Symptomatic Anemia

The development of anemia is possible with a number of pathological conditions, seemingly not related to the hematopoietic system. Diagnostic difficulties, as a rule, do not occur if the underlying disease is known and the anemic syndrome does not prevail in the clinical picture. The significance of symptomatic (secondary) anemia is explained by their relative frequency in pediatrics and the possible resistance to therapy. The most common symptomatic anemia is observed in chronic infections, systemic connective tissue diseases, liver diseases, endocrine pathology, chronic renal failure, tumors.

[1], [2], [3], [4], [5],

Anemia in chronic inflammatory processes, infections

The most common are with purulent-inflammatory processes, protozoal infections, HIV infection. It was found that with any chronic infection lasting more than 1 month, hemoglobin decreased to 110-90 g / l.

In the origin of anemia, several factors are important:

1. Blockade of iron transition from reticuloendothelial cells to bone marrow erythroblasts;
2. An increase in the costs of iron for the synthesis of iron-containing enzymes and, correspondingly, a decrease in the amount of iron going to hemoglobin synthesis;
3. Shortening of the lifespan of erythrocytes, caused by increased activity of cells of the reticuloendothelial system;
4. Violation of erythropoietin release in response to anemia in chronic inflammation and, as a consequence, reduction of erythropoiesis;
5. Reduction of iron absorption during fever.

Depending on the duration of chronic inflammation, normochromic normocytic anemia is detected, less often hypochromic normocytic anemia and hypochromic microcytic anemia for very long duration of the disease. Morphological signs of anemia are nonspecific. Anisocytosis is found in the blood smear. Biochemically, a decrease in serum iron and iron binding capacity of serum is observed at normal or elevated iron levels in the bone marrow and reticuloendothelial system. In the differential diagnosis of true iron deficiency anemia helps the level of ferritin: in secondary hypochromic anemia, the ferritin level is normal or elevated (ferritin is the protein of the acute phase of inflammation), with true iron deficiency, the ferritin level is low.

Treatment is aimed at arresting the underlying disease. Iron preparations are prescribed for patients with low serum iron. To treat use of vitamins (especially group B). In patients with AIDS who have a cirrhotic level of erythropoietin, its administration in large doses can correct anemia.

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

[6], [7], [8], [9], [10], [11], [12],

Anemia in systemic connective tissue diseases

According to the literature, anemia is observed in approximately 40% of patients with systemic lupus erythematosus and rheumatoid arthritis. The main cause of the development of anemia is considered insufficient compensatory response of the bone marrow, due to impaired secretion of erythropoietin. Additional factors of anemia are the development of iron deficiency caused by persistent latent bleeding through the intestine on the background of taking nonsteroidal anti-inflammatory drugs and depleting the reserves of folate (the need for folic acid is increased due to the proliferation of cells). In patients with systemic lupus erythematosus, in addition, there may be autoimmune hemolytic anemia and anemia due to renal failure.

Anemia is usually 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, iron binding ability is also low.

Therapy with iron preparations in the active phase can be effective in children under 3 years of age, because they often have a previous iron deficiency, as well as in patients with extremely low serum iron levels and a low iron transferrin saturation ratio. Reducing the activity of the disease under the influence of pathogenetic therapy leads to a rapid increase in serum iron and an increase in the transport of iron to the bone marrow. Patients may be prescribed therapy with erythropoietin, but patients require large doses of erythropoietin and even a high dose shows a different degree of response. It was found that the higher the level of basal erythropoietin circulating in the patient's plasma, the less effectiveness of erythropoietin therapy.

Secondary autoimmune hemolytic anemia in patients with systemic connective tissue diseases is often stopped in the treatment of the underlying disease. The first stage of treatment is corticosteroid therapy and, if necessary, splenectomy. With hemolysis resistance, cytostatics (cyclophosphamide, azathioprine), cyclosporin A, large doses of immunoglobulin for intravenous administration are added to these therapies. To quickly reduce the titer of antibodies, plasmapheresis can be used.

[13], [14], [15], [16], [17], [18], [19]

Anemia in liver diseases

With cirrhosis of the liver in patients with portal hypertension syndrome, the development of anemia is due to iron deficiency due to periodic blood loss from varicose veins of the esophagus and stomach and hypersplenism. Cirrhosis can be accompanied by a "sarcoidosis anemia" with the fragmentation of erythrocytes. Hypoproteinemia aggravates anemia due to increased plasma volume.

With Wilson-Konovalov disease, chronic hemolytic anemia is possible due to the accumulation of copper in erythrocytes.

When viral hepatitis can develop aplastic anemia.

In some patients, folic acid deficiency is possible. The level of vitamin B ₁₂ in severe liver diseases is pathologically elevated, since the vitamin "exits" from the hepatocytes.

Treatment of anemia is symptomatic and depends on the main mechanism of its development - iron deficiency, folate, etc.; operative treatment in the syndrome of portal hypertension.

[20], [21], [22], [23], [24], [25], [26]

Anemia in endocrine pathology

Anemia is often diagnosed with hypothyroidism (congenital and acquired), due to a decrease in the production of erythropoietin. More often anemia is normochromic normocytic, may be hypochromic due to iron deficiency caused by a violation of its absorption in hypothyroidism, or hyperchromic macro-cytopathic because of a deficiency of vitamin B ₁₂, which develops as a result of the damaging effect of antibodies directed against cells of not only the thyroid gland but also parietal cells stomach, which leads to a deficiency of vitamin B ₁₂. Substitution therapy with thyroxine leads to an improvement and a gradual normalization of hematologic indices, according to indications prescribe iron preparations and vitamin B ₁₂

The development of anemia is possible with thyrotoxicosis, chronic insufficiency of the adrenal cortex, hypopituitar-tarizm.

[27], [28], [29], [30], [31], [32]

Anemia in chronic renal failure

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

With the loss of the mass of functioning nephrons, a progressive loss of renal functions occurs, including the production of erythropoietin. The development of anemia in patients with chronic renal failure is mainly due to a decrease in the synthesis of erythropoietin. It was found that the decrease in the ability of the kidneys to produce erythropoietin coincides, as a rule, 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 (hemorrhage, hemolysis, imbalance of iron, calcium, phosphorus, influence 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; the level of hemoglobin can be reduced to 50-80 g / l; when there is a deficiency of iron - hypochromic microcirculatory.

Treatment is carried out by recombinant human erythropoietn (epokrin, rekormon), which is prescribed in the presence of anemia as patients who still do not need hemodialysis, and in the late stages of chronic renal failure. If necessary, prescribe iron preparations, folic acid, ascorbic acid, vitamins of group B (B ₁, B ₆, B ₁₂ ), anabolic steroids. Blood transfusions are performed mainly for emergency correction of progressive severe anemia (decrease in hemoglobin level below 60 g / l), for example, with massive bleeding. The effect of blood transfusion is only temporary, further conservative therapy is needed. 

[33], [34], [35], [36], [37]

Anemia with cancer

The following causes of anemia develop in malignant diseases:

1. Hemorrhagic status
2. Deficiency conditions
3. Dyserothyrotytic anemia
   • anemia similar to that observed in chronic inflammation;
   • sideroblastic anemia
   • erythroid hypoplasia
4. Hemodulation
5. Hemolysis
6. Leukoerythroblast anemia and bone marrow infiltration
7. Treatment with cytostatics.

In patients with lymphoma or lymphogranulomatosis, refractory hypochromic anemia is described, characterized by biochemical and morphological signs of iron deficiency, but which can not be treated with iron preparations. It has been established that iron is not transferred to the plasma from the reticuloendothelial system involved in the pathological process.

Metastasis of tumors in the bone marrow - most often in the bone marrow metastasizes neuroblastoma, 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 leukoerythroblast anemia, which is characterized by the presence of myelocyte-bearing erythroid cells, reticulocytosis, and in the late stage - thrombocytopenia and neutropenia, that is, pancytopenia. The leucoerythroblast picture of blood is explained by the fact that with bone marrow infiltration, extramedullary erythropoiesis occurs, as a result of which the early myeloid and erythroid cells are ejected into the peripheral blood. Although anemia is usually present, it may be absent in the early stages.

Treatment of anemia, in addition to the temporary effect of transfusion, is not very successful if the main process can not be stopped. It is possible to use erythropoietin.

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

[38], [39], [40], [41]