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B-12-Folic deficiency anemia

B-12 folic-deficient anemia is associated with a disruption in the synthesis of RNA and DNA. Previously, this anemia was named for the authors who described it - Addison in 1849 and Birmer in 1872. Before the discovery of hepatic therapy, this disease was fatal, with which the old term "pernicious anemia" is associated, which means fatal or malignant anemia. Even at the end of the last century there were works on the use of raw liver of cattle in clinical practice.

Subsequent experimental studies by William Castle, a prominent American physiologist, revealed the relationship between the stomach and hematopoietic activity of the liver. A series of experiments with combined and separate feeding of patients with pernicious anemia with beef meat and gastric juice allowed Castl to state a number of provisions.

The presence of two components of the hematopoietic substance was revealed: the extraneous, contained in beef meat and internal, located in gastric juice. As a result of the interaction of two factors: external or exogenous and internal or endogenous, hemopoietin 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 development of the internal factor of Kastla - glycoprotein are the parietal cells of the base glands - gastromucoprotein. The main function of the internal factor is the formation with vitamin B-12 of a fragile aggregate complex - protein-cyanocobalamin, which binds to specific receptors in the lower and middle parts of the ileum, which

promotes the absorption of vitamin in the small intestine, then vitamin B-12 combines with cyanocobalamin, which regulate the formation of hematopoietin in the liver, which in turn promotes the transition of folic acid into a physiologically active reconstituted form that participates

in the metabolism of hematopoietic cells, affecting the formation of DNA. The B-12 reserves in the body are so great that it takes 3-6 years to develop a deficiency of B-12 if its absorption is impaired. Stocks of folic acid are consumed in 4 months.

Exogenous insufficiency of vitamin B-12 and folic acid can be nutritive or nutritional, for example, when feeding children with goat milk, milk powder. There may be radiation anemia, medication (phenobarbital), and also as a result of intracellular metabolism of folates in patients taking cytostatic and anti-tuberculosis drugs, and in individuals who consume alcohol.

Endogenous insufficiency of vitamin B-12 occurs due to impaired assimilation of food vitamin B-12 due to loss of secretion of gastric mucoprotein. This can be true Addison-Birmer anemia, symptomatic anemia of the pernicious type in cancer, syphilis, lymphogranulomatosis, polyposis of the stomach. Disrupted assimilation of the vitamin in the intestine takes place during helminthic (diphyllobothrious) anemia, with sprue, after resection of the small intestine. Increased consumption of the vitamin is noted in pregnancy, with cirrhosis of the liver. There are hereditary causes of insufficient secretion of the internal factor. In some patients antibodies to parietal cells of the stomach and internal factor are detected.

The clinical picture of the disease consists of a triad of symptoms: violations of the hematopoietic system, the digestive tract and the nervous system. Patients quickly become tired, complain of dizziness, noise in the ears, "flying flies" in the eyes, a feeling of cotton feet, shortness of breath, palpitation, drowsiness. Then the dyspeptic

symptoms in the form of anorexia and diarrhea. There is a burning sensation in the tongue, paresthesia - a feeling of crawling, numbness in the distal parts of the limbs, pain in the radicular nature.

Appearance of patients in the period of exacerbation is characterized by a sharp pallor of the skin with a lemon-yellow hue. The scleras are subiclinic. Sometimes on the face there is a pigmentation. Patients are usually not depleted. Hemorrhagic rashes, as a rule, do not happen. Typical is the defeat of the language - glossitis of Genter. The language is bright red

sites of inflammation, very sensitive to food and medication, causing the patient a feeling of pain and burning.
When the inflammation covers the entire tongue, it becomes as "scalded." Subsequently, the inflammatory phenomena subsided, and the papillae of the tongue become atrophied. Language becomes

smooth and shiny ("lacquered tongue").

Gastroscopy reveals nesting nests, rarely - total atrophy of the gastric mucosa. A characteristic symptom is the presence of so-called mother-of-pearl plaques - areas of mucosal atrophy.

The analysis of gastric contents, as a rule, reveals a sword and an increased amount of mucus. Since the introduction into clinical practice of a sample with histamine, cases of pernicious anemia with conserved free hydrochloric acid in the gastric juice, that is, the absence of achlorhydria, began to occur more often. The liver is mostly enlarged and

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

Particularly striking are the changes in the blood, leading to the development of severe anemia. As low hemoglobin decreases, the number of red blood cells decreases even lower, so that the color index always exceeds unity, that is, the main hematological sign is hyperchromic anemia of a megaloblastic nature. The main mass of red blood cells has a diameter of 9-10 μm (macro-cells). There are erythrocytes with a diameter of 12 to 15 μm (megalocytes), which are excessively saturated with hemoglobin. As the exacerbation progresses, the megaloblasts appear in the peripheral blood in various degrees of their maturation; there may be red blood cells with preserved core remains in the form of Jolly bodies, Cabot rings, erythrocytes with a basophilic position. No less characteristic are the changes in white blood. Leukopenia is noted (up to 1.5 x 10.9 / L and less), neutropenia, eosinopenia. Among the cells of the neutrophilic series, a shift to the right is determined: the presence of unique giant polysegmented forms containing up to 8-10 nuclear segments. At the same time, there may be a shift to the left before metamyelocytes and myelocytes.

Moderately expressed thrombocytopenia is noted.

Bone marrow point macroscopically appears abundant, bright red, which contrasts with the pale appearance of peripheral blood. In some patients there are no 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, the absolute predominance of erythroblasts is observed. The bone marrow picture in these cases is compared with embryonic hematopoiesis. In fact, this comparison is not quite accurate, since with pernicious anemia, megaloblasts differ from those in human embryos. A characteristic feature of the ineffectiveness of megaloblastic erythropoiesis is intracranial decomposition of hemoglobin-containing megaloblasts, which creates a picture of hemolytic jaundice, but without reticulocytosis accompanying typical hemolytic jaundice.

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

Still, SP Botkin drew attention to the possibility of developing megaloblastic anemia when infecting with a wide ribbon. The parasite, being in the upper part of the small intestine of a person, consumes huge resources of vitamin B-12, supplied with food.

Under the name of B-12 folic-anhremic anemia, that is, anemia from non-use, we mean the state when the bone marrow is unable to use the 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 jaundice, no increase in liver and spleen. The liver of the deceased from acrid anemia contains vitamin B-12 and folic acid, but these vitamins are not absorbed by the bone marrow. At present, this condition is considered a 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-Birmer anemia. With the disease .addison-birmer, a multifaceted clinico-hematological syndrome is fully realized, characterizing the state of endogenous B12-avitaminosis in a "pure" form (Figure 41). To endogenous B12-avitaminosis we also include perinic-anemic
  2. Vitamin B12- and folate-deficient anemia
    Vitamin B12- and folic-deficient anemia belong to the group of macrocytic anemia. In their essence, they are two different anemia, 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 B2, folic acid, and some rare hereditary enzymopathies.
  3. Enterogenic FOSSIL-B12-deficient anemia
    Symptomatic folic-B12-deficiency anemia associated with chronic intestinal diseases (enteritis such as sprue, celiac disease), as well as with functional deactivation of a more or less significant segment of the small intestine (resection, atresia, diverticulosis) is combined under this name. ANEMIES WITH SPRA Sprue (spru, Dutch sprew-foam ") synonyms: aphtae tropicae, psilolis
    Hyperchromic macrocytic anemia of pregnant women in our country is relatively rare. Significantly, this anemia is found in women of the subtropical and tropical countries, 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-deficiency anemia
    The metabolically active (coenzyme) form of folic acid is tetrahydrofolic acid, which is necessary for the regulation of the formation of thymidine monophosphate, which is part of the DNA structure, the synthesis of glutamic acid, pyrimidine and purine bases. The cause of this disease is insufficient intake of folic acid in the body with food (starvation, especially in children
    This name describes severe anemia of pernicious type, progressing during pregnancy and leading to death in untreated cases. Pathogenesis. Pernicious anemia of pregnant women, as a rule, occurs on the 4th-5th month of pregnancy, ie, at a time when embryonic hematopoiesis in the liver of the fetus is replaced by normoblastic (EV Kravkova, our observations). As it was already
    B12 - folic-deficiency anemia. Hyperchromic anemia. The presence of megaloblasts (giant erythrocytes containing the nucleus) and megalocytes (giant erythrocytes with complete enucleation), and giant ones with polysegmented nuclei of neutrophils. Detection of Jolly bodies in macrocytes - remains of nuclear substance and Kebot rings - remains of nuclear envelope. Iron deficiency anemia. Hypochromatic
  8. Deficiency anemia in young children
    Questions for recurrence: 1. Hemogram of healthy children of different ages. 2. Indicators of red blood sprouts in healthy children (life expectancy, size and form of red blood cells, calculation and value of color index). Control 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
    They combine a large group of hereditary, congenital and acquired anemia, which develop as a result of a violation of the synthesis of nucleic acids, a common feature is the appearance in the bone marrow and peripheral blood of megaloblasts. Often observed anemia due to a deficiency of vitamin B12, less often - a deficiency of folic acid. Children are more likely to have a deficiency of folic acid Anemia due to
    Pernicious anemia develops as a result of vitamin B12 deficiency (daily requirement is 1-5 μg). In most cases, it is combined with a base gastritis and achlorhydria. Pernicious anemia is an autoimmune disease with the formation of AT to parietal cells of the stomach or the internal factor of the Castle, but there are B | 2-deficient anemias of alimentary origin. Pernicious anemia can be congenital
  11. Deficiency anemia
    -amnesis: eating disorders, digestive disorders -c-m anemia: pallor of the skin and mucous membranes, decrease in the amount of hemoglobin and erythrocytes -hyperplastic s-m: an increase in the liver and spleen according to the degree of severity of the disease-hemolytic c-m: jaundice, splenomegaly, bilirubin in the blood-hemorrhagic с-m is expressed only in severe forms-laboratory
  12. Vitamin B6-deficient anemia
    Develop with a deficiency or increased intake of vitamin B6. Vitamin B6 is found in large quantities in fresh vegetables, cereals, yeast, meat, egg yolks and other products. Therefore, the true hypo- or vitamin deficiency of vitamin B6 is very rare and mainly in infants. The causes of vitamin B deficiency are unilateral breastfeeding, long-term intestinal
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