Leukopenia

Leukopenia or neutropenia is a syndrome in which the absolute number of circulating neutrophils in the blood is below 1.5x10 ⁹ / L. The extreme manifestation of leukopenia is agranulocytosis, a condition in which the number of granulocytes in the blood is below 0.5 x ^{10 9} / L.

Synonyms: neutropenia, leukopenia, granulocytopenia, agranulocytosis.

ICD-10 code

D70 leukopenia, agranulocytosis.

Epidemiology of leukopenia

The prevalence of leukopenia and agranulocytosis caused by chemotherapy is determined by the epidemiology of oncological and hematological diseases. Severe chronic leukopenia occurs with a frequency of 1 per 100 000 population, congenital and idiopathic leukopenia - 1 per 200 000, cyclical leukopenia - 1 per 1 million population. Leukopenia is a frequent manifestation of aplastic anemia. In Europe, two new cases of this disease per 1 million people are annually identified, and in East Asia and Africa - 2-3 times more.

The frequency of drug agranulocytosis caused by the appointment of non-chemotherapeutic drugs in the UK is 7 cases per million people per year, in Europe - 3.4-5.3 cases, in the USA - from 2.4 to 15.4 per 1 million people. The risk of developing drug agranulocytosis rises with age only in 10% of cases it occurs in children and young people, more than half of the cases - in people over 60 years old. In women, this complication develops 2 times more often than in men. Vancomycin-induced neutropenia is observed in 2% of patients receiving the drug in patients taking antithyroid drugs - in 0.23% of cases, with clozapine treatment - in 1% of cases.

[1], [2], [3], [4]

Causes of leukopenia

• In congenital forms of leukopenia, the cause of the development of the disease is one or another genetic defect transmitted autosomal recessive or autosomal dominant, and sporadic cases of the disease.
• With oncological diseases, including oncohematological, the cause of development of leukopenia is most often - in ongoing chemotherapy, radiation therapy (myelotoxic agranulocytosis).
• Aplastic anemia, myelofibrosis - acquired aplasia of hematopoiesis.
• Suppression of normal hematopoiesis by tumor cells - tumor diseases of the blood system, tumor metastases in the bone marrow of IDR.
• Metabolic disorders, in particular deficiency of vitamin B12, folic acid, copper, kwashiorkor, violations of glycogen deposits of type 2b lead to leukopenia.
• Infections - severe sepsis, viral infection (Epstein-Barr virus, cytomegalovirus, HIV, hepatitis, parvovirus B19, rubella virus), fungal and protozoal infections (leishmaniasis, histoplasmosis, malaria), tuberculosis, brucellosis - cause neutropenia.
• Non-chemotherapeutic drugs used in clinical practice, including intensive care, cause severe neutropenia - agranulocytosis.

Non-chemotherapeutic drugs that cause agranulocytosis

Class of drugs	Preparations
Heavy metals	Preparations containing arsenic, gold, mercury diuretics
Analgesics of NSAIDs	Acetylsalicylic acid paracetamol, diclofenac, indomethacin ibuprofen, phenylbutazone, piroxicam, tenoxicam, phenazone
Antipsychotic, sedative antidepressant drugs	Chlordiazepoxide, clozapine, diazepam, haloperidol, imipramine, meprobamate, phenothiazine, risperidone, tiaprid, barbiturates
Anticonvulsant drugs
Antithyroid drugs	Thiamazole potassium perchlorate, thiouracil derivatives
Antihistamines	Brompheniramine, mianserin
Different drugs	Acetazolamide, allopurinol, colchicine, famotidine, cimetidine, ranitidine, metoclopramide, levodopa, oral sugar reducing drugs (glibenclamide), fully retinoic acid, tamoxifen, aminoglutethimide, flutamide, sulfasalazine, penicillamine, glucocorticoids
Different chemicals and drugs	Paint for hair, insecticides, mustard gas, DCT, medicinal herbs
Drugs used in cardiology	Captopril, flurbiprofen furosemide hydralazine, methyldopa, nifedipine, phenindione, procainamide, propafenone, propranolol spironolactone, thiazide diuretics, lisinopril, ticlopidine, quinidine ethambutol, tinidazole, gentamicin, isoniazid, lincomycin, metronidazole, nitrofurans, penicillin, rifampicin, streptomycin, thioacetazone, vancomycin , flucytosine, dapsone, chloroquine, hydroxychloroquine levamisole, mebendazole pyrimethamine, quinine, acyclovir, zidovudine, terbinafine, sulfonamides (salazosulfapyridine, etc.)

The risk of agranulocytosis is especially great when taking sulfasalazine, antithyroid drugs, ticlopidine, gold salts, penicillamine, dipyridone, metamizole sodium, sulfamethoxazole + trimethoprim (biseptol). For some drugs, the risk of agranulocytosis is associated with the presence of a histocompatibility antigen. Agranulocytosis caused by levamisole occurs in persons with HLA-B27. In Jews taking clozapine, the drug agranulocytosis is associated with HLA-B38 haplotypes, DRB1 * 0402, DRB4 * 0101, DQB1 * 0201, DQB1 * 0302, in Europe, when clozapine is administered, agranulocytosis occurs with HLA-DR * 02, DRB1 * 1601, DRB5 * 02 DRB1 * 0502. It is important and the disease, against which agranulocytosis develops. The risk of agranulocytosis is high in patients with rheumatoid arthritis who receive captopril, in patients with renal failure receiving probenecid.

[5], [6], [7], [8], [9]

How is leukopenia developing?

Leukopenia can occur as a result of impaired production, circulation or redistribution of neutrophils. Neutrophils in the body are distributed in three spaces - the bone marrow, peripheral blood and tissues. Produced neutrophils in the bone marrow, leaving which enter the blood. In the blood there are two pools of neutrophils - freely circulating and marginal, adhering to the vascular wall. The latter make up about half of the blood neutrophils. Neutrophils leave the bloodstream for 6-8 hours and enter the tissues.

When chemotherapy and radiation therapy, young, actively proliferating cells die, i.e., a bone marrow pool, myelotoxic agranulocytosis develops. Disturbance of bone marrow hemopoiesis is also observed with a tumor lesion of the bone marrow, in which the bone marrow is displaced and suppressed by tumor cells. With aplastic anemia, a decrease in the number of progenitors of the myeloid series is noted, and the remaining cells are functionally inferior, lack adequate proliferative capacity and are apoptotic.

With sepsis, intravascular stimulation of neutrophils by activated complement 5 (C5a) and endotoxin causes increased neutrophil migration to the vascular endothelium, a decrease in the number of circulating neutrophils. With sepsis, the expression of G-CSF receptors is also decreased, myeloid differentiation is disrupted.

With some congenital forms of leukopenia, aplastic anemia, acute leukemia, myelodysplastic syndrome, polypotent myeloid stem cells are disrupted, which leads to a decrease in neutrophil production.

Leukopenia in parasitic infections with splenomegaly (malaria, kala-azar) occurs as a result of increased sequestration of neutrophils in the spleen. In HIV infection, hematopoietic progenitor cells and stromal cells are infected in the bone marrow, which leads to a decrease in the production of neutrophils, the production of autoantibodies, and increased apoptosis of mature leukocytes.

In congenital leukopenia, there is a mutation in the G-CSF receptor gene, as well as a defect in other molecules responsible for signal transmission under the action of G-CSF. As a result, G-CSF does not stimulate granulocytopoiesis in physiological doses. Cyclic neutropenia is caused by a mutation of the gene that codes for neutrophil elastase, as a result of which the interaction between neutrophil elastase, serpins and other substances that affect hematopoiesis is disturbed.

The development of drug agranulocytosis, not associated with chemotherapy, may be due to toxic, immune, allergic mechanisms.

Symptoms of leukopenia

Leukopenia has no specific manifestations and can be asymptomatic, its manifestations are caused by the attachment of infectious complications, the risk of development of which depends on the depth and duration of leukopenia. With the number of neutrophils below 0.1x10 ⁹ / L during the first week, the infection is detected in 25% of patients, and within 6 weeks - in 100% of patients. The rate of development of leukopenia is important for patients whose neutrophil count has decreased rapidly, are more prone to infectious complications than patients with long-standing neutropenia (eg, chronic neutropenia, aplastic anemia, cyclic neutropenia, etc.).

The appearance of fever in leukopenia is the first and often the only sign of infection. In 90% of patients with neutropenia, fever is a manifestation of infection, in 10% it occurs due to non-infectious processes (reaction to drugs, tumor fever, etc.). In patients receiving glucocorticoid hormones, the infection can occur without increasing body temperature. Almost half of patients with leukopenia have a fever with an unidentified focus of infection. 25% of febrile neutropenic patients have a microbiologically proven infection, most of them have bacteremia. Even in 25% of patients, the infection is diagnosed clinically, but it can not be confirmed by microbiology. Infection of patients with leukopenia is mainly due to the endogenous flora that colonized the foci of infection.

From isolated leukopenia, neutropenia should be distinguished from a cytostatic disease that occurs under the influence of chemotherapy. Cytostatic disease is caused by the death of dividing cells of the bone marrow, epithelium of the digestive tract, intestines, skin. A frequent manifestation of cytostatic disease is liver damage. In addition to infectious complications, anemia, thrombocytopenia, hemorrhagic syndrome, oral syndrome (swelling of the oral mucosa, ulcerative stomatitis), intestinal syndrome (necrotic enteropathy or neutropenic enterocolitis) are found along with infectious complications. Necrotizing enteropathy is an acute inflammatory process caused by the death of epithelial cells of the intestine, which is manifested by flatulence, frequent loose stools, and abdominal pain. Enteropathy leads to the translocation of microbial flora with the subsequent development of sepsis, septic shock. The development of septic shock in the state of agranulocytosis necrotic enteropathy precedes in 46% of patients.

The course of the infectious process in patients with leukopenia has its own distinctive features

Transience

A few hours pass from the first signs of infection to the development of severe sepsis. In septic shock in the state of agranulocytosis, one third of patients begin to fever only a day before the onset of arterial hypotension. The outcome of septic shock in patients with hemoblastosis in the state of agranulocytosis occurs 2 times faster than in the same category of patients without leukopenia.

Features of the inflammatory process in conditions of leukopenia

With soft tissue infection, there is no suppuration, local manifestations of inflammation (redness, edema, pain syndrome) can be negligible, with a general intoxication. Necrotic enteropathy often leads to perianal lesions and inflammations, which are found in 12% of patients in agranulocytosis. Pneumonia in the state of agranulocytosis occurs without neutrophilic infiltration of the lung tissue. In 18% of cases in the first 3 days with bacterial pneumonia there are no changes on the radiographs, it can be detected only with CT. Peritonitis, which complicates the course of necrotic enteropathy, is often erased, without pronounced pain syndrome, there may be no peritoneal symptoms.

[10], [11], [12], [13], [14], [15]

Features of pathogens

In the state of agranulocytosis, along with common bacterial pathogens, infectious complications can be caused by pathogens that are rare in patients without leukopenia. With prolonged leukopenia, spontaneous myoclostridial necrosis may occur, manifested by pain in the muscles, their edema, fulminant sepsis, septic shock. The diagnosis is established when a free gas is detected in the intermuscular tissue on an X-ray or ultrasound scan, revealing the pathogen in the blood and the affected tissues. Often, herpesvirus complications caused by herpes simplex viruses, cytomegalovirus, Epstein-Barr virus are recorded. The frequency of mycotic infections caused by Candida spp and Aspergillus spp. Is high. For every tenth patient with ODN, developed in agranulocytosis, the cause of lung damage is Pneumocystis carinii. More than half of patients in agranulocytosis pneumonia leading to ODN are caused by several pathogens.

[16], [17], [18], [19], [20], [21], [22], [23]

Classification of leukopenia

By duration:

• Acute leukopenia - duration does not exceed 3 months.
• Chronic leukopenia - if its duration exceeds 3 months.

There are four main types of chronic neutropenia:

1. congenital,
2. idiopathic,
3. autoimmune,
4. cyclic.

By time of occurrence:

• Leukopenia can be congenital (Costman's syndrome, cyclic neutropenia) or acquired throughout life.

By severity of leukopenia:

• The depth of the decrease in the level of neutrophils determines the risk of developing infectious complications.

Classification of leukopenia by severity

Absolute number of blood neutrophils	Degree of leukopenia	Risk of infectious complications
1-1.5x10 9 / l	Lightweight	Minimum
0.5-1x10 9 / L	Moderate	Moderate
<0.5x10 9 / l	Severe (agranulocytosis)	High risk

[24], [25], [26], [27],

Etiopathogenetic classification of leukopenia

Violation of the formation of neutrophils in the bone marrow

• hereditary diseases (congenital, cyclic leukopenia),
• tumor diseases,
• some medicines (LS), irradiation,
• deficiency of vitamin B12 or folic acid,
• aplastic anemia.

Increased destruction of neutrophils

• autoimmune leukopenia,
• chemotherapy,
• sequestration of neutrophils - in the apparatus of artificial circulation, in the apparatus "artificial kidney" in the conduct of HD,
• leukopenia in viral infections.

[28], [29], [30], [31], [32], [33]

Diagnosis of leukopenia

For the diagnosis of leukopenia, an absolute count of blood neutrophils is needed, only the number of leukocytes is sufficient for this. In a number of diseases, the absolute number of neutrophils can be sharply reduced, while the number of blood leukocytes remains normal or even increased due to, for example, lymphocytes, blast cells, etc. To do this, the leukocyte formula is counted, then the percentage of all granulocytes and the resulting the sum, divided by 100, is multiplied by the number of leukocytes. Neutropenia is diagnosed with a neutrophil count below 1.5 × ^{10 9} / L. It is also necessary to count the red blood cells and platelets. Association of leukopenia with anemia, thrombocytopenia indicates a possible tumor disease of the blood system. The diagnosis is confirmed by the detection of blast cells in the peripheral blood or in the bone marrow.

The study of bone marrow punctate and trepanobioptate allows differential diagnosis and establishment of a mechanism for the development of leukopenia (impaired neutrophil production in the bone marrow, increased destruction in the blood, detection of atypical or blast cells, etc.).

With an unclear diagnosis, it is necessary to further examine the blood for antinuclear antibodies, rheumatoid factor, anti-granulocyte antibodies, conduct liver tests (transaminases, bilirubin, markers of viral hepatitis, etc.), examine the levels of vitamin B12, folates.

Difficulties may be the diagnosis of drug agranulocytosis, not related to the appointment of chemotherapy. Almost 2/3 of the patients take more than two drugs, so it is always difficult to unequivocally determine which of them led to agranulocytosis.

[34], [35], [36], [37], [38], [39]

Criteria for agranulocytosis caused by non-chemotherapeutic drugs

• The number of neutrophils is <0.5 × ^{10 9} / L in the presence or absence of fever, clinical signs of infection and / or septic shock.
• Initiation of agranulocytosis during treatment or within 7 days after the first administration of the drug and complete recovery of granulocytopoiesis (> 1.5x10 ⁹ / L neutrophils in the blood) within no more than a month after discontinuation of the drug.
• Exclusion criteria are congenital or immune leukopenia in a history, a recent infectious disease (in particular, a viral infection), recent chemotherapy or radiation therapy, immune therapy, blood system diseases.
• With medicinal non-cytotoxic agranulocytosis, the number of platelets, erythrocytes and hemoglobin levels are usually normal. The study of bone marrow allows you to exclude other possible causes of agranulocytosis.
• With drug agranulocytosis in the bone marrow, usually normal or moderately reduced total cellularity, there are no myeloid progenitor cells.
• In some cases, a lack of mature myeloid cells is observed while the immature forms (up to the myelocyte stage) are preserved-the so-called "myeloid block", which may be a consequence of selective drug / antibody interaction on mature cells or represent the initial stage of recovery.
• The absence of myeloid progenitors means that at least 14 days should pass before the recovery of leukocytes in the peripheral blood.
• In contrast, with a myeloid block, the recovery of the number of white blood cells can be expected within 2-7 days.

The occurrence of fever in patients with agranulocytosis is an indication for conducting a diagnostic search for an infectious agent. Microbiological diagnosis determines the choice of adequate regimens of antibiotic therapy. Infection in patients with agranulocytosis is often polyethylene, so identifying only one pathogen should not stop the diagnostic search. Along with traditional microbiological studies, the examination of a patient in agranulocytosis includes:

• detection of antigens of fungi (mannans, galactomannans) in the blood, BAL, CSF,
• detection in blood cells, lavage fluid and CSF of herpes simplex virus, cytomegalovirus, Epstein-Barr virus, and antibodies to them in serum.

Diagnosis of sepsis in this category of patients is often a probabilistic nature. A reliable diagnosis of sepsis is based on the following symptoms:

• clinical manifestations of infection or isolation of the pathogen,
• CER,
• detection of laboratory markers of systemic inflammation.

However, in 44% of patients in agranulocytosis, fever appears without an established focus of infection, only 25% of febrile neutropenic patients have a microbiologically proven infection. One of the SRER criteria - neutropenia - is always present in these patients. The occurrence of fever in a patient in agranulocytosis, even in the absence of a foci of infection, should be considered as a possible manifestation of sepsis. Such a laboratory marker of inflammatory reaction, like procalcitonin of blood, can be used to diagnose sepsis in patients with agranulocytosis. However, the attachment of fungal, viral infections occurring with a clinical picture of severe sepsis may be accompanied by a normal or slightly elevated level of procalcitonin.

The most frequent infection complication in patients with agranulocytosis is pneumonia. Diagnosis of infectious lung lesions in patients with agranulocytosis should also include the most likely pathogens.

[40], [41], [42], [43]

Screening for leukopenia

Counting the number of blood leukocytes, the leukocyte formula, the absolute number of blood granulocytes.

Treatment of leukopenia

The patient is placed in a separate ward (isolator). When dealing with sick personnel, it is necessary to carefully follow measures of asepsis and antiseptics (wearing facial masks, washing hands with antiseptics, etc.).

In most cases, leukopenia and agranulocytosis in specific treatment is not necessary. The main preventive and curative measures are reduced to the prevention of infection, the treatment of already emerging infectious complications and the underlying disease that led to leukopenia. Erroneous should be considered undertaken for the treatment of leukopenia transfusion of whole blood or erythrocyte mass, leukocyte suspension, the appointment of glucocorticoid hormones. The latter can be used only in the treatment of the underlying disease that led to the development of leukopenia, for example systemic lupus erythematosus, rheumatoid arthritis, some forms of acute leukemia, autoimmune leukopenia, etc. It should be borne in mind that the appointment of glucocorticoids in agranulocytosis sharply increases the risk of developing infectious complications. Depending on the underlying disease (eg, with aplastic anemia, Felty syndrome, autoimmune agranulocytosis), splenectomy, immunosuppressive therapy (cyclosporine, cyclophosphamide, azathioprine, methotrexate, etc.) can be used to treat leukopenia.

When folate deficiency, vitamin B12 deficiency is indicated the appointment of vitamin B12, folic acid in a dose of up to 1 mg / day, leucovorin at 15 mg per day. With medicinal non-chemotherapeutic agranulocytosis, it is necessary to cancel the drug, which could cause it.

Features of treatment of infectious complications

The main method of combating complications caused by neutropenia is the implementation of measures aimed at the prevention and treatment of infection. Patients in the state of agranulocytosis in case of attachment of infectious complications need to be placed in isolated chambers. In most cases, the source of infection, especially bacterial and fungal etiology, is the gastrointestinal tract, so when developing agranulocytosis, decontamination of the intestine is carried out. For this purpose, antibacterial drugs sensitive to gram-negative flora (ciprofloxacin), trimethoprim / sulfamethoxazole are used. The latter also has activity against pneumocystis infection.

In the absence of bacterial infection, antibiotics are not prescribed for prophylactic purposes. When signs of infection appear, immediately begin empirical antibiotic therapy, which can then be changed to take into account a clinically identified focus of infection and / or microbiologically confirmed pathogens. The delayed administration of antibiotics in agranulocytosis, especially with gram-negative infection, significantly increases mortality from sepsis and septic shock.

Treatment for sepsis and septic shock is carried out according to accepted rules. In case of septic shock for the invasive monitoring, even in the presence of thrombocytopenia after transfusion of the platelet concentrate, the radial or femoral artery is catheterized, necessarily the central vein. For invasive monitoring in these patients, in spite of leukopenia, pulmonary artery catheterization with the help of Svan-Hans catheter, transpulmonary thermodilution using a special arterial catheter can be used.

In 16% of patients who died of septic shock, in the state of agranulocytosis, massive hemorrhages to the adrenal glands are detected, in the vast majority of patients who received glucocorticoid hormones in chemotherapy courses, septic shock reveals relative adrenal insufficiency. Consequently, the inclusion of small doses (250-300 mg / day) in septic shock therapy for hydrocortisone is pathogenetically justified.

[44], [45], [46], [47], [48], [49]

Features of respiratory therapy

The success of respiratory therapy in ODN in patients with leukopenia is associated primarily with the use of non-invasive ventilation of the lungs. It avoids intubation of the trachea in a third of patients whose agranulocytosis is complicated by the development of ODN.

With intubation of the trachea and transfer of the patient to the ventilator, it is recommended to perform an early (in the first 3-4 days) tracheostomy, which is especially important when the patient has a concomitant hemorrhagic syndrome due to thrombocytopenia.

[50], [51], [52], [53], [54], [55]

Features of nutritional support

Leukopenia is not a contraindication to enteral nutrition. Patients in agranulocytosis are prescribed a sparing diet without canned foods, excess fiber. As in patients without leukopenia, enteral nutrition prevents the translocation of microflora from the intestine, the development of dysbiosis, increases the protective properties of the mucous membrane, reducing the risk of secondary infectious complications. In addition to the generally accepted indications for the transfer of patients to full parenteral nutrition, in patients with agranulocytosis, it is prescribed for expressed mucositis, necrotizing enteropathy, clostridial enterocolitis.

The issue of access to enteral nutrition is important. With expressed mucositis, esophagitis, which often occur in patients with agranulocytosis, enteral nutrition can be carried out through the nasogastric tube, and with concomitant gastroparesis, which occurs after chemotherapy courses, especially with the use of vincristine, methotrexate, with sepsis through the naso-intestinal probe. With long-lasting mucositis, esophagitis is the method of choice for enteral nutrition - gastrostomy. In a number of cases, after chemotherapy courses (especially with methotrexate), mucositis, salivation, a decrease in the cough reflex are so pronounced that tracheostomy is performed for patients without respiratory insufficiency to divide the airways and prevent aspiration. Application of colony-stimulating factors.

The duration and depth of leukopenia can be reduced by the use of CSF, in particular G-CSF. Efficacy and indications for CSF application are different depending on the cause of agranulocytosis and the patient's condition.

In oncology, indications for the appointment of CSF for the prevention of leukopenia and the occurrence of febrile leukopenia depend on the patient's condition, age, intensity of chemotherapy, nosology and the stage of the underlying disease.

With medicinal agranulocytosis, the use of CSF can shorten the duration of drug agranulocytosis by an average of 3-4 days. G-CSF or granulocyte-macrophagal CSF (GM-CSF, filgrastim, molgamostim) is prescribed at a dose of 5 μg / kg per day until the level of granulocytes (leukocytes) higher than 1,5-2х109 / l. However, G-CSF can not be recommended for routine use in drug agranulocytosis, since along with data confirming the effectiveness of this drug, there are also results of its unsatisfactory use in drug agranulocytosis. Application of transfusions of granulocyte concentrate.

The severity of infectious complications during agranulocytosis can be reduced by transfusion of granulocyte concentrate. Concentrate of granulocytes, in contrast to the concentrate of leukocytes and leukemia, is obtained after special preparation of donors. 12 hours before the collection of granulocytes, glucocorticoid hormones (usually 8 mg of dexamethasone) and 5-10 μg / kg of G-CSF are administered subcutaneously, after which granulocyte apheresis is performed on special automatic blood fractionators. This regime allows one to collect from one donor to (70-80) x10 ⁹ cells. There are no legislative norms in Russia that allow hormones and CSF to be administered to donors. Data on the effectiveness of granulocyte transfusions for the treatment of sepsis in patients with agranulocytosis are contradictory. In addition, this method of treatment has a large number of side effects (the risk of transmission of a viral infection, alloimmunization, pulmonary complications). Thus, transfusion of granulocyte concentrates can not yet be recommended for routine use in the treatment of sepsis in patients with agranulocytosis.

[56], [57], [58], [59]

How is leukopenia prevented?

Prevention of leukopenia caused by chemotherapy, as a rule, is not carried out. If the renal and / or liver function is impaired, doses of chemotherapeutic drugs should be reduced, since cumulation of drugs is possible, which can lead to prolonged, sometimes irreversible agranulocytosis. Preventive administration of granulocyte colony-stimulating factor (G-CSF) is carried out in certain categories of oncological and oncohematological patients during chemotherapy to prevent leukopenia and / or shorten its duration.

For the prevention of agranulocytosis caused by non-chemotherapeutic drugs, it is necessary to take into account the history and indication of the development of leukopenia when prescribing medications.

Prognosis of leukopenia

Mortality in the complications of leukopenia, which occurred during the treatment of cancer, ranges from 4 to 30%. With medicinal non-chemotherapeutic agranulocytosis in recent decades, mortality has decreased from 10-22% in the 1990s to 5-10% at the present time. This decline was due to better care of patients, adequate antibiotic therapy of infectious complications, in some cases, the application of CSF. A higher mortality is observed with medicinal agranulocytosis in the elderly, as well as in patients in whom it developed against a background of renal insufficiency or complicated by bacteremia, septic shock.

Information for Patient

When verifying a patient with leukopenia or agranulocytosis, the doctor must inform the patient that he should avoid receiving unprocessed meat, raw water, use juices, dairy products only in factory packaging, and pasteurized. It is forbidden to take unwashed raw fruits and vegetables. When visiting public places, the patient should wear a facial mask and avoid contact with people suffering from respiratory diseases. When there is an increased body temperature - immediate access to medical personnel and, as a rule, emergency hospitalization.