Anemia in HIV-infected people. Blood diseases due to AIDS (HIV infection) Anemia due to HIV infection causes

Anemia is a common companion to HIV infection. Pathology not only significantly worsens the patient’s quality of life, but also increases mortality rates. Most often this is a normocytic normochromic form, characterized by the accumulation of iron in soft tissues body. In this case, the hemoglobin level in the blood is significantly reduced.

Causes of anemia in HIV infection

Among the factors that contribute to a drop in blood hemoglobin levels in an HIV-infected person, medicine includes:

decrease in total CD4+ cell count below 200/μl;
(significant) weight loss;
history of bacterial pneumonia;
candidal inflammation of the oral cavity;
high level viral load;
taking zidovudine;
being female;
Negroid race;
history of AIDS.

In order not to miss the onset of an anemic state, patients with HIV need constant monitoring of blood hemoglobin levels. If a decrease is detected, additional tests should be ordered.

Symptoms of low hemoglobin

With a decrease in blood hemoglobin and the formation of anemia, patients with HIV infection experience unexplained weakness. Additional feature it is worth mentioning a deterioration in overall health.

How to treat anemia in HIV-infected people?

For elimination pathological condition Highly active antiretroviral therapy (abbreviated HAART) may be used. The technique is one of the treatment options for an anemic condition (and not only) in HIV infection, combining the use of three to four medications simultaneously. The effect of HAART for anemia is recorded after a six-month course.

The next drug that can be prescribed is erythropoietin. The product has received good recommendations from doctors for eliminating anemia caused by the following conditions:

when suppressing the functionality of the bone marrow;
infectious/inflammatory processes occurring in a chronic format;
taking the drug zidovudine, as well as medications from the category of antitumor chemotherapy.

Erythropoietin is prescribed for subcutaneous administration. When calculating the dosage, the formula is used: 100...200 microns per kilogram of the patient’s weight.

Application regimen: three times a week. After the level of red blood cells is restored, maintenance therapy is prescribed - injections are given once for two weeks.

Anemia is a common companion to HIV infection. Pathology not only significantly worsens the patient’s quality of life, but also increases mortality rates. Most often, this is a normocytic normochromic form, characterized by the accumulation of iron in the soft tissues of the body. In this case, the hemoglobin level in the blood is significantly reduced.

Causes of anemia in HIV infection

Among the factors that contribute to a drop in blood hemoglobin levels in an HIV-infected person, medicine includes:

decrease in total CD4+ cell count below 200/μl;

(significant) weight loss;

history of bacterial pneumonia;

candidal inflammation of the oral cavity;

high level of viral load;

taking zidovudine;

feverish conditions;

being female;

history of AIDS.

In order not to miss the onset of an anemic state, patients with HIV need constant monitoring of blood hemoglobin levels. If a decrease is detected, additional tests should be ordered.

Symptoms of low hemoglobin

With a decrease in blood hemoglobin and the formation of anemia, patients with HIV infection experience unexplained weakness. An additional sign is a deterioration in overall health.

How to treat anemia in HIV-infected people?

Highly active antiretroviral therapy (HAART) can be used to eliminate the pathological condition. The technique is one of the treatment options for an anemic condition (and not only) in HIV infection, combining the use of three to four medications simultaneously. The effect of HAART for anemia is recorded after a six-month course.

The next drug that can be prescribed is erythropoietin. The product has received good recommendations from doctors for eliminating anemia caused by the following conditions:

when suppressing the functionality of the bone marrow;

infectious/inflammatory processes occurring in a chronic format;

taking the drug zidovudine, as well as medications from the category of antitumor chemotherapy.

Erythropoietin is prescribed for subcutaneous administration. When calculating the dosage, the formula is used: 100...200 microns per kilogram of the patient’s weight.

Application regimen: three times a week. After the level of red blood cells is restored, maintenance therapy is prescribed - injections are given once for two weeks.

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Types of anemia: symptoms and treatment

The human body is quite vulnerable to various diseases. Questions about what anemia is, the symptoms and treatment of this disease are asked quite often. Low level hemoglobin in the blood is a rather unpleasant phenomenon that can seriously complicate a person’s full life activity. Hemoglobin is a complex organic compound protein with iron molecules. This substance is responsible for delivering oxygen trapped in the lungs to all parts of the body. Treatment of anemia of various origins is a separate area in modern medicine. In order to know how to treat anemia, it is necessary to understand the mechanism of occurrence of this disease in the body.

Causes of anemia

A decrease in the level of red cells in the blood cannot occur without the influence of significant internal and external factors.

The reasons for a decrease in hemoglobin levels may be the following:

Bleeding. They can be obvious or hidden. Obvious blood loss includes such blood loss, the source of which can be determined without testing. This can be prolonged discharge in women during their menstrual periods, bleeding during and after surgical operations. External hemorrhoids, in turn, can be accompanied by heavy blood loss. Hidden bleeding is characteristic of the gastrointestinal tract. Anemia is more common in women than in men due to their anatomical and reproductive structure.
Heredity. Anemia can be quite painful a large number of close relatives. It is quite difficult to resist the gene factor.
Chronic and infectious diseases, which affect the lifespan of red blood cells. Worms in the intestines actively absorb vitamin B-12, which serves to form hemoglobin.
Blood donation. After a donor's blood is taken, the patient's blood volume and quality are significantly reduced. It takes some time to produce enough hemoglobin.
Poor nutrition. A similar reason is more typical for a growing child’s body. But, with a lack of sufficient funds in adults, they are not able to provide their body with the necessary amount of nutritious food.

As a result of these factors, anemia occurs, which has the following degrees:

Mild, in which the hemoglobin level is from 90 g to 110 g per liter of blood.
Average. This figure is in the range of 70-90 g/l.
Heavy. It poses a serious threat to health, since the hemoglobin content is less than 70 g/l.

Knowing the basic conditions that cause the disease, it is not difficult to understand why quite specific and varied symptoms arise.

Signs of anemia

A decrease in the level of hemoglobin in the blood causes certain changes in the processes occurring in the body and in the behavior of the patient. Depending on the type of anemia, they can be expressed by general or purely specific symptoms.

Common symptoms of anemia are:

apathy and malaise;

general weakness;

increased fatigue;

rolling lightheadedness;

rapid pulse;

constant headache;

elevated temperature;

sudden fainting;

increased fragility of nails and hair, the appearance of gray hair;

change taste qualities and sense of smell.

As the level of hemoglobin in the blood continues to decrease, the following signs of anemia appear:

drying of the tongue and its redness;

yellowing of the skin;

loss of appetite;

bowel dysfunction (diarrhea or constipation);

absent-mindedness;

memory losses;

insomnia;

change from normal skin color to sallow;

drying out of the throat, which leads to difficulty swallowing chewed food.

Further progression of the disease causes the following symptoms:

blood in urine and stool;

decreased muscle functionality, which leads to involuntary urination and defecation;

swelling and loss of sensation in the limbs;

decreased mental abilities;

loss of balance when walking;

decreased immunity, which leads to persistent infectious diseases;

ulcers in the corners of the mouth that do not heal despite all efforts.

The last symptom that indicates anemia is severe darkening of the urine, associated with increased removal of dead red blood cells from the body.

If such syndromes are detected, you should contact medical care. Delay can have fatal consequences.

By nature, anemia in men and women is a consequence of one or more diseases. Based on this, the cause of the decrease in hemoglobin is targeted in order to get rid of the consequences of the disease. The prerequisites for the onset of the disease can only be determined by conducting a comprehensive examination.

Diagnostics is carried out in the following ways:

Examination by a specialist. During a personal conversation, the doctor can establish basic data about the course of the disease: the onset of the disease, its main symptoms and possible reasons. An external physical examination will allow you to determine the extent of damage to the body.
Carrying out a blood test. The test results will indicate the level of hemoglobin in the blood, the size of red blood cells and the number of reticulocytes. The level of iron concentration in the blood is also determined.
Fibrogastroscopy. This procedure, associated with the introduction of a probe into the gastrointestinal tract, makes it possible to identify the presence of areas of hidden bleeding. They can be an ulcer or gastritis.
Intestinal examination. With the help of an external examination and a sigmoidoscope, the condition of the large and small intestines is established. This allows you to find pathologies and check the rectum for the presence of hemorrhoids.
X-ray examination. By introducing a contrast agent, any abnormalities in intestinal development can be detected.
Magnetic resonance imaging examination. 3D image internal organs will give the most accurate picture of the patient's condition.

After specific examinations, consultations are held with an infectious disease specialist, oncologist, gastroenterologist and nephrologist. Women must undergo an examination by a gynecologist. When a diagnosis such as anemia is made, comprehensive treatment is prescribed. You need to be prepared for the fact that it will last quite a long time.

Procedure for treating anemia

Treatment for anemia is aimed at normalizing hemoglobin levels in the blood. This implies restoration of the required concentration of red blood cells and iron. But before these vital indicators are restored, all diseases that caused pathological changes in the body are cured. These treatments may include surgery, antibiotics, and immune-boosting medications. After the sources of bleeding and factors that destroy red blood cells are eliminated, a restorative course is carried out.

Depending on the type of disease, the patient is prescribed the following types of treatment:

For bleeding. In case of heavy bleeding, its cause is determined, and urgent measures are taken to stop blood loss. The loss of hemoglobin can be compensated by the introduction of donor blood. Infusion of physiological fluids and preparations with a high iron content is used. As a rule, after wounds heal, the hemoglobin concentration quickly returns to normal.
With a low level of red blood cells. If the level of red blood cell production is reduced, the patient is prescribed medications containing ferrous iron. They are well absorbed by the body. But this solution does not give quick results, since iron is initially absorbed by the mucous membrane of the gastrointestinal tract. When taking such drugs, you should strictly follow your doctor's recommendations. An overdose of iron can cause severe poisoning and problems with the musculoskeletal system. Taking such drugs on an empty stomach is not allowed. They should be consumed with meals. This will avoid unpleasant sensations.
With vitamin B12 deficiency. This substance can be introduced into the body using injections, tablets or nasal spray. As a rule, relief occurs quite quickly after the start of the administration of vitamin preparations. If a person's body is unable to absorb vitamin B12 from foods, they will need constant injections or pills throughout their lives.
With bone marrow damage. Disturbances in the functioning of the bone marrow cause numerous disturbances in the functioning of many internal organs. One of these consequences may be anemia. The solution to this problem may be a complete blood transfusion or a bone marrow transplant from a donor.

In cases where all treatment methods have failed, surgery is performed. The patient's spleen, an organ in which a large number of red blood cells die, is removed.

Disease prevention

You can avoid a pathological decrease in the level of hemoglobin in the blood if you follow certain norms and rules of behavior.

Prevention of anemia of various origins involves performing the following procedures:

Regular examinations by a specialist with tests. This will help detect relapse of the disease at its early stage. You may need to adjust your medication intake.
Regular visits to sanatoriums. Therapeutic procedures and fresh air will significantly strengthen the body and cardiovascular system.
Getting rid of bad habits such as smoking and drinking alcohol. They negatively affect the immune system and blood composition.
Balanced diet. You should include foods rich in vitamin B12 and iron in your diet. These include fish, seafood, milk, oysters. Quite a bit of folic acid found in fresh vegetables (cabbage, lettuce, tomatoes). Eating eggs and nuts will significantly increase your blood iron levels.
Losing excess weight. Supplying the body with a large volume of blood leads to a heavy load on the cardiovascular system and a decrease in blood quality.
Change of place of work. Quite often, the cause of anemia is harmful working conditions. If lead enters the body, this inevitably leads to a decrease in hemoglobin levels.
Maintaining an active lifestyle. Regular walks in the fresh air help train and strengthen the heart muscle and blood vessels. In the event of a relapse, they will more easily tolerate the increased load.
Regularly taking preventive medications prescribed by your doctor.
Timely response to all symptoms indicating hidden bleeding. To stop open bleeding you should always have on hand necessary funds. All family members should learn the rules of first aid for open wounds.

It should be remembered that any disease can cause a recurrence of anemia. As soon as the first symptoms appear, you must seek medical help.

We should not forget about centuries of experience traditional medicine. To increase hemoglobin levels, it is recommended to eat apples, strawberries, rose hips and currants. For heavy bleeding during menstruation and hemorrhoids, it is recommended to drink a tincture of rowan berries and rose hips, yarrow leaves and nettles. 100 grams of this liquid, drunk 3 times a day, will bring significant relief.

Anemia is not a sentence according to which a person must give up his life. If you consult a doctor in a timely manner, you can quickly return the patient to a normal state.

Proper treatment and constant preventive measures will allow you to forget about this disease forever and live a long, fulfilling life.

krovetvorenie.ru

Anemia in HIV-infected persons

Anemia in HIV-infected people can have serious consequences, ranging from decreased quality of life to progression of the underlying disease, worsening prognosis and survival.

Factors associated with development in HIV-infected patients include:

history of AIDS;
CD4+ cell count<200/мкл;
female;
Negroid race;
treatment with zidovudine;
reduced body mass index;
history of bacterial pneumonia;
oral candidiasis;
fever.

Observation of 32,867 patients showed a decrease in survival with hemoglobin levels<100 г/л. Рабочей группой по анемии при ВИЧ-инфекции разработаны следующие доказательно-обоснованные рекомендации по выявлению анемии и ведению ВИЧ-инфицированных пациентов:

Monitor hemoglobin levels and question for weakness.
At hemoglobin level<130 г/л у мужчин и <120 г/л у женщин выявить и, по возможности, устранить причины.
The need for highly active antiretroviral therapy is indicated.
Therapy with erythropoietin (EPO) at a dose of 40,000 units once a week for uncorrectable hemoglobin levels<130 г/л у мужчин и <120 г/л у женщин.
Therapy should continue until symptoms resolve and hemoglobin increases >130 g/l in men and >120 g/l in women.

Comments: The authors correctly point to anemia as a contributing factor to the development of weakness in some HIV-infected people. They also indicate that anemia is associated with a poor prognosis, although the direct cause-and-effect relationship is not entirely clear. Most AIDS-related conditions also adversely affect prognosis, and a clear limitation of the recommendations described above is the lack of evidence of a change in survival prognosis when anemia is corrected. With regard to weakness, it is classically thought to develop in chronic anemia when the hemoglobin level<110 г/л у мужчин и <100 г/л у женщин. При почечной недостаточности руководства рекомендуют начинать терапию эритропоэтином при гемоглобине <120 г/л у мужчин и <110 г/л у женщин.

Volberding P.A., Levine A.M., Dieterich D., Mildvan D., Mitsuyasu R., Saag M;

Anemia in HIV Working Group.

Anemia in HIV infection: clinical impact and evidence-based management strategies.

Clin Infect Dis 2004; 38: 1454-63

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Many chronic diseases in most cases can be accompanied by the development of anemic syndrome. For example, anemia is often diagnosed in CKD - chronic kidney disease. Many patients are concerned about an important question: is anemia a blood cancer or not? We can say for sure that anemia is a blood disease that can only develop into blood cancer. This is precisely the reason why it is worth starting slow treatment and eliminating the cause of anemia.

Anemia with uterine fibroids

Despite the fact that uterine fibroids are not a very dangerous disease, this pathology can lead to serious complications. Anemia due to uterine fibroids is a common condition that is caused by complications. In this condition, the hemoglobin content in red blood cells is significantly reduced. A characteristic symptom of uterine fibroids is menstrual irregularity, which manifests itself as long and heavy periods.

Prolonged menstruation can lead to significant blood loss, which causes anemia with uterine fibroids. As a result, the level of hemoglobin in the blood drops, and the patient begins to complain of signs of anemia. With heavy bleeding, patients complain of severe thirst and dry mouth. If left untreated, this dangerous condition can be fatal.

Anemia in rheumatoid arthritis

Anemic syndrome is a common companion with rheumatoid arthritis. According to statistics, anemia in rheumatoid arthritis develops in almost 50% of patients. Often it is the chronic course of the disease that is diagnosed, sometimes iron deficiency anemia or anemia due to a lack of vitamin B12. The development of hemolytic or mixed anemia is much less common.

It has been established what factors lead to the development of anemia in rheumatoid arthritis. These include:

Changes in iron metabolism.
Reduced life expectancy of red blood cells.
In some cases, the toxic effects of cytokines lead to anemia.
Some cases of anemia are caused by medications.

Preventing the occurrence of anemia in rheumatoid arthritis lies mainly in correct and adequate treatment tactics. Only effective and successful treatment of the underlying disease can eliminate the cause of anemia. An additional method of treatment is taking iron supplements.

Anemia in liver cirrhosis

The appearance of anemia in liver cirrhosis is considered common. Anemia is caused by various factors that are directly related to problems of the liver or endocrine system. Elimination of anemia and therapeutic measures are carried out only in the treatment of the underlying disease that provoked the development of anemia.

Microcytic anemia is often observed, which is caused by the following factors: chronic inflammation of the liver leads to portal hypertension, cases of venous bleeding occur in the liver, esophagus and stomach. The disease also leads to problems in the metabolic process of folic acid and vital vitamin B12 - all these reasons cause a drop in hemoglobin in the blood.

Anemia due to hypothyroidism

Almost half of all patients with hypothyroidism may suffer from a mild form of anemia. Anemia is caused by a lack of hormones. An active decrease in plasma volume may masquerade as a decrease in the total level of red blood cells in hypothyroidism. There is also iron deficiency anemia, which occurs in a mild form. Hypothyroidism often causes atrophic gastritis, and as a result the patient may have a deficiency of iron or vitamin B12.

Clinical manifestations may vary from person to person. Therapeutic therapy consists of prescribing thyroxine. Long-term use of this drug can significantly normalize the course of all processes, as well as effective treatment. Additionally, therapy is prescribed that eliminates iron and vitamin B12 deficiency.

Anemia in HIV patients can lead to a significant decrease in standard of living, worse prognosis and survival, as well as serious consequences and progression of the disease. There are some factors that lead to the development of anemia with this diagnosis: viral load, bacterial pneumonia, oral candidiasis, fever.

Anemia due to HIV infection causes patients to feel weak and worsens their overall health. In more severe cases, anemia due to HIV becomes the cause of AIDS. To quickly identify and treat anemia, patients are diagnosed with hemoglobin levels in the blood and the necessary tests. Then therapy is prescribed that eliminates all symptoms of anemia.

With properly selected and adequate treatment, it is quite possible to achieve a good result by eliminating the disease. However, without the necessary measures and proper treatment, hemorrhoids can lead to the development of serious complications, including anemia. Therefore, at the first signs of the disease, it is extremely important to begin timely treatment so as not to miss dangerous complications. Often, frequent, even minor bleeding can lead to the development of secondary anemia.

Severe hemorrhoidal bleeding causes acute anemia. In this case, there is a sharp decrease in the amount of hemoglobin, which carries oxygen to the tissues. As a result, all internal organs are affected due to lack of oxygen in the body. Patients with such complications complain of increased fatigue, weakness, and rapid pulse. The chronic course of anemia develops over several months.

The acute form is accompanied by the release of whole blood clots, the patient’s skin becomes pale, and the lips turn blue. In the chronic form, only certain areas of the body turn pale. Also, the acute form is accompanied by dizziness and tinnitus. Dry mouth, rapid breathing, frequent fainting, and low body temperature are observed. With such a complication, immediate intervention by a specialist is required.

Gastritis occurs in almost every third person - this disease is so common. Many patients live for a long period of time without the necessary treatment and diet. However, some forms of gastritis can have dangerous manifestations for human health. The atrophic form of gastritis can cause such a serious complication as anemia. For diagnosis, colonoscopy may be prescribed for anemia to take samples for histology.

Any form of gastritis predisposes the patient to anemia. But with atrophic gastritis, this symptom almost always appears. There are some reasons why iron deficiency occurs in the patient's body: unbalanced nutrition or impaired absorption of iron. Anemia manifests itself with the following manifestations: fatigue, fatigue, problems with skin, hair and nails.

Anemia in cancer is quite common, especially after chemotherapy. There are three factors that cause anemia in oncology: slow production of red blood cells, rapid destruction of blood elements or internal bleeding. Also, all methods of cancer treatment, be it chemotherapy or radiation, have a rather negative effect on hematopoiesis. Cases of anemia in leukemia are often recorded.

Lack of appetite and bouts of vomiting lead to a lack of essential elements and poor nutrition. Breast or lung cancer causes a negative effect on the bone marrow, which displaces healthy material. In some cases, the immune reaction leads to anemia. Anemia in stomach cancer occurs as a result of a lack of hematopoietic elements. Any therapeutic therapy should be carried out only with proper and healthy nutrition.

Anemia with pneumonia

Normochromic anemia develops as a result of chronic lung diseases. The reaction of the immune system to its own healthy cells is the cause of anemia in most cases. Anemia with pneumonia often does not require correction. Only in rare cases does anemia occur due to drug allergies. The drop in hemoglobin is noted as moderate, the anemic syndrome is normochromic in nature. With anemia caused by pneumonia, patients complain of low performance, shortness of breath and tinnitus.

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Anemia - symptoms and treatment

Anemia is a decrease in the number of red blood cells - red blood cells - below 4.0 x 109 / l, or a decrease in hemoglobin level below 130 g / l in men and below 120 g / l in women. Anemia during pregnancy is characterized by a decrease in hemoglobin below 110 g/l.

This is not an independent disease; anemia occurs as a syndrome in a number of diseases and leads to disruption of the oxygen supply to all organs and tissues of the body, which, in turn, provokes the development of many other diseases and pathological conditions.

Depending on the concentration of hemoglobin, it is customary to distinguish three degrees of severity of anemia:

Grade 1 anemia is registered when the hemoglobin level decreases by more than 20% of the normal value;
anemia of the 2nd degree is characterized by a decrease in hemoglobin content by approximately 20–40% of the normal level;
Anemia of the 3rd degree is the most severe form of the disease, when hemoglobin decreases by more than 40% of the normal value.

Only a blood test can clearly show that a patient has stage 1 or a more severe stage.

What is it: anemia, that is, anemia, is nothing more than a lack of hemoglobin in the blood. Namely, hemoglobin carries oxygen throughout all tissues of the body. That is, anemia is caused precisely by a lack of oxygen in the cells of all organs and systems.

Nature of nutrition. With insufficient consumption of iron-containing foods, iron deficiency anemia can develop, this is more common in population groups where there is already a high level of nutritional anemia;
Disturbances in the gastrointestinal tract (in case of disturbances in the absorption process). Since iron absorption occurs in the stomach and upper part of the small intestine, if the absorption process is disrupted by the mucous membrane of the digestive tract, this disease develops.
Chronic blood loss (gastrointestinal bleeding, nosebleeds, hemoptysis, hematuria, uterine bleeding). Belongs to one of the most important causes of iron deficiency conditions.

Iron-deficiency anemia

The most common form of anemia. It is based on a violation of the synthesis of hemoglobin (oxygen carrier) due to iron deficiency. It is manifested by dizziness, tinnitus, flickering of spots before the eyes, shortness of breath, and palpitations. Dry skin, pallor are noted, and cracks and cracks appear in the corners of the mouth. Typical manifestations are brittleness and layering of nails, their pepper striations.

Aplastic anemia

This is often an acquired acute, subacute or chronic disease of the blood system, which is based on a violation of the hematopoietic function of the bone marrow, namely a sharp decrease in its ability to produce blood cells.

Sometimes aplastic anemia begins acutely and develops quickly. But more often, the disease occurs gradually and does not manifest itself with clear symptoms for quite a long time. The symptoms of aplastic anemia include all the symptoms characteristic of a lack of red blood cells, platelets and leukocytes in the blood.

B12 deficiency anemia

It occurs when there is a lack of vitamin B12 in the body, which is necessary for the growth and maturation of red blood cells in the bone marrow, as well as for the proper functioning of the nervous system. For this reason, one of the hallmark symptoms of B12 deficiency anemia is tingling and numbness in the fingers, and an unsteady gait.

Hemolysis occurs under the influence of antibodies. These may be maternal antibodies directed against the child’s red blood cells if the child and mother are incompatible with the Rh antigen and, much less frequently, with the ABO system antigens. Antibodies against one's own red blood cells can be active at normal temperatures or only when cooled.

They can appear for no apparent reason or due to the fixation of incomplete hapten antigens, foreign to the body, on red blood cells.

We list the main signs of anemia that can worry a person.

pale skin;
increased heart rate and breathing;
fast fatiguability;
headache;
dizziness;
noise in ears;
spots in the eyes;
muscle weakness;
difficulty concentrating;
irritability;
lethargy;
slight increase in temperature.
Among the symptoms of anemia, the leading ones are those directly related to hypoxia. The degree of clinical manifestations depends on the severity of the decrease in hemoglobin number.
With a mild degree (hemoglobin level 115-90 g/l), general weakness, increased fatigue, and decreased concentration may be observed.
With moderate levels (90-70 g/l), patients complain of shortness of breath, rapid heartbeat, frequent headaches, sleep disturbances, tinnitus, decreased appetite, and lack of sexual desire. Patients are distinguished by pale skin.
In severe cases (hemoglobin less than 70 g/l), symptoms of heart failure develop.

With anemia, in many cases there are no symptoms. The disease can only be detected through laboratory blood tests.

Diagnosis of the disease

In order to understand how to treat anemia, it is important to determine its type and cause of development. The main method of diagnosing this disease is to test the patient’s blood.

for men 130-160 grams per liter of blood.
for women 120-147 g/l.
for pregnant women, the lower limit of the norm is 110 g/l.

Naturally, methods of treating anemia differ radically depending on the type of anemia, its cause and severity. But the basic principle of treating anemia of any kind is the same - it is necessary to fight the cause that caused the decrease in hemoglobin.

If you have anemia caused by blood loss, you need to stop the bleeding as quickly as possible. In case of large blood loss that threatens life, donor blood transfusion is used.
For iron deficiency anemia, you should eat foods rich in iron, vitamin B12 and folic acid (they improve iron absorption and hematopoietic processes); your doctor may also prescribe medications containing these substances. Folk remedies are often effective.
In case of anemia caused by infectious diseases and intoxication, it is necessary to treat the underlying disease and take urgent measures to detoxify the body.

In case of anemia, an important condition for treatment is a healthy lifestyle - proper balanced nutrition, alternating exercise and rest. It is also necessary to avoid contact with chemical or toxic substances and petroleum products.

An important component of treatment is a diet with foods rich in substances and microelements that are necessary for the process of hematopoiesis. What foods should be eaten for anemia in a child and an adult? Here is the list:

meat, sausages;
offal - especially liver;
fish;
egg yolks;
whole grain flour products;
seeds - pumpkin, sunflower, sesame;
nuts - especially pistachios;
spinach, cabbage, Brussels sprouts, fennel, parsley leaves;
beet;
black currant;
sprouts, wheat germ;
apricots, prunes, figs, dates;

You should avoid drinking drinks containing caffeine (for example, tea, coffee, cola), especially during meals, because caffeine interferes with iron absorption.

Iron supplements for anemia

Iron supplements for anemia are much more effective. The absorption of this microelement in the digestive tract from iron preparations is 15-20 times higher than from food.

This allows you to effectively use iron supplements for anemia: quickly increase hemoglobin, restore iron reserves, eliminate general weakness, fatigue and other symptoms.

Ferretab composite (0154g ferrous fumarate and 0.0005g folic acid). Additionally, it is advisable to take ascorbic acid in a daily dose of 0.2-0.3 g).
Sorbifer durules (0.32 g of ferrous sulfate and 0.06 g of vitamin C) is available in tablets, daily dosage depending on the degree of anemia, 2-3 times a day.
Totema - available in 10 milliliter bottles, the content of elements is the same as in the sorbifer. It is used internally, can be diluted with water, it can be prescribed for intolerance to tablet forms of iron. Daily dose 1-2 doses.
Fenyuls (0.15g, ferrous sulfate, 0.05g vitamin C, vitamins B2, B6, 0.005g calcium pantothenate.
Vitamin B12 in 1 ml ampoules of 0.02% and 0.05%.
Folic acid in tablets 1 mg.
Ampoule iron preparations for intramuscular and intravenous administration are sold only by prescription and require injections only in hospital settings due to the high frequency of allergic reactions to these drugs.

You should not take iron supplements together with medications that reduce their absorption: Levomycytin, Calcium supplements, Tetracyclines, Antacids. As a rule, iron supplements are prescribed before meals; if the drug does not contain vitamin C, then an additional intake of ascorbic acid is required in a daily dose of 0.2-0.3 g.

For each patient, the daily requirement for iron is specially calculated, as well as the duration of the course of treatment, and the absorption of the specific drug prescribed and the iron content in it are taken into account. Usually long courses of treatment are prescribed, therapeutic doses are taken for 1.5-2 months, and prophylactic doses are taken in the next 2-3 months.

Iron deficiency anemia, if not treated early, can have serious consequences. A severe degree progresses to heart failure associated with tachycardia, edema, and low blood pressure. Sometimes people end up in the hospital with a sudden loss of consciousness, the cause of which is undertreated or not detected in time anemia.

Therefore, if you suspect that you have this disease or are prone to low hemoglobin, then you should take a blood test every three months.

simptomy-treatment.net

WHAT IS ANEMIA?

WHAT CAUSES ANEMIA?

HOW IS ANEMIA TREATED?

WHAT IS ANEMIA?

Anemia is a lack of hemoglobin. Hemoglobin is a protein (protein) in red blood cells. It carries oxygen from the lungs to the rest of the body.

Anemia can cause lethargy, shortness of breath and dizziness. People with anemia do not feel as well as people with normal hemoglobin levels. It's harder for them to work. This is called "deterioration in quality of life."

Hemoglobin levels are measured as part of a complete blood count. See Fact Sheet 121 for more information about these laboratory tests. Hemoglobin is measured in grams per deciliter, the amount in a given blood sample.

Anemia is determined by the level of hemoglobin. Most doctors agree that a hemoglobin level below 6.5 indicates life-threatening anemia. A normal hemoglobin level is at least 12 in women and 14 in men.

Women have lower hemoglobin levels. The same can be said for old people and very young people. Africans have a higher incidence of anemia than other ethnic groups.

WHAT CAUSES ANEMIA?

The bone marrow produces red blood cells. This process requires the presence of iron, vitamin B12 and folic acid (vitamin B6). Erythropoietin stimulates the production of red blood cells. Erythropoietin is a hormone produced by the kidneys.

Anemia can be caused by the body not making enough red blood cells. This can also be caused by their destruction or death. Several factors can cause anemia:

Lack of iron, vitamin B12 or folic acid. A lack of folic acid can cause megaloblastic anemia, in which the red blood cells become large but pale (see fact sheet 121).

Bone marrow or kidney damage

Blood loss due to internal bleeding or the menstrual cycle in women.

Destruction of red blood cells (hemolytic anemia)

HIV infection can cause anemia. This can also be done by opportunistic infections (see fact sheet 500), so-called. HIV-associated diseases. Many drugs commonly used to treat HIV and related diseases can cause anemia.

Anemia was much more common in the past. More than 80% of people diagnosed with AIDS had some degree of anemia. People with more advanced HIV infection or lower CD4 cell counts had higher levels of anemia.

Rates of anemia began to decline when people started taking combination antiretroviral therapy (ART). Severe forms of anemia have become rare. However, ART did not eliminate anemia. A large study was conducted that showed that about 46% of patients had mild or moderate forms of anemia after a year of taking ART.

Several factors are associated with increased rates of anemia among people with HIV:

Low CD4 cell count (see fact sheet 124)

Taking AZT (Retrovir Fact Sheet 411)

HIV progresses faster in people diagnosed with anemia. The rate is about five times higher among people with anemia compared to those without. Anemia is also associated with a high risk of death. Treatment of anemia has been reported to eliminate these risks.

HOW IS ANEMIA TREATED?

The method of treating anemia depends on the cause of its occurrence.

First, treat all chronic bleeding. This could be internal bleeding, hemorrhoids, or even frequent nosebleeds.

Stop taking or reduce the dose of the drug causing anemia

These methods may not work. For example, it may not be possible to stop taking all medications that cause anemia. There are two additional treatments: erythropoietin injections and blood transfusions.

Erythropoietin stimulates the production of red blood cells. In 1985, scientists found a way to produce synthetic erythropoietin. It is administered subcutaneously, usually once a week. The most well-known brand of erythropoietin is Procrit®.

A large study among people living with HIV found that erythropoietin injections reduced the risk of death. Blood transfusions seem to increase it. Because of these risks, blood transfusions are rarely used to treat anemia.

Blood transfusions were previously the only way to treat severe forms of anemia. However, transfusion can cause infection and suppress the immune system. Transfusion appears to cause rapid progression of HIV and increase the risk of death in patients with HIV.

Anemia increases fatigue and makes people feel unwell. It increases the risk of disease progression and death. It can be caused by HIV infection or other diseases. Many drugs used to treat HIV and related diseases can also cause anemia.

Anemia has always been a problem for people with HIV/AIDS. The number of serious, severe cases of anemia dropped incredibly when people started using ART. However, almost half of PLHIV still have mild or moderate anemia.

Treating anemia improves the health and survival of PLHIV. Treatment of bleeding, lack of iron, or vitamins are the first steps. If possible, you should stop taking medications that cause anemia. If necessary, the patient should receive treatment with erythropoietin, or in extremely rare cases, a blood transfusion.

These data indicate a high incidence of anemia among HIV-infected patients at all stages of the disease before the use of HAART. Thus, the use of HAART has recently been associated with a decrease in the incidence and severity of anemia.

Etiology of Anemia
^

Anemia associated with decreased red blood cell production

Another cause of hypoproliferative anemia in HIV-infected patients is infection of the bone marrow with parvovirus B19 (infection at the level of early erythrocyte precursors - pronormoblasts).

Thus, bone marrow failure of red cells, platelets, and neutrophils has been described in association with parvovirus B19. This may be pure anemia with no or minimal manifestations of thrombocytopenia and neutropenia. Parvovirus infection is usually acquired in childhood and is one of the five most common childhood exanthems. An antiviral antibody response with the development of late resistance to infection is known. Approximately 85% of adults had serological evidence of previous parvovirus infection. However, the serological prevalence of such antibodies among HIV-infected patients is only 64%. This suggests an inability of these individuals to maintain adequate humoral immunity, resulting in reactivation of latent infection. Diagnosis of parvovirus (B19) infection can be based on the detection in the bone marrow of giant pronormoblasts with an accumulation of basophilic chromatin and light cytoplasmic vacuoles. The diagnosis can be confirmed by FISH using DNA probes specific for parvovirus B19. Therapy for parvovirus-induced red cell aplasia involves intravenous gammaglobulin infusions. Gammaglobulin contains antibodies from the plasma of many donors, most of whom have been exposed to parvovirus. Infusion of these antibodies can neutralize the virus and restore normal hematopoiesis. Recurrence of anemia induced by parvovirus B19 requires repeated treatment.

^ Incidence of anemia in HIV-infected patients (Table 1)

Cause of anemia	mechanism
Decreased red blood cell production (low reticulocyte count, normal or decreased free bilirubin)	A) neoplastic infiltration of bone marrow Lymphoma Kaposi's sarcoma Lymphogranulomatosis Other B) infections Mycobacterium avium complex Mycobacterium tuberculosis Cytomegalovirus B19 parvovirus Fungal infection Other C) medications (see Table 2) D) direct effect of HIV Abnormal growth of BOE-E Anemia of chronic disease Impaired production and/or use of erythropoietin. E) iron deficiency anemia due to chronic blood loss.
Ineffective production (low reticulocytes, high conjugated bilirubin)	A) folic acid deficiency Nutritional Pathology of the jejunum. Malabsorption B) B12 deficiency Malabsorption in the ileum Pathology of the stomach with decreased production of internal factor Production of antibodies to intrinsic factor, for example in pernicious anemia.
Hemolysis (increased levels of reticulocytes and indirect bilirubin)	A) hemolytic anemia with a positive Coombs test. B) hemophagocytic syndrome. C) thrombotic thrombocytopenic purpura D) disseminated intravascular coagulation E) medications. Sulfonamides, dapsone Oxidants in patients with glucose-6-phosphate dehydrogenase deficiency.

^ Hemolytic anemia.

Increased destruction of red blood cells may occur in HIV-infected patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency who have been exposed to oxidants, and in HIV-infected patients with disseminated intravascular coagulation and TTP. In the last two situations, thrombocytopenia and fragmented red blood cells are observed in the peripheral blood smear; Heinz bodies are observed in association with G6PD deficiency. Hemophagocytic syndrome has also been described in association with HIV, with significant phagocytosis of red blood cells by bone marrow macrophages. In addition, the destruction of red blood cells, leading to anemia in HIV-infected patients, is due to the production of autoantibodies with a positive Coombs test and reduced resistance of red blood cells. Interestingly, the presence of antibodies on the membrane of red blood cells (positive direct Coombs test) is reported in 18% to 77% of cases of HIV-infected patients, despite the fact that hemolysis or destruction of red blood cells is negligible. Anti-I antibodies and antibodies against anti-U antigens have been described in 64% and 32% of HIV-infected patients, respectively. A high incidence of a positive direct Coombs test can also be found in patients with other hypergammaglobulinemic conditions, which, however, indicates the secondary nature of a positive direct Coombs test in polyclonal hypergammaglobulinemia, which is known to occur in HIV infection.

^ Anemia due to ineffective red blood cell production (B12 and/or folate deficiency anemia)

Folic acid is absorbed in the jejunum and is responsible for carboxylation during DNA synthesis. FA deficiency results in megaloblastic anemia with large oval red blood cells in the peripheral blood, hypersegmented polys and abnormalities in all three lineages of hematopoiesis, resulting in anemia, neutropenia and thrombocytopenia. Folic acid is mainly found in green vegetables and is unstable in heat. Since tissue stores of folate are relatively small, a lack of folate in the diet over a period of 6-7 months can lead to anemia. Thus, it is clear that HIV-infected patients who cannot eat well, as well as patients with jejunal insufficiency, are not able to absorb the required amount of folic acid. This insufficient absorption can lead to anemia, neutropenia and thrombocytopenia. In folate deficiency anemia, reticulocyte levels are low, but unconjugated bilirubin is increased. RBC MCV is high. Classic changes in megaloblastic anemia are found on bone marrow examination, with low red blood cell and serum folate levels.

Ineffective erythropoiesis, pancytopenia in the blood, increased free bilirubin levels and low reticulocyte levels are also observed with vitamin B12 deficiency. In the stomach, vitamin B12 binds to intrinsic factor secreted by parietal cells, then the B12+intrinsic factor complex is absorbed in the ileum. Thus, malabsorption of B12 can easily develop in various gastric disorders (for example, achlorhydria), in the production of antibodies to intrinsic factor of parietal cells ("pernicious anemia"), or in various disorders of the small and ileal intestine (infections, Crohn's disease). Thus, while B12 deficiency is highly unlikely to occur solely due to poor diet, patients with HIV infection are predisposed to malabsorption, which appears to be caused by a variety of infections and other disorders affecting the small intestine. An imbalance of vitamin B12 is documented in almost one in three AIDS patients, clearly demonstrating defective absorption of the vitamin. The diagnosis of B12 deficiency is made based on a reported low serum vitamin B12 level, while an early sign of a negative B12 balance is the detection of low B12 levels in the blood of patients receiving transcobalamin II. Monthly administration of parenteral B12 should correct the deficiency, and absolutely anemia and pancytopenia in the peripheral blood. The consequence of B12 deficiency can be neurological dysfunctions (subacute combined degeneration of the cord) with motor, sensory and higher cortical dysfunctions. Possible B12 deficiency is often considered the cause of these neurological syndromes in HIV-infected people.

^ Causes and prevalence of anemia in HIV-infected women.

In an attempt to develop a prediction system for HIV-infected patients receiving HAART, Lingren and colleagues at EuroSIDA assessed 2027 patients initiating HAART among an initial cohort of 8457 subjects. The data were substantiated in two additional groups: 1946 and 1442 people, respectively. A total of 9.9% of subjects experienced clinical progression (either a new AIDS-defining illness or death), representing an incidence of 3.9 per 100 person-years. According to the results of a multidisciplinary study, 4 independent factors of disease progression were recognized: CD4+ cell count, HIV-1 load, AIDS clinic before starting HAART and hemoglobin level. Thus, mild anemia (Hb80-140 g/l in men and 80-120 g/l in women) is associated with a risk of disease progression or death of 2.2 (95%CI1.6-2.9, P

Anemia in rheumatoid arthritis

It has been established what factors lead to the development of anemia in rheumatoid arthritis. These include:

Changes in iron metabolism.
Reduced life expectancy of red blood cells.
In some cases, the toxic effects of cytokines lead to anemia.
Some cases of anemia are caused by medications.

Anemia in liver cirrhosis

Anemia due to hypothyroidism

Anemia with HIV

Anemia with hemorrhoids

Anemia with gastritis

Anemia in cancer

Anemia with pneumonia

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Anemia, neutropenia and thrombocytopenia. Pathogenesis and approaches to therapy in HIV-infected patients

Translation: postgraduate student of the Department of Hematology and Intensive Care of the Russian Medical Academy of Postgraduate Education

A.O. Tuaeva,

Essay

HIV infection is associated with numerous disorders of hematopoiesis, affecting both lymphoid and myeloid lineages of hematopoiesis at the level of hematopoietic stem cells. Anemia develops in 70-80% of HIV-infected patients; neutropenia can be observed in more than 50% of individuals with advanced HIV-associated immunodeficiency. Thrombocytopenia is also common, affecting approximately 40% of patients, and in 10% of patients with HIV it is the first symptom or sign of infection.

The etiology of these disorders is different. It is controversial that hematopoietic stem cells or CD34+ progenitor cells are resistant to HIV infection. However, many myeloid progenitor cells can become infected and become functionally defective, with a marked reduction in colony growth. Moreover, the bone marrow microenvironment necessary for the growth and development of normal blood cells is disrupted. Cells such as T cells and macrophages that make up this microenvironment (stroma) are susceptible to infection by HIV, resulting in decreased production of various hematopoietic growth factors, which further impairs the growth of progenitor cells. All of these factors, together with numerous additional disorders, ultimately lead to the frequent development of cytopenia, including anemia, neutropenia and/or thrombocytopenia.

Treatment for HIV-associated cytopenias is variable and depends on the specific causes that led to the disorder. The validity of the use of hematopoietic growth factors, such as erythropoietin, G-CSF, GM-CSF, has been proven. The effectiveness of highly active antiretroviral therapy (HAART) is also manifested in an improvement in hemoglobin levels after at least 6 months from the start of therapy. HAART is also associated with the prevention of anemia. Erythropoietin can correct anemia during HIV infection in patients whose endogenous erythropoietin levels are less than 500 units. Erythropoietin use may be associated with increased survival and improved quality of life. G-CSF increases neutrophil levels in HIV-infected patients undergoing anticancer chemotherapy or in cases of neutropenia caused by antiviral drugs such as gancicorvir.

Knowledge related to diagnosis, technique, and therapeutic management of various hematological complications of HIV infection is important for clinicians caring for patients with HIV.

Topics discussed:

· Pathogenesis of specific hematological disorders associated with HIV infection.

Assessment of clinical significance

· Appropriate therapy

· Clinical tactics based on the example of medical history.

hematological virus immunodeficiency anemia

1 . Requirements for normal hematopoiesis

Stem cells and hematopoietic progenitor cells.

The first requirement for hematopoiesis is the presence of stem cells and, to a greater extent, progenitor cells. Stem cells differ from all other cells of the body in their ability to reproduce themselves, as well as to differentiate pluripotently, forming tissues from numerous germ layers. Multipotent cells, such as lymphohematopoietic cells, are capable of self-reproduction and simultaneously differentiate into different types of tissues, but within a specific germ layer. Progenitor cells are even more differentiated, with a more limited ability to regenerate, and less ability to differentiate into different cell types. The remaining cells are only capable of differentiation, and this is how the process of programmed cell death begins.

The terminology surrounding stem cells is quite confusing and is based on early experiments with hematopoiesis in mice. In 1963, Becker and colleagues first demonstrated that a single cell (stem cell) was able to regenerate the hematopoietic system in lethally irradiated mice. After irradiation, some of these animals were injected with bone marrow isolated from normal genetically identical (from the same litter) mice. Several weeks later, the mice were dissected and independent colonies of hematological cells were noted in the spleen tissue. Some colonies consisted of only red blood cells, others consisted of granulocytes, monocytes and megakaryocytes, and some consisted of all of the above cells. Interestingly, genetic marks from the donor bone marrow were visible in the spleen colonies. This study showed that a single cell (CFU-C or spleen colony-forming unit in mice) can completely restore the hematopoietic and immune systems. It has now been established that the early hematopoietic cell is the precursor of myelopoiesis (colony-forming unit of granulocytes, eosinophils, monocytes, megakaryocytes in humans CFU-GEMM) is necessary for hematopoiesis in both humans and mice. Multipatent lymphohematopoietic stem cells, even less differentiated than CFU-GEMM, give rise to lymphocytes and CFU-GEMM.

CFU-HEMMs are formed not only in the bone marrow, but also in the organs of embryonic hematopoiesis, including the liver, spleen, and peripheral blood. There, in adults, they are in a non-functioning state, except in extreme stressful situations. The vast majority of CFU-GEMMs reside in the bone marrow in a quiescent state, with only about 5% dividing periodically. However, these cells are entirely responsible for the reproduction of red blood cells, platelets, granulocytes, monocytes, eosinophils and basophils throughout the life of the organism. These cells are difficult to distinguish morphologically, since in appearance they resemble small lymphocytes. They can be identified by specific markers on the cell surface, including CD34 antigen (which they express) and c-Kit.

Depending on the differentiation of CFU-GEMMs, many closely related progenitor cells arise, with a more limited capacity for self-renewal and a narrower range of lineage differentiation (Table 1). Thus, CFU-GEMM surrounded by GM-CSF (granulocyte-macrophage colony-stimulating factors) ultimately give rise to CFU-GM (colony-forming unit of granulocytes and macrophages), which in turn form colony-forming unit of granulocytes (CFU-G) and granulocytes , as well as colony-forming unit monocytes (CFU-M) and monocytes. Surrounded by erythropoietin, CFU-GEMM gives rise to a burst-forming unit of erythropoiesis (BFU), then a colony-forming unit of erythropoiesis (CFU-E), and, ultimately, a pronormoblast, recognized as the precursor of an erythrocyte in the bone marrow, capable only of differentiation into a mature erythrocyte, with programmed death after approximately 120 days. In the presence of thrombopoietin, CFU-GEMM differentiates into burst-forming unit of megakaryocytopoiesis (BFU-MEG), then into colony-forming unit of megakaryocytopoiesis (CFU-MEG), and then into megakaryocyte and platelet.

Hematological stem and progenitor cells (vol. 1)

Bone marrow microenvironment

Along with the presence of CFU-GEMM, normal hematopoiesis requires an appropriate bone marrow microenvironment. This environment consists of T lymphocytes, macrophages, endothelial cells and fibroblasts. Despite the importance of these cells, they have only recently been appreciated. It is now obvious that outside this normal microenvironment, normal hematopoiesis cannot occur. The cells that make up the microenvironment are responsible for the production of various hematopoietic growth factors necessary for the production of all blood cells. T lymphocytes produce stem cell factor and Flt3 ligand, which serves as an early activator of “pan” growth factor, allowing early initiation of growth of all cell types. Interleukin (IL-3), also produced by T cells in the bone marrow stroma, acts on early bone marrow progenitors at subsequent stages of differentiation. Macrophages produce tumor necrosis factor (TNF) and IL-1, which activate fibroblasts and endothelial cells, inducing the production of GM-CSF, G-CSF and M-CSF.љљ

Hematological growth factors.

The clinical significance of the bone marrow microenvironment lies in the ability to produce various hematopoietic growth factors (GM-CSF, G-CSF, M-CSF) necessary for the proliferation, differentiation and functioning of mature granulocytes, monocytes, basophils and eosinophils. Erythropoietin, synthesized by interstitial cells of the kidney, plays a role in the production of red blood cells. Thrombopoietin, created by the liver, stimulates platelet production. In addition, thrombopoietin, Flt3 and stem cell factor (kit ligand) are early activators of hematopoietic stem factors that help initiate the growth of all hematopoietic lineages (erythrocytes, granulocytes and megakaryocytes/monocytes).

GM-CSF also affects adult cells by stimulating the cytotoxic and phagocytic activity of granulocytes and monocytes against infectious agents, stimulating the production of granulocyte superoxide, and inhibiting the migration of granulocytes from the site of infection or injury. Likewise, G-CSF increases the functionality of mature granulocytes by accelerating the production of CFU-G by these cells. M-CSF similarly increases the functionality of mature monocytes and stimulates the production of CFU monocytes.

Hematopoietic growth factors (vol. 2).

2. Basic hematologistslogical disorders caused by HIV

Hematopoietic progenitor cells (CFU-HEMM)

There is currently doubt as to whether CFU-GEMMs can be infected by HIV. While the results are controversial, it has been shown that CD34+ progenitor cells have receptors for CD4 and CXCR4 (fusin), which are necessary for HIV entry. So, some qualities of infection can potentially cause hematopoietic disorders. However, no convincing evidence of CFU-HEMM infection has been demonstrated even at an advanced stage.

So, the possibility of infection by CFU-GEMM has been questioned, but it is obvious that during HIV infection, numerous defects in the growth of progenitor cells occur. It has been shown that as a result of the interaction of the cell surface with the HIV envelope protein gp120/160, the growth of BOE-E, CFU-GM, CFU-G and CFU-M colonies is reduced. Contact of CD34+ cells with HIV also promotes their apoptosis, with a marked reduction in colony growth. Also, the cause of decreased growth in hematopoietic colonies is dysregulation of cytokines with excessive production of inhibitory cytokines TNF-a (tumor necrosis factor) and interferon g in HIV-infected stromal cells of the bone marrow microenvironment. Other factors potentially responsible for the suppression of colonial growth may also be inhibitory factors in some HIV-infected individuals.

Bone marrow microenvironment and production of hematopoietic growth factors.

It is clear that stromal elements of the bone marrow microenvironment, such as T lymphocytes, fibroblasts, endothelial cells and macrophages, are easily infected by HIV. Thus, HIV-1 infected stromal cells produce a reduced volume of G-CSF and IL-3, which leads to a decrease in the ability of normal hematopoiesis. In addition, HIV-infected patients with anemia have reduced tolerance to erythropoietin, which leads to severe anemia in some patients. Laboratory studies by Bachner and colleagues showed that infection of human bone marrow with HIV-1 is sufficient to suppress all hematopoietic lineages.

Disease history:

A 41-year-old man with an asymptomatic HIV carrier diagnosed for the first time in 1998. (during routine HIV testing as being at risk). CD4+ cells were 614 per mm3, no antibodies to toxoplasma, hepatitis B and C were detected.

This condition lasted until February 1999, when a decrease in platelet levels to 54 thousand per mm3 was detected. At this time, hemoglobin was 140 g/l, leukocytes were 4.3 thousand. There were episodes of nosebleeds, gum bruising and bruises on the skin. No evidence of internal bleeding was found during the examination. CD4+ cells were 340 m mm3, and plasma HIV-1 levels were 55 copies per ml. The peripheral blood smear showed a decreased level of platelets; all circulating platelets were large. The bone marrow showed megakaryocytosis with normal white and red lineages. Bala was diagnosed with HIV-induced idiopathic thrombocytopenic purpura, and the patient was started on treatment with zidovudine/lamividine/nelfinavir. A month later, the platelet level was 430 thousand per mm3, and the CD4+ cells were 513 per mm3. The patient was released for observation.

3. Anemia due to HIV infection

Prevalence

Anemia is common in HIV-infected individuals, accounting for approximately 30% during the initial asymptomatic stage of infection, and reaching 80-90% during the course of the disease. In an attempt to determine the exact cause of anemia in HIV-infected patients pretreated with HAART, Sullivan and colleagues evaluated data from 32,867 clinical records of HIV-infected individuals receiving therapy from January 1990 to August 1996. The HIV surveillance program includes two groups - adults and adolescents, consists of individuals undergoing HIV treatment in hospitals and HIV clinics in 9 major cities in the United States, and is based at a treatment and prevention center. Defining anemia as a decrease in hemoglobin below 100 g/l, or clinical manifestations of anemia, the researchers concluded that anemia lasting for a year can be regarded as a result of HIV infection. Anemia lasting a year accompanies 37% of patients with clinical manifestations of AIDS, occupies 12% of patients with immunological manifestations of AIDS (such as a decrease in the level of CD4+ cells to 200 per mm3 in the absence of clinical conditions specific to AIDS), and 3% of patients among HIV-positive patients. infected, without any clinical and immunological manifestations of AIDS.

These data indicate a high incidence of anemia among HIV-infected patients at all stages of the disease before the use of HAART. Thus, the use of HAART has recently been associated with a decrease in the incidence and severity of anemia.

Etiology of Anemia

Anemia associated with decreased red blood cell production

Decreased red blood cell production may be the result of CFU-GEMM suppressive factors, such as inflammatory cytokines or HIV itself. Decreased erythropoietin production may also be documented in anemic HIV-infected patients. Similar suppression may occur in other infections and inflammatory processes. The presence of antibodies to erythropoietin has been described in HIV-infected patients with anemia. Tumor infiltration of the bone marrow (such as lymphoma), or infection (such as Mycobacterium avium complex (MAC)) may also be leading causes of decreased red blood cell production. In addition, MAC may be associated with cytokine-induced bone marrow suppression. Involvement of the gastrointestinal tract in various infectious or tumor processes can cause chronic blood loss, with possible iron deficiency anemia. Another obvious cause of hypoproliferative anemia in HIV-infected patients is the large number of drugs, many of which have the ability to suppress bone marrow and/or red blood cells. Zidovudine (AZT), one of the drugs often associated with microcytosis (mean red blood cell volume > 100 fl), which can be used as an objective criterion that a patient may experience complications from treatment. Anemia requiring replacement transfusion therapy (hemoglobin below 85 g/l) is found in approximately 30% of AIDS patients receiving zidovudine at a dose of 600 mg/d. However, severe anemia occurs in only one percent of asymptomatic patients taking zidovudine. It should be noted that despite the fact that stavudine is also associated with microcytosis of erythrocytes, there is no threat of developing anemia when taking this drug.љ

Another cause of hypoproliferative anemia in HIV-infected patients is infection of the bone marrow with parvovirus B19 (infection at the level of early erythrocyte precursors - pronormoblasts).

Incidence of anemia in HIV-infected patients (Table 1)

Cause of anemia	mechanism
Decreased red blood cell production (low reticulocyte count, normal or decreased free bilirubin)	A) neoplastic infiltration of bone marrow Lymphoma Kaposi's sarcoma Lymphogranulomatosis · Other B) infections Mycobacterium avium complex Mycobacterium tuberculosis · Cytomegalovirus B19 parvovirus Fungal infection · Other C) medications (see Table 2) D) direct effect of HIV Abnormal growth of BOE-E Anemia of chronic disease · Impaired production and/or use of erythropoietin. E) iron deficiency anemia due to chronic blood loss.
Ineffective production (low reticulocytes, high conjugated bilirubin)	A) folic acid deficiency · Nutritional · Pathology of the jejunum. Malabsorption B) B12 deficiency Malabsorption in the ileum Pathology of the stomach with decreased production of internal factor · Production of antibodies to intrinsic factor, for example in pernicious anemia.
Hemolysis (increased levels of reticulocytes and indirect bilirubin)	A) hemolytic anemia with a positive Coombs test. B) hemophagocytic syndrome. C) thrombotic thrombocytopenic purpura D) disseminated intravascular coagulation E) medications. Sulfonamides, dapsone · Oxidants in patients with glucose-6-phosphate dehydrogenase deficiency.

Hemolytic anemia.

Anemia due to ineffective red blood cell production (B12 and/or folate deficiency anemia)

Causes and prevalence of anemia in HIV-infected women.

Levine and colleagues reported the prevalence and proportion of anemia in a group of 2056 HIV-infected women enrolled in the National Institutes of Health's sponsored Women's Interagency HIV Study (WIHS), compared with 569 HIV-infected women. -negative women. Anemia was defined as a decrease in hemoglobin below 120 g/l. It was detected in 37% of HIV-infected women, versus 17% in HIV-negative women. Factors associated with anemia in both groups were African-American race and MCV<80fl. Среди ВИЧ-инфицированных женщин анемия встречалась статистически чаще при уровне CD4+клеток менее 200 в 1мм3, высоким плазматическим уровнем РНК вируса, с клиническими проявлениями СПИДа, а также среди тех, кто принимал зидовудин.

Consequences of anemia in HIV-infected people. Survival.

More than 32,000 medical records were reviewed to identify the consequences of anemia in HIV-infected patients under the auspices of the Multistate Adult and Adolescent Spectrum of HIV Disease Surveillance Project. In this study, anemia was defined as a decrease in hemoglobin below 100 g/L or clinical manifestations of anemia. Importantly, in this group, anemia was associated with an increased risk of death. Thus, the relative risk of death in anemic patients who started the study with a CD4+ cell count >200 per mm3 was 148% higher than in patients with the same CD4 cell levels who started without anemia, while the risk of death increased by 58%. in those who began the examination with a CD4+ cell level below 200 mm3 and severe anemia. Interestingly, the risk of death is reduced in those patients who, for any reason, have restored their red blood, while the risk of death remains high (170%) in those who do not recover from anemia. A similar relationship between anemia and increased risk of death was also observed by Moore et al. This study, including 2348 patients, was conducted at a large urban HIV clinic in Baltimore, Maryland. The development of anemia was associated with decreased survival, independent of other prognostic factors. Importantly, use of erythropoietin was associated with a reduced risk of death, as was use of antiretroviral therapy. An additional study carried out by EuroSIDA among 6725 HIV-infected patients found that severe anemia (SA)<80г/л) является веским независимым прогностическим фактором смертности, регулируемый уровнем CD4+клеток и ВИЧ-1 РНК уровень в плазме. В большом WIHS исследовании 2056 ВИЧ-инфицированных женщин, анемия была расценена как самостоятельный маркер укорочения выживаемости. Все исследователи пришли к единому мнению о клинической значимости анемии на ВИЧ-инфекции. Итак четыре крупных исследования выявили, что анемия является самостоятельным фактором риска, приводящем к укорочению жизни у ВИЧ- инфицированных пациентов.љ

Consequences of anemia in HIV-infected people. Progression of the disease.

The relationship between anemia and HAART

Recent studies have shown that HAART helps correct or eliminate anemia. In a study of 6725 HIV-infected patients in Europe, Mocroft et al found that HAART was statistically associated with adjustment of hemoglobin levels. When HAART is used for a long time, the likelihood of correcting anemia is high. Thus, 65% of the study group were anemic before starting HAART, 53% remained anemic for 6 months of HAART, and 46% of those receiving this therapy for 12 months. In a study of 905 HIV-infected patients conducted by Johns Hopkins Medical Center in Baltimore, use of HAART also demonstrated a reduction in anemia. Normal hemoglobin levels were observed in 42% of patients receiving HAART and in 31% of patients without HAART. A multivariate study of HAART use showed a clear relationship with relief from anemia, subject to regulation of CD4+ cell levels, HIV-1 viral load, taking into account gender, race, drugs used, and use of antianemic therapy. The large WHIS study of HIV-infected women receiving HAART for at least 6 months found a trend toward resolution of anemia, and longer duration of HAART use was associated with greater improvement.

The use of HAART is also associated with the prevention of anemia, but long-term use is required (more than 18 months). Interestingly, HAART may also be associated with early prevention of anemia.

The mechanism of the antianemic and preventive action of HAART is not completely clear. However, there is a strong suggestion that when the viral load is reduced, the growth of common hematopoietic progenitors improves, the level of HIV-1 in bone marrow stromal cells decreases, and tolerance to erythropoietin improves. In addition, Isgro et al showed that HAART is associated with increased growth of hematopoietic progenitor cells. Moreover, ritonavir, as a protease inhibitor, is associated with a decrease in apoptosis of hematopoietic progenitor cells, and stimulates the growth of these cells in vitro.

Brief evolution of anemia in HIV-infected patients.

4. Treatment of anemia in HIV infection

Numerous studies have shown that anemia can occur in patients with HIV. Appropriate treatment for these conditions depends on the diagnosis.

Use of HAART to correct anemia in HIV-infected patients.

The cohort studies described above documented the effectiveness of HAART on anemia in most patients when used for longer than six months.

Use of erythropoietin to treat anemia in HIV-infected patients.

A blurred response to erythropoietin often accompanies HIV infection, leading to anemia that requires treatment. In a normal situation, when anemia develops, increasing the production of erythropoietin corrects it. However, in HIV infection, the normal compensatory response of erythropoietin to a decrease in the number of red blood cells is disrupted, resulting in the inability of the bone marrow to respond to the anemic state. The mechanism for this defect in erythropoietin production is a posttranscriptional defect in erythropoietin production, with normal erythropoietin RNA molecule but reduced production of normal erythropoietin protein. In addition, the development of autoantibody reactions to erythropoietin, which leads to anemia, has been described in HIV-infected patients. Multiple studies have now shown the beneficial effects of erythropoietin in HIV-infected patients with anemia, whose bone marrow function has been suppressed by HIV, or other chronic infections or inflammatory processes.

Erythropoietin is also effective in treating anemia caused by zidovudine or other drugs, including anticancer chemotherapy drugs that suppress bone marrow. Baseline serum endogenous erythropoietin levels predict which patients will respond to therapeutic use of erythropoietin. Patients with endogenous erythropoietin levels500 - no. Erythropoietin is prescribed subcutaneously at a dose of 100-200 mg/kg body weight, three times a week until the level of red blood cells normalizes, then once every one to two weeks the hemoglobin concentration is normal. Recent trials have demonstrated equivalent effectiveness of 40,000 units of erythropoietin administered once a week compared with three times a day. Such prescriptions promise an increase in hematocrit, significantly reduce the number of red blood cell replacement transfusions and significantly improve the quality of life. Recent data from the Spectrum of Disease Study and a study by Moore et al showed that correction of anemia is associated with increased survival. Toxicity of erythropoietin is extremely rare and consists mainly of local soreness at the injection site, a slight increase in temperature and rash. However, in the control study, these side effects were also observed when using placebo.

Recently, a council of AIDS specialists approved the effectiveness of the use of erythropoietin in the treatment of anemia in HIV-infected patients. In patients whose endogenous erythropoietin level is less than 500 IU/L and there is no response to drugs, provided that hidden deficiency of iron, B12, folate and other similar causes is excluded.

Effect of erythropoietin therapy on life expectancy and quality of life.

As previously discussed, the Spectrum of Disease Study documented that 36.9% of HIV-1-infected patients with clinical AIDS were likely to develop anemia, 12.1% of patients with immunologic AIDS (CD4+ cell count)<200 в мм3) и у 3,2% ВИЧ-инфицированных людей без каких-либо проявлений. Анемия ассоциирована с повышенным риском смерти при отсутствии других факторов. Риск смерти у анемизированных пациентов с уровнем CD4+ клеток<200 - на 148%, выше чем у тех CD4+клетки которых>200 in mm3, and in them it is correspondingly 58% higher than in the observed non-anaemic patients. Interestingly, the risk of death is 170% higher in patients with recurrent anemia compared to those with persistent anemia.љ

The importance of treating anemia in HIV-infected patients was demonstrated by Moore et al, who followed 2,348 HIV-infected patients from 1989 to 1996. Among them, 21% developed anemia (Hb<94 г/л). Как и в исследовании Салливана с коллегами развитие анемии при условии контроля других прогностических факторов было связано с сокращением жизни. Примечательно, что применение эритропоэтина было причастно к снижению смертности.

It has also been demonstrated that treatment of anemia is always associated with improved quality of life. Research has been completed regarding the quality of life of patients undergoing chemotherapy for oncology. So in a study of 2342 patients conducted by Glasby and colleagues, erythropoietin was prescribed 3 times a week for 4 months. Erythropoietin was effective in improving functional status and quality of life in anemic cancer patients in addition to its effect of raising hemoglobin levels. The second large study was conducted by Demetri and colleagues among 2289 anemic cancer patients who received chemotherapy, taking erythropoietin at a dose of 10,000 units three times a week for four months.

љA significant improvement in quality of life was found, directly related to an increase in the level of hemoglobin associated with erythropoietin. Interestingly, improvement in quality of life was independent of response to chemotherapy, with clear improvement in both responders and non-responders to each specific chemotherapy regimen. Gabrilov et al also showed significant improvements in quality of life in 3012 patients with nonmyeloid malignancy who received 40,000–60,000 units of erythropoietin weekly. These data help to understand the importance of hemoglobin values in improving the lives of cancer patients and the additional importance of hemoglobin values in determining the standard of living in patients with HIV infection.

Several researchers have assessed the effect of erythropoietin on anemia and quality of life in patients with HIV. Abrams and colleagues examined 221 people in a community-based, multicenter, open-label study. Patients received 4200 mg/week zidovudine in addition to other antiretroviral agents, and all had hemoglobin levels<110 г/л. В среднем уровень гемоглобина поднимался на 25 г/л. Более того, статистически значимое улучшение качества жизни было связано с улучшением уровня гемоглобина. Интересно, что положительная динамика не была связана с какими-либо изменениями уровняљ CD4+клеток. Еще ранее Ревиски и коллеги установили эффективность применения эритропоэтина в отношении уровня жизни у 251 пациента с ВИЧ-инфекцией и анемией (гематокрит<30%). Коррекция анемии при уровне гематокрита 38% и выше без дополнительных гемотрансфузий наблюдалась в течение 24 недель у 34% пациентов. Эти пациенты были в значительной мере удовлетворены уровнем своего здоровья, общим самочувствием, энергичностью и наблюдались амбулаторно. Также была показана эффективность еженедельного приема эритропоэтина в отношении уровня гемоглобина и объективного улучшения качества жизни в группе из 786 человек, получавших профилактическое лечение. В этом исследовании 75% пациентов отреагировали подъемом уровня гемоглобина как минимум на 10 г/л, с подъемом через четыре месяца среднем на 27 г/л.љ The mean Linear Analogue Scale (LASA) Quality of Life measure increased by 41%, while the MOS-HIV overall quality-of-life measure increased by 37%.

Potential role of Darbopoetin Alpha.

Darbopoietin alfa is known as a new erythropoiesis stimulating protein (NESP), which acts on red blood cells in the same way as erythropoietin, but differs from it in chemical structure. The additional presence of a sialic acid residue increases its half-life, allowing a reduced dosage compared to conventional erythropoietin. Recent studies have established the effectiveness of NESP at a dose of 2.25-4.5 mcg/kg once a week in patients with cancer, among whom approximately 70-80% of hemoglobin returned to normal levels. Another dosing regimen where NESP was given every 2 or 3 weeks was also found to be effective. There is currently no declaration on the use of NESP in HIV/AIDS. Multiple prospective studies are being conducted to determine the efficacy and toxicity of NESP in the treatment of anemia in HIV-infected patients. Results similar to those already demonstrated with recombinant human erythropoietin are expected.

The use of blood replacement transfusions in the correction of anemia in HIV-infected patients.

Blood transfusions play an important role in the management of acute blood loss, and periodic transfusions are also necessary as symptomatic therapy for chronic blood loss or drug suppression of erythropoiesis. However, transfusions are always associated with various risks, such as infection, alloimmunization, transfusion reactions and febrile non-hemolytic transfusion reactions. In a group of HIV-infected patients receiving blood replacement transfusions for 1-2 weeks, increased levels of HIV-1 p24 antigen and HIV-1 RNA were documented. Also in such a situation, an increase in opportunistic infections is documented. Importantly, HIV-infected patients receiving blood transfusions have an increased risk of death. A prospective study of 531 patients with HIV and SMV infections was recently conducted. Transfusions of red blood cells were randomized using a leukocyte filter and without a filter, and the effect in each of them was established in relation to the plasma level of HIV-1 RNA, CD4+ cells, and cytokines. In addition, filter transfusions were found to be disadvantageous compared with unmodified transfusions. While there is no scientific basis for the pathological immunomodulatory effects of blood transfusions, observational data suggest the possibility of some of these effects being possibly associated with an increased risk of cancer recurrence or infection. Therefore, blood transfusions should be reserved for HIV-infected patients in need of urgent correction of anemia in the presence of cardiovascular and other symptoms.

5. Medical history

In July 2000, the patient was diagnosed with anemia with a hemoglobin level of 90 g/l. Erythrocyte indices corresponded to the use of zidovudine, MCV=114fl (N-80-100fl). The platelet level was 350 thousand, leukocytes 3.4 thousand. The reticulocyte level was low - 0.1%, free bilirubin was normal.. A month later Hb-75 g/l, Tp-300 thousand, leuk-3 thousand. The reticulocyte level remained low (0.1%), and free bilirubin normal. Bone marrow puncture and trephine biopsy were performed and showed pathological giant pronormoblasts with light cytoplasmic vacuoles. The PCR method using specific DNA samples revealed infection of the bone marrow with parvovirus B19. Then, for 4 days, the patient received intravenous gamma globulin. Two weeks later, the reticulocyte level rose to 5%, and hemoglobin to 86 g/l. The level of platelets was 450 thousand, leukocytes - stable 3.2 thousand. Hemoglobin levels returned to normal over the next month.

In August 2000, the patient again experienced a drop in hemoglobin, accompanied by a decrease in the level of reticulocytes. A second course of IV gamma globulin again led to an increase in reticulocyte and hemoglobin levels. Antiretroviral therapy was changed to abacavir, efavirenz and amprenavir.

Neutropenia

Etiology of neutropenia and decreased granulocyte function in HIV infection.

Neutropenia occurs in approximately 10% of cases of early asymptomatic HIV carriage and in more than 50% of cases with significant HIV-induced immunodeficiency. Neutropenia in HIV infection is caused by the same etiological factors as other peripheral cytopenias. Thus, a decrease in colonial growth of common progenitor cells, CFU-GM, can lead to a decrease in the production of granulocytes and monocytes. A soluble inhibitory substance produced by HIV-infected cells can inhibit neutrophil production in vitro. Decreased serum G-CSF levels have been described in HIV-seropositive subjects with nonfebrile neutropenia (less than 10,000 neutrophils per liter). This demonstrates the relative deficiency of hematopoietic growth factors and helps maintain neutropenia. Finally, myelosuppression and neutropenia can result from the use of a number of drugs. (vol. 2).

Drugs commonly associated with myelosuppression in patients with HIV (vol. 2)

antiretroviral	Zidovudine, Lamivudine, Didanosine, Zalcitabine, Stavudine
antiviral	Ganciclovir, Foscarnet, Cidofovir
antifungal	Flucytosine, Amphotericin
Against pneumjcystis carinii	Sulfonamide, trimethoprim, pyrimethamine, pentamidine
cytostatics	Cyclophosphamide, doxorubicin, methotrexate, paclitaxel, vinblastine, liposomal doxorubicin, liposomal daunorubicin.
immunomodulators	a-interferon.

In addition to absolute neutropenia, patients with HIV infection may experience decreased function of granulocytes and monocytes, opsonization and intracellular death of bacteria.

Factors contributing to the development of infection in HIV-infected patients with neutropenia.

Multiple studies have shown that in cancer patients who received chemotherapy, the risk of developing infectious complications increased when the absolute neutrophil level (ANL) was less than 10,000 per 1 L, and worsened when the ANL was less than 500 per 1 L. A number of studies have demonstrated in patients with HIV infection that the risk of infection during neutropenia is lower than in patients receiving anticancer chemotherapy. Moore and colleagues found that the risk of bacterial infection increases by 2.3 times in HIV-infected people with a blood level of less than 10,000 per liter, and 8 times more in those with a blood level of less than 5,000 per liter. A low level of SUN is associated with the risk of hospitalization for serious infections among HIV-infected patients, as shown by Jacobs et al., who studied 2047 discharges from HIV-positive patients (San Francisco General Hospital's AIDS clinic).

In a study of 62 HIV-infected patients with SUN less than or at a level of 10,000/L, 24% developed infectious complications, usually developing within 24 hours from the onset of neutropenia. Multidisciplinary analyzes revealed 3 factors independently associated with infectious complications: a central venous catheter, neutropenia during the previous three months, and a low granulocyte count (250 cells per μl with infection and 620 cells per μl without infection). Among the drugs that cause neutropenia, zidovudine comes first, followed by biseptol and ganciclovir. Neutropenia associated with infection is less pronounced than neutropenia caused by antitumor chemotherapy.

Moore et al. reported on a laboratory study of 87 HIV-infected patients with neutropenia and OUN less than 10,000 per liter. All but three cases of neutropenia were caused by myelosuppressive treatment. The average neutrophil level in these patients is 6600 per liter. and the average duration of neutropenia was 13 days. Despite significant neutropenia, unproven infection was noted in 17% of cases, and culture-proven infections in only 8%. Not a single patient died from the infection. Patients with infection had a significantly reduced level of OUN (on average 4600-7200 per 1 L) and a significantly reduced level of CD4+ cells (on average 64-126 cells/mm3), but the duration of neutropenia was no longer than in patients without infectious complications.

Impact of effective antiretroviral therapy on neutropenia.

Building on the concept that HIV may directly influence the growth of common hematopoietic progenitor cells, recent work has shown that HAART may lead to improvements in neutropenia and leukopenia. In a group of 66 HIV-infected patients treated with HAART, a statistically significant increase in total white blood cell and absolute granulocyte levels was evident over six months. Whether OUN increased in the early or later stages of treatment does not make much difference statistically. Sloand et al. previously showed a direct stimulatory effect of protease inhibitors on human hematopoiesis. These data suggest that low to moderate neutropenia can be controlled by HAART alone, even if it may take several months to achieve the goal.

The use of G-CSF and GM-CSF for neutropenia in patients with HIV infection.

When GM-CSF is administered subcutaneously to HIV-infected patients with neutropenia, an increase in granulocytes, monocytes and eosinophils is observed, depending on the dose. GM-CSF stimulates the proliferation, differentiation and release of these cells from the bone marrow. GM-CSF therapy results in increased neutrophil function with increased superoxide production, phagocytosis, bacteriolysis by mature granulocytes, and antibody-induced cellular cytotoxicity (ADCC). The recommended dose of GM-CSF is 5 mcg/kg/day - subcutaneously. After 5-6 days of therapy, the dose is adjusted depending on the effect.љ

Application of hematopoietic growth factors. (vol. 3)

	erythropoietin
Indications	Anemia caused by HIV inflammatory or infectious diseases · use of anti- retroviral anti-infective and/or anti-tumor chemotherapy.	HIV-induced neutrophil level<10000 в1л · Antitumor chemotherapy. · Anti-infective drugs.
Required initial data	Serum erythropoietin level · No other causes of anemia.
Initial dosages	100 mcg/kg subcutaneously three times a week.	1 mg/kg subcutaneously daily
Further dosing	Selection of dosage if necessary to maintain the effect (approximately 10,000 U/week)	Selection of dosage if necessary to maintain the effect
Side effects	Pain at the site of infection, fever.	High LDH levels High ALP level Bone pain
Expected effect	Hemoglobin level >/=110 g/l in women, >/= g/l in men.	OUN >/= 10000 in 1 liter.

Early studies combined the use of GM-CSF with prolongation of HIV replication. Many in vitro studies have demonstrated that GM-CSF significantly inhibits HIV-1 replication, Brights et al. conducted a randomized placebo-controlled study of GM-CSF among 105 HIV-infected patients who received a nucleoside analogue HIV reverse transcriptase inhibitor. GM-CSF was administered at a dose of 125 μg/m2 twice a week for six months. It is extremely interesting that in patients receiving HAART and GM-CSF, a greater reduction in plasma HIV levels was achieved - the level of HIV-1 was significantly lower than detectable. A decrease in the frequency of mutations leading to HIV resistance to zidovudine has also been demonstrated among those who took antiretroviral drugs with placebo.љ

G-CSF also demonstrated an increase in granulocyte levels in HIV neutropenia caused by antitumor chemotherapy, antiretroviral, and/or anti-infective therapy. The use of G-CSF leads to an increase in the functional activity of mature granulocytes. Recently, Kaiser et al. conducted a retrospective analysis of 152 HIV-infected patients with neutropenia to evaluate the therapeutic efficacy of G-CSF. From medical records, 71 patients who received G-CSF were compared with 81 patients who did not receive G-CSF from 1991 to 1994. The two groups were similar in baseline characteristics, including CD4+ cell counts of 37 and 40 per μL, respectively. љThe risk of bacteremia decreased significantly (p=.02). In addition, a reduction in the risk of death was found in those patients receiving G-CSF who were taking antiretroviral therapy and were receiving prophylaxis for pneumonia (p. carinii).

The initial recommended dose of G-CSF is 5 mcg/kg subcutaneously. However, previous data suggest the effectiveness of G-CSF in HIV-infected patients at a much lower dose. Thus, an initial dose of 1 mcg/kg/day is used frequently and is used until the level of neutrophils rises to acceptable levels (more than 10,000 per liter). The dosage is adjusted individually, usually 1 or 2 times a week, depending on the need to maintain the response.

G-CSF does not support HIV replication in vitro and its use cannot lead to increased HIV replication in vivo. The toxicity of G-CSF is negligible and consists mainly of bone pain. It is important to remember that LDH and ALP levels may increase during G-CSF therapy.

Anemia in HIV-infected people. Blood diseases due to AIDS (HIV infection) Anemia due to HIV infection causes

Causes of anemia in HIV infection

How to treat anemia in HIV-infected people?

Causes of anemia in HIV infection

How to treat anemia in HIV-infected people?

Types of anemia: symptoms and treatment

Causes of anemia

Signs of anemia

Procedure for treating anemia

Disease prevention

Anemia in HIV-infected persons

Anemia with uterine fibroids

Anemia in rheumatoid arthritis

Anemia in liver cirrhosis

Anemia due to hypothyroidism

Anemia with pneumonia

Anemia - symptoms and treatment

Iron-deficiency anemia

Aplastic anemia

B12 deficiency anemia

Diagnosis of the disease

Iron supplements for anemia

Anemia associated with decreased red blood cell production

Anemia in rheumatoid arthritis

Anemia in liver cirrhosis

Anemia due to hypothyroidism

Anemia with HIV

Anemia with hemorrhoids

Anemia with gastritis

Anemia in cancer

Anemia with pneumonia

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Bone marrow microenvironment

Hematological growth factors.

Prevalence

These data indicate a high incidence of anemia among HIV-infected patients at all stages of the disease before the use of HAART. Thus, the use of HAART has recently been associated with a decrease in the incidence and severity of anemia.

Etiology of Anemia

Anemia associated with decreased red blood cell production

Another cause of hypoproliferative anemia in HIV-infected patients is infection of the bone marrow with parvovirus B19 (infection at the level of early erythrocyte precursors - pronormoblasts).

Incidence of anemia in HIV-infected patients (Table 1)

A) neoplastic infiltration of bone marrow

Lymphoma

Kaposi's sarcoma

Lymphogranulomatosis

· Other

B) infections

Mycobacterium avium complex

Mycobacterium tuberculosis

· Cytomegalovirus

B19 parvovirus

Fungal infection

· Other

C) medications (see Table 2)

D) direct effect of HIV

Abnormal growth of BOE-E

Anemia of chronic disease

· Impaired production and/or use of erythropoietin.

A) folic acid deficiency

· Nutritional

· Pathology of the jejunum. Malabsorption

B) B12 deficiency

Malabsorption in the ileum

Pathology of the stomach with decreased production of internal factor

Hemolysis

A) hemolytic anemia with a positive Coombs test.

B) hemophagocytic syndrome.

C) thrombotic thrombocytopenic purpura

D) disseminated intravascular coagulation

E) medications.

Sulfonamides, dapsone

· Oxidants in patients with glucose-6-phosphate dehydrogenase deficiency.

Hemolytic anemia.

The relationship between anemia and HAART

The use of HAART is also associated with the prevention of anemia, but long-term use is required (more than 18 months). Interestingly, HAART may also be associated with early prevention of anemia.

Brief evolution of anemia in HIV-infected patients.

5. Medical history

In August 2000, the patient again experienced a drop in hemoglobin, accompanied by a decrease in the level of reticulocytes. A second course of IV gamma globulin again led to an increase in reticulocyte and hemoglobin levels. Antiretroviral therapy was changed to abacavir, efavirenz and amprenavir.

Neutropenia

Etiology of neutropenia and decreased granulocyte function in HIV infection.

Drugs commonly associated with myelosuppression in patients with HIV (vol. 2)

Serum erythropoietin level
· No other causes of anemia.