Lack of vitamin B12 and folic acid. Anemia due to deficiency of vitamin B12 and folic acid. Damage to the digestive system

It appears due to a lack of vital vitamin B12 in the body.

Most of it is found in the bone marrow, tissues of the nervous system, so the lack of a substance leads to a malfunction of almost all organs.

Symptoms of the disease are individual. For example, one person may feel a sharp weakness, while another patient may not notice the course of the disease. In both cases, surgical treatment is necessary, since ignoring its signs leads to dangerous consequences, including disability or death.

Absolutely everyone can get sick with anemia, so you need to know what preventive measures and methods of treatment exist.

Causes of anemia due to a lack of vitamin B12

There are many reasons that can provoke the appearance of the disease. The etiological factors of the disease can manifest themselves in cyanocobalamin or folic acid deficiency, which is caused by:

vegetarianism;
low absorption capacity of the gastrointestinal tract;
gastrectomy;
neuropsychiatric disorders;
many diseases and viral infections;
improper, unbalanced diet;
atrophic processes in the intestines and stomach.

Only a specialist in the laboratory can identify the true cause of a vitamin deficiency. A blood test gives a complete clinical picture of the disease and allows you to make an accurate diagnosis. If you find symptoms of B12 deficiency anemia, seek immediate medical attention.

Chronic alcoholism and other bad habits can cause vitamin B12 deficiency, as they significantly weaken the human immune system and worsen the state of human health. Disease prevention is a balanced diet, healthy lifestyle life, personal hygiene.

Vitamin B12 deficiency is normal during pregnancy, so there is no need to panic if symptoms are detected. AT this case you need to visit a local gynecologist who will prescribe a complex of vitamins or a drug that contains the maximum amount of a deficient substance.

There are two main causes that provoke anemia. These include insufficient intake of the required amount of vitamin B12 from food and disturbances in the functioning of the gastrointestinal tract, which lead to a decrease in absorption and absorption capacity.

Symptoms, distinctive features of the disease

B12 deficiency anemia proceeds slowly and without manifestations. It is extremely rare that it manifests itself very sharply, but this is possible only with a running form. The main symptoms of the disease are:

shortness of breath even with light work, loads;
heart palpitations;
staggering gait;
increased blood pressure;
pale skin;
a state of general weakness;
fatigue, decreased physical activity.

In addition, the patient may feel irritated and overwhelmed. At the first sign of illness, it is recommended to take a complete blood count to confirm or exclude the presence of anemia.

In addition to external changes in the body, internal pathological processes occur. For example, inflammation of the papillae in the tongue, an increase in some organs, such as the spleen, liver. Outwardly, it is impossible to determine the pathology, therefore, a comprehensive examination is necessary, which consists of an ultrasound examination, blood and urine tests.

Moreover, the patient may be seen disorders of the nervous system. In particular, a slow reaction, instability, a tendency to a depressive state, a decrease in sensitivity.

Symptoms of the disease may appear in different phases. At the beginning of anemia, they may be absent, but over time, the symptoms increase and can appear sharply and abruptly. In each case, different symptoms are observed. It all depends on the individual characteristics, the state of the human immune system.

Diagnostic methods

A blood test can determine if a person has anemia, which is characterized by a lack of vitamin B12. With it, you can identify the following signs:

decrease in the level of red blood cells, hemoglobin;
an increased color index that exceeds 1.05 units;
the presence of macrocytosis, characteristic of the group of anemias of the macrocytic type;
leukopenia;
a decrease in such cells in the blood as reticulocytes, monocytes;
thrombocytopenia.

If these indicators are identified, the attending physician may prescribe effective treatment, which is based on drug therapy, diet and additional procedures. In addition, an increased level of bilirubin in the blood can indicate the presence of anemia.

To confirm the diagnosis, the patient may be assigned a bone marrow puncture. It is necessary to make it in order to exclude the course of other diseases that have similar symptoms. If a this procedure showed hyperchromia, then there is no doubt in the diagnosis, since it is characteristic of B12 deficiency anemia. Diagnosis of the disease is carried out both in a paid clinic and in a state clinic.

In order to know whether there is a risk of developing the disease, it is necessary to conduct a routine examination and take a blood test once a year. This will allow timely detection of signs and symptoms of anemia and take the necessary measures to eliminate it.

Medical treatment

Anemia due to vitamin B12 deficiency is quickly and easily treatable. Her symptoms are eliminated promptly and without the use of complex manipulations. In most cases, the disease is treated with medications that make up for the lack of vitamins and minerals. Substitution therapy is designed to eliminate not only the manifestations and first signs, but also the source of the disease.

Preparations containing vitamin B12

To date, there are 3 types of drugs that treat anemia. These include drugs such as:

The drug Cyano-cobalamin is administered by intramuscular injection every day for 14 days. Oxycobalamin, which has a stronger bond with proteins, is administered 1 time in 2 days. But the drug Adenosylcobalamin has a more effective effect. It has an active effect on funicular myelosis, but has no effect on erythropoiesis.

The result of injections is noticeable after several procedures. At the same time, the patient feels an improvement in well-being, vigor and an increase in physical and mental performance. Moreover, blood counts improve, megaloblasts, which are concentrated in the bone marrow, disappear. After the administration of the drug, the level of reticulocytes increases after 5-6 days. Treatment continues for at least 4 weeks. The average dosage of the drug varies by micrograms per day.

If the patient has funicular myelosis, then the dose is increased to 1000 mcg. The effectiveness of treatment is evidenced by stable remission. If it is absent, then such a phenomenon indicates that the diagnosis was made incorrectly, and the treatment is ineffective.

Fixing therapy is prescribed after the main course of treatment. For two months, it is necessary to inject Cyanocobalamin 1-2 times a week. After that, a preparation containing vitamin B12 is administered for 6 months. Injections should be done 2 times a month, and the dose of the drug is 500 mcg.

People who suffer from chronic anemia due to a lack of vitamin B12 can alleviate their condition with a complete cure for the disease. In most cases, Epogen injections are recommended. Epogen is a hormone that stimulates the production of cells such as red blood cells. If anemia is caused by kidney failure, then dialysis, Epogen procedures, are prescribed. In extreme cases, a kidney transplant is needed.

Folk remedies

Treatment with folk remedies is allowed only after consulting a doctor. Improper treatment at home can lead to serious consequences, the elimination of which will take a lot of time and cost. First of all, folk remedies are aimed at the causes of the disease, which include atrophic gastritis and helminthiasis.

To eliminate anemia due to B12 deficiency, you need to eat animal products. Diet is the most effective way to improve the patient's condition and return the hematopoietic process to normal functioning.

Foods rich in vitamin B12 include:

Vegetable products practically do not contain this vitamin. But to make up for the lack of folic acid, you need to eat leafy greens, cereals, beans, cauliflower, mushrooms. Proper nutrition based on animal products can help eliminate the symptoms of the disease and reduce vitamin deficiency. After a 2-week diet, a person will feel relief and return to normal health. But this is possible only at the initial stage of anemia.

In addition, to folk remedies includes the reception of various decoctions, infusions from medicinal herbs and natural preparations. So, decoctions from meadow clover and wild rose help well. It also helps to improve the condition of freshly squeezed juice from beets, carrots, radishes. Treatment of the disease should be complex, so it is necessary to combine both drug therapy and diet.

Preventive measures

Treatment of anemia, which is based on a lack of vitamin B12, will be favorable, effective only with timely treatment. Therefore, at the first symptoms of the disease, you need to come to an appointment with a local therapist who will conduct an examination, examination and refer you to a specialist.

Also, every person who wants to exclude the development of anemia should strengthen the immune system and follow the rules of personal hygiene. You can increase the function of the immune system with the help of vitamin complexes, which are sold in every pharmacy. A balanced diet plays an important role in disease prevention. Various diets and hunger strikes can change the composition of the blood and lead to serious complications.

Treatment of B12 deficiency anemia is carried out for a long time. Therefore, it is better to prevent the disease than to spend a huge amount of money on treatment. If signs of the disease are found, it is necessary to contact a hematologist who treats blood diseases. Hardening and other methods of increasing immunity can help in preventing the disease.

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Megaloblastic anemia: causes, symptoms and treatment

One type of anemia is megaloblastic, or B12-folate deficiency anemia. This is a disease that develops as a result of a violation of the process of maturation of erythrocytes due to a violation of the synthesis of RNA and DNA in the cell, accompanied by the presence in the bone marrow of a large number of modified erythrocyte precursors - megaloblasts.

The frequency of megaloblastic anemia is 9-10% of all cases of anemia. People of all ages suffer from it, but it is more common in older people than in young people (4% and 0.1%, respectively). Megaloblastic anemia is a condition that can and should be treated. The causes, symptoms and treatment of this disease will be considered in this article.

Causes and mechanism of development of megaloblastic anemia

The reason for the development of B12-folate deficiency anemia is a lack of vitamin B12 (cyanocobalamin) and folic acid (vitamin B9) in the body.

Folic acid deficiency usually occurs for the following reasons:

insufficient intake of vitamin with food during fasting;
insufficient absorption in the intestine due to various diseases such as celiac disease and other enteropathies;
partial or complete absence of the patient's small intestine as a result of resection (removal);
increased need for vitamin B9 during pregnancy and lactation, as well as in some forms of hemolytic anemia, with exfoliative dermatitis or in the case of broad tapeworm invasion - with diphyllobothriasis;
increased loss of it, for example, during hemodialysis;
chronic hepatitis, cirrhosis of the liver;
chronic pancreatitis;
alcohol abuse;
long-term use of certain medications - combined oral contraceptives, anticonvulsants, drugs that slow down metabolism.

The reasons for the lack of cyanocobalamin in the body are:

vegetarianism;
polyposis or cancer of the fundus of the stomach;
chronic gastritis A;
partial or complete removal of the stomach;
Zollinger-Ellison syndrome;
pregnancy and lactation period;
helminthic invasion;
enteropathy, in particular, celiac disease;
resection of the small intestine;
Crohn's disease;
cirrhosis of the liver and chronic hepatitis;
enzyme deficiency - transcobalamin II.

With a deficiency in the body of vitamins B9 and B12, the synthesis of genetic material in cells - DNA and RNA - is disrupted. In this case, the cells of the bone marrow and the epithelium of the digestive tract suffer more than others - that is, cells with a high renewal rate. RBC progenitor cells lose their ability to differentiate (transition from younger to more mature forms), but their cytoplasm develops as before: as a result, huge cells called megaloblasts are formed.

Vitamin B12 enters the human body with all kinds of animal products. Once in the stomach, it binds to a special substance - gastromucoprotein, with which it moves further along the digestive tract - into the small intestine, where it is absorbed. The daily requirement for vitamin B12 is 3-7 mcg. Its reserves are in the liver and amount to 3-5 mg. The need for folic acid is higher - 100 micrograms per day, but more of it enters the body - with a standard diet - micrograms. The reserves of vitamin B9 are 5-10 mg.

Vitamin B12 consists of 2 important parts - coenzymes. With a lack of the first, DNA synthesis is disrupted - the maturation of erythroid cells is disrupted - a megaloblastic type of hematopoiesis is formed. In addition to erythrocytes, the formation of leukocytes and platelets is disrupted, but these changes are less pronounced.

Also, a deficiency of the first coenzyme leads to a disruption in the synthesis of an essential amino acid - methionine, which is responsible for the normal functioning of the nervous system. Due to the lack of the second coenzyme in the body, the metabolism of fatty acids is disturbed - toxic substances accumulate, partially affecting the spinal cord - a condition called funicular myelosis develops.

Clinical features of megaloblastic anemia

The vast majority of megaloblastic anemias are B12-deficient. Their clinical manifestations can be combined into 4 groups - signs of damage to the digestive tract, symptoms of funicular myelosis, circulatory-hypoxic syndrome, psycho-neurological disorders. Let's consider in more detail.

1. Signs of damage to the digestive tract (occur due to atrophy of the gastric mucosa, damage to the mucous membrane of the upper intestine, insufficient production of enzymes and the disturbances in the processes of digestion and absorption of food caused by these changes):

loss of appetite;
complete aversion to meat food;
tingling and pain of the tip of the tongue, taste disturbance, "varnished" tongue - these symptoms were combined by the term Hünter's atrophic glossitis;
nausea, vomiting;
stool disorders.

2. Symptoms of funicular myelosis:

headache;
sensations of tingling, tingling, burning in the skin - paresthesia;
feeling cold;
wobbly, unsteady gait;
feeling of numbness in the limbs;
lethargy in the lower extremities;
limitation motor activity- paresis and, in especially severe cases, paralysis.

3. Circulatory-hypoxic syndrome:

4. Psycho-neurological disorders:

irritability;
hallucinations;
convulsions;
the complexity of performing simple mathematical functions.

The disease, as a rule, proceeds in 2 stages - subclinical and clinical. At the first stage, there are no obvious signs of hypovitaminosis, and patients complain of mild malaise and minor dyspeptic symptoms. Despite the absence of external clinical signs, a decrease in the content of vitamins in the blood is already present. When the reserves of vitamins in the body are depleted or earlier, but after exposure to a strong provoking factor (for example, against the background of psycho-emotional stress or after a serious surgical intervention), the disease enters the second stage - clinical.

Against the background of megaloblastic anemia, chronic somatic diseases - angina pectoris, arrhythmias - become aggravated and actively progress. Edema appears.

It is worth noting the peculiarity of the course of megaloblastic anemia in the elderly. This category of patients, even at sufficiently low hemoglobin values, makes few complaints, while in iron deficiency anemia, a decrease in this indicator to only 110 g/l is accompanied by a significant deterioration in the patient's condition and many complaints.

Diagnosis of megaloblastic anemia

The doctor will suspect the presence of anemia even at the stage of collecting complaints, anamnesis and an objective examination of the patient.

The following changes will be noticed:

pallor, sometimes yellowness of the skin; skin color in this disease is compared with the color of parchment;
enlarged lacquered tongue;
with auscultation of the heart - an increase in its contractions - tachycardia, systolic murmur;
palpation of the abdomen - an increase in the spleen - splenomegaly;
neurological examination showed signs of funicular myelosis.

In the general blood test, there is a decrease in the level of hemoglobin and erythrocytes, an increase in the color index above 1.1 (that is, anemia is hyperchromic). In some patients, thrombocytopenia and leukopenia are detected in parallel with erythropenia. Also in the blood are determined modified precursors of erythrocytes - megaloblasts, macrocytes. Characterized by anisocytosis (change in cell size) and poikilocytosis (change in their shape). In the cytoplasm of erythrocytes, specific elements are determined - Kebbot's rings and Jolly bodies. Reticulocytopenia is also noted.

The level of vitamins B9 and / or B12 in the blood serum, of course, is below normal values.

Since megaloblastic anemia is often accompanied by hemolysis of erythrocytes, the level of iron in the blood serum is not reduced, but is within the normal range or elevated. For the same reason, the level of free bilirubin in the blood serum is also increased.

To confirm the diagnosis, a sternal puncture is performed. In the punctate, megaloblastic transformation of the bone marrow is determined. It is important to carry out a puncture before starting therapy of a patient with vitamin B12, since within a few hours after its administration, the composition of the bone marrow begins to return to normal, and after 1-2 days, the manifestations of the megaloblastic type of hematopoiesis disappear altogether.

In almost all patients, in addition to the changes described above, atrophic changes in the gastric mucosa are determined, a reduced content of hydrochloric acid in it - hypo- or even achlorhydria.

In general, the entire process of examining a patient for the presence of megaloblastic anemia can be divided into 3 stages:

A clinical blood test, in which the above-described changes characteristic of this type of anemia are determined.
Determination of the level of vitamins B9 and B12, sternal puncture followed by examination of the punctate.
Establishment of the causative factor of anemia - a detailed study of the history data, examination of the stomach (fibrogastroscopy, determination of acidity, and so on), intestines, liver, determination of the presence or absence of helminthiases (examination of feces). The scope of ongoing clinical trials is individual for each patient and is determined by the specific clinical situation.

Treatment of megaloblastic anemia

If the exact cause is determined - the etiological factor of anemia, the main direction of therapy is to eliminate it. This can be deworming (if worms are found), surgical removal of polyps or other tumors of the stomach, adequate treatment of intestinal diseases, the fight against alcoholism, and so on.

In parallel with the etiological treatment, the patient should pay much attention to nutrition. The diet of a patient with megaloblastic anemia should include a sufficient amount of meat and dairy products, liver, leafy vegetables, and fruits.

The essence of pathogenetic therapy is the parenteral administration of vitamin B12 - cyanocobalamin. The dose required for treatment depends on the initial blood counts and varies within micrograms per day.

Such therapy continues until the onset of hematological remission, that is, until the dynamics in relation to the normalization of red blood counts is determined. Starting from this period, the dose of administered cyanocobalamin is recommended to be reduced or administered at the same dosage, but not every day, but once every 48 hours, and later - 2 times a week until the hemoglobin level normalizes.

Usually, the first sign of hematological remission appears 6-10 days after the start of therapy and is a sharp - up to 2-3% - increase in the level of reticulocytes. This phenomenon is called "reticular crisis". In the future, the indicators of hemoglobin, erythrocytes, as well as leukocytes and platelets gradually return to normal, the color index decreases.

When indicators general analysis blood levels are normalized, the dose of cyanocobalamin is reduced to a maintenance dose - it is administered pomg once every 1-2 weeks. If a patient is diagnosed with Addison-Birmer anemia, vitamin B12 is recommended for him for life.

In some cases of the disease - for example, with already developed funicular myelosis - higher doses of vitamin B12 - mg are prescribed every day. Reduce the dose of the drug only when not only the indicators of peripheral blood have returned to normal, but the neurological symptoms of this condition have completely disappeared.

In especially severe clinical situations - when the patient is in a pre-coma state or has already fallen into a coma - he is prescribed blood transfusions. As a rule, washed erythrocytes are administered. With a proven autoimmune mechanism of the disease (this occurs in a number of patients), the patient is shown the introduction of glucocorticoids in minimal therapeutic dosages in a short course.

In case of folic acid deficiency, preparations containing it are administered. The daily dose of the drug is usually 1-5 mg. The route of administration is oral.

To prevent the recurrence of the disease in the future, the patient should be prescribed prophylactic courses of vitamin B9, while its dose is one third of the therapeutic one.

Prevention of megaloblastic anemia

Among the measures that reduce the risk of developing this type of anemia, rational nutrition should be noted - eating enough foods containing vitamins B9 and B12, fighting bad habits - in particular, alcoholism, preventing helminthiasis, timely treatment of diseases of the digestive tract, the introduction of vitamin B12 patients after surgery to remove the stomach or small intestine.

Prognosis for megaloblastic anemia

Subject to the timely start of adequate treatment, the prognosis for both types of megaloblastic anemia (both B12 and folate deficiency) is favorable.

Which doctor to contact

If you are concerned about the symptoms described above, or you have already donated blood and know that you have some kind of anemia, contact your physician. After additional diagnostics, a patient with megaloblastic anemia is referred to a hematologist, who prescribes treatment. In addition, a consultation with a neurologist (for funicular myelosis) and a gastroenterologist (for indigestion) is often required. Since liver diseases and helminthic invasions are a common cause of anemia, an examination by a hepatologist and infectious disease specialist is recommended. Of great importance in the treatment is nutrition, it will be useful to consult a nutritionist.

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Anemia associated with impaired DNA synthesis can be both hereditary and acquired. common feature of these anemias is the presence of megaloblastic hematopoiesis in the bone marrow. These are megaloblastic anemias. More often there is an isolated deficiency of vitamin B 12, less often - folic acid.

Anemia due to vitamin B12 deficiency

Pernicious anemia was described in 1849 by Addison. Somewhat later, in 1872, Birmer defined it as "progressive pernicious anemia." Ehrlich discovered large cells with a peculiar chromatin structure in the bone marrow and called them "megaloblasts". In 1926, Minot and Murphy showed the possibility of curing pernicious anemia by administering raw liver containing an external factor, vitamin B 12 . Almost simultaneously, Castle (1929) discovered the internal gastric factor, and Smith and Rickes (1948) discovered vitamin B 12, which contributed to the establishment of the pathogenesis of pernicious anemia.

The frequency of occurrence of B 12 deficiency anemia increases with age and is 0.1% in young people, 1% in the elderly, after 75 years it is recorded in 4% of people.

Reasons for the development of vitamin B 12 deficiency

Malabsorption:
- Absence of intrinsic factor of Castle (atrophic gastritis, gastric resection, gastric irradiation).
- Small bowel disease (enteritis, jejunal resection, celiac disease, polyposis, cancer, Imerslund-Gresbeck syndrome)
Insufficient intake from food:
Strict vegetarian diet
Competitive Consumption:
- Wide tapeworm (diphylobothriasis).
- Pathological microflora in the presence of diverticulosis or "blind loop"
Increased utilization of vitamin B 12:
- Malignant neoplasms.
- hyperthyroidism
Hereditary deficiency of transcobalamin II.

Vitamin B 12 exchange [show]

The chemical structure of vitamin B 12 is presented in the form of two parts - one resembles a nucleotide, the second, the most characteristic part, is a corrin structure containing 4 pyrrole rings, in the center of which there is a cobalt atom (Co +3). Vitamin B 12 is also known as cobalamin. Vitamin B 12 is found in foods rich in protein: meat, eggs, cheese, milk, especially a lot of it in the liver and kidneys. In food, it is associated with protein.

In order for vitamin B12 to be absorbed, it is first released from food proteins by acid hydrolysis in the stomach or trypsin proteolysis in the intestine and binds to the R-protein produced by the salivary glands. Under the influence of pancreatic secretion proteases, the RB 12 complex is destroyed and vitamin B 12 is released.

Then vitamin B 12 combines with the internal factor of the Castle (WF, IF - intrinsic factor) - a protein secreted by the parietal cells of the mucosa of the fundus and body of the stomach. A VF-B 12 complex is formed, which dimerizes and binds to specific receptors in the ileum. The number of receptors in the ileum is a factor limiting the rate of intake of vitamin B 12 into the body. In the presence of Ca 2+ and pH 7.0, this complex is cleaved, and vitamin B 12 penetrates into the cells of the intestinal mucosa. From here, vitamin B 12 enters the blood, where it combines with transport proteins transcobalamin I, II and III, which deliver the vitamin to the cells of the liver, bone marrow and other cells (Fig. 36).

The release of vitamin B 12 from the complex with transcobalamin II in the cell occurs in three stages:

binding of the complex to cell receptors;
its endocytosis;
lysosomal hydrolysis to release vitamin

Transcobalamins I and III release vitamin B 12 only in the liver. The main depot of the vitamin is the liver, 1 g of which contains 1 μg of vitamin B12. The daily requirement for a vitamin for an adult is 5-7 mcg. Vitamin B 12 is mainly excreted in the bile, its loss also occurs in the feces. 0.1% of the total amount of the deposited vitamin is lost per day. The existence of the intestinal-hepatic circulation of vitamin B 12 has been proven - about % of the vitamin excreted with bile is reabsorbed again. This explains the development of megaloblastic anemia 1-3 years after the complete cessation of vitamin intake into the body.

In humans, two biochemical reactions are known that require the participation of vitamin B 12: 1) the formation of tetrahydrofolate from N5-methyltetrahydrofolate, in the same process homocysteine is converted to methionine, 2) a derivative of vitamin B 12 - 5'-deoxyadenosylcobalamin acts as a the transition of methylmalonyl-CoA to succinyl-CoA (Fig. 37).

The first reaction is key in the development of megaloblastic anemia with a lack of vitamin B 12 or folate. The main thing is the impossibility of N5-methyltetrafolate to go into tetrafolate (the so-called tetrafolate block develops), the formation of folates necessary for the synthesis of purine and pyrimidine decreases. Violation of the formation of thymidine leads to a slowdown in DNA synthesis, cell division, and the appearance of a megaloblastic type of hematopoiesis. Violation of DNA synthesis in B 12 deficiency can be expected in almost all nucleated cells, however, vitamin B 12 deficiency primarily affects hematopoiesis, since hematopoietic cells have the highest proliferative activity compared to other systems.

The second reaction, in which vitamin B 12 is involved, is necessary for the normal metabolism of fatty acids. During the breakdown of fatty acids, propionic acid is formed, during the metabolism of which a number of intermediate products are synthesized, in particular methylmalonic acid, the latter, under the influence of 5'-deoxyadenosylcobalamin, turns into succinic acid. In the absence or deficiency of this enzyme, methylmalonic acidemia is noted, the synthesis of fatty acids is disrupted, which results in neurological disorders.

The main reason for the development of vitamin B12 deficiency is atrophic gastritis, in which the synthesis of intrinsic factor stops or decreases. There is no parallelism between a violation of the production of an internal factor and a decrease in the acid- and enzyme-forming function of the stomach. Perhaps a combination of several factors is necessary for the occurrence of the disease.

Essential in the development of vitamin B12 deficiency is hereditary predisposition, 20-30% of patients have relatives with a similar disease. In the appearance of atrophic gastritis, the role of immune mechanisms is important. Autoantibodies directed to the antigens of parietal cells of the stomach, to the intrinsic factor, immunocomplex deposits in the wall of the stomach were found. Immune mechanisms may play a leading role in the development of B12 deficiency anemia in young adults. Often, it is combined with other autoimmune diseases (Hashimoto's goiter, hemolytic anemia).

Megaloblastic anemia can occur while taking anticonvulsants and cytostatics.

Clinical picture consists of symptoms of damage to the hematopoietic system, nervous system, gastrointestinal tract. Patients complain of fatigue, weakness, palpitations, shortness of breath. In severe anemia, slight yellowness of the sclera is noted. Some patients complain of pain and burning sensation in the tongue, however, the symptom of glossitis is not an absolutely pathognomonic sign of vitamin B12 deficiency, as it can also be with IDA. There is hepato- or splenomegaly. Gastric secretion is sharply reduced. Achilia is manifested by unstable appetite, aversion to food, dyspepsia.

The basis of neurological disorders is funicular myelosis of the lateral and / or posterior columns of the spinal cord, which is a consequence of demyelination, and then degenerative changes in nerve fibers in the spinal cord and peripheral nerves. Disturbances from the nervous system are detected in the form of peripheral polyneuropathy: leg weakness, crawling sensation, numbness of the fingers, impaired sensitivity in the limbs, a feeling of constant coldness in the legs. Muscle weakness is often observed, muscle atrophy is possible. First of all, the lower limbs are affected symmetrically, then the abdomen, upper limbs are less frequently affected. In the most severe cases, areflexia develops, persistent paralysis of the lower extremities, dysfunction of the pelvic organs. With B 12 deficiency anemia, convulsive seizures, hallucinations, memory loss, spatial orientation, mental disorders, psychoses with depressive or manic states are possible. A severe complication is the development of pernicious coma resulting from rapid anemia and cerebral ischemia.

Bone marrow. Characterized by megaloblastic type of hematopoiesis with a high level of ineffective erythropoiesis. The bone marrow is hypercellular due to an increase in the number of nucleated red cells. The ratio of leuco/erythro is 1:2-1:3 (the norm is 3:1-4:1). As a result of a violation of cell division, erythroid cells become very large (megaloblasts) and their structure changes qualitatively. The nuclei of megaloblasts always have a characteristic soft-mesh distribution, asynchronous maturation of the nucleus and cytoplasm. The nucleus, as the polychromatophilic and oxyphilic megaloblast matures, is more often located eccentrically.

Quantitative ratios between megaloblasts of varying degrees of maturity are highly variable and depend on the activity of bone marrow hematopoiesis. The predominance of promegaloblasts and basophilic megaloblasts creates a picture of "blue" bone marrow (Fig. 38). A characteristic feature of megaloblasts is the early hemoglobinization of their cytoplasm with the preserved delicate structure of the nucleus (Fig. 39, 41). There are significant degenerative changes in the nuclei of cells, ugliness, karyorrhexis, mitosis. The life span of megaloblasts is 2-4 times less than normal, so most cells die in the bone marrow without maturing.

Violation of cell division in the normal synthesis of hemoglobin creates a condition for enhancing ineffective erythropoiesis. The results of autoradiographic and cytophotometric studies showed an elongation of the S-G 2 phase of the cell cycle and cell death in this period. Megaloblasts develop into megalocytes and macrocytes. Intramedullary hemolysis of erythrokaryocytes (ineffective hematopoiesis) and the short lifespan of megalocytes lead to an increase in the level of indirect bilirubin.

Lack of vitamin B 12 entails changes in leukopoiesis, since DNA synthesis is disturbed in all cells. The slowing down of proliferation processes leads to an increase in the size of myelocytes, metamyelocytes, stab and segmented neutrophils (Fig. 40). The number of megakaryocytes is usually normal, in severe cases it decreases. In megakaryocytes, platelet lacing may be impaired.

peripheral blood. The result of megaloblastic hematopoiesis is the development of macrocytic hyperchromic anemia (Hb concentration may decrease to dog/l). The number of erythrocytes is sharply reduced (1.0-1.5 x/l). There is a high color index (1.1-1.4), an increase in the average volume of erythrocytes (MCV> 100 fl) and the average content of hemoglobin in the erythrocyte (MCH> 32 pg) with normal values of the average hemoglobin concentration in one erythrocyte (MCHC). The erythrocyte histogram is significantly shifted to the right, flattened, stretching along the X axis (Fig. 42).

Erythrocytes differ in saturation with hemoglobin - hyperchromic, without central enlightenment, with a diameter of more than 10 microns (macrocytes and megalocytes). They are characterized by anisocytosis, poikilocytosis, schizocytosis, there are erythrocytes with remnants of the nuclear substance (Kebot rings, Jolly bodies) (Fig. 43), basophilic puncture (RNA remnants) (Fig. 44), polychromatophilic erythrocytes. Megaloblasts are often present. The number of reticulocytes may be normal, but as differentiation is impaired, it sharply decreases.

B12 deficiency anemia is characterized by leukopenia, neutropenia with relative lymphocytosis, monocytopenia, aneosinophilia or abasophilia may be observed. There is an appearance in the blood of giant hypersegmented neutrophils (the number of segments is more than 5) (Fig. 45), sometimes a shift to the left to myelocytes and metamyelocytes.

Thrombocytopenia is of a moderate nature, platelets are rarely less than 100 x 109 / l, giant forms are found, but their function is not impaired, and hemorrhagic syndrome is rarely observed. Depending on the severity of anemia, the ESR is accelerated by domm/h. In the blood serum, there is a decrease in the content of vitamin B 12 (the norm for adults pmol / l, over 60 years pmol / l).

The diagnosis of B 12 deficiency anemia can only be established by a morphological study of the bone marrow, which is advisable to perform before the administration of vitamin B 12. Injection of vitamin B 12 within 1-2 days changes the type of hematopoiesis in the bone marrow. Megaloblasts decrease in size, the structure of the nucleus changes, the cells become macronormoblasts. Only by the presence of giant forms of neutrophils, it can be assumed that megaloblastic hematopoiesis took place.

The reticulocyte crisis occurs 5-7 days after the start of treatment, ahead of the rise in hemoglobin concentration and the number of erythrocytes and indicates a switch from megaloblastic hematopoiesis to normoblastic. Hematological remission is determined by the normalization of bone marrow hematopoiesis and peripheral blood parameters. In patients who receive vitamin therapy for a long time, iron deficiency anemia may develop over time due to the activation of hemoglobin synthesis. In these cases, normo- or moderately hypochromic erythrocytes are noted (color index 0.8-0.9). Normalization of red blood counts usually occurs after one to two months of treatment with vitamin B 12 .

Imerslund-Griesback syndrome. Rare hereditary pathology (there are about 100 observations). Absorption of vitamin B 12 is impaired due to the lack of receptors in the jejunum that bind the B 12 complex, an intrinsic factor. Manifested by megaloblastic anemia, normal gastric secretion, normal levels of intrinsic factor, proteinuria without other changes in the urine and without the development of renal failure.

In humans, folic acid is contained in an amount of 5-10 mg. Daily requirement for folic acid. Its reserves are depleted 3-4 months after the cessation of its receipt.

Folates are widely distributed in liver, yeast, meat, spinach, chocolate, raw vegetables and fruits. More than 50% of folic acid can be destroyed during cooking, hence the deficiency in people who eat cooked foods.

Folic acid is absorbed in the duodenum and proximal jejunum. The ability of the intestine to absorb folic acid exceeds the daily requirement for the vitamin.

In plasma, it binds to various proteins (β 2 -macroglobulin, albumin). Most of the folate is transported to the liver, where it is deposited in the form of polyglutamates, a small amount is excreted in the urine. Folates, like vitamin B 12, occupy a key position in many types of cellular metabolism, including the synthesis of amino acids and nucleic acids, which are especially important for proliferating cells. Their penetration into cells is a vitamin-B 12 -dependent process, therefore, with a deficiency of B 12, an increase in the level of folate in the blood and a decrease in it in erythrocytes are observed.

The pathogenesis of folate deficiency anemia is associated with its participation, together with vitamin B 12, in the synthesis of purine bases necessary for the formation of DNA.

Clinic. People of young age, pregnant women get sick more often. Signs of anemia predominate: pallor of the skin with mild subicteria, tachycardia, weakness. Neurological symptoms are not characteristic of these patients, disorders of the gastrointestinal tract are minor.

In people with epilepsy and schizophrenia, folic acid deficiency leads to an increase in seizures.

Changes in the blood and bone marrow are similar to B 12 deficiency anemia. In the blood serum, there is a decrease in the level of folate (the norm is 6-20 ng / ml), its concentration is also reduced in erythrocytes (normang / ml).

Bercow R. The Merck manual. - M.: Mir, 1997.
Guide to Hematology / Ed. A.I. Vorobyov. - M.: Medicine, 1985.
Dolgov V.V., Lugovskaya S.A., Pochtar M.E., Shevchenko N.G. Laboratory diagnosis of iron metabolism disorders: Tutorial. - M., 1996.
Kozinets G.I., Makarov V.A. Study of the blood system in clinical practice. - M.: Triada-X, 1997.
Kozinets G.I. Physiological systems of the human body, the main indicators. - M., Triada-X, 2000.
Kozinets G.I., Khakimova Y.Kh., Bykova I.A. Cytological features of erythron in anemia. - Tashkent: Medicine, 1988.
Marshall W.J. Clinical biochemistry. - M.-SPb., 1999.
Mosyagina E.N., Vladimirskaya E.B., Torubarova N.A., Myzina N.V. Kinetics of blood cells. - M.: Medicine, 1976.
Ryaboe S.I., Shostka G.D. Molecular genetic aspects of erythropoiesis. - M.: Medicine, 1973.
Hereditary anemia and hemoglobinopathies / Ed. Yu.N. Tokareva, S.R. Hollan, F. Corral-Almonte. - M.: Medicine, 1983.
Troitskaya O.V., Yushkova N.M., Volkova N.V. Hemoglobinopathies. - M.: Publishing House of the Russian University of Friendship of Peoples, 1996.
Schiffman F.J. Pathophysiology of the blood. - M.-SPb., 2000.
Baynes J., Dominiczak M.H. medical biochemistry. - L.: Mosby, 1999.

Treatment of vitamin B12 deficiency should begin with the appointment of parenteral vitamin B12 preparations: cyanocobalamin or hydroxycobalamin. The recommended initial dose is 0.1-1 mg / day intramuscularly for 1-2 weeks. The maintenance dose is a monthly injection of 1 mg of cyanocobalamin throughout life. Oral intake of 1 mg of vitamin B12 5 times a week is comparable effective.

Despite the lack internal factor, absorption by passive diffusion can meet a daily requirement of 2-5 mcg. Applications of vitamin B12 intranasally in gel form are justified as an addition to the diet, but not as a treatment for pernicious anemia, although it does increase serum levels of vitamin B12 equally.
Serum K+ concentration may fall after treatment with vitamin B12 due to increased use of intracellular K+ to support new cell synthesis.

Megaloblastic anemia as a result of vitamin B12 deficiency may be the result of high doses of folate. Conversely, excess doses of vitamin B12 can turn megaloblastic anemia into folate deficiency. It is important to remember that the neurological damage caused by vitamin B12 deficiency is irreversible through the use of folate. Therefore, an accurate diagnosis of the type of deficiency is necessary.

folic acid deficiency

folate(folic acid) belongs to the B-vitamin family and is found in most fresh foods, but is rapidly destroyed by heat. Folic acid is widely present in nature in the form associated with one or more molecules of glutamic acid. Naturally, existing folate must be separated from mono- and diglutamates by conjugas available in the stomach before it can be effectively absorbed in the proximal small intestine.

folate transported to the liver, where it is stored and transformed into 5-methyltetrahydrofolate, a form that can penetrate into tissue cells. In the cell, 5-methyltetrahydrofolate is transformed into the metabolically active form, tetrahydrofolate, by vitamin B12-dependent methyltransferase. The daily intake of folate is approximately 100 micrograms, with a tissue reserve of approximately 10 mg. Inadequate folate intake therefore leads to megaloblastic anemia faster than vitamin B12 deficiency.

The dangers of using folic acid. Large doses of folic acid can reverse the course of megaloblastic anemia caused by vitamin B12 deficiency, but the neurological damage due to this deficiency will be irreversible.

Inadequate reception drug is the most common cause of folate deficiency. During pregnancy, the need for folate increases markedly. folate deficiency in early period pregnancy leads to birth defects of the neural tube in the fetus. Folate supplementation is recommended for all pregnant women, or those who are planning a pregnancy, as there is an increased need for folate in the first days after conception. Alcoholism is a common cause of folate deficiency anemia due to reduced folate intake and reduced absorption.

Since the concentration folate in bile several times greater than in plasma, a deficiency will reduce plasma folate concentrations. Patients with long-term bile drainage should also receive folate. People taking phenytoin and similar anticonvulsants tend to have reduced folate absorption, but they rarely develop megaloblastic anemia. Antifolate drugs such as methotrexate are actively used to treat hematological and inflammatory diseases. Methotrexate competes with dihydrofolate for the enzyme dihydrofolate reductase and even in relatively small doses is used in the treatment of rheumatoid arthritis; at the same time macrocytosis of red blood cells is proved.

History, examination and discovery macrocytosis allow a doctor to diagnose folate deficiency. Although folate and vitamin B12 deficiencies cause similar morphological changes in red blood cells, characteristic neurological changes are observed only in cases of megaloblastic anemia caused by vitamin B12 deficiency. Diagnosis of folate deficiency requires measurement of serum folate or red blood cell folate; the latter is of greater diagnostic value.

Folate deficiency requires 1-5mg daily folate orally. The injectable form is also acceptable. Because vitamin B12 deficiency can cause concomitant folate deficiency, it is important to ensure that the patient is not deficient in vitamin B12 before treatment. Folate can correct megaloblastic anemia caused by vitamin B12 deficiency, but will not correct neurological damage. Indiscriminate use of folate may therefore mask the symptoms of vitamin B12 deficiency and lead to irreversible neurological damage.

Folic acid can prevent atherosclerosis. Serum homocysteine concentration is inversely correlated with serum folate levels. Elevated serum homocysteine has been shown to be an independent risk factor for atherosclerosis. Therefore, homocysteine-lowering folic acid therapy is useful for the prevention of atherothrombosis.

and adolescent gynecology

and evidence-based medicine

and health worker

and folic acid

Russian Medical Academy

Anemia associated with impaired DNA synthesis can be both hereditary and acquired.

A common feature of these anemias is the presence of megaloblastic hematopoiesis in the bone marrow. These are megaloblastic anemias. More often there is an isolated deficiency of vitamin B 12, less often - folic acid.

Anemia due to vitamin B12 deficiency

The frequency of occurrence of B 12 deficiency anemia increases with age and is 0.1% in young people, 1% in the elderly, after 75 years it is recorded in 4% of people.

Reasons for the development of vitamin B 12 deficiency

Malabsorption:
- Absence of intrinsic factor of Castle (atrophic gastritis, gastric resection, gastric irradiation).
- Small bowel disease (enteritis, jejunal resection, celiac disease, polyposis, cancer, Imerslund-Gresbeck syndrome)
Insufficient intake from food:
Strict vegetarian diet
Competitive Consumption:
- Wide tapeworm (diphylobothriasis).
- Pathological microflora in the presence of diverticulosis or "blind loop"
Increased utilization of vitamin B 12:
- Malignant neoplasms.
- hyperthyroidism
Hereditary deficiency of transcobalamin II.

Vitamin B 12 exchange [show]

The release of vitamin B 12 from the complex with transcobalamin II in the cell occurs in three stages:

binding of the complex to cell receptors;
its endocytosis;
lysosomal hydrolysis to release vitamin

Megaloblastic anemia can occur while taking anticonvulsants and cytostatics.

The basis of neurological disorders is funicular myelosis of the lateral and / or posterior columns of the spinal cord, which is a consequence of demyelination, and then degenerative changes in nerve fibers in the spinal cord and peripheral nerves. Disturbances from the nervous system are detected in the form of peripheral polyneuropathy: leg weakness, crawling sensation, numbness of the fingers, impaired sensitivity in the limbs, a feeling of constant coldness in the legs. Muscle weakness is often observed, muscle atrophy is possible. First of all, the lower limbs are affected symmetrically, then the abdomen, the upper limbs are affected less frequently. In the most severe cases, areflexia develops, persistent paralysis of the lower extremities, dysfunction of the pelvic organs. With B 12 deficiency anemia, convulsive seizures, hallucinations, memory loss, spatial orientation, mental disorders, psychoses with depressive or manic states are possible. A severe complication is the development of pernicious coma resulting from rapid anemia and cerebral ischemia.

Violation of cell division in the normal synthesis of hemoglobin creates a condition for enhancing ineffective erythropoiesis. The results of autoradiographic and cytophotometric studies showed an elongation of the S-G 2 phase of the cell cycle and cell death in this period. Megaloblasts develop into megalocytes and macrocytes. Intramedullary hemolysis of erythrokaryocytes (ineffective hematopoiesis) and the short lifespan of megalocytes lead to an increase in the level of indirect bilirubin.

In humans, folic acid is contained in an amount of 5-10 mg. Daily requirement for folic acid. Its reserves are depleted 3-4 months after the cessation of its receipt.

Folic acid is absorbed in the duodenum and proximal jejunum. The ability of the intestine to absorb folic acid exceeds the daily requirement for the vitamin.

The pathogenesis of folate deficiency anemia is associated with its participation, together with vitamin B 12, in the synthesis of purine bases necessary for the formation of DNA.

In people with epilepsy and schizophrenia, folic acid deficiency leads to an increase in seizures.

Bercow R. The Merck manual. - M.: Mir, 1997.
Guide to Hematology / Ed. A.I. Vorobyov. - M.: Medicine, 1985.
Dolgov V.V., Lugovskaya S.A., Pochtar M.E., Shevchenko N.G. Laboratory diagnosis of iron metabolism disorders: Textbook. - M., 1996.
Kozinets G.I., Makarov V.A. Study of the blood system in clinical practice. - M.: Triada-X, 1997.
Kozinets G.I. Physiological systems of the human body, the main indicators. - M., Triada-X, 2000.
Kozinets G.I., Khakimova Y.Kh., Bykova I.A. Cytological features of erythron in anemia. - Tashkent: Medicine, 1988.
Marshall W.J. Clinical biochemistry. - M.-SPb., 1999.
Mosyagina E.N., Vladimirskaya E.B., Torubarova N.A., Myzina N.V. Kinetics of blood cells. - M.: Medicine, 1976.
Ryaboe S.I., Shostka G.D. Molecular genetic aspects of erythropoiesis. - M.: Medicine, 1973.
Hereditary anemia and hemoglobinopathies / Ed. Yu.N. Tokareva, S.R. Hollan, F. Corral-Almonte. - M.: Medicine, 1983.
Troitskaya O.V., Yushkova N.M., Volkova N.V. Hemoglobinopathies. - M.: Publishing House of the Russian University of Friendship of Peoples, 1996.
Schiffman F.J. Pathophysiology of the blood. - M.-SPb., 2000.
Baynes J., Dominiczak M.H. medical biochemistry. - L.: Mosby, 1999.

Source: V.V.Dolgov, S.A.Lugovskaya, V.T.Morozova, M.E.Pochtar. Laboratory diagnosis of anemia: A guide for doctors. - Tver: "Provincial medicine", 2001

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B12-deficiency anemia and folate deficiency: causes, manifestations, diagnosis, treatment

Previously, B12-deficiency anemia (Addison-Birmer disease) was called pernicious anemia or pernicious anemia. The first to declare the existence of such a disease and describe this option was a doctor from England, Thomas Addison, and this happened back in 1855. Later, the German Anton Birmer reported the disease in more detail, but it happened only 17 years later (1872). However, the scientific world recognized the primacy of Addison, therefore, at the suggestion of the French physician Armand Trousseau, the pathology began to be called by the name of the author, that is, Addison's disease.

A breakthrough in the study of this serious illness happened already in the 20s of the last century, when American doctors George Whipple, William Murphy and George Minot, based on their research, stated that the disease can be treated if raw liver is present in the patient's diet. They proved that B12-deficiency anemia is a congenital failure of the stomach to secrete substances that ensure the absorption of vitamin B12, for which they were awarded the Nobel Prize in Physiology or Medicine in 1934.

Currently, we know megaloblastic anemia associated with a lack of cyanocobalamin (vitamin B12) as B12-deficiency anemia, and the combined form caused by a deficiency of both vitamin B12 and folic acid (vitamin B9) as B12-folic deficiency anemia.

What is the similarity and what is the difference

As noted above, B12-deficiency and B12-folate deficiency anemias are included in the group of megaloblastic anemias, which are characterized by a decrease in DNA production, which, in turn, leads to a violation of the proliferation of cells capable of rapid division. These are the cells:

bone marrow;
Skin;
mucous membranes;
Gastrointestinal tract.

Among all rapidly proliferating cells, hematopoietic (hematopoietic) cells show the greatest tendency to accelerate reproduction, so the symptoms of anemia are among the first clinical manifestations of these megaloblastic anemias. There are frequent cases when, in addition to anemia (a decrease in the level of red blood cells and hemoglobin), other signs of hematological pathology are observed, for example, a decrease in the number of platelets - platelets (thrombocytopenia), neutrophilic leukocytes (neutropenia, agranulocytosis), as well as monocytes and reticulocytes.

blood for B12 deficiency anemia

Why are these variants of anemia so interconnected and what is their difference? The fact is that:

The presence and direct participation of vitamin B12 is very necessary for the formation of the active form of folic acid, which, in turn, is very necessary for the production of thymidine, an important component of DNA. This biochemical interaction with the participation of all the necessary factors allows you to fully ensure the normal formation of blood cells and cells of the gastrointestinal tract (gastrointestinal tract);
Other tasks are also assigned to vitamin B12 - with its participation, individual fatty acids (FA) are decomposed and synthesized. With an insufficient content of cyanocobalamin, this process is disrupted, and harmful, neuron-killing methylmalonic acid begins to accumulate in the body, and at the same time, the production of myelin, a substance that forms a myelin sheath that carries an electrically insulating function for nerve cells, decreases.

As for folic acid, the breakdown of fatty acids does not need its participation, and with its deficiency, the nervous system does not suffer. Moreover, if a patient with a B12 deficiency is prescribed folic acid as a treatment, then for a short time it will stimulate erythropoiesis, but only until it is in excess. An excessive amount of the drug will force all B12 present in the body to work, that is, even the one that was intended to ensure the breakdown of fatty acids. Of course, such a situation does not lead to good - nervous tissues are even more affected, deep degenerative changes in the spinal cord develop with loss of motor and sensory functions (combined sclerosis, funicular myelosis).

Thus, a lack of vitamin B12, along with a violation of the proliferation of hematopoietic cells and the development of anemia, has a negative effect on the nervous system (NS), while a deficiency of folic acid only affects the division of hematopoietic cells, but does not affect the health of the nervous system.

Significance of the internal factor

Cyanocobalamin from food that has entered the gastrointestinal tract is absorbed with the help of the so-called intrinsic factor (IF). Here's how it goes:

In the stomach, B12 is not in a hurry to be absorbed with an internal factor, as it was previously thought, it finds protein-R and combines with it in order to go to the duodenum in the form of the Vit B12 + protein-R complex and already there, under the influence of proteolytic enzymes, break down;
In the duodenum 12, cyanocobalamin is released from protein-R and in a free state meets with the internal factor that arrived there, interacts with it and forms another complex - “Vit B12 + WF”;
The complex "Vit B12 + VF" is sent to the jejunum, finds receptors intended for intrinsic factor, connects to them and is absorbed;
After absorption, cyanocobalamin “sits down” on the transport protein transcobalamin II, which will deliver it to the places of main activity or to the depot to create a reserve (bone marrow, liver).

It is obvious why such great importance is given to the internal factor, because if everything is in order with it, then almost all cyanocobalamin that comes with food will safely reach its destination. Otherwise (in the absence of WF), only 1% of vitamin B12 will diffuse through the intestinal wall by diffusion, and then the person will not receive the amount of such an important vitamin he needs.

The body's daily need for cyanocobalamin is from 3 to 5 mcg, and its reserve is from 4 to 5 grams, therefore, it can be calculated that if the intake of vitamin B12 is completely excluded (for example, during gastrectomy), then the reserves will run out after 3- 4 years. In general, the supply of vitamin B12 is designed for 4-6 years, while folic acid will disappear in 3-4 months if there is no intake. From this we can conclude that B12 deficiency during pregnancy does not threaten if before that its level was normal, but folic acid, if a woman did not eat raw fruits and vegetables, is quite capable of falling below the permissible limit and creating a deficient state (development of folic acid deficiency anemia ).

Vitamin B12 is found in animal products, folic acid - in almost all foods, however, cyanocobalamin remarkably tolerates heat treatment for a long time and is stored for entry into the body, which cannot be said about folic acid - after 15 minutes of boiling, this vitamin does not there will be a trace...

What is the reason for the deficiency of these vitamins?

The lack of cyanocobalamin can be caused by the following reasons:

Low dietary intake of vitamin B12 (when a person, on his own initiative or for other reasons, does not receive enough foods that carry cyanocobalamin to the body: meat, liver, eggs, dairy products), or a complete transition to vegetarianism (vitamin B12 is difficult to find in food of plant origin);
Violation of the secretion of the internal factor due to atrophy of the mucosa, which is formed due to hereditary predisposition, exposure to toxic substances, the influence of antibodies and the development of atrophic gastritis as a result of this. Similar consequences lie in wait for the patient in the event of a complete removal of the stomach (gastrectomy), while the loss of only part of the organ leaves the secretion intact;
The absence of receptors that the internal factor needs in order to bind itself, which occurs with Crohn's disease affecting all parts of the gastrointestinal tract, diverticula and tumors of the small intestine, tuberculosis and resection of the ileum, intestinal infantilism (celiac disease), chronic enteritis;
Competitive absorption of cyanocobalamin in the gastrointestinal tract by helminths or microorganisms that multiply intensively after the imposition of anastomoses;
A disorder of the exocrine function of the pancreas and, as a result, a violation of the cleavage of protein-R, which prevents the binding of vitamin B12 to the internal factor;
A rather rare, inherited anomaly - a decrease in the level of transcobalamin and a violation of the movement of cyanocobalamin to the bone marrow.

With vitamin B9, everything is much simpler: it is found in almost all foods, is remarkably absorbed in a healthy intestine and does not need any internal factor. Problems arise if:

The diet due to various circumstances of the patient is extremely poor;
A person suffering from anorexia nervosa deliberately refuses to eat;
The age of the patient is regarded as old;
The alcoholic "shakes" from the withdrawal syndrome when long binge(not up to a full meal - it does not climb);
There is a syndrome of impaired intestinal absorption (diseases of the gastrointestinal tract: Crohn's disease, celiac disease, intestinal tumors, etc.) - the main cause of B12-folic deficiency anemia;
The need for folic acid increases, which happens during pregnancy, certain skin diseases (psoriasis, dermatitis), impaired utilization (alcoholism, congenital diseases of folate metabolism).

By the way, a lack of vitamin B9 is not so rare in people who are forced to take anticonvulsants for a long time, including phenobarbital, so this fact should be taken into account when prescribing such therapy.

How do B12- and B9-deficient states manifest themselves?

If the described conditions are referred to as anemia, then it goes without saying that they will be characterized by all the symptoms of anemia:

Rapid onset of fatigue even with minimal physical activity, weakness, decreased performance;
Episodes of darkening in the eyes;
Tendency to hypotension (lowering blood pressure);
Respiratory failure (the desire to accelerate the step or other movements cause shortness of breath);
Periodic headaches, often dizzy;
Often there is a violation of the rhythm (tachycardia);
The skin is pale, gives off a slight yellowness (subicteric);
In the oral cavity, problems develop with signs characteristic of glossitis: the papillae are atrophied, the surface of the tongue is varnished, the tongue swells and hurts;

Due to the fact that with a lack of cyanocobalamin there is a triad of syndromes (damage to the blood, gastrointestinal tract and nervous system), and with a deficiency of folic acid, the suffering of the nervous system is not observed, the following symptoms, indicating involvement in the pathological process of the nervous system, will apply only to B12- scarce state:

Funicular myelosis (degenerative pathology of the spinal cord), which in severity does not correlate with the clinical manifestations of anemia;
Peripheral polyneuropathy with muscle weakness, sensory disturbance and decreased tendon reflexes;
In other cases, on the basis of anemia, depressive states, memory impairment, and rarely, mental disorders are observed.

It should be noted that B12- and folate-deficiency states do not differ in a rapidly progressive course and are not particularly rich in symptoms. Diseases until recently were attributed to the pathology of old age, however, in last years there has been a tendency towards "rejuvenation" - this kind of anemia began to occur in young people.

Diagnostics

Clinically manifested icterus of the sclera and yellowness of the skin are signs that give grounds to immediately send the patient to the laboratory, where the diagnosis of folic and B12 deficiency states begins.

The first stage of laboratory research makes one suspect megaloblastic anemia:

Complete blood count (CBC) - typical for such conditions: low levels of erythrocytes and hemoglobin, thrombocytopenia, neutropenia with polysegmentation, CP is usually higher than 1, macrocytosis, poikilocytosis, anisocytosis, in erythrocytes - Jolly bodies, Kebot rings;
Elevated values of bilirubin due to the unbound fraction in a biochemical blood test (BAC).

Considering that another hematological pathology (hypoplastic and aplastic conditions, hemolytic anemia, leukemia) can give a similar picture of peripheral blood, the patient is prescribed a puncture of the spinal cord, in which megaloblasts are found (a characteristic sign of B12-deficiency anemia), giant megakaryocytes and granulocytic cells.

As a rule, after laboratory tests (or in parallel with them), the patient is waiting for a “terrible procedure” - fibrogastroscopy (FGS), according to which it is clear that the gastric mucosa is atrophied.

Meanwhile, further diagnosis of B12-deficiency anemia requires its dissociation from anemia associated with a lack of vitamin B9. It is very important to carefully collect the patient's history: to study his lifestyle and nutrition, to thoroughly identify the symptoms, to examine the state of the cardiovascular and nervous system, but the diagnosis still requires laboratory tests. And here it should be noted that in any case, the differential diagnosis of these two anemias is difficult for ordinary laboratories, because it creates the need to determine the quantitative values of vitamins, however:

The microbiological method is far from perfect and gives only approximate results;
Radioimmunoassay research is not available to residents of villages and small towns, since analysis requires the participation of modern equipment and highly sensitive reagents, which are the privilege of large cities.

In this case, a urine test that determines the amount of methylmalonic acid in it would be useful for differential diagnosis: in B12-deficient anemia, its content increases markedly, while in a folate-deficient state, the level remains unchanged.

Treatment

Treatment of folic acid deficiency is mainly limited to the appointment of vitamin B9 tablets at a dose of 5-15 mg / day. True, if the diagnosis of folate deficiency anemia still remains in question, then it is advisable to start treatment with intramuscular injection of cyanocobalamin. However, on the contrary, it is impossible, because with B12-deficiency anemia, the use of folic acid will further aggravate the situation.

As for the treatment of B12-deficiency anemia, it is based on three principles:

To fully saturate the body with cyanocobalamin, so that it is enough for the performance of functional duties and deposited in the reserve;
Due to maintenance doses, constantly replenish stocks;
If possible, try to prevent the development of an anemic state.

It goes without saying that the main thing in the treatment of B12 deficiency will be the appointment of cyanocobalamin, taking into account changes in the blood and the severity of neurological symptoms, if any.

Usually, treatment begins with intramuscular injection of cyanocobalamin at a dose of 500 mcg every day and oxycobalamin - 1000 mcg every other day;
If there are pronounced symptoms of damage to the nervous system (funicular myelosis), then the dose of B12 is increased to 1000 mcg (every day), and, in addition, 500 mcg of adenosylcobalamin is added in tablets, which takes part in the exchange, but does not affect hematopoiesis;
The appearance in the blood test of hypochromia of red blood cells against the background of therapeutic measures or in the case of mixed forms of the disease (B12- + Iron-deficiency anemia) is the basis for the appointment of iron preparations;
Red blood cell transfusion is resorted to in special cases: if signs of oxygen starvation of the brain and symptoms of anemic encephalopathy are clearly indicated, there is progressive heart failure and if an anemic coma is suspected, a condition that is very dangerous for the patient's life;
At the same time, a therapeutic effect is prescribed on the factors that may have caused vitamin B12 deficiency, for this purpose it is carried out: deworming (drugs and doses depend on the type of helminths), treatment of diseases of the gastrointestinal tract, surgery for stomach cancer, normalization intestinal flora, a diet is being developed that provides for sufficient intake of vitamin B12 in the body.

Literally a few days after the start of therapy, a control count of reticulocytes is performed - a reticulocyte crisis will be evidence that the treatment tactics have been chosen correctly.

After the blood condition is recognized as normal, the patient is transferred to maintenance therapy: first, every week, and then every month, the patient is given 500 mcg of B12, and, in addition, every six months, a 2-3 week course of vitamin therapy is prescribed (supportive treatment with vitamin B12 ).

B12 deficiency anemia dangerous disease, which is associated with a violation of the normal processes of hematopoiesis that occur against the background of a deficiency of cobalamin in the body. Today, many people are interested in questions about under the influence of what factors anemia develops and what symptoms accompany the disease.

What is a disease?

In fact, B12-deficiency anemia is known by various terms - it is percinious or megaloblastic anemia, pernicious anemia, and Addison-Birmer disease. A similar disease is accompanied by a decrease in the number of red blood cells, which is associated with a deficiency of vitamin B12 (cyanocobalamin). It should be noted that not only bone marrow structures, but also nervous tissues are especially sensitive to the lack of this substance, which, in fact, makes the disease extremely dangerous.

In most cases, patients are diagnosed with B12-folic deficiency anemia, in which the symptoms of the disease are observed and were described for the first time relatively recently - in 1855, the English physician T. Addison was studying an unknown disease. And already in 1926, researchers W. Murphy, J. Will and J. Minot noted in their studies that the symptoms of the disease disappear if raw liver is introduced into the patient's diet.

The main causes of the development of B12-deficiency anemia

Immediately it is worth noting that there are many reasons for the development of this type of anemia. Some of them are related to the way of life, while others are related to changes in the body itself.

First you need to mention the so-called alimentary deficiency, which develops as a result of insufficient intake of a vitamin in the body along with food. For example, such a disease can develop against the background of starvation or strict vegetarianism. In an infant, this form of anemia is observed if the nursing mother refuses animal products.
In some patients, there is a violation of the normal absorption of cyanocobalamin.
The causes of B12 deficiency anemia may lie in the lack of the so-called intrinsic factor of Castle. a complex substance that is secreted by the intestinal mucosa, combines with cyanocobalamin and ensures its absorption. In turn, the deficiency of this substance can be caused by some congenital anomalies, as well as autoimmune diseases. In addition, the lack of the Castle factor is observed with various structural changes in the stomach, for example, with gastritis, surgical operations, etc.
Risk factors can also include various changes in the structure of intestinal tissues, which is observed in the presence of tumors or develops as a result of surgical excision of part of the intestine.
The absorption functions of the intestine can change in the presence of dysbacteriosis, in which the composition of the microflora changes.
In some cases, cyanocobalamin, which enters the body with food, is absorbed by other "inhabitants" digestive system such as pathogenic bacteria or worms.
Risk factors include diseases of the liver and kidneys, since against their background there is often an increase in the release of vitamin B12 or its incomplete use.
Deficiency can also develop if tissues or organs absorb too much of the vitamin. A similar phenomenon is observed, for example, in the presence of a rapidly growing malignant tumor. Risk factors include hormonal changes and some as well as pathologies associated with the active death of red blood cells.

Disease pathogenesis

How does B12 deficiency anemia develop? The pathogenesis of the disease is directly related to the main functions of cyanocobalamin. This vitamin plays an important role in the process of hematopoiesis. Its deficiency results in a condition known as megablastosis. It is accompanied by the accumulation of large forms of platelets and leukocytes, as well as their premature destruction in the bone marrow.

In addition, vitamin B12 is a cofactor in the most important metabolic reactions that are necessary for the vital activity of nerve cells. That is why the nervous system suffers from its deficiency.

B12-deficiency anemia: symptoms of the disease

Such a disease is accompanied by a mass of symptoms, which are usually combined into three main groups.

To begin with, it is worth talking about the anemic syndrome, which develops against the background of a decrease in the number of red blood cells. At first, patients complain of severe weakness, rapid fatigue and a noticeable decrease in performance. As the disease progresses, intermittent tinnitus is observed, as well as dizziness, and often fainting. Sick people also note the appearance of "flies" before their eyes. Signs of anemia can also include increased heart rate and severe shortness of breath, which occur even with the slightest physical exertion. Sometimes there are unpleasant, stabbing pains in the chest area.

Of course, with a vitamin deficiency, disorders of the digestive system are also observed. In particular, patients experience a sharp decrease in appetite and, as a result, loss of body weight. Periodically occurring nausea and vomiting also bring a lot of inconvenience to a person's life. In addition, stool disorders are also possible - most often these are prolonged constipation. Changes in the tongue are also considered very characteristic, the surface of which is smoothed out and acquires a bright red, and sometimes crimson hue.

Of course, these are not all the changes that accompany B12 deficiency anemia. Symptoms also appear in the nervous system. First of all, damage to the peripheral nerves is observed. Patients report an unpleasant tingling in the arms and legs, as well as temporary numbness of the extremities. Gradually, muscle weakness develops. In connection with the stiffness of the legs, a gradual change in gait is observed - it becomes more unstable.

Prolonged deficiency of vitamin B12 leads to damage to the spinal cord, and then the brain. The symptoms of these disorders can vary. For example, damage to the fibers in the spinal cord, as a rule, leads to a loss of sensitivity - a person no longer feels vibrations in the skin (the skin on the legs is most often affected). Some patients develop seizures. But increased irritability, uncontrolled mood changes, color perception disorders indicate brain damage. In the absence of therapy, the patient may fall into a coma.

Forms of the disease

Of course, there are several schemes for classifying the disease. It is important to know that in modern medicine, B12-deficiency anemia can be of two types, depending on the cause of development:

The primary form of the disease, as a rule, is associated with some genetic characteristics of the organism. It is this B12-deficient infancy that is observed most often.
The secondary form of the disease develops already in the process of growing up and human life, under the influence of factors of the external or internal environment.

Stages of development of anemia

The main symptoms of the disease directly depend on the stage of its development. The severity of the patient's condition is usually determined based on the number of erythrocytes (red blood cells) in the blood. Depending on this indicator, three stages of the disease are distinguished:

With a mild form of anemia, the number of red blood cells ranges from 90 to 110 g / l.
The average form of severity is characterized by a more significant decrease in the number of red blood cells - from 90 to 70 g / l.
If the patient's red blood cell count is 70 g/l or less, then we are talking about a severe form of B120-deficiency anemia, which is extremely dangerous for health and even life.

Why is this form of anemia dangerous? Possible Complications

Vitamin B12 deficiency anemia can be extremely dangerous if left untreated. As already mentioned, first of all, the lack of this substance affects the state of the nervous system. Complications of this type of anemia include damage to the spinal cord and peripheral nerves. In turn, such violations are accompanied by discomfort and tingling in the limbs, complete and partial loss of sensation, incontinence of feces or urine.

Against the background of a chronic deficiency of cyanocobalamin, the work of the whole organism worsens - the appearance of various diseases of the kidneys, heart and other organs is possible. Sometimes, against the background of a sharp decrease in the number of red blood cells, it develops, which leads to a pernicious coma.

If you start treatment in the early stages, then all the above complications can be avoided. Late therapy can eliminate vitamin deficiency, but, alas, changes in the nervous system are already irreversible.

Modern diagnostic methods

If you have the above symptoms, you should definitely consult a doctor. After all, only a specialist can accurately determine the disease. To begin with, a medical history is compiled. B12-deficiency anemia most often develops under the influence of certain external factors, so the doctor will definitely take an interest in information about the patient's life, his diet, etc. A physical examination follows. In patients with a similar disease, as a rule, pallor of the skin can be noticed. Often there is a decrease in blood pressure and a rapid heartbeat.

Naturally, other studies follow in the future, with the help of which it is possible to determine whether B12-deficiency anemia really takes place. A blood test with a similar disease will demonstrate a decrease in the number of red blood cells and their precursor cells (reticulocytes). Along with this, there is a decrease in the number of platelets. Naturally, the level of hemoglobin in the blood is also reduced. A biochemical blood test can also provide valuable information. With this type of anemia, an increase in the level of iron and bilirubin in the blood is observed.

Diagnosis of B12 deficiency anemia includes other procedures. In particular, for laboratory tests, bone marrow is taken (in most cases, a puncture of the sternum is performed). In addition, the patient takes urine and stool tests. Electrocardiography, electroencephalography, computed tomography, and sometimes some other procedures are shown - these tests are necessary in order to assess the degree of damage to other organ systems, as well as determine the cause of anemia.

B12 deficiency anemia: treatment

In addition, it is important to compensate for the deficiency of cyanocobalamin. In the first few days, the vitamin solution is administered intramuscularly. For an adult, the average daily dose is 200 to 500 mcg. In especially severe conditions, the amount of the drug is increased to 1000 mcg - this scheme is followed for three days. Upon reaching stable improvements, the dose is reduced to 100-200 mcg - injections are carried out once a month for 1-2 years.

Naturally, it is extremely important to proper diet, including in it foods rich in cyanocobalamin and folic acid - this is primarily the liver, meat and eggs.

Require urgent replenishment of the number of red blood cells. For this purpose, patients are injected with red blood cells isolated from donor blood. The same procedure is necessary for anemic coma.

According to statistics, the prognosis for patients is quite favorable. The only exceptions are those cases when a person seeks help in a very serious condition, since it is impossible to restore the affected parts of the nervous system.

Are there effective methods of prevention?

As you can see, B12 deficiency anemia is an extremely dangerous disease. That is why it is much easier to try to avoid it. And in this case, a properly composed diet is very important. Make sure that your menu regularly contains foods rich in cyanocobalamin. In particular, vitamin B12 is found in eggs, meat, liver and dairy products.

All diseases of the gastrointestinal tract should be treated in time - it is extremely important to follow the doctor's recommendations and not refuse the medicines prescribed by him. From time to time it is recommended to take multivitamin complexes as a preventive measure (every six months).

After surgery to remove parts of the intestine or stomach, the doctor must prescribe cyanocobalamin preparations to the patient in the appropriate dose.

They unite a large group of hereditary, congenital and acquired anemias that develop as a result of a violation of the synthesis of nucleic acids, their common feature is the appearance of megaloblasts in the bone marrow and peripheral blood. Anemia due to vitamin B12 deficiency is more common, less often due to folic acid deficiency. Folic acid deficiency is more common in children Anemia due to a combined deficiency of vitamin B12 and folic acid is rare.

AT 12 - deficiency anemia. The classic variety is anemia in Addison-Birmer disease (malignant, pernicious), manifested by a triad of symptoms: 1) a violation of the hematopoietic process; 2) atrophic changes in the mucosa of the gastrointestinal tract; 3) disorders of the nervous system.

Etiology. Exogenous vitamin B12 deficiency is rare. Endogenous deficiency may occur with a decrease or complete suppression of the production of gastromucoprotein by the parietal cells of the stomach, which is caused by: a) a hereditary defect transmitted autosomal recessively (detected in 1/3 of patients); b) immune mechanisms (50% of patients have antibodies against the internal anti-anemic factor or parietal cells of the stomach); c) toxic effects on the gastric mucosa; d) gastrectomy; e) stomach cancer, etc. Endogenous deficiency also occurs when the process of absorption of vitamin B 12 in the intestine is disturbed (resection of the small intestine, enteropathy, etc.), with increased consumption of vitamin B 12 (pregnancy, broad tapeworm invasion).

Pathogenesis. Normally, vitamin B 12 (external anti-anemic factor) forms a complex with gastromucoprotein (intrinsic anti-anemic factor), which interacts with specific receptors in the lower and middle parts of the ileum, which ensures the absorption of vitamin B 12. About 1% of vitamin B 12 can be absorbed regardless of the intrinsic factor. One of the coenzymes of vitamin B 12, methylcobalomin, is involved in normal hematopoiesis. With its participation, thymidine monophosphate, which is part of DNA, is formed from uridine monophosphate. Folic acid is also required for the synthesis of thymidine monophosphate. In the absence of methylcobalamin, DNA is not formed, the processes of division of actively regenerating cells are disrupted, which are most pronounced on the part of erythropoiesis; normoblastic type of hematopoiesis becomes megaloblastic. The latter is characterized by a relatively smaller number of mitoses (instead of three mitoses characteristic of normoblastic erythropoiesis, one mitosis occurs), lengthening the time of the mitotic cycle, early hemoglobinization of megaloblasts, a decrease in the osmotic resistance of megalocytes, a reduction in their lifespan, an increase in ineffective erythropoiesis, a reduction in the lifespan of erythrocytes, an increase in activity hemolytic properties of blood plasma, which leads to the development of bilirubinemia. Extramedullary foci of megaloblastic hematopoiesis appear. Leuko- and thrombocytopenia is also disturbed. The second coenzyme - deoxyadenosylcobalamin is involved in the metabolism of fatty acids, in the conversion of methylmalonic acid to succinic. With a deficiency of vitamin B 12, methylmalonic acid accumulates in the body, causing degeneration of the posterolateral columns of the spinal cord, the development of funicular myelosis, and dysfunction of the central nervous system.

The blood picture is characterized by a pronounced hyperchromic anemia (CP > 1.0). The number of erythrocytes decreases more than Hb, leukopenia with neutropenia, relative lymphocytosis, thrombocytopenia. In the smear, megaloblasts, megalocytes, anisocytosis, poikilocytosis, macrocytosis, erythrocytes with Jolly bodies, Kabo rings, basophilic granularity, giant polysegmentonuclear neutrophils are detected, the number of reticulocytes decreases (an increase indicates remission), ESR increases. In the bone marrow, oxyphilic megaloblasts are sometimes absent, basophilic forms predominate (“blue bone marrow”). Cells show degenerative changes.

Disturbances in the gastrointestinal tract and nervous system exacerbate the course of anemia. Gunter's glossitis develops (inflammation followed by the formation of a "varnished" tongue due to atrophy of its papillae), stomatitis, and gastroenterocolitis. The neurological syndrome is manifested by mental disorders (delusions, hallucinations), unsteady gait, paresthesia, pain, numbness of the extremities, paraparesis, the occurrence of pathological reflexes, etc.