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 0.5x10 ⁹ /l.

Synonyms: neutropenia, leukopenia, granulocytopenia, agranulocytosis.

ICD-10 code

D70 leukopenia, agranulocytosis.

Epidemiology of leukopenia

The prevalence of chemotherapy-induced leukopenia and agranulocytosis 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, cyclic leukopenia - 1 per 1 million population. Leukopenia is a frequent manifestation of aplastic anemia. In Europe, 2 new cases of this disease are detected annually per 1 million population, and in the countries of East Asia and Africa - 2-3 times more.

The incidence of drug-induced agranulocytosis caused by non-chemotherapeutic drugs in the UK is 7 cases per 1 million population annually, 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-induced agranulocytosis increases with age: only in 10% of cases it occurs in children and young people, and in more than half of cases - in people over 60 years of age. 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, during treatment with clozapine - in 1% of cases.

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Causes of leukopenia

• In congenital forms of leukopenia, the cause of the disease is one or another genetic defect, transmitted autosomal recessively or autosomal dominantly; sporadic cases of the disease are also noted.
• In oncological diseases, including oncohematological ones, the cause of leukopenia development is most often the chemotherapy and 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 to the bone marrow IDR.
• Metabolic disorders, in particular vitamin B12 deficiency, folate deficiency, copper deficiency, kwashiorkor, glycogen storage disorder type 2b lead to leukopenia.
• Infections - severe sepsis, viral infection (Epstein-Barr virus, cytomegalovirus, HIV, hepatitis, parvovirus B19, rubella virus), fungal and protozoal (leishmaniasis, histoplasmosis, malaria) infections, tuberculosis, brucellosis - cause neutropenia.
• Non-chemotherapeutic drugs used in clinical practice, including intensive therapy, cause severe neutropenia - agranulocytosis.

Non-chemotherapeutic drugs that cause agranulocytosis

Class of drugs	Preparations
Heavy metals	Preparations containing arsenic, gold, mercury diuretics
Analgesics NSAIDs	Acetylsalicylic acid paracetamol, diclofenac, indomethacin ibuprof fen, phenylbutazone, piroxicam, tenoxicam, phenazone
Antipsychotics, sedatives, antidepressants	Chlordiazepoxide, clozapine, diazepam, haloperidol, imipramine, meprobamate, phenothiazine, risperidone, tiapride, barbiturates
Anticonvulsants
Antithyroid drugs	Thiamazole potassium perchlorate, thiouracil derivatives
Antihistamines	Brompheniramine, mianserin
Various LS	Acetazolamide, allopurinol, colchicine, famotidine, cimetidine, ranitidine, metoclopramide, levodopa, oral hypoglycemic agents (glibenclamide), all retinoic acid, tamoxifen, aminoglutethimide, flutamide, sulfasalazine, penicillamine, glucocorticoids
Various chemicals and drugs	Hair dye, 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 developing agranulocytosis is especially high 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 individuals with HLA-B27. In Jews taking clozapine, drug-induced agranulocytosis is associated with the haplotypes HLA-B38, DRB1*0402, DRB4*0101, DQB1*0201, DQB1*0302, in Europeans taking clozapine, agranulocytosis occurs with HLA-DR*02, DRB1*1601, DRB5*02 DRB1*0502. The disease against which agranulocytosis develops is also important. The risk of developing agranulocytosis is high in patients with rheumatoid arthritis receiving captopril, in patients with renal failure receiving probenecid.

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How does leukopenia develop?

Leukopenia may occur due to a disruption in the production, circulation or redistribution of neutrophils. Neutrophils in the body are distributed in three spaces - bone marrow, peripheral blood and tissues. Neutrophils are produced in the bone marrow, leaving which they enter the blood. There are two pools of neutrophils in the blood - freely circulating and marginal, adherent to the vascular wall. The latter make up approximately half of the neutrophils in the blood. Neutrophils leave the bloodstream within 6-8 hours and penetrate into the tissues.

During chemotherapy and radiation therapy, young, actively proliferating cells die, i.e. the bone marrow pool, and myelotoxic agranulocytosis develops. Bone marrow hematopoiesis is also impaired in tumor lesions of the bone marrow, in which bone marrow hematopoiesis is displaced and suppressed by tumor cells. In aplastic anemia, a decrease in the number of myeloid progenitor cells is observed, and the remaining cells are functionally defective, lack adequate proliferative capacity, and are subject to apoptosis.

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

In some congenital forms of leukopenia, aplastic anemia, acute leukemia, and myelodysplastic syndrome, there is a disruption of pluripotent myeloid stem cells, 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 in the bone marrow are infected, which leads to a decrease in neutrophil production, the development 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 when G-CSF acts. As a result, G-CSF in physiological doses does not stimulate granulocytopoiesis. Cyclic neutropenia is caused by a mutation in the gene encoding neutrophil elastase, as a result of which the interaction between neutrophil elastase, serpins and other substances that affect hematopoiesis is disrupted.

The development of drug-induced agranulocytosis not associated with chemotherapy may be caused by toxic, immune, and allergic mechanisms.

Symptoms of leukopenia

Leukopenia has no specific manifestations and can be asymptomatic, its manifestations are caused by the addition 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, infection is detected in 25% of patients, and within 6 weeks - in 100% of patients. The rate of development of leukopenia is important - patients whose neutrophil count has decreased quickly are more susceptible to infectious complications than patients with long-term neutropenia (for example, 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, infection can occur without an increase in body temperature. Almost half of patients with leukopenia have fever with an unspecified source of infection. 25% of febrile patients with neutropenia have a microbiologically proven infection, most of them have bacteremia. In another 25% of patients, infection is diagnosed clinically, but it cannot be confirmed microbiologically. Infection of patients with leukopenia occurs mainly due to the endogenous flora that has colonized the foci of infection.

Isolated leukopenia should be distinguished from neutropenia in cytostatic disease caused by chemotherapy. Cytostatic disease is caused by the death of dividing cells of the bone marrow, gastrointestinal epithelium, intestines, and skin. A frequent manifestation of cytostatic disease is liver damage. Along with infectious complications, anemia, thrombocytopenia, hemorrhagic syndrome, oral syndrome (swelling of the oral mucosa, ulcerative stomatitis), and intestinal syndrome (necrotic enteropathy or neutropenic enterocolitis) are detected. Necrotic enteropathy is an acute inflammatory process caused by the death of intestinal epithelial cells, which manifests itself as flatulence, frequent loose stools, and abdominal pain. Enteropathy leads to the translocation of microbial flora with the subsequent development of sepsis and septic shock. The development of septic shock in a state of agranulocytosis is preceded by necrotic enteropathy in 46% of patients.

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

Transience

Several hours pass from the first signs of infection to the development of severe sepsis. In septic shock in a state of agranulocytosis, a third of patients begin to have a fever only a day before the onset of arterial hypotension. The outcome of septic shock in patients with hemoblastoses in a 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

In soft tissue infection, there is no suppuration, local manifestations of inflammation (redness, swelling, pain) may be insignificant, while general intoxication is expressed. Necrotic enteropathy often leads to perianal damage and inflammation, which are detected 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 of bacterial pneumonia, there are no changes in radiographs, it can only be detected by CT. Peritonitis, complicating the course of necrotic enteropathy, often occurs in an erased manner, without pronounced pain syndrome, peritoneal symptoms may be absent.

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Features of pathogens

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

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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. cyclical.

By time of occurrence:

• Leukopenia can be congenital (Kostmann syndrome, cyclic neutropenia) or acquired during life.

By the severity of leukopenia:

• The depth of the decrease in neutrophil levels determines the risk of developing infectious complications.

Classification of leukopenia by severity

Absolute neutrophil count	Degree of leukopenia	Risk of infectious complications
1-1.5x10 9 /l	Easy	Minimum
0.5-1x10 9 /l	Moderate	Moderate
<0.5x10 9 /l	Severe (agranulocytosis)	High risk

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Etiopathogenetic classification of leukopenia

Impaired formation of neutrophils in the bone marrow

• hereditary diseases (congenital, cyclic leukopenia),
• tumor diseases,
• some medications (medicines), radiation,
• vitamin B12 or folate deficiency,
• aplastic anemia.

Increased destruction of neutrophils

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

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Diagnosis of leukopenia

To diagnose leukopenia, it is necessary to count the absolute number of neutrophils in the blood; determining the number of leukocytes alone is not enough. In a number of diseases, the absolute number of neutrophils may be sharply reduced, while the number of leukocytes in the blood remains normal or even increased due to, for example, lymphocytes, blast cells, etc. To do this, calculate the leukocyte formula, then sum up the percentage of all granulocytes and divide the resulting sum by 100, multiplying it by the number of leukocytes. Neutropenia is diagnosed when the number of neutrophils is below 1.5x10 ⁹ /l. It is also necessary to count erythrocytes and platelets. The association of leukopenia with anemia, thrombocytopenia indicates a possible tumor disease of the blood system. The diagnosis is confirmed by detecting blast cells in the peripheral blood or bone marrow.

The study of bone marrow puncture and trephine biopsy allows for differential diagnosis and the establishment of the mechanism of leukopenia development (impaired production of neutrophils in the bone marrow, increased destruction in the blood, detection of atypical or blast cells, etc.).

If the diagnosis is unclear, it is necessary to additionally test the blood for antinuclear antibodies, rheumatoid factor, antigranulocyte antibodies, conduct liver tests (transaminases, bilirubin, markers of viral hepatitis, etc.), and examine the levels of vitamin B12 and folates.

Difficulties may arise in diagnosing drug-induced agranulocytosis that is not associated with the administration of chemotherapy drugs. Almost 2/3 of patients take more than two drugs, so it is always difficult to clearly determine which of them led to agranulocytosis.

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Criteria for non-chemotherapeutic drug-induced agranulocytosis

• Neutrophil count <0.5x10 ⁹ /L with or without fever, clinical signs of infection and/or septic shock.
• Onset of agranulocytosis during treatment or within 7 days after the first dose of the drug and complete restoration of granulocytopoiesis (>1.5x10 ⁹ /l neutrophils in the blood) no later than one month after stopping the drug.
• Exclusion criteria: history of congenital or immune leukopenia, recent infectious disease (in particular, viral infection), recent chemotherapy or radiation therapy, immune therapy, blood diseases.
• In drug-induced non-cytotoxic agranulocytosis, platelet counts, red blood cell counts, and hemoglobin levels are usually normal. Bone marrow examination can rule out other possible causes of agranulocytosis.
• In drug-induced agranulocytosis, the bone marrow usually has normal or moderately reduced total cellularity and no myeloid progenitor cells.
• In some cases, a deficiency of mature myeloid cells is observed while immature forms (up to the myelocyte stage) are preserved - the so-called "myeloid block", which may be a consequence of the selective interaction of the drug/antibody on mature cells or represent the initial stage of recovery.
• The absence of myeloid precursors means that at least 14 days must pass before leukocytes in the peripheral blood are restored.
• In contrast, with myeloid block, recovery of the white blood cell count can be expected within 2-7 days.

The occurrence of fever in patients with agranulocytosis is an indication for diagnostic search for the infectious agent. Microbiological diagnostics determines the choice of adequate antibacterial therapy regimens. Infection in patients with agranulocytosis is often polyetiological, therefore, detection of only one pathogen should not stop the diagnostic search. Along with traditional microbiological studies, examination of a patient with agranulocytosis includes:

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

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

• clinical manifestations of infection or isolation of the pathogen,
• SSVR,
• identification of laboratory markers of systemic inflammation.

However, 44% of patients with agranulocytosis develop fever without an established source of infection, and only 25% of febrile patients with neutropenia have a microbiologically proven infection. One of the SIRS criteria, neutropenia, is always present in these patients. The development of fever in a patient with agranulocytosis, even in the absence of a source of infection, should be considered as a possible manifestation of sepsis. Such a laboratory marker of the inflammatory reaction as blood procalcitonin can be used to diagnose sepsis in patients with agranulocytosis. However, the addition of fungal or viral infections, which occur with a clinical picture of severe sepsis, can be accompanied by a normal or slightly elevated level of blood procalcitonin.

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

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Leukopenia screening

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

Treatment of leukopenia

The patient is placed in a separate ward (isolation room). When communicating with the patient, the staff must carefully observe aseptic and antiseptic measures (wearing face masks, washing hands with antiseptics, etc.).

In most cases of leukopenia and agranulocytosis, there is no need for specific treatment. The main preventive and therapeutic measures are limited to preventing infection, treating infectious complications that have already arisen, and the underlying disease that has led to leukopenia. Transfusions of whole blood or red blood cell mass, leukocyte suspension, and administration of glucocorticoid hormones undertaken to treat leukopenia should be considered erroneous. The latter can only be used as part of the treatment of the underlying disease that has led to the development of leukopenia, such as systemic lupus erythematosus, rheumatoid arthritis, some forms of acute leukemia, autoimmune leukopenia, etc. It should be borne in mind that administration of glucocorticoids in the presence of agranulocytosis dramatically increases the risk of infectious complications. Depending on the underlying disease (for example, aplastic anemia, Felty's syndrome, autoimmune agranulocytosis), splenectomy and immunosuppressive therapy (cyclosporine, cyclophosphamide, azathioprine, methotrexate, etc.) can be used to treat leukopenia.

In case of folate deficiency, vitamin B12, vitamin B12, folic acid in a dose of up to 1 mg/day, leucovorin at 15 mg per day are indicated. In case of drug-induced non-chemotherapeutic agranulocytosis, it is necessary to discontinue the drug that could cause it.

Features of treatment of infectious complications

The main method of combating complications caused by neutropenia is to carry out measures aimed at preventing and treating infection. Patients with agranulocytosis in the case of infectious complications need to be placed in isolated wards. In most cases, the source of infection, primarily bacterial and fungal etiology, is the gastrointestinal tract, therefore, when agranulocytosis develops, the intestines are decontaminated. For this purpose, antibacterial drugs sensitive to gram-negative flora (ciprofloxacin), trimethoprim/sulfamethoxazole are used. The latter is also active against pneumocystis infection.

In the absence of bacterial infection, antibiotics are not prescribed for prophylactic purposes. When signs of infection appear, empirical antibacterial therapy is started immediately, which can then be modified taking into account the clinically identified source of infection and/or microbiologically confirmed pathogens. Delayed administration of antibiotics in the setting of agranulocytosis, especially in gram-negative infections, significantly increases mortality from sepsis and septic shock.

Treatment of sepsis and septic shock is carried out according to accepted rules. In septic shock, to carry out invasive monitoring even in the presence of thrombocytopenia after transfusion of platelet concentrate, the radial or femoral artery is catheterized, and the central vein is mandatory. To carry out invasive monitoring in these patients, despite leukopenia, catheterization of the pulmonary artery using a Swan-Ganz catheter, transpulmonary thermodilution using a special arterial catheter can be used.

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

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Features of respiratory therapy

The success of respiratory therapy in ARF in patients with leukopenia is associated primarily with the use of noninvasive ventilation. It allows avoiding tracheal intubation in a third of patients whose agranulocytosis is complicated by the development of ARF.

When intubating the trachea and transferring the patient to mechanical ventilation, it is recommended to perform an early (in the first 3-4 days) tracheostomy, which is especially important if the patient has concomitant hemorrhagic syndrome due to thrombocytopenia.

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Features of nutritional support

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

The issue of access for enteral nutrition is important. In cases of severe mucositis and esophagitis, which often occur in patients with agranulocytosis, enteral nutrition can be administered through a nasogastric tube, and in cases of concomitant gastroparesis, which occurs after chemotherapy courses, especially with the use of vincristine, methotrexate, and in sepsis - through a nasointestinal tube. In cases of long-term mucositis and esophagitis, the method of choice for enteral nutrition is gastrostomy. In some cases, after chemotherapy courses (especially with methotrexate), mucositis, salivation, and decreased cough reflex are so severe that tracheostomy is performed in patients even without signs of respiratory failure to separate the airways and prevent aspiration. Use of colony-stimulating factors.

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

In oncology, indications for the use of CSF for the prevention of leukopenia and in the event of febrile leukopenia depend on the patient’s condition, age, intensity of chemotherapy, nosology and stage of the underlying disease.

In drug-induced agranulocytosis, the use of CSF can shorten the duration of drug-induced agranulocytosis by an average of 3-4 days. G-CSF or granulocyte-macrophage CSF (GM-CSF, filgrastim, molgramostim) is prescribed at a dose of 5 mcg / kg per day until the level of granulocytes (leukocytes) increases above 1.5-2x109 / l. However, G-CSF cannot be recommended for routine use in drug-induced agranulocytosis, since along with data confirming the effectiveness of this drug, there are also results of its unsatisfactory use in drug-induced agranulocytosis. Use of granulocyte concentrate transfusions.

The severity of infectious complications during agranulocytosis can be reduced by transfusing granulocyte concentrate. Granulocyte concentrate, unlike leukocyte concentrate and leukocyte suspension, is obtained after special preparation of donors. Donors are given glucocorticoid hormones (usually 8 mg dexamethasone) and 5-10 μg/kg G-CSF subcutaneously 12 hours before granulocyte collection, after which granulocyte apheresis is performed on special automatic blood fractionators. This regimen allows collecting up to (70-80)x10 ⁹ cells from one donor. In Russia, there are no legislative norms allowing the administration of hormonal drugs and CSF to donors. Data on the effectiveness of using granulocyte transfusions to treat sepsis in patients with agranulocytosis are contradictory. In addition, this treatment method has a large number of side effects (risk of viral infection transmission, alloimmunization, pulmonary complications). Thus, transfusion of granulocyte concentrates cannot yet be recommended for routine use in the treatment of sepsis in patients with agranulocytosis.

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How is leukopenia prevented?

Prevention of chemotherapy-induced leukopenia is generally not performed. In case of renal and/or hepatic dysfunction, the doses of chemotherapeutic drugs should be reduced, since drug accumulation is possible, which can lead to prolonged, sometimes irreversible agranulocytosis. In certain categories of oncological and oncohematological patients, prophylactic administration of granulocyte colony-stimulating factor (G-CSF) is performed during chemotherapy to prevent leukopenia and/or shorten its duration.

To prevent agranulocytosis caused by non-chemotherapeutic drugs, it is necessary to take into account the anamnesis data, indications of the development of leukopenia when prescribing drugs.

Leukopenia prognosis

Mortality from complications of leukopenia that arise during the treatment of oncological diseases ranges from 4 to 30%. Mortality from drug-induced non-chemotherapeutic agranulocytosis has decreased in recent decades from 10-22% in the 1990s to 5-10% at present. This decrease occurred due to better patient care, adequate antibacterial therapy for infectious complications, and in some cases, the use of CSF. Higher mortality is observed in drug-induced agranulocytosis in the elderly, as well as in patients who developed it against the background of renal failure or were complicated by bacteremia, septic shock.

Information for the patient

When verifying that a patient has leukopenia or agranulocytosis, the doctor must inform the patient that he should avoid undercooked meat, raw water, use juices, dairy products only in factory packaging, and pasteurized products. It is prohibited to eat unwashed raw fruits and vegetables. When visiting public places, the patient should wear a face mask and avoid contact with people suffering from respiratory diseases. If a high body temperature appears, immediately contact medical personnel and, as a rule, emergency hospitalization.