eosinophilia

This term refers to the infiltration (impregnation) of lung tissue with eosinophils. This is the most common tissue localization of eosinophils.

The disease combines the following conditions:
1. Eosinophilic granulomas.
2. Pulmonary infiltrates (volatile).
3. Eosinophilic pulmonary vasculitis caused by various causes.
4. Eosinophilic pneumonia.

To determine the nature of the disease that led to eosinophilia, it is necessary to conduct a biochemical blood test (levels of proteins, liver enzymes, etc.), a general urine test, and a stool test for worm eggs. One of the methods for confirming allergic rhinitis is a Wright-stained smear for eosinophilia of discharge cells in the nasal mucosa.

It is necessary to perform an X-ray of the lungs if indicated, a puncture of the affected joint in rheumatoid arthritis to detect eosinophilic infiltration, and bronchoscopy.

Treatment

Treatment of eosinophilia as an independent disease does not make sense. First of all, it is necessary to find out the reason for the increase in the level of eosinophils in the blood, and, together with the attending physician, develop a rational treatment regimen for the underlying disease. Which medications will be included in the course of treatment will depend on the type of disease, severity and stage of its course, the presence of concomitant diseases and conditions. You may need to do the opposite - stop taking some medications prescribed earlier.

Eosinophilia in cats and dogs

Detection of an increase in the number of eosinophils in cats and dogs may indicate infestation with worms, allergic and skin diseases. Some of these diseases can also be contracted by people who keep animals at home. Therefore, it is necessary to carefully consult with your veterinarian about the possibility of quality treatment for your pet.

Expressed blood eosinophilia, often with pulmonary infiltrates, occurs in strongyloidiasis, ascariasis, trichinosis, opisthorchiasis and schistosomiasis. In parallel, the patient should be examined to exclude clonal diseases of the blood system. It is necessary to perform aspiration and trepanation bone marrow biopsy and cytogenetic analysis. Often the malignant clone cannot be detected by available methods.

In this case, the presence of dysplastic signs in myelogram, pronounced fibrosis on histological examination of the bone marrow, low levels of alkaline phosphatase in neutrophils, and normal levels of cytokines may be indirect signs of clonal damage.

Due to the fact that hypereosinophilic syndrome is a diagnosis of exclusion and its formulation depends on the availability of sophisticated research methods; the greatest difficulty is in excluding chronic eosinophilic leukemia (CEL). Severe eosinophilia and damage to internal organs, primarily the heart, can be observed with hypereosinophilic syndrome and with CEL. Such morphological changes in eosinophils, such as vacuolization and zones of degranulation, hypo- and hypersegmentation of the nucleus, are also not pathognomonic exclusively for hypereosinophilic syndrome.

If the patient has the listed criteria chronic eosinophilic syndrome should be diagnosed. In some patients, signs of clonality may be absent at the time of diagnosis, but are detected later as the disease progresses. There are no specific chromosomal aberrations for chronic eosinophilic leukemia. The most common are trisomy of chromosome 8, isochromosome 17q, monosomy 7, breakages of chromosomes 4, 6, 10, 15 and t(5;12)(q31-q33;p12-13), t(5;7), t(5; 10).

Chromosomal damage involving chromosomes 5 are most often associated with myeloproliferative diseases occurring with eosinophilia, since it is on chromosome 5 that the genes encoding cytokines responsible for eosinophilopoiesis (IL-3, IL-5, GM-CSF) are located. It was shown that eosinophils in these patients were part of the malignant clone. Chronic eosinophilic leukemia is characterized by a chronic course, but by analogy with chronic myeloid leukemia or myelodysplastic syndromes, blast transformation may occur in some patients.

Due to the complexity differential diagnosis, and also due to the fact that some patients with hypereosinophilic syndrome are actually patients with chronic eosinophilic syndrome or hypereosinophilic syndrome can transform over time into chronic eosinophilic syndrome (CHEL_, in the latest WHO classification both diagnoses belong to the same category.

It is also necessary to remember about rare reactive conditions, which are characterized by increased levels eosinophils:
1) Kimura disease;
2) Wells syndrome;
3) Spanish toxic syndrome;
4) eosinophilic myalgia caused by tryptophan;
5) treatment with IL-2;
6) AIDS;
7) kidney transplant rejection;
8) acute and chronic graft-versus-host disease (GVHD) after hematopoietic stem cell transplantation;
9) chronic hemodialysis.

The mechanism of development and characteristics of individual rare eosinophilias are given below.

When conducting differential diagnosis it must be remembered that approximately half of patients on chronic hemodialysis and 70-80% of patients receiving peritoneal dialysis have eosinophilia in the blood and peritoneal fluid. To date, the reason for this phenomenon is unclear.

Versions are being put forward about allergies to the various anticoagulants that this category of patients receives, to the material included in the dialysis membranes, as a reaction to a concomitant catheter infection. Interestingly, cases of the development of Kimura disease in patients on chronic hemodialysis have been described.

It should be noted that for many symptomatic for a long time existing eosinophilia, damage to internal organs is observed. For patients with hypereosinophilic syndrome, it is a mandatory sign of the disease. In this regard, special attention is paid to a thorough examination of the patient.

Recommended ultrasound examination of the heart, abdominal organs, if symptoms are present - computed tomography, nuclear magnetic resonance imaging, as well as other imaging methods, such as endoscopic. In some cases, a biopsy of organs and tissues is indicated. In the absence of damage to internal organs, a full examination should be repeated every six months, since it is not always possible to detect pathological changes in the early stages of the disease using the available means.

You should also repeat the search malignant clone, determine the cytokine profile. If known causes are excluded, a diagnosis of hypereosinophilic syndrome can be made. It must be remembered that the basis of hypereosinophilic syndrome is most likely either a lymphoproliferative disease with a clone of T cells producing IL-5, or a myeloproliferative disease caused by a breakage of chromosome 4: a deletion in the region of the long arm (q12) and the formation of a new oncogene FIP1L1/ PDGFRa, but in many cases the cause cannot be determined.

According to the latest data, the defeat internal organs with hypereosinophilic syndrome is largely associated with the development of fibrosis (primarily in such vital organs as the heart and lungs), in the pathogenesis of which the enzyme tryptase plays a role. In this regard, it is necessary to determine it in blood serum. This is also important for prognostic purposes: a high level of tryptase may indicate a poor prognosis of the disease.

More than 90% of patients are men, usually older. WHO classifies hypereosinophilic syndrome as a myeloproliferative disorder, recognizing that not all cases arise at the stem cell level. It can be almost impossible to distinguish clonal proliferation of eosinophils from reactive ones caused by causeless excessive production of cytokines. If there are no signs of clonality (eg, chromosomal abnormalities), a diagnosis of hypereosinophilic syndrome is made; otherwise, eosinophilic leukemia is diagnosed.

The etiology of hypereosinophilic syndrome is unknown. It is assumed that GM-CSF, IL-5 and IL-7 are responsible for the excessive formation of eosinophils. Despite the pronounced tendency to thrombosis, no specific disorders were found in the coagulation and fibrinolytic systems.

Damage to internal organs:

Hematopoietic disorders. The absolute number of eosinophils usually ranges from 3000 to / μl; The diagnosis is made if the eosinophil count exceeds 1/µL for 6 months or longer and there are no other causes of eosinophilia. Eosinophils are usually small mature cells with a reduced number of granules. In half of the patients, normocytic normochromic anemia is detected. In the bone marrow, the number of myeloid cells is increased, 25-75% of them are eosinophils with an increase in the number of immature elements. The content of myeloblasts is not increased, there are no chromosomal abnormalities.

Damage to the nervous system (40-70% of cases) is manifested by cerebral embolism, encephalopathy and sensory neuropathy. Only nonspecific changes are detected in biopsy specimens.

Lung involvement (40-50% of cases) usually manifests as a prolonged, non-productive cough. In the absence of heart failure and pulmonary embolism, pulmonary function tests are unchanged. On radiographs, focal or diffuse lung damage is detected in only 20% of patients. Bronchial asthma with hypereosinophilic syndrome is rare.

Other myeloproliferative diseases. Hypereosinophilic syndrome is rarely accompanied by severe myelofibrosis and hyperplasia of other cell lineages.

Eosinophilia with damage to individual organs is not accompanied by multiple organ damage, often observed in hypereosinophilic syndrome.

III. Diagnostics. Criteria for hypereosinophilic syndrome:

1. Persistent eosinophilia more than 1500 μl"6 for 6 months.

2. Absence of helminthiasis, allergic reactions and other causes of eosinophilia.

3. Signs of damage to internal organs.

4. Absence of chromosomal abnormalities (otherwise the diagnosis of eosinophilic leukemia is made).

Detailed history and physical examination, complete blood count, liver and kidney function tests, urinalysis.

IgE level and serological tests for collagenoses.

Chest X-ray.

Cytological, histological and cytogenetic examination of bone marrow.

Biopsy of skin lesions.

Repeated stool examinations for helminths and their eggs.

Examination of duodenal contents and serological testing for strongyloidiasis.

Inoculation on media for bacteria, mycobacteria and fungi.

IV. Forecast. More than 75% of patients survive 5 years, and 40% survive 10 years or longer, depending on the success of treatment of lesions of internal organs. The prognosis is unfavorable for refractory heart failure and leukocytosis above / µl.

V. Treatment. As long as there are no signs of damage to internal organs, therapy should be abstained. Glucocorticoids are the most effective. When organ function is restored and the number of eosinophils decreases to the upper limit of normal, treatment is stopped. If prednisone is ineffective, monochemotherapy with hydroxyurea, vincristine or chlorambucil is prescribed. Polychemotherapy should be avoided. Leukapheresis is useless, since the level of eosinophils returns to baseline within 24 hours. Antiplatelet drugs (aspirin) or anticoagulants (warfarin) are often prescribed, but their effectiveness has not been proven.

Hypereosinophilic syndrome, literature:

Bain B.J. Eosinophilic leukaemias and the idiopathic hypereosinophilic syndrome. Br J Haematol 1996; 95:2.

Vardiman JW, Harris NL, Brunning RD. The World Health Organization (WHO) classification of the myeloid neoplasms. Blood 2002; 100:2292.

Weller PF, Bubley GJ. The idiopathic hypereosinophilic syndrome. Blood 1994; 83:2759.

Autoimmune symptoms

It is currently debated whether there are significant differences between ES and acute eosinophilic leukemia (AEL). No agreement has been reached, but there appear to be some overlapping symptoms. Two types of clinical outcome and degrees of visceral involvement are observed. In patients with symptoms of primary damage to the heart and lungs, as well as vasculitis, a subsequent clinical course most likely corresponds to disseminated vasculitis. On the other hand, patients with primary hepatoeplenomegaly, unusually high blood eosinophil counts, and rapid clinical deterioration appear to have malignant ALE.

ES is very rare in children. Variants of the disease may be observed, which are characterized by isolated damage to certain organs. The primary cardiac lesion that is diagnosed as endocarditis with endomyocardial fibrosis may actually be a variant of ES.

Other autoimmune conditions that occur with eosinophilia are also known: eosinophilic fasciitis, rheumatoid arthritis, periarteritis nodosa, chronic hepatitis, regional enteritis, eosinophilic cystitis, eosinophilic gastroenteritis and infected gastroperitoneal shunt (see table). There is agreement on the issue that eosinophilia in chronic peritoneal dialysis is of an autoimmune nature. A full discussion of each of the clinical options is beyond the scope of this chapter; some of them are mentioned below in the context of differential diagnosis for patients who have the symptom of eosinophilia.

In addition to systemic autoimmune diseases, eosinophilia can be observed during local inflammatory processes, which can be difficult to distinguish from the early stages of ES. Some of these immune diseases are described below.

Eosinophilic fasciitis. Eosinophilic fasciitis is a disease that affects the face and skin and is difficult to distinguish from scleroderma. It differs from scleroderma in its relatively acute onset, appearance after unusual physical activity, and sensitivity to corticosteroid hormones. Eosinophilia is usually found in the blood and skin tissue. In contrast to scleroderma, in the pathogenesis of the inflammatory process in eosinophilic fasciitis, degranulation of mast cells is more important than deposits of immune complexes.

Eosinophilic gastroenteritis. Apparently, in eosinophilic gastroenteritis, an autoimmune mechanism of activation of the complement cascade by mast cells operates. Patients present with symptoms such as afternoon nausea, vomiting, cramps, periumbilical pain, and loose, watery stools. Charcot-Leyden crystals, which are products of eosinophil degradation, may be present in the stool. Rectoscopy or rectosigmoid biopsy often reveals thickening of the intestinal wall. The pathogenesis of this disease is not fully understood, but there is strong evidence in favor of an autoimmune mechanism for its development.

Eosinophilic cystitis. Inflammation of the bladder is known to resemble other forms of intractable cystitis, such as interstitial cystitis due to tuberculosis and bladder neoplasms, which occurs secondary to allergic or immune disorders. A constant feature is eosinophilia in the blood and bladder wall. The disease usually has a chronic course and in some patients is caused by food allergens.

Hepatitis. Hepatitis can also occur with eosinophilia. In most cases, the possibility of hepatitis is indicated by general symptoms and signs; with isolated eosinophilia without such symptoms, it is difficult to make a correct diagnosis.

Eosinophilia in malignant neoplasms

It is known that eosinophilia can be a symptom accompanying various tumor lesions. Most often, eosinophilia is observed in combination with cancer of the nasopharynx and bronchial tubes, as well as with adenocarcinoma of the stomach, colon, uterus and thyroid gland. In addition, it is observed in Hodgkin's disease and histiocytoma.

In all likelihood, eosinophilia in malignant neoplasms has clinical significance. It has been noted that eosinophilia can be observed in tumor tissue and in the blood. Tumors in which isolated eosinophilia is observed in the neoplasm tissue have a more favorable prognosis than those without eosinophilia. However, often tumors that occur with eosinophilia in the blood spread quickly and have an unfavorable prognosis.

Malignant transformation of eosinophils is observed in AEL (Fig.). However, eosinophilia is not uncommon in other leukemias, such as acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML). It can sometimes be very difficult to differentiate AEL from reactive eosinophilia associated with ALL or AML. The most definitive answer to distinguishing between these types is provided by studies of special cell markers. The difficulties in differentiating ES from eosinophilia associated with leukemia have been discussed previously. In this regard, it is important to note that chloromas and blastomas (i.e., accumulations of eosinophils and blast cells) are very rare in ES, but are often observed in leukemia. In addition, when comparing patients with ES, in whom chromosomal studies were performed, with the carpotypes of patients with a confirmed diagnosis of leukemia, it was found that ES is usually not accompanied by any disorders, unlike ALL, AML AEL, in which aneuploid and polyploid changes are observed. Because of this, karyotype studies can be critical in differentiating these conditions.

Bone marrow preparation from a patient with acute eosinophilic leukemia.

Blast forms of eosinophils infiltrating the bone marrow dominate over other cell types.

Eosinophilia in pediatric practice

Eosinophilic gastroenteritis is predominantly a disease of childhood, and most patients are under 20 years of age. An allergic history is not always available.

Eosinophilia usually occurs in premature infants and persists until they reach normal body weight. Currently, a high eosinophil count is considered a sign of an anabolic state.

Acute myeloid leukemia - symptoms of promyelocytic, monoblastic, myelomonocytic myeloid leukemia

The concept of acute myeloblastic (or myeloid) leukemia (abbreviated as AML) combines several types of cancer of the human hematopoietic system, in which the bone marrow becomes the focus of cancer.

Until today, oncohematologists do not have a single confidence in the exact causes of disruption of the hematopoietic system, so it is quite difficult to identify special risk groups, and even more so to predict the likelihood of developing myeloid leukemia, or blood cancer. Science is making every effort to create effective methods for diagnosing and treating AML, as a result of which acute myeloid leukemia, diagnosed in the early stages, today has a favorable prognosis for survival.

How does myeloid leukemia develop?

If you imagine the role of the bone marrow as a producer of the entire variety of blood cells, then myeloid leukemia will look like a kind of sabotage in this well-functioning production.

The fact is that disruption of the bone marrow in myeloid leukemia is accompanied by the release into the blood production system of a huge number of “immature” or underdeveloped white blood cells - myeloblasts - leukocytes that have not yet acquired their immune function, but at the same time began to multiply uncontrollably. As a result of such a mutation, the coordinated process of regular renewal of leukocytes in the blood is disrupted and the rapid displacement of full-fledged blood cells by abnormal precursor cells begins. In this case, not only leukocytes are displaced, but also red blood cells (erythrocytes) and platelets.

Types of myeloid leukemia

Due to the fact that the mutation of blood cells itself rarely develops in the body in a “pure” form, but is most often accompanied by other mutations of stem cells and other pathologies, there are many different forms and types of myeloid leukemia.

If until recently there were 8 main types, divided according to the origin of leukemic formations, today mutations that have occurred in cells at the genetic level are also taken into account. All these nuances affect the pathogenesis and prognosis of life expectancy in one form or another of the disease. In addition, determining the type of acute myeloid leukemia disease allows you to select an appropriate treatment regimen.

According to the FAB, variants of myelocytic lecosis are divided into the following subgroups:

Features of acute promyelocytic leukemia

APL, or APML, which stands for acute promyelocytic leukemia, is a subtype of myeloid leukemia M3 according to the FAB (French-American-British classification). With this malignant disease, abnormal numbers of promyelocytes, which are immature granulocytes, accumulate in the blood and bone marrow of patients.

Acute promyelocytic leukemia is defined by a typical chromosome translocation, leading to the formation of abnormal oncoproteins and uncontrolled division of mutated promyelocytes. It was discovered in the middle of the 20th century and for a long time was considered one of the fatal and ultra-acute forms of myeloid leukemia.

Currently, acute promyelocytic leukemia shows a unique response to treatments such as arsenic trioxide and trans-retinoic acid. Thanks to this, APL has become one of the most favorably predicted and curable subtypes of the disease acute myeloid leukemia.

The life expectancy forecast for this variant of AML in 70% of cases is 12 years without exacerbations.

Promyelocytic leukemia is diagnosed by bone marrow tests, blood tests and additional cytogenetic studies. The most accurate diagnostic picture can be obtained through PCR (polymerase chain reaction) research.

Characteristics of acute monoblastic leukemia

Acute monoblastic leukemia belongs to the interregional form of AML in accordance with the FAB classification - variant M5, which occurs in 2.6% of cases in children and in 6-8% of cases in adults (most often the elderly).

The clinical picture indicators are practically no different from acute myeloid leukemia, although the general symptoms are supplemented by more severe intoxication and high body temperature.

The disease is also characterized by signs of neutropenia with a predominance of necrotic changes in the mucous membrane of the nasopharynx and oral cavity, as well as inflammation of the tongue.

The main site of localization of the disease is the bone marrow, but an enlargement of the spleen and certain groups of lymph nodes is also observed. In the future, infiltration of the gums and tonsils, as well as metastasis of the tumor to the internal organs, may occur.

However, with timely testing, detection of malignant pathology and the use of modern treatment regimens, in 60% of cases a significant improvement in the patient’s condition is predicted.

Characteristics of eosinophilic leukemia

Acute eosinophilic leukemia develops as a result of malignant transformation of eosinophils and can occur against the background of adenocarcinoma of the thyroid gland, uterus, intestines, stomach, bronchial and nasopharyngeal cancer. This type of myeloid leukemia is similar to the reactive eosinophilia inherent in acute lymphoblastic leukemia (ALL) or myeloblastic leukemia. Therefore, to differentiate diagnostics, they resort to studies of specific cellular blood markers.

The most characteristic features of this subtype of myeloid leukemia are an increase in the number of eosinophils and basophils in a blood test, and an increase in the size of the liver and spleen.

Features of myelomonocytic leukemia

Of particular concern to modern oncohematologists is such a subgroup of AML as myelomonocytic leukemia, varieties of which most often affect children. Although among the elderly population the risk of contracting this type of myeloid leukemia is also high.

Myelocytic leukemia is characterized by an acute and chronic course, and one of the chronic forms is juvenile myelomonocytic leukemia, characteristic of children from the first year of life to 4 years. The peculiarity of this subtype is the frequency of its development in young patients and the greater predilection for the disease in boys.

Why does myeloid leukemia develop?

Despite the fact that the exact causes of leukemia have still not been established, in hematology there is a certain list of provoking factors that can have a destructive effect on the activity of the bone marrow:

radiation exposure;
unfavorable environmental living conditions;
work in hazardous production;
influence of carcinogens;
side effects from chemotherapy for other forms of cancer;
chromosomal pathologies – Fanconi anemia, Bloom and Down syndromes;
the presence of pathologies such as Epstein-Barr virus, lymphotropic virus or HIV;
other immunodeficiency conditions;
bad habits, especially smoking, of parents of a sick child;
hereditary factor.

How does myeloid leukemia manifest?

Due to the fact that the symptoms of myeloid leukemia vary depending on the forms and types of AML, the allocation of general clinical indicators to the category of symptoms is very arbitrary. As a rule, the first alarming signals are detected in the results of a blood test, which forces the doctor to prescribe additional diagnostic methods.

AML in children

In the case of young children, who are most susceptible to juvenile myelomonocytic leukemia, the presence of the following symptoms should alert parents and force them to see a doctor:

If your child is not gaining weight well;
If there are delays or deviations in physical development;
Increased fatigue, weakness, pale skin due to iron deficiency anemia;
Presence of hyperthermia;
Frequent infections;
Enlarged liver and spleen;
Swelling of peripheral lymph nodes.

Of course, the presence of one or more of the above symptoms does not mean that the child is definitely developing juvenile myelocytic leukemia, because such indicators are characteristic of many other diseases. But, as you know, treatment of complex diseases is most effective in the early stages, so taking blood tests and undergoing other diagnostic procedures will not be superfluous.

AML in adults

chronic fatigue, general weakness;
loss of weight and appetite;
tendency to internal hemorrhages, bruising, increased bleeding;
increased bone fragility;
frequent dizziness and chills;
instability to infectious pathologies;
nausea;
constant pallor.

It is clear that these symptoms cannot serve as the only factor in determining AML, so you should not self-diagnose cancer.

Diagnostic procedures for AML

The first and fundamental diagnostic measure for verifying myeloid leukemia is a complete blood test. If a pathological proliferation of certain groups of blood cells is detected, a bone marrow biopsy is prescribed. To determine the spread of cancer cells in the body, the following are used:

X-ray and ultrasound examinations;
skeletal scintigraphy;
computed and magnetic resonance imaging.

As a rule, all diagnostic procedures are carried out in hematology and oncology clinics, and when the diagnosis of AML is confirmed, a treatment plan is immediately drawn up. Since the pathogenesis (course) of different forms of the disease differs at the cellular and molecular level, the prognosis of the patient’s life expectancy depends entirely on the accuracy of the diagnosis and the adequacy of the chosen treatment method.

Therapeutic measures

Today, treatment of myeloid leukemia consists of 4 stages of therapeutic measures:

Induction with intensive use of chemotherapy designed to destroy as many myeloid cells as possible in the shortest possible time to achieve a remission period.
Consolidation with intensive therapy of combined and additional chemotherapy doses to destroy remaining tumor cells and reduce the risk of disease return.
Treatment of the central nervous system, carried out to prevent leukemia cells from reaching the spinal cord and brain, to prevent metastasis. If leukemia cells fall into the central nervous system, a course of radiation therapy may be prescribed.
Long-term maintenance therapy, prescribed for a long period (a year or more) and carried out on an outpatient basis with the aim of destroying surviving cancer cells.

Side effects of chemotherapy

Despite the effectiveness of chemotherapy treatment, not every patient agrees to use high doses of chemotherapy, since this technique has a significant drawback - side complications.

The most common side effect is cytopenia, which develops as a result of a disruption of the hematopoietic process (myelotoxicity). The occurrence of leukopenia is of great danger, since due to a lack of white blood cells, the body loses its immune defense against infectious lesions that are life-threatening.
No less of a problem (sometimes even fatal) are thrombocytopenia and iron deficiency anemia confirmed by tests, in the fight against which the body is sometimes oversaturated with iron elements, which leads to secondary changes in internal organs.
Taking cytostatics leads to nausea and vomiting, which is extremely poorly tolerated by patients. Prolonged vomiting leads to dehydration and electrolyte imbalance, anorexia (complete loss of appetite) and even stomach bleeding.
A common side effect is alopecia (baldness), damage to the kidneys and heart muscle, jaundice, ulceration of the mucous membranes and other symptoms of side complications that arise depending on the patient’s age, stage of the disease, combination of drugs and other factors.

Is it possible to defeat leukemia?

Today it is too early to talk about a complete victory over leukemia. But an increase in life expectancy after intensive therapy by at least 5-7 years is noted on average in 60% of patients. True, the forecasts for patients over 60 years of age do not rise above a 10% indicator. Therefore, you should not wait until you reach old age in order to take serious care of your own health. You need to undergo preventive examinations, monitor your diet and lifestyle, and donate blood and urine tests regularly.

eosinophilic leukemia

Russian-Italian medical dictionary with indexes of Russian and Latin terms. - M.: “Russo”. C.C. Prokopovich. 2003.

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EOSINOPHILIC LEUKEMIA

(l. eosinophilica) chronic myeloid leukemia, the morphological substrate of which is represented predominantly by acidophilic granulocytes (eosinophils).

Medical terms. 2012

Reasons

The causes of leukemia in children are not fully understood. Some scientists are proponents of the viral theory. The genetic origin of the disease is also being recognized.

It is possible that mutant genes (oncogenes) are formed under the influence of retroviruses and are inherited. These genes begin to act during the perinatal period. But up to a certain point, leukogenesis cells are destroyed. Only when the child’s body’s defenses are weakened does leukemia develop.

Confirmation of a hereditary predisposition to blood cancer are the facts of a more frequent development of leukemia in identical twins compared to fraternal twins. In addition, the disease more often affects children with. There is an increased risk of developing leukemia in children and with other hereditary diseases (Klinefelter syndrome, Bloom syndrome, primary immunodeficiency, etc.).

Factors of physical (radiation exposure) and chemical exposure are important. This is evidenced by the increased incidence of leukemia after the nuclear explosion in Hiroshima and the Chernobyl nuclear power plant.

In some cases, secondary leukemia develops in children who have received radiation therapy and chemotherapy as a treatment for another cancer pathology.

Classification

Based on the morphological characteristics of tumor cells, lymphoblastic and non-lymphoblastic leukemia in children is distinguished. With lymphoblastic leukemia, uncontrolled proliferation (reproduction, growth) of lymphoblasts (immature lymphocytes) occurs, which are of 3 types - small, large and large polymorphic.

Children predominantly (in 97% of cases) develop an acute form of lymphoid leukemia, that is, a lymphoblastic type of disease. Chronic lymphoid leukemia does not develop in childhood.

According to their antigenic structure, lymphoblastic leukemias are:

0-cell (account for up to 80% of cases);
T-cell (15 to 25% of cases);
B-cell (diagnosed in 1-3% of cases).

Among the non-lymphoblastic leukemias, myeloblastic leukemias are distinguished, which in turn are divided into:

poorly differentiated (M 1);
highly differentiated (M 2);
promyelocytic (M 3);
myelomonoblastic (M 4);
monoblastic (M 5);
erythromyelocytosis (M 6);
megakaryocytic (M 7);
eosinophilic (M 8);
undifferentiated (M 0) leukemia in children.

Depending on the clinical course, there are 3 stages of the disease:

I Art. – this is the acute phase of the disease, ranging from initial manifestations to improvement in laboratory parameters due to treatment;
II Art. - achieving incomplete or complete remission: in case of incomplete remission, normalization of parameters in the peripheral blood, the clinical condition of the child is achieved, and in the myelogram of blast cells no more than 20%; with complete remission, the number of blast cells does not exceed 5%;
Stage III – relapse of the disease: with favorable hemogram indicators, foci of leukemic infiltration are detected in the internal organs or nervous system.

Symptoms

One of the signs of leukemia may be recurring sore throat.

The onset of the disease can be either acute or gradual. In the leukemia clinic in children, the following syndromes are distinguished:

intoxication;
hemorrhagic;
cardiovascular;
immunodeficient.

Quite often the disease begins suddenly and develops rapidly. The temperature rises to high levels, general weakness is noted, signs of infection in the oropharynx (,), and nosebleeds appear.

With a slower development of leukemia in children, intoxication syndrome is a characteristic manifestation:

pain in bones or joints;
increased fatigue;
significant decrease in appetite;
sleep disturbance;
sweating;
unexplained fever;
against the background of a headache, vomiting and convulsions may appear;
weight loss.

Hemorrhagic syndrome is typical in the clinic of acute leukemia in children. Manifestations of this syndrome may be:

hemorrhages on the mucous membranes and skin or in the joint cavities;
bleeding in the stomach or intestines;
the appearance of blood in the urine;
pulmonary hemorrhage;
(decrease in hemoglobin and number of red blood cells in the blood).

Anemia is also aggravated due to the suppression of the red line of the bone marrow by blast cells (that is, inhibition of the formation of red blood cells). Anemia causes oxygen starvation in the body tissues (hypoxia).

Manifestations of cardiovascular syndrome are:

increased heart rate;
cardiac arrhythmias;
expanded borders of the heart;
diffuse changes in the heart muscle on the ECG;
reduced ejection fraction by .

A manifestation of immunodeficiency syndrome is the development of a severe form of inflammatory processes that threaten the child’s life. The infection can become generalized (septic) in nature.

Neuroleukemia, the clinical manifestations of which are severe headache, dizziness, vomiting, double vision, and neck rigidity (tension), also poses an extreme danger to a child’s life. With leukemic infiltration (impregnation) of the brain substance, paresis of the limbs, dysfunction of the pelvic organs, and sensitivity disorders can develop.

During a medical examination of a child with leukemia, the following is revealed:

pallor of the skin and visible mucous membranes, there may be an earthy or jaundiced tint to the skin;
bruising on the skin and mucous membranes;
lethargy of the child;
and spleen;
enlarged lymph nodes, parotid and submandibular salivary glands;
rapid heartbeat;
dyspnea.

The severity of the condition increases very quickly.

Diagnostics

In most cases of leukemia, there are characteristic changes in the blood.

It is important that the pediatrician promptly suspects leukemia in the child and refers him for a consultation to an oncohematologist, who will further clarify the diagnosis.

The basis for diagnosing blood cancer is a laboratory study of peripheral blood (hemogram) and bone marrow punctate (myelogram).

Changes in the hemogram:

anemia (decreased number of red blood cells);
(reduced number of blood platelets involved in blood clotting);
reticulocytopenia (decrease in the number of blood cells - the precursors of red blood cells);
increased ESR (erythrocyte sedimentation rate);
leukocytosis of varying severity (increased number of white blood cells) or leukopenia (decreased number of white blood cells);
blastemia (an immature form of leukocytes that predominates in the blood); It is often very difficult to determine the myeloid or lymphoid nature of this pathologically altered immature cell, but more often in acute leukemia they are lymphoid;
absence of intermediate (between blast and mature forms of leukocytes) types of white blood cells - young, rod, segmented; there are no eosinophils either: these changes are typical for leukemia, they are called “leukemic failure”.

It should be noted that in 10% of children with acute leukemia, peripheral blood test results are absolutely normal. Therefore, if there are clinical manifestations that allow one to suspect an acute form of the disease, it is necessary to conduct additional studies: bone marrow puncture, cytochemical tests. And specific markers, for the detection of which labeled monoclonal antibodies are used, will help determine the variant of lymphoblastic leukemia.

The final confirmation of the diagnosis is a myelogram obtained by sternal puncture (puncture of the sternum to remove a piece of bone marrow). This analysis is mandatory. The bone marrow contains virtually no normal elements; they are replaced by leukoblasts. Confirmation of leukemia is the detection of blast cells over 30%.

If convincing data for diagnosis are not obtained from a myelogram study, then a puncture of the iliac bone, cytogenetic, immunological, and cytochemical studies are necessary.

If neuroleukemia manifests itself, the child is examined by an ophthalmologist (to perform an ophthalmoscopy), a neurologist, a spinal puncture is performed and the resulting cerebrospinal fluid is examined, and a skull x-ray is performed.

In order to identify metastatic foci in various organs, additional studies are performed: MRI, ultrasound or CT (liver, spleen, lymph nodes, scrotum in boys, salivary glands), X-ray examination of the chest organs.

Treatment

For treatment, children with leukemia are hospitalized in a specialized oncohematology department. The child is in a separate box, where conditions close to sterile are provided. This is necessary to prevent bacterial or viral infectious complications. Providing your baby with a balanced diet is of great importance.

The main treatment method for leukemia in children is the administration of chemotherapy, the goal of which is to completely get rid of the leukemia clan of cells. For acute myeloblastic and lymphoblastic leukemia, chemotherapy drugs are used in different combinations, doses and methods of administration.

For the lymphoid variant of leukemia, the drugs Vincristine and Asparaginase are used. In some cases, a combination with Rubidomycin is used. Upon achieving remission, Leupirin is prescribed.

For myeloid acute leukemia, drugs such as Leupirin, Cytarabine, Rubidomycin are used. In some cases, a combination with Prednisone is used. For neuroleukemia, treatment with Amethopterin is used.

To prevent relapses, intensive courses of treatment are prescribed for 1-2 weeks every 2 months.

Chemotherapy can be supplemented with immunotherapy (active or passive): smallpox vaccine, immune lymphocytes, interferons are used. But immunotherapy has not yet been fully studied, although it gives encouraging results.

Promising methods for treating leukemia in children are bone marrow transplantation, stem cells, and umbilical cord blood transfusions.

Along with specific treatment, symptomatic treatment is carried out, including (depending on the indications):

transfusion of blood products (platelet and red blood cells), administration of hemostatic drugs for hemorrhagic syndrome;
use of antibiotics (in case of infections);
detoxification measures in the form of infusions of solutions into a vein, hemosorption, plasma sorption or plasmapheresis.

For acute leukemia in children, step-by-step treatment is carried out: after achieving remission and treating complications, maintenance therapy and relapse prevention are carried out.

Forecast

The prognosis for children with the development of leukemia is quite serious.

In the case of early diagnosis, with the help of modern treatment methods, it is possible to achieve stable remission and even complete recovery (up to 25%) in a child with lymphoid type of leukemia. With the myeloblastic variant of the disease, remission is achieved in 40% of cases.

However, even after prolonged remission, relapses can occur. Child mortality from leukemia remains high. The cause of death is often infections that develop due to the fact that both the disease itself and intensive therapy lead to a significant decrease in the body's resistance.

Often death is associated with severe diseases such as tuberculosis, cytomegalovirus infection,