Symptomatic anemias

Anemia may develop in a number of pathological conditions that seem to be unrelated to the hematopoietic system. Diagnostic difficulties, as a rule, do not arise if the underlying disease is known and the anemic syndrome does not prevail in the clinical picture. The importance of symptomatic (secondary) anemias is explained by their relative frequency in pediatrics and possible resistance to therapy. Symptomatic anemias are most often observed in chronic infections, systemic connective tissue diseases, liver diseases, endocrine pathology, chronic renal failure, and tumors.

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Anemia in chronic inflammatory processes, infections

Most often encountered in purulent-inflammatory processes, protozoal infections, HIV infection. It has been established that with any chronic infection lasting more than 1 month, a decrease in hemoglobin to 110-90 g/l is observed.

Several factors play a role in the origin of anemia:

1. Blockade of iron transfer from reticuloendothelial cells to bone marrow erythroblasts;
2. Increased iron consumption for the synthesis of iron-containing enzymes and, accordingly, a decrease in the amount of iron used for the synthesis of hemoglobin;
3. Shortening of the lifespan of red blood cells due to increased activity of cells of the reticuloendothelial system;
4. Impaired erythropoietin secretion in response to anemia during chronic inflammation and, as a consequence, decreased erythropoiesis;
5. Decreased iron absorption during fever.

Depending on the duration of chronic inflammation, normochromic normocytic anemia is detected, less often hypochromic normocytic anemia and, if the disease has been going on for a very long time, hypochromic microcytic anemia. Morphological signs of anemia are nonspecific. Anisocytosis is detected in the blood smear. Biochemically, a decrease in serum iron and iron-binding capacity of the serum is detected with a normal or increased iron content in the bone marrow and reticuloendothelial system. The ferritin level helps in differential diagnostics from true iron deficiency anemias: in secondary hypochromic anemias, the ferritin level is normal or increased (ferritin is an acute phase protein of inflammation), while in true iron deficiency, the ferritin level is low.

Treatment is aimed at stopping the underlying disease. Iron preparations are prescribed to patients with low serum iron levels. Vitamins (especially group B) are used for treatment. In AIDS patients with low erythropoietin levels, its administration in large doses can correct anemia.

Acute infections, especially viral ones, can cause selective transient erythroblastopenia or transient bone marrow aplasia. Parvovirus B19 is the cause of aregenerative crises in patients with hemolytic anemia.

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Anemia in systemic connective tissue diseases

According to literature data, anemia is observed in approximately 40% of patients with systemic lupus erythematosus and rheumatoid arthritis. The main cause of anemia is considered to be an insufficient compensatory response of the bone marrow, caused by impaired secretion of erythropoietin. Additional factors of anemia are the development of iron deficiency caused by constant hidden bleeding through the intestines against the background of taking non-steroidal anti-inflammatory drugs and depletion of folate reserves (the need for folic acid is increased due to cell proliferation). In addition, patients with systemic lupus erythematosus may have autoimmune hemolytic anemia and anemia due to renal failure.

Anemia is most often normochromic normocytic, sometimes hypochromic microcytic. There is a correlation between the concentration of hemoglobin and ESR - the higher the ESR, the lower the hemoglobin level. The level of iron in the serum is low, the iron-binding capacity is also low.

Iron therapy in the active phase may be effective in children under 3 years of age, as they often have pre-existing iron deficiency, and in patients with extremely low serum iron and low transferrin saturation. Reduction in disease activity under the influence of pathogenetic therapy leads to a rapid increase in serum iron and increased iron transport to the bone marrow. Patients may be prescribed erythropoietin therapy, but patients require high doses of erythropoietin and even to high doses there is a variable response. It has been established that the higher the level of basal erythropoietin circulating in the patient's plasma, the less effective is erythropoietin therapy.

Secondary autoimmune hemolytic anemia in patients with systemic connective tissue diseases is often stopped by treating the underlying disease. The first stage of treatment is corticosteroid therapy and, if necessary, splenectomy. If hemolysis is resistant, cyclostatics (cyclophosphamide, azathioprine), cyclosporine A, and large doses of immunoglobulin for intravenous administration are added to the above methods of therapy. Plasmapheresis can be used to quickly reduce the antibody titer.

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Anemia in liver diseases

In patients with cirrhosis of the liver and portal hypertension syndrome, anemia develops due to iron deficiency due to periodic blood loss from varicose veins of the esophagus and stomach and hypersplenism. Cirrhosis may be accompanied by "spur cell anemia" with fragmentation of red blood cells. Hypoproteinemia worsens anemia due to an increase in plasma volume.

In Wilson-Konovalov disease, chronic hemolytic anemia is possible due to the accumulation of copper in red blood cells.

Viral hepatitis can cause aplastic anemia.

Some patients may have a folic acid deficiency. The level of vitamin B ₁₂ in severe liver diseases is pathologically elevated, since the vitamin "leaves" the hepatocytes.

Treatment of anemia is symptomatic and depends on the underlying mechanism of its development - replenishment of iron deficiency, folates, etc.; surgical treatment for portal hypertension syndrome.

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Anemia in endocrine pathology

Anemia is often diagnosed in hypothyroidism (congenital and acquired), caused by a decrease in the production of erythropoietin. Most often, anemia is normochromic normocytic, it can be hypochromic due to iron deficiency caused by impaired absorption in hypothyroidism, or hyperchromic macrocytic due to vitamin B ₁₂ deficiency, which develops as a result of the damaging effect of antibodies directed against cells of not only the thyroid gland, but also the parietal cells of the stomach, which leads to vitamin B ₁₂ deficiency. Thyroxine replacement therapy leads to improvement and gradual normalization of hematological parameters, iron preparations and vitamin B _{12 are prescribed according to indications.}

The development of anemia is possible with thyrotoxicosis, chronic adrenal cortex insufficiency, and hypopituitarism.

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Anemia in chronic renal failure

Chronic renal failure (CRF) is a syndrome caused by irreversible death of nephrons due to primary or secondary kidney disease.

With the loss of the mass of functioning nephrons, there is a progressive loss of renal function, including a decrease in erythropoietin production. The development of anemia in patients with chronic renal failure is mainly due to a decrease in the synthesis of erythropoietin. It has been established that a decrease in the ability of the kidneys to produce erythropoietin usually coincides with the appearance of azotemia: anemia develops at a creatinine level of 0.18-0.45 mmol / l and its severity correlates with the severity of azotemia. With the progression of renal failure, complications of uremia and program hemodialysis (blood loss, hemolysis, imbalance of iron, calcium, phosphorus, the effect of uremic toxins, etc.) are added, which complicates and individualizes the pathogenesis of anemia in chronic renal failure and aggravates its severity.

Anemia is usually normochromic normocytic; hemoglobin level can be reduced to 50-80 g/l; if iron deficiency occurs, hypochromic microcytic.

Treatment is carried out with recombinant human erythropoietin (epocrine, recormon), which is prescribed in the presence of anemia both to patients who do not yet need hemodialysis and in the late stages of chronic renal failure. If necessary, iron preparations, folic acid, ascorbic acid, B vitamins (B ₁, B ₆, B ₁₂ ), anabolic steroids are prescribed. Blood transfusions are carried out mainly for emergency correction of progressive severe anemia (decrease in hemoglobin level below 60 g/l), for example, in case of massive bleeding. The effect of blood transfusion is only temporary, conservative therapy is required in the future.

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Anemia in cancer

The following causes of anemia development in malignant diseases are identified:

1. Hemorrhagic status
2. Deficiency states
3. Dyserythropoietic anemias
   • anemia similar to that observed in chronic inflammation;
   • sideroblastic anemia
   • erythroid hypoplasia
4. Hemomodulation
5. Hemolysis
6. Leukoerythroblastic anemia and bone marrow infiltration
7. Treatment with cytostatics.

Refractory hypochromic anemia has been described in patients with lymphoma or lymphogranulomatosis, characterized by biochemical and morphological signs of iron deficiency, but not amenable to treatment with iron preparations. It has been established that iron is not transferred from the reticuloendothelial system involved in the pathological process into the plasma.

Metastasis of tumors to the bone marrow - most often neuroblastoma metastasizes to the bone marrow, less often retinoblastoma and rhabdomyosarcoma, lymphosarcoma. In 5% of patients with lymphogranulomatosis, infiltration into the bone marrow is detected. Bone marrow infiltration can be assumed in leukoerythroblastic anemia, which is characterized by the presence of myelocytes and nucleated erythroid cells, reticulocytosis, and in the late stage - thrombocytopenia and neutropenia, i.e. pancytopenia. The leukoerythroblastic blood picture is explained by the fact that during bone marrow infiltration, extramedullary erythropoiesis occurs, as a result of which early myeloid and erythroid cells are released into the peripheral blood. Despite the fact that anemia is usually present, it may be absent in the early stage.

Treatment of anemia, apart from the temporary effect of transfusion, is not very successful if the underlying process cannot be stopped. Erythropoietin may be used.

Premature infants with anemia during the period of clinical and hematological changes should be observed by a physician at least once a week with clinical blood test control every 10-14 days against the background of treatment with iron preparations. If therapy is ineffective and in cases of severe anemia, hospitalization is indicated to determine refractoriness to iron preparations and treatment.

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