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B-12-folic deficiency anemia

B-12-folic deficiency anemias are associated with impaired RNA and DNA synthesis. Previously, this anemia was named after the authors who described it — Addison in 1849 and Birmer in 1872. Prior to the discovery of hepatic therapy, this disease was fatal, with which the old term "pernicious anemia" is connected, which means fatal or malignant anemia. At the end of the last century, work appeared on the use of raw liver of cattle in clinical practice.

Subsequent experimental studies of William Castl, a major American physiologist, found out the relationship between the stomach and the hematopoietic activity of the liver. A series of experiments with combined and separate feeding of patients with pernicious anemia of beef meat and gastric juice allowed Kastlou to express a number of provisions.

The presence of two components of a hematopoietic substance was revealed: an external one contained in beef meat and an internal one found in gastric juice. As a result of the interaction of two factors: external or exogenous and internal or endogenous, hematopoietin is formed, which is deposited in the liver and regulates the processes of physiological maturation of bone marrow elements, primarily erythroblasts.

The external factor of Kastla is cyanocobalamin (vitamin B-12). The place of production of the internal factor of Kastl - the glycoprotein is the parietal cells of the fundal glands - gastromucoprotein. The main function of the internal factor is the formation of a fragile aggregate complex, protein cyanocobalamin with vitamin B-12, which binds to specific receptors in the lower and middle part of the ileum, which

promotes the absorption of vitamin in the small intestine, then vitamin B-12 is combined with cyanocobalamin, which regulate the formation of hematopoietin in the liver, which in turn contributes to the transition of folic acid to the physiologically active restored form, which participates

in the metabolism of hematopoietic cells, affecting the formation of DNA. The reserves of B-12 in the body are so large that it takes 3-6 years to develop a deficiency of B-12 in violation of its absorption. Folic acid reserves are consumed in 4 months.

Exogenous deficiency of vitamin B-12 and folic acid can be nutritive or nutritional in nature, for example, when feeding children with goat milk, milk powder. There may be radiation anemia, medication (phenobarbital), as well as due to impaired intracellular folate metabolism in patients taking cytotoxic and anti-tuberculosis drugs, and in persons who consume alcohol.

Endogenous vitamin B-12 deficiency occurs due to impaired assimilation of dietary vitamin B-12 due to loss of secretion of gastric mucoprotein. This may be true Addison-Birmer anemia, symptomatic anemia of pernicious type in cancer, syphilis, lymphogranulomatosis, gastric polyposis. Disturbed assimilation of the vitamin in the intestine occurs with helminthic (difillobotrioznoy) anemia, with sprue, after resection of the small intestine. Increased consumption of vitamin is observed during pregnancy, with cirrhosis of the liver. There are hereditary reasons for insufficient secretion of the internal factor. In some patients, antibodies to parietal cells of the stomach and intrinsic factor are detected.

The clinical picture of the disease consists of a triad of symptoms: disorders of the hematopoietic system, digestive tract and nervous system. Patients quickly get tired, complain of dizziness, tinnitus, "flying flies" in the eyes, feeling of cotton legs, shortness of breath, palpitations, drowsiness. Then join dyspeptic

symptoms in the form of anorexia and diarrhea. There is a burning sensation in the tongue, paresthesia - crawling, numbness in the distal extremities, pain of radicular character.

The appearance of patients in the period of exacerbation is characterized by a sharp paleness of the skin with a lemon-yellow shade. Sclera subicteric. Sometimes there is pigmentation on the face. Patients usually are not exhausted. Hemorrhagic rash, as a rule, does not happen. The typical is the defeat of the language - glossit Genter. The language appears bright red

areas of inflammation that are very sensitive to food and medicine, causing the patient to feel pain and burning.
When the inflammation engulfs the entire tongue, it becomes like a scalded. In the future, the inflammatory phenomena subside, and the nipples of the tongue atrophy. Language becomes

smooth and shiny ("lacquered tongue").

Gastroscopy reveals the nest nest, less often - total atrophy of the gastric mucosa. A characteristic symptom is the presence of so-called nacreous plaques - areas of mucosal atrophy.

An analysis of the gastric contents usually reveals an achilia and an elevated mucus content. Since the introduction of histamine into clinical practice, cases of pernicious anemia with preserved free hydrochloric acid in the gastric juice, that is, the lack of achlorhydria, have become more frequent. The liver is mostly enlarged and

sensitive to palpation. As a rule, the lower pole of the spleen is palpable by 2-3 cm from under the edge of the costal arch. The pathomorphological basis of the nervous syndrome is the degeneration and sclerosis of the posterior and lateral columns of the spinal cord, or the so-called funicular myelosis with typical spastic paraparesis.

Especially bright are the changes in the blood, leading to the development of pronounced anemia. However low hemoglobin decreases, the number of erythrocytes decreases even lower, so the color index always exceeds unity, that is, the main hematological sign is hyperchromic anemia of a megaloblastic nature. The bulk of red blood cells has a diameter of 9-10 microns (macrocytes). There are red blood cells with a diameter of 12 to 15 microns (megalocytes), which are excessively saturated with hemoglobin. As the aggravation in peripheral blood progresses, megaloblasts appear in varying degrees of maturation, there may be red blood cells with preserved remnants of the nucleus in the form of Jolly bodies, Cabot rings, red blood cells with basophilic puncture. No less characteristic and changes in white blood. There is leukopenia (up to 1.5 x 10.9 / l and less), neutropenia, eosinopenia. A shift to the right is determined among the cells of the neutrophilic series: the presence of peculiar giant polysegmented forms containing up to 8-10 nuclear segments. At the same time, there may be a shift to the left to metamyelocytes and myelocytes.

There is moderately severe thrombocytopenia.

Bone marrow puncture macroscopically seems to be abundant, bright red, which contrasts with the pale appearance of peripheral blood. Some patients lack oxyphilic forms - "blue bone marrow". The ratio between leukocytes and erythroblasts instead of 3: 1, 4: 1 becomes 1: 2 and even 1: 3, that is, absolute predominance of erythroblasts is observed. The picture of the bone marrow in these cases is compared with the fetal hematopoiesis. In essence, this comparison is not entirely accurate, since with pernicious anemia, megaloblasts differ from those in human embryos. A characteristic feature of the ineffectiveness of megaloblastic erythropoiesis is intraosseous cerebral disintegration of hemoglobin-containing megaloblasts, creating a picture of hemolytic jaundice, but without reticulocytosis, accompanying typical hemolytic jaundice.

In blood tests, the content of vitamin B-12 is reduced, the content of unbound bilirubin, which gives an indirect reaction, is increased.

S.P. Botkin also drew attention to the possibility of the development of megaloblastic anemia during invasion with a wide tapeworm. The parasite, being in the upper part of the human small intestine, consumes huge resources of vitamin B-12, coming from food.

Called B-12-folic-achrestic anemia, that is, anemia from non-use, refers to a condition where the bone marrow is unable to use antianemic substances in the blood, that is, vitamin B-12 and folic acid. At the same time, there are no signs of damage to the digestive tract, gastric juice contains both hydrochloric acid and pepsin, and there are no signs of damage to the nervous system.

There is no yellowness, not enlarged liver and spleen. The liver of the dead from achrestic anemia contains vitamin B-12 and folic acid, but these vitamins are not absorbed by the bone marrow. Currently, this condition is considered as pre-leukemia.
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B-12-folic deficiency anemia

    The classic form of B12-deficient anemia is the so-called malignant, or pernicious, Addison-Birmere anemia. In Addison-Birmere disease, a diverse clinical and hematological syndrome, which characterizes the state of endogenous B12-avitaminosis in “pure” form (Fig. 41), is fully realized. To endogenous B12-avitaminosis, we also include perinitic-anemic
  2. Vitamin B12- and folic deficiency anemias
    Vitamin B12- and folic-deficient anemias belong to the group of macrocytic anemias. In essence, they are two different anemias, and they are rarely found in the same person at the same time. These anemias have similar pathogenetic mechanisms. They are associated, ultimately, with a violation of the synthesis of DNA and RNA with a deficiency of vitamin B! 2, folic acid, and some rare hereditary fermentopathies.
  3. Enterogenic folic-B12-deficient anemias
    Symptomatic folic-B12-deficient anemias, associated with chronic intestinal diseases (enteritis such as sprue and celiac disease), as well as with the functional shutdown of a more or less significant segment of the small intestine (resection, atresia, diverticulosis), are combined under this name. ANEMIA AT THE SPRU Sprue (spru, dutch sprew — foam ”synonyms: aphtae tropicae, psilolis
    Hyperchromic macrocytic anemia of pregnant women in conditions of our country is relatively rare. Much more often this anemia occurs in women of subtropical and tropical countries, and often against the background of malaria, helminthic invasion or intestinal lesions. According to the observations of Layrisse, in Venezuela, macrocytic anemia of pregnant women is a relatively frequent complication
  5. Folic acid deficiency anemia
    The metabolically active (coenzyme) form of folic acid is tetrahydrofolic acid, which is necessary for regulating the formation of thymidine monophosphate, which is part of the DNA structure, for the synthesis of glutamic acid, pyrimidine and purine bases. The cause of the development of this disease is insufficient intake of folic acid with food (starvation, especially in children
    Under this name, severe pernicious type anemia is described, progressing during pregnancy and resulting in untreated cases of death. Pathogenesis. Pernicious anemia of pregnant women, as a rule, occurs in the IV — V month of pregnancy, that is, during the period when the fetal hematopoiesis in the fetal liver is replaced by normoblastic (E.V. Kravkova, our observations). As already been
    B12 - folic acid deficiency anemia. Hyperchromic anemia. The presence of megaloblasts (giant erythrocytes containing the nucleus) and megalocytes (giant erythrocytes with completed enucleation), and gigantic with polysegmented neutrophil nuclei. Detection in macrocytes of Jolly Taurus - remnants of the nuclear substance and Kebot rings - remnants of the nuclear membrane. Iron deficiency anemia. Hypochromic
  8. Deficient anemia in young children
    Questions for repetition: 1. Hemogram of healthy children of different ages. 2. Indicators of red blood sprout in healthy children (life expectancy, the size and shape of red blood cells, the calculation and value of the color index). Test questions: 1. Deficiency anemia in children. Classification. 2. Iron deficiency anemia (IDA): 2.1. predisposing factors, risk groups. 2.2. etiopathogenesis of IDA.
  9. Anemia associated with deficiency of vitamin B12 and folic acid
    A large group of hereditary, congenital and acquired anemias, developing as a result of a violation of the synthesis of nucleic acids, is combined; their common feature is the appearance of megaloblasts in the bone marrow and peripheral blood. More often observed anemia due to a deficiency of vitamin B12, at least - a deficiency of folic acid. Folic acid deficiency is more common in children. Anemia due to
    Pernicious anemia develops due to vitamin B12 deficiency (daily requirement of 1-5 μg). In most cases, combined with fundal gastritis and achlorhydria. Pernicious anemia is an autoimmune disease with the formation of AT to the parietal cells of the stomach or the internal factor of Castle, however, there are B2-deficient anemias of alimentary genesis. Pernicious anemia can be congenital
  11. Deficient anemia
    -Anamnesis: eating disorders, digestive disorders -sm anemia: pallor of the skin and mucous membranes, reducing the amount of hemoglobin and red blood cells -hyperplastic sm: an increase in the liver and spleen according to the severity of the disease -hemolytic cm: jaundice, splenomegaly, increase in indirect bilirubin in the blood - hemorrhagic sm is expressed only in severe forms - laboratory
  12. Vitamin B6-deficient anemia
    Develop with deficiency or increased intake of vitamin B6. Vitamin B6 is found in large quantities in fresh vegetables, cereals, yeast, meat, egg yolks and other foods. Therefore, the true hypo-or vitamin B6 vitamin deficiency is very rare and mostly in infants. Causes of vitamin Ba deficiency are unilateral milk feeding, long-term intestinal
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