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Thyroid wave anemia

Thioprivial anemia - anemia that develops on the basis of hypothyroidism. Experimental work confirms the important role of thyroid hormone - thyroxin - in stimulating normal blood formation. Animals deprived of the thyroid gland, quickly anemiziruyutsya, the introduction of the same thyroid preparations thyroidectomized animals cures them from the effects of thyroid-void cachexia, in particular from anemia.

The clinical picture of anemia in myxedema (hypothyroidism) is heterogeneous. There are three types of anemia: 1) normochromic (macrocytic), 2) hypochromic, 3) hyperchromic (pernicious).

The pathogenesis of thyroid-free anemia is heterogeneous. Thyroxine deficiency is thought to lead to a disorder in the utilization of specific hematopoietic factors (iron, folic acid, vitamin B12.

Anemia in thyroiditis Hashimoto (struma lymphomatosa) is considered by modern authors in the aspect of autoimmune conflict. In this regard, the combination of hypothyroidism with pernicious (B12-deficient) anemia can be interpreted as a result of organ-specific immunization, as evidenced by specific immunological studies that detect the presence of antibodies directed against the thyroid cells (or thyroglobulin) and the parietal fundus glands (or internal factor a).

Treatment. Clinical experience shows that with anemia occurring on the background of hypothyroidism, the best effect is achieved through the use of combination therapy with iron and vitamin B12 in the usual dosage in combination with thyroidin (0.1—0.2 g 3 times a day).


From true anemia, which is a consequence of renal failure (with chronic nephritis, wrinkled kidney, etc.), one should distinguish between “false anemia”, which depends both on the degree of skin edema and poor blood filling of the skin vessels, and on hydremia, i.e. swelling of the blood itself.

In most cases, anemia is hypochromic normo-or microcytic in nature, characteristic of iron deficiency anemia. However, in some patients with chronic nephritis with symptoms of renal failure, hyperchromic macrocytic, pernicious-like anemia develops.

Anemia in renal insufficiency is accompanied by changes in white blood in the form of neutrophilic leukocytosis (with preservation of eosinophils), reaching with uremia (not even complicated by infection), especially high numbers (12000—20000 in 1 mm3).

The lifetime study of bone marrow hematopoiesis in the case of anemia of brayts (G. A. Alekseev) revealed a picture of a deep disorder of erythropoiesis in the form of a violation of hemoglobinization and delayed maturation of erythroblasts.

What is the pathogenesis of anemia of the bratiks? With the exception of relatively rare cases, when patients with nephritis have prolonged gross hematuria and anemia is mainly post-hemorrhagic, anemia of braic is the result of autointoxication of the body associated with renal failure.

It can be assumed that azotemic gastritis and enterocolitis, which is observed during azotemia, is a known role in the development of anemia of brightkeys. A change in the function of the stomach, which becomes primarily an excretory organ (“the stomach urinates,” according to the figurative expression of M. P. Konchalovsky), as well as the intestine, cannot but adversely affect

secretion of free hydrochloric acid and gastromucoprotein, which in turn should lead to a breakdown of iron absorption.

In the light of the latest data on erythropoietin plasma (see above), it is suggested that the cause of anemia of the braic can be impaired function of the juxtaglomerular apparatus of the kidneys in the production of erythropoietin.


In chronic diffuse lesions of the liver (chronic hepatitis), regardless of the etiology of the process, macrocytic anemia of the normochromic or slightly hyperchromic type occurs.

Studies by our employees (N. T. Fokina) and other authors who have found elevated levels of vitamin B12 in plasma give the right to argue that macrocytic anemia in chronic liver damage is associated with impaired deposition and utilization of vitamin B12, as well as folic acid.

In subacute liver dystrophy, hyperchromic macrocytic anemia is one of the most important indicators of severe liver dysfunction and has a serious prognostic value.

The development of severe pernicious anemia in metastatic liver cancer may indicate the primary localization of cancer in the stomach.


Anemias in infectious diseases are very diverse both in etiology and pathogenesis, and in clinical features.
Anemia in infectious diseases can occur because of a violation of the normal absorption of iron or hematopoietic substances (vitamin B12, folic acid). It may be associated with hemolysis, bleeding, hypersplenism, developing avitaminosis, finally, with the anemizing effect of chemotherapy drugs.

The development of iron deficiency anemia in infectious diseases is mainly due to the fact that iron is not used for the needs of erythropoiesis, but for the fight against infection. Being fixed in the tissues, iron participates as a catalyst of oxidative processes, increasing in febrile conditions, and as a stimulator of reticulohistiocytic (lymphoid) elements that produce immune antibodies. Additional factors contributing to the development of infectious hyposiderosis are reduced iron adsorption in the gastrointestinal tract, as well as impaired iron absorption and heme disorder in erythroblasts, as evidenced by the increased content of protoporphyrin in them and increased excretion of coproporphyrin.

An undoubted role in the development of hyposiderosis in infectious patients is also played by protein deficiency, in particular, deficiency of? -Globulin (transferrin), which plays a role in the delivery of iron to the bone marrow.

The above anemizing factors can be combined, for example, with a prolonged septic endocarditis, the toxic effect of the infective (streptococcus) on the bone marrow and its hemolytic effect and the development of hypersplenism takes place. Anemia is a characteristic symptom for many infections. These are protozoal diseases: malaria, trypanosomiasis, internal leishmaniasis, in which either red blood cells are affected, or reticulohistiocytic, resp. the hematopoietic system, as well as some acute and chronic bacterial septic infections, the causative agents of which cause anemia due to myelotoxic action. According to their pathogenesis, these anemias are either hemolytic (malaria, acute anaerobic or streptococcal sepsis), or anemia from impaired blood formation due to the direct toxic effects of pathogens on the bone marrow (visceral leishmaniasis).

Treatment. Therapy of infectious anemia consists in the treatment of the underlying disease.


Despite the relative rarity of drug-induced anemia, which indicates the role of the individual sensitivity of the organism in their occurrence, the issue of drug-induced anemia becomes particularly relevant, given the current scale of chemotherapeutic agents.

As it is known, chemotherapy drugs and some antibiotics (chloramphenicol) in relation to the macroorganism are antivitamins that, in affinity for microbes, compete with vitamins essential for the microbial cell - the so-called essential metabolites, such as para-aminobenzoic acid.

The bacteriostatic effect of sulfonamides and PAS is based on the structural similarity of these drugs with para-aminobenzoic acid. Replacing the latter of the association with a specific microbial protein, respiratory enzyme, and thus destroying the biologically active enzyme system vital for the microorganism, the chemotherapy drugs themselves bind to the same specific proteins, forming a biologically inactive system.

The bacteriostatic effect of chemotherapy drugs (sulfonamides) and some antibiotics (chloramphenicol) also extends to the intestinal flora useful for the microorganism, which is involved in the synthesis of a number of vitamins, in particular folic acid.

This explains the role of sulfonamides and antibiotics in the occurrence of disorders of hematopoiesis, especially with prolonged use of massive doses.

According to some reports, sulfonamides violate the synthesis of folic acid and directly, preventing the connection of para-aminobenzoic and pteroylglutamic acids.

It was experimentally possible to obtain macrocytic anemia in pigs by turning off folic acid from the diet and prescribing its antagonists simultaneously with sulfathiazole.

The anti-vitamin effect of sulfonamides and antibiotics on the human body is manifested, especially in weak, exhausted patients, in the form of pellagroznyh phenomena (glossitis, hyperkeratosis, enteritis) and macrocytic anemia, indicating deficiency of B vitamins, in particular nicotinic and folic acids.

Currently, most medicinal anemias, especially hemolytic, are considered in the aspect of the innate inferiority of the erythrocyte enzyme structures, which determine their "hemolytic readiness" in connection with taking certain medications (see Enzyme Deficiency Hemolytic Anemias).
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    Despite the large number of studies devoted to the study of hypo-and aplastic anemias, it is still not possible to create a rational classification of these conditions, since not only the issues of pathomorphogenesis, but even the definition of the very concept of "hypo (a) plastic anemia" is debatable. In accordance with modern concepts of the genesis of hypo-
  2. Anemia due to blood loss, post-hemorrhagic anemia
    Anemia due to blood loss, post-haemorrhagic
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    This group of diseases includes: a) anemia, combined by a common mechanism of occurrence associated with impairment or termination of erythropoiesis as a result of a deficiency of substances necessary for normal blood formation - deficient anemia (B12 -, B6 -, B2 - folic acid, iron-copper cobalt-deficient, protein-deficient), as well as anemia, arising from the inability of the bone marrow
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