B12 deficiency anemia signs. Pernicious (B12-deficiency) anemia

B 12 deficiency anemia is a disease, the essence of which is a disorder of hematopoiesis associated with a deficiency of vitamin B 12 (cyanocobalamin) in the child’s body. It belongs to the variety. It is also called pernicious, that is, translated from Latin language dangerous.

This vitamin enters the body from food products. Cyanocobalamin, or vitamin B 12, binds in the stomach with glucoprotein produced by the mucous membrane and other R-proteins (proteins) that make up saliva and gastric juice. These binding factors protect the vitamin from destruction in the digestive tract.

IN small intestine Pancreatic enzymes promote the detachment of cyanocobalamin from transport R proteins and connection with intrinsic factor. IN ileum this complex connects with the epithelial cells of the mucosa.

The release of the vitamin from Castle factor and epithelium is carried out with the help of special blood serum proteins (transcobalamins), which deliver cyanocobalamin to the tissues.

The vitamin is carried in the blood:

  • to the bone marrow, where its participation is necessary in the production of red blood cells;
  • to the liver to create its reserve;
  • in the central nervous system, where it participates in the synthesis of the myelin sheath around nerve fibers.

The reserve of cyanocobalamin in the body is approximately 5 mg, and its daily loss is 5 mcg.

How does anemia develop with cyanocobalamin deficiency?

On the left are normal blood cells, on the right are those in megaloblastic anemia.

The nervous system and red bone marrow are most sensitive to vitamin B12 deficiency. First of all, hematopoiesis suffers. The formation of red blood cells becomes ineffective - they appear instead normal cells megaloblasts.

Some of them are destroyed by the body immediately, the life expectancy of the rest is also less than that of normal red blood cells. In this regard, the number of red blood cells in the blood decreases significantly - anemia occurs. Increased destruction (hemolysis) of failed cells leads to an enlargement of the spleen, increased level bilirubin in the blood and urobilin in the urine.

A decrease in the number of platelets in the blood increases the risk of bleeding. And the reduced content of leukocytes in the bloodstream creates a risk of developing infections.

Insufficient oxygen supply to tissues leads to the development dystrophic changes in the heart muscle, liver and other organs, mucosal atrophy digestive tract. The myelin sheath in nerve fibers is destroyed, which leads to disruption of conduction nerve impulses.

Vitamin B 12 deficiency can also cause insufficient levels in the body folic acid. Without these two components, the process of DNA synthesis in cells is impossible. Defeat nervous system B 12 deficiency anemia differs from megaloblastic folate deficiency anemia. But since cyanocobalamin and folates are closely related to each other, a double deficiency often occurs in the body - a lack of these two substances at the same time.

Causes

There are many causes of pernicious anemia:

  1. Insufficient vitamin content in diet products:
  • unbalanced child nutrition;
  • (many parents with early childhood accustom children to a food system that excludes, depending on the type of vegetarianism, the consumption of milk, etc.);
  • in an infant, a deficiency can be created when breastfeeding vegetarian mother.
  1. Violation of vitamin absorption and absorption:
  • insufficient release of Castle factor as a result of:

A) birth defect the gastric mucosa or the structure of the factor itself;

b) inflammation of the mucous membrane during;

c) due to the destruction of cells secreting internal factor by autoantibodies;

  • decreased pancreatic secretion, which leads to disruption of the breakdown of protein R, necessary for the connection of vitamin B 12 with gastromucoprotein;
  • changes in the small intestine that reduce absorption:

a) inflammatory process (with chronic enterocolitis);

b) surgical removal of part of the intestine;

c) dysbiosis of intestinal microflora;

d) malignant neoplasms;

e) gluten enteropathy (celiac disease);

g) diverticulitis of the jejunum (structural disorder, protrusion of the intestinal wall).

  1. Increased needs for vitamin B 12:
  • with increased production of thyroid hormones;
  • during periods of intensive growth of the body;
  • when the number of red blood cells decreases due to their increased destruction;
  • when the vitamin is absorbed by bacteria or (especially when infested with tapeworm).
  1. Inadequate use of vitamin B 12 in the body:
  • lack of vitamin depot in liver pathology.
  1. Increased vitamin loss:
  • its increased excretion from the body due to insufficient binding with protein in some congenital pathologies;
  • at .
  1. Long-term treatment medications such as:
  • Fluorouracil;
  • Azathioprine;
  • Methotrexate;
  • 6-Mercaptopurine;
  • Cytosar;
  • Sulfasalazine;
  • Colchicine;
  • Acyclovir;
  • Triamterene;
  • Phenobarbital;
  • Neomycin and others.

Symptoms


The first symptoms of anemia in children are dizziness, weakness, absent-mindedness, and tinnitus.

Anemia can be mild, moderate or severe in severity. All clinical manifestations of pernicious anemia in children can be combined into 3 groups: damage to the hematopoietic system is manifested by anemic syndrome, the digestive system - gastroenteric or dyspeptic syndrome, the central nervous system and peripheral nerve fibers - neurological symptoms.

The clinical picture of anemia develops gradually, symptoms appear and increase unnoticeably.

Anemic syndrome is characterized by:

  • weakness;
  • dizziness;
  • pale skin has a jaundiced tint;
  • possible slight yellowness of the sclera;
  • pallor of visible mucous membranes;
  • flashing black dots before the eyes;
  • noise in ears;
  • perversion of taste (children can eat soil, chalk).

The resulting tissue hypoxia leads to a deterioration in the condition of the skin (it becomes dry, rough), hair (they lose their shine and split), nails (delamination, fragility and striations appear).

Due to a decrease in the number of platelets, frequent nosebleeds are characteristic. With a slight load, children quickly get tired, shortness of breath and an increase in heart rate are noted. With advanced anemia, severe swelling appears.

Damage to the gastrointestinal tract, or dyspeptic syndrome, manifests itself:

  • (sometimes even aversion to food);
  • phenomena of glossitis (inflammation of the tongue): the tongue with smoothed papillae becomes bright pink color(“varnished” tongue), pain and burning of the tongue;
  • violation of stool in the form of diarrhea and;
  • nausea and vomiting;
  • bloating due to deterioration of food digestion due to a decrease in the secretory function of the digestive organs;
  • an increase in the size of the spleen and liver;
  • heaviness or pain in the abdomen;
  • reduction in body weight.

These manifestations are not specific; they are observed in all types of anemia. In contrast, at B 12 - deficiency anemia manifestations of funicular myelosis are characteristic (due to the loss of the myelin sheath of the nerves and disruption of the transmission of nerve impulses to organs):

  • impaired coordination and gait;
  • stiffness of movements;
  • muscle weakness;
  • intercostal neuralgia (pain along the intercostal spaces);
  • tingling sensation in the hands and feet;
  • There may be enuresis (urinary incontinence).

Brain hypoxia is clinically expressed by fainting, intellectual disorders, memory impairment, and inability to concentrate. As a result, schoolchildren's academic performance suffers. The auditory, visual, and olfactory nerves may be affected, resulting in impaired smell, hearing, vision, and color perception. Children become emotionally labile and easily irritated.

With long-term untreated pernicious anemia, the development of coma associated with severe ischemia due to cerebral hypoxia is possible.

Diagnostics

A doctor may suspect anemia in a child based on complaints (the little patient or parents) and examination, and will help confirm the diagnosis of anemia and determine its type laboratory methods research. Correct diagnosis is very important, since only it allows you to prescribe adequate treatment.

B12-deficiency anemia is characterized by the following changes in laboratory tests:

In a blood test (clinical):

  • decreased number of red blood cells;
  • low hemoglobin level;
  • increased color index;
  • macrocytosis (blood cells large sizes);
  • the presence of Jolly bodies and Cabot rings in erythrocytes;
  • the presence of megaloblasts (immature red blood cells);
  • decreased level of platelets (blood platelets);
  • decrease in the number of leukocytes;
  • increased number of hypersegmented leukocytes;
  • decrease in reticulocytes (young red blood cells).

Typical for any anemia is anisocytosis (the presence, along with normal red blood cells, of overly large cells and reduced cells - microcytes; as well as poikilocytosis: red blood cells with an altered shape (oval, pear-shaped instead of round).

With B 12 deficiency anemia distinctive characteristic is hyperchromia (intense coloring of red blood cells due to high content they contain hemoglobin).

Considering that changes in peripheral blood are not specific and occur in other types of anemia or leukemia, a sternal puncture and bone marrow examination are required.

The myelogram (analysis of the obtained bone marrow punctate) is characterized by the megaloblastic type of hematopoiesis:

  • the number of erythroid cells is increased by 2-3 times;
  • the presence of megaloblasts with characteristic nuclear-cytoplasmic dissociation: mature cytoplasm and a delicate mesh structure of the nucleus with unusually located chromatin in the form of nucleoli.

The biochemical blood test method is used to assess the condition internal organs. The results can help determine the cause of the disease, and they are taken into account when choosing the optimal treatment.

With this type of anemia, the content of bilirubin in the blood (mainly its indirect fraction), iron, and ferritin may increase. Activity LDH enzyme(lactate dehydrogenase) is high and increases as the disease progresses.

To determine the cause of developed anemia, hardware can be used diagnostic studies: Ultrasound, FGDS, colonoscopy, MRI.

Treatment

Treatment is prescribed depending on the severity of anemia, the age of the child, and the presence of neurological pathology.

Principles of treating anemia in children:

  • identifying and eliminating (if possible) the causes of anemia;
  • saturating the body with cyanocobalamin;
  • supportive treatment;
  • diet therapy.

If gastrointestinal pathology is detected, appropriate therapy is prescribed, including enzymatic preparations(Creon, Festal, Panzinorm) to eliminate fermentative and putrefactive dyspepsia. At helminthic infestation deworming is carried out. Eubiotics (Bifidumbacterin, Bifiform, Linex, Lactobacterin, etc.) will help normalize the composition of microflora in the intestines.

Complex treatment includes the injection of cyanocobalamin. The dose of the drug and the duration of the course are determined by the doctor. After the main course, maintenance therapy is carried out. Children with B 12 deficiency anemia need dispensary observation pediatrician or hematologist. They need monitoring of peripheral blood parameters, and if necessary, repeated courses of treatment are prescribed.

Blood transfusion (erythrocyte mass) is indicated only in critical situations with hemoglobin levels less than 70 g/l and a threat to the child’s life.

If there is a simultaneous deficiency of folic acid, it is prescribed to be administered in the form of medications, and this fact is also taken into account when preparing the diet. If autoantibodies to gastromucoprotein are detected, the pediatric hematologist prescribes corticosteroid drugs.

A long course of cyanocobalamin can lead to a decrease in potassium levels in the body. That is why this indicator should be periodically monitored and, if necessary, adjusted by prescribing potassium supplements.

In the presence of neurological symptoms, other B vitamins (B 1, B 6) are additionally prescribed.

The treatment complex certainly includes a balanced diet that can provide the child’s body with sufficient quantities of not only vitamins, but also proteins. Eating foods rich in vitamin B12 will help you replenish your supply of vitamin B12. The consumption rates of cyanocobalamin depend on the age of the child.

Children's daily requirement for vitamin B 1:

  • Liver (beef – 60; chicken – 16.6; pork – 30).
  • Meat (pork – 2; beef – 2.6; rabbit – 4.3; lamb – 2; heart (offal) – 25).
  • Fish (mackerel – 12; carp – 1.5; sardine – 11; cod – 1.6).
  • – 20.
  • – 1,0.
  • Cheese cheese – 1.0.
  • Cheese (Dutch – 1.4; Russian – 1.5).
  • Bifidolact – 1.4.
  • Acidophilus – 0.33.
  • Kefir – 0.34.
  • Sour cream – 0.36.
  • Butter – 0.07.
  • Milk – 0.4.
  • Chicken egg - 0.52.

The treatment improves the condition and well-being of the child. 12 hours after the injection of cyanocobalamin, hematopoiesis in the bone marrow becomes normoblastic.

An increase in reticulocytes is observed from the 3rd day of treatment, and from 4 to 10 days a reticular crisis is possible (a significant increase in them). If reticulosis does not appear, then the diagnosis is incorrect. Hypersegmentation of leukocytes lasts up to 2 weeks.

All blood counts return to normal after 1-2 months. Neurological symptoms disappear after six months.

Prevention


The diet of a child suffering from B12 deficiency anemia should contain foods rich in this vitamin.

Prevention of anemia in a child should be taken care of even before the baby is born. A pregnant woman should, firstly, eat right and adhere to all recommendations for the regimen, and secondly, regularly monitor blood tests. With the development of anemia in a pregnant woman, the risk of its occurrence in the infant increases significantly.

After birth, the optimal nutrition for the baby is. During lactation, it is also very important for a nursing mother to provide. From the age of 6 months, it should be administered to the baby, while following all the recommendations of the pediatrician. At 6 and 12 months, the child undergoes a blood test.

Older children should be under the supervision of a pediatrician and have an annual blood test. Children's nutrition should be balanced, providing the child with all the nutrients and vitamins necessary for a growing body. It is important to promptly identify and treat helminthiasis, inflammatory diseases Gastrointestinal tract, which can cause anemia.

Summary for parents

The reasons for the development of megaloblastic B 12 deficiency anemia are varied. Some of them are manifestations hereditary pathology, but many can be prevented by taking care of this before the baby is born.

Rational nutrition of the expectant mother and children throughout life, regular medical supervision- these are the basics that will help raise a healthy child.

An important point is the timely diagnosis and treatment of developed B 12 deficiency anemia, which prevents the development of serious neurological and dystrophic disorders.


B12 deficiency anemia is a disease characterized by impaired hematopoiesis and caused by a deficiency of vitamin B12 in the human body. This pathology is quite rare, but women suffer from vitamin B12 deficiency more often, and this may be associated with pregnancy.

Causes of B12 deficiency anemia

Modern medicine knows quite a lot of reasons that provoke the development of the pathological condition in question, but they all boil down to a lack of vitamin B12 in the human body. Therefore, the causes of B12 deficiency anemia should be considered in conjunction with the causes of the lack of the vitamin mentioned above.

The main reasons for the development of the disease in question are:


It is worth noting that most often the cause of B12 deficiency anemia is insufficient intake of the vitamin in question in the body.

Symptoms of B12 Deficiency Anemia

The reserves of the vitamin in question in the human body are quite large, so there may not be clinical manifestations of B12 deficiency anemia for a long time. The disease develops very slowly and in the initial stages is characterized by weakness, increased fatigue and drowsiness - completely nonspecific symptoms.

The main clinical manifestations of B12 deficiency anemia include:

  1. Impaired blood cell formation. This manifests itself as dizziness and frequent headaches, pallor and yellowness of the mucous membranes/skin, intolerance physical activity, rapid heartbeat, the appearance of “floaters” before the eyes and an enlarged spleen. In principle, if only one of the above manifestations appears, a person should seek qualified help, because it is not at all necessary that a complex of symptoms of impaired blood cell formation will be present at the same time.
  2. Damage to the digestive system. This symptom is the earliest sign of B 12 deficiency anemia, and it will manifest itself:
    • indigestion;
    • decreased appetite;
    • pain and burning in the mouth;
    • taste disturbance;
    • after eating;
    • frequent infections in the oral cavity.
  3. Damage to the nervous system. Usually they appear only in the case of an advanced form of B12 deficiency anemia and are:
    • sensory disturbances in the fingers and wrists;
    • paresthesia - “tingling” in certain places of the body;
    • decreased muscle strength;
    • problems with urination and bowel movements.

The most dangerous manifestation B12 deficiency anemia is a mental disorder, as evidenced by hallucinations,.

Note:all symptoms of the disease in question are nonspecific, that is, they may indicate the development of other diseases. Therefore, doctors always consider them only in conjunction with other diagnostic data.

Diagnosis of B12 deficiency anemia

Merely the patient’s complaints about the symptoms described above are not a reason to diagnose the disease in question. The process of diagnosing B12 deficiency anemia is quite complex, since the following measures will need to be taken:

  • examine blood by conducting general and laboratory analysis;
  • do a bone marrow puncture.

And a patient with suspected or already established B12 deficiency anemia must be thoroughly examined, since it will be necessary to find out the cause of the pathology.

Treatment for B12 deficiency anemia

Treatment of the disease in question is carried out only comprehensively, because doctors are faced with the task of restoring it as quickly as possible. normal functioning hematopoietic, digestive and nervous systems.

Drug treatment

The essence of this type of therapy is to administer vitamin B 12 externally. Indications for such treatment are a confirmed diagnosis of B12 deficiency anemia and severe clinical picture the disease in question.

Most often, vitamin B12 is administered intramuscularly, but it can also be taken orally in the form of tablets if the fact of insufficient intake of vitamin B12 from food is accurately established.

Treatment of the disease begins with intramuscular administration of 500-1000 mcg of vitamin B12 once a day. The duration of drug treatment is at least 6 weeks, then doctors transfer the patient to maintenance therapy - the dosage in this case will be 200-400 mcg of the drug 2-4 times a month. In some cases, such maintenance therapy is carried out throughout the patient's life.

Note:During the period of drug treatment for B12 deficiency anemia, the patient must monitor the effectiveness of therapy - blood is drawn 2-3 times a week for laboratory research. As a rule, after 1 month, complete normalization of peripheral blood parameters occurs, neurological manifestations weaken, and the functioning of the digestive system is restored. As soon as the patient is transferred to maintenance therapy, blood is drawn for analysis once a month.

Blood transfusion

This treatment method involves giving a blood transfusion to the patient, but more often red blood cells are used. Because this method is considered quite severe and even dangerous in some sense, so it is used only if the patient’s life is in direct danger due to the development of vitamin 12 deficiency anemia . Unconditional indications for blood transfusion:

  • severe anemia, when the patient's hemoglobin level is less than 70 g/l;
  • anemic coma manifesting itself.

Since blood transfusion is prescribed only with a confirmed diagnosis, simultaneously with this procedure, intramuscular injection vitamin B12 preparation. But blood or red blood cell transfusions are stopped as soon as the life-threatening condition of the patient is eliminated.

Nutrition correction

Very often, B12 deficiency anemia is treated with diet, but this is only possible with timely diagnosis of the disease. The patient's menu should include foods rich in vitamin B12 and important for the treatment of anemia:

It is important to eat nutritiously and variedly. Here is a sample daily menu for patients diagnosed with B12 deficiency anemia:

  • 1 breakfast – fresh cabbage salad with apples and sour cream, omelette, oatmeal porridge with milk;
  • 2nd breakfast – tea and 100 grams of cheese (maximum amount);
  • lunch - borscht meat broth with sour cream, fried chicken with boiled rice and compote;
  • afternoon snack - rosehip decoction;
  • dinner - meat zrazy with onion and egg, carrot puree, buckwheat casserole with cottage cheese, weak tea;
  • at night - kefir.

Note:A specialist should draw up a dietary menu for patients diagnosed with B12 deficiency anemia, since the general state of health, the presence of general pathologies and the individual sensitivity of the body to different products.

Prognosis for B12 deficiency anemia

If the disease in question was diagnosed on early stage of its development, treatment was immediately prescribed and carried out, and the normalization of peripheral blood parameters occurred within a month to a month and a half, then the prognosis will be extremely favorable. As soon as the basic therapy is carried out, the health condition is restored and the patient returns to the usual rhythm of life. But if there is:

  • late start of treatment;
  • symptoms of damage to the central nervous system;
  • lack of effect from the treatment;
  • hereditary form of B12 deficiency anemia,

then the forecasts will be unfavorable. Most likely, the patient will be forced to undergo treatment throughout his life; often a severe form of B12 deficiency anemia ends in coma and death.

B12 deficiency anemia is a condition that is not life-threatening, but very insidious. If a person pays attention to the earliest signs of the condition in question, then the doctor will be able to quickly establish the cause of the disease and carry out effective treatment.

07.09.2017

Anemia is a clinical and hematological pathology, during which there is a decrease in hemoglobin concentration per unit of circulating blood. And the lack of hemoglobin leads to a decrease in the number of red blood cells, as a result, all organs begin to receive the missing amount of oxygen, which leads to hypoxia. Anemia or anemia develops at any age and is considered not an independent disease, but pathological condition, which appears due to the influence of a group of factors on the body.

There are several types of anemia. One of the severe types of anemia is B12 deficiency anemia - a disease when hematopoiesis is impaired due to a lack of vitamin B12. Other names for anemia are pernicious or megaloblastic anemia.

B12 anemia is rare and occurs in 0.1% of the world's population, but among older people the rate reaches 1%. Women are most susceptible to this disease, especially during pregnancy. Under what circumstances does B12 deficiency anemia develop, what are the symptoms and is it possible to get rid of this problem forever? You will learn about all this and much more regarding pernicious anemia from this article.

Features of the development of B12 deficiency anemia

Anemia is a pathology of a weak body, during which hemoglobin in the blood significantly decreases and at the same time the number of red blood cells decreases, which causes oxygen starvation. The formation of red blood cells occurs in the red bone marrow under the influence of a substance synthesized by the kidneys. They are created from protein and non-protein components. For 3 days after formation, red blood cells transport oxygen, carbon dioxide and various nutrients from cells to tissues.

Red blood cells live for 120 days, after which they are destroyed. Having become unusable, red blood cells accumulate in the spleen, where they are divided into protein and non-protein fractions. After separation, the non-protein components are destroyed, and the protein components enter the red bone marrow, where they participate in the production of new red blood cells. Red blood cells are made up of hemoglobin and various vitamins, in particular vitamin B12, which is involved in the formation of DNA. Ordinary anemia develops due to a lack of hemoglobin, which allows for better transport of oxygen and carbon dioxide throughout the body. But if there is a lack of vitamin B12 in the body, the formation of red blood cells in the bone marrow is disrupted, which leads to the development of megaloblastic anemia.

Mechanism of development of B12 deficiency anemia

Vitamin B12 (cobalamin) enters the body of a living being, including humans, through food of animal origin, since the body itself is not able to synthesize this vitamin. With a normal balanced diet, 30 to 50 micrograms of vitamin B12 are absorbed into the intestines of an average person daily, while daily requirement body is from 3 to 5 micrograms. When absorbed, cobalamin is deposited in the liver, which can contain up to 5 mg of the vitamin in an adult. That is, it is not at all surprising that the first symptoms of malignant anemia appear several years after the start of cobalamin intake in insufficient quantities.

Vitamin B12 deficiency provokes a violation of DNA synthesis in all cells of the body

Vitamin B12 deficiency provokes a disruption of DNA synthesis in all cells of the body. And first of all, this becomes noticeable in the mucous membranes and hematopoietic tissues, the processes of cell division in which occur more intensively. After the vitamin enters the cell, it takes on one of the following forms:

  • deoxyadenosylcobalamin. He takes part in education fatty acids, the deficiency of which leads to damage to the nervous system;
  • Methyl-B12. Actively participates in the synthesis of DNA components, in particular thymidine. And the lack of cobalamin in the body leads to a stop in the synthesis of this nucleoside, resulting in the formation of a DNA molecule with an inferior structure. This molecule is prone to rapid destruction, which prevents normal cell division.

Lack of vitamin B12 leads to disruption of DNA synthesis in the process of hematopoiesis. initial stage development of red blood cells, which is why they further development becomes impossible. What is also very important, cobalamin deficiency leads to disruption of the formation of not only red blood cells, but also platelets and leukocytes. This disruption process is much less pronounced than the disruption of red blood cell formation. But if this phenomenon occurs over a long period of time, then there is a high probability of developing a syndrome characterized by a lack of all important blood components.

Causes of B12 deficiency anemia

There are many reasons for the development of B12 deficiency anemia, but they all involve a lack of cobalamin in the body. The following are the main causes of B12 deficiency anemia:

Increased use of vitamin B12 by the body can develop deficiency anemia

Risk factors include older people, as well as patients suffering from stomach diseases. Pernicious anemia is also very common in vegetarians. This is explained by the fact that in plant products this vitamin is not contained. Therefore, vegans are advised to take vitamin supplements.

Symptoms of B12 deficiency anemia

The human body is capable of accumulating quite large reserves of cobalamin, so even if there is insufficient intake of vitamin B12 in the body, the first symptoms will appear several years after the onset of the pathology. On initial stage progression of the disease, weakness may be observed, constant drowsiness And increased fatigue. But that's how it is nonspecific signs that a person cannot suspect the development of anemia. First of all, the process of hematopoiesis is disrupted, and then other body systems are damaged.

The most common symptoms include dizziness and frequent fainting.

In the presence of B12 deficiency anemia, symptoms are divided into 3 groups:

  • disruption of blood cell formation. A disruption of hematopoiesis occurs, due to which the number of red blood cells per unit of circulating blood is significantly reduced. As a result, the transportation of gases in the body is significantly deteriorated, which leads to oxygen starvation of organs and tissues. This is accompanied by the following symptoms:
  • heartache;
  • exercise intolerance;
  • pallor or yellowness of the skin;
  • cardiopalmus;
  • increase in the size of the spleen;
  • flickering of flies before the eyes;
  • damage to the digestive system. First clinical manifestations B12 deficiency anemia is precisely a lesion of the gastrointestinal system, which is expressed in:
    • disruption of the digestive process;
    • decreased appetite;
    • violation of taste perception;
    • sudden weight loss;
    • problems with stool;
    • infections in the oral cavity;
    • burning and pain in the mouth;
    • abdominal pain after eating;
    • the tongue becomes bright crimson and smooth;
  • damage to the nervous system. These disorders occur in advanced stages of malignant anemia. The greatest danger is damage to the brain and spinal cord. This process is accompanied by the following symptoms:
    • impaired hand sensitivity;
    • numbness and tingling in some parts of the body;
    • muscle dysfunction;
    • retention or incontinence of feces or urine;
    • mental problems: from ordinary insomnia to severe psychosis and hallucinations.
  • The above symptoms are nonspecific and may indicate the presence of both B12 deficiency anemia and other diseases. Therefore, to identify pernicious anemia, symptoms need to be considered only in conjunction with diagnostic measures.

    Diagnosis and treatment of B12 deficiency anemia

    Megaloblastic anemia develops for a very long time and is asymptomatic, which makes diagnosing the disease at the initial stage of development difficult. But if treatment is not started in a timely manner, the disease will further progress, affecting more and more systems and organs. Therefore, it is very important to consult a hematologist immediately if you suspect anemia. After a thorough interview and physical examination, your doctor will order the following diagnostic tests:

    • general blood analysis;
    • blood chemistry;
    • Analysis of urine;
    • bone marrow puncture;
    • CT and MRI of the liver and spleen;
    • ECG, ultrasound and some other clinical and instrumental diagnostic methods;
    • identifying the cause of anemia.

    The first step is to undergo a series of tests to identify the cause of the pathology.

    You may also need to consult specialists in other fields: a therapist, a neurologist and a gastroenterologist. After B12 deficiency anemia has been diagnosed, treatment is selected strictly by a doctor and must be comprehensive. First of all, treatment is aimed at restoring the functions of damaged systems, and is based on 3 principles:

    • complete saturation of the body with cyanocobalamin. Its quantity should be sufficient both to perform functions and to be stored in reserve;
    • constant replenishment of vitamin reserves using maintenance doses;
    • preventing the development of anemia.

    Treatment for B12 deficiency anemia involves replenishing the required amount of cobalamin in the body. And therefore, first of all, it is necessary to get rid of the cause that provoked the development of this pathology. Complex treatment of malignant anemia consists of the following points:

    • drug treatment. Vitamin B12 is in most cases administered intramuscularly, but in case of cobalamin deficiency due to poor diet, the doctor may prescribe it in tablets. Drug treatment B12 deficiency anemia involves administering 0.5-1 mg of vitamin B12 intramuscularly once a day. The duration of the course is at least 6 weeks, after which the dosage is reduced to 02.-0.4 mg of the drug several times a month. In advanced cases, such therapy is carried out throughout the patient’s life;
    • nutrition correction. Timely diagnosis of the disease makes it possible to cure anemia only with the help of special diet, which includes foods rich in cobalamin. Such products include meat, fish, offal, plum juice and much more;
    • blood transfusion. The patient is transfused with blood or red blood cells. This method of treatment is used only in conditions that threaten the patient’s life, as it is extremely dangerous procedure. Such conditions with anemia that pose a serious threat are:
      • severe anemia, when the hemoglobin level is below 70 g/l;
      • anemic coma, that is, complete loss of consciousness.

    Megaloblastic anemia leads to disruption of the functioning of all organs and systems of the body. And if, in the presence of pernicious anemia, treatment was started in a timely manner, then all violations are quickly eliminated with the help of complex treatment. But without treatment, the disease continues to progress, leading to the development of such severe consequences, such as malignant coma and funicular myelosis.

       (from the Latin perniciosus - disastrous, dangerous) or B12-deficiency anemia or megaloblastic anemia or Addison-Biermer disease or (outdated name) malignant anemia- a disease caused by impaired hematopoiesis due to a lack of vitamin B12 in the body. Bone marrow and tissue of the nervous system are especially sensitive to deficiency of this vitamin.

    In 1855, the English physician Thomas Addison, and then in 1872, the German physician Anton Birmer, described the disease in more detail, which was called pernicious (pernicious) anemia. Soon, the French doctor Armand Trousseau proposed calling these diseases Addison's anemia and Addison's disease.

    In 1926, J. Whipple, J. Minot and W. Murphy reported that pernicious anemia was treated by introducing raw liver into the diet and that the disease was based on the congenital inability of the stomach to secrete the substance necessary for the absorption of vitamin B12 in the intestine. For this discovery they received the Nobel Prize in 1934.

    Megaloblastic anemias are a group of diseases characterized by weakened DNA synthesis, as a result of which the division of all rapidly proliferating cells (hematopoietic cells, skin cells, gastrointestinal cells, mucous membranes) is disrupted. Hematopoietic cells are among the most rapidly multiplying elements, which is why anemia often comes to the fore in the clinic. The main cause of megaloblastic anemia is a deficiency of cyanocobalamin or folic acid.


    Symptoms:

    B12 deficiency anemia develops relatively slowly and may be asymptomatic. Clinical signs of anemia are nonspecific: weakness, fatigue, palpitations. Patients are pale and subicteric. There are signs - with areas of inflammation and atrophy of the papillae, a varnished tongue, and there may be an enlargement of the spleen and liver. Gastric secretion sharply decreases. Fibrogastroscopy reveals the gastric mucosa, which is confirmed histologically. There are also symptoms of damage to the nervous system (funicular myelosis), which do not always correlate with the severity of anemia. The main neurological manifestations are demyelination of nerve fibers. Distal and peripheral polyneuropathy, sensitivity disorders, and increased tendon reflexes are noted.

    Thus, B12 deficiency anemia is characterized by a triad:
    - blood damage;
    - damage to the gastrointestinal tract;
    - damage to the nervous system.


    Causes:

    Various etiological factors can cause deficiency of cyanocobalamin or folic acid (less commonly, combined deficiency of both) and the development of megaloblastic anemia.

    Cyanocobalamin deficiency can be caused by the following reasons:
    - low content in the diet;
    - vegetarianism;
    - low absorption;
    - deficiency of internal factor;
    - pernicious anemia;
    - ;
    - damage to the gastric epithelium by chemicals;
    - infiltrative changes in the stomach; (lymphoma or carcinoma);
    - Crohn's disease;
    - ;
    - resection of the ileum;
    - atrophic processes in the stomach and intestines;
    - increased utilization of vitamin B12 by bacteria during their excessive growth;
    - condition after gastrointestinal anastomosis;
    - diverticula of the jejunum;
    - intestinal stasis or obstruction due to strictures;
    - helminthic infestation;
    - broad tapeworm (Diphyllobotrium latum);
    - pathology of the absorbent area;
    - ileum;
    - small intestine;
    - ;
    - regional;
    - other reasons.
    - congenital absence of transcobalamin 2 (rare)
    - abuse of nitrous oxide (inactivates vitamin B12 by oxidizing cobalt);
    - malabsorption caused by the use of neomycin, colchicine.

    Causes of folate deficiency may include:
    1. Insufficient intake
    - poor diet;
    - alcoholism;
    - neuropsychic;
    - ;
    - unbalanced diet in the elderly.

    2. Malabsorption
    - malabsorption
    - changes in the intestinal mucosa
    - celiac disease and sprue
    - Crohn's disease
    - regional ileitis
    -
    - reduction of the reabsorbing surface after resection of the jejunum
    - taking anticonvulsants

    3. Increased need
    - pregnancy
    - hemolytic anemia
    - exfoliative and

    4. Violation of disposal
    - alcoholism;
    - folate antagonists: trimethoprim and methotrexate;
    - congenital disorders of folate metabolism.


    Treatment:

    For treatment the following is prescribed:


    Complex therapeutic event for B12 deficiency anemia should be carried out taking into account the etiology, severity of anemia and the presence of neurological disorders. When treating, you should focus on the following points:
    - an indispensable condition for the treatment of B12-deficiency anemia due to helminthic infestation is deworming (to expel the broad tapeworm, phenosal is prescribed according to a certain scheme or male fern extract).
    - for organic intestinal diseases and diarrhea, enzyme preparations (panzinorm, festal, pancreatin) should be used, as well as fixing agents (calcium carbonate in combination with dermatol).
    - normalization of intestinal flora is achieved by taking enzyme preparations(panzinorm, festal, pancreatin), as well as the selection of a diet that helps eliminate putrefactive or fermentative syndromes.
    - a balanced diet with sufficient vitamins, protein, and an absolute prohibition of alcohol is an indispensable condition for the treatment of B12 and folate deficiency anemia.
    - pathogenetic therapy is carried out using parenteral administration of vitamin B12 (cyanocobalamin), as well as normalization of altered indicators of central hemodynamics and neutralization of antibodies to gastromucoprotein (" internal factor") or gastromucoprotein + vitamin B12 complex (corticosteroid therapy).

    Blood transfusions are carried out only when there is a significant decrease in hemoglobin and symptoms of a coma appear. It is recommended to administer 250 - 300 ml of red blood cells (5 - 6 transfusions).

    Principles of therapy:
    - saturate the body with vitamins
    - maintenance therapy
    - warning possible development anemia

    Cyanocobalamin is most often used in doses of 200-300 micrograms (gmm). This dose is used if there are no complications (funicular myelosis, coma). Now they use 500 micrograms daily. Administer 1-2 times a day. If there are complications, 1000 micrograms. After 10 days, the dose is reduced. The injections continue for 10 days. Then, 300 micrograms are administered weekly for 3 months. After this, 1 injection is given every 2 weeks for 6 months.


    Vitamin B12 deficiency is one of the most common micronutrient deficiencies worldwide.

    It is most confirmed by older people and strict vegetarians who do not eat animal products.

    The important role it plays in the body determines the nature and severity of the consequences of its deficiency, including, among other things, a decrease in sports performance.

    In this article we will talk about the symptoms of vitamin B12 deficiency.

    The important role of vitamin B12

    Vitamin B12 or cobalamin is a water-soluble vitamin that plays important role in the creation of red blood cells and DNA, and in the proper functioning of the nervous system.

    Neither humans nor animals are able to synthesize it on their own. Food is its only source 1 .

    In its natural form Vitamin B12 is present in animal products, including meat, fish, poultry, eggs and dairy products. It is also used to enrich a fairly large number of finished products, including sports nutrition, breakfast cereals, bread, non-animal milks (soy, rice, almond).

    Groups at risk of vitamin B12 deficiency

    Vitamin B12 deficiency is one of the most common worldwide 1 .

    The reasons may be insufficient intake from food or the body’s inability to absorb it.

    People at risk of vitamin B12 deficiency:

    • aged people;
    • vegetarians (those who completely exclude animal products from their diet, in particular, vegans and raw foodists);
    • those who have undergone surgery to remove part of the intestine responsible for the absorption of B12;
    • those who take certain medications (metformin for diabetes, antacids for heartburn).

    The only source of vitamin B12 for humans is food, animal products. Vegetarians and the elderly are at risk of deficiency

    Difficulties in diagnosing vitamin B12 deficiency

    The main difficulty is that signs of vitamin B12 deficiency may appear years after its formation.

    Also there is no single symptom that can be used to diagnose it unambiguously 1 . This cannot be done only with the help of a blood test: the content of this vitamin in the blood is not an unambiguous indicator 1, as it is determined by the type of deficiency.

    The symptoms of vitamin B12 deficiency are very similar to vitamin B9 (folate) deficiency.

    The concentrations of B9 and B12 are interrelated: if the body lacks vitamin B12, then the level of B9 also drops. If you start taking vitamin B9 at the same time, this can “mask” the lack of vitamin B12 2 .

    Listed below are 9 signs of vitamin B12 deficiency. Any of them (and even more so if there are several of them) is a reason to consult a doctor.

    Signs of vitamin B12 deficiency can take years to appear and there is no single symptom that can be used to diagnose it.

    Symptoms of vitamin B12 deficiency

    1 Pale yellowish skin

    People who are deficient in vitamin B12 often have pale skin with a slight yellowish tint; yellow appears on the cornea of ​​the eyes (the white visible part).

    The reason for this is a decrease in the production of red blood cells (erythrocytes), which are actually red in color and are “responsible” for the pink, healthy color of the skin 3 . In the language of doctors, this condition is called anemia.

    Vitamin B12 plays a very important role in the creation of DNA molecules, in which the mechanism of erythrocyte synthesis is “recorded” 3.

    Its deficiency leads to a type of anemia in which very large non-functional red blood cells are produced in the bone marrow: they simply cannot get out of the bone marrow and into blood system. As a result, the blood becomes less red and the skin loses its pink tint.

    These dysfunctional blood cells are easily destroyed, leading to increased levels of bilirubin, a red-brown substance produced by the liver when it disposes of red blood cells.

    It is bilirubin that colors the normally white cornea of ​​the eye yellow 4 . (The same thing happens with jaundice, by the way.)

    With a deficiency of vitamin B12, the skin becomes pale, and the cornea of ​​the eye (the white visible part of the eye) acquires a yellowish tint due to anemia

    2 Weakness and fatigue

    This is another characteristic symptom of vitamin B12 deficiency.

    The reason is the same: anemia, due to a disruption in the production of red blood cells, which in the body are responsible for transporting oxygen to the cells, without which their functioning and life are impossible.

    (To illustrate the importance of oxygen, completely depriving brain cells of oxygen will cause them to die within minutes.)

    Oxygen is necessary to obtain energy from food. Its deficiency naturally leads to a feeling of lethargy and weakness.

    In sports, a lack of vitamin B12 means decreased performance: oxygen supply to muscles is a determining factor in physical performance; that is why the action of many types of doping is aimed at improving the transport function of the blood in the transfer of oxygen; in case of B12 deficiency, the opposite effect occurs.

    The cause of weakness and lethargy due to vitamin B12 deficiency is a disruption in the supply of oxygen to muscles and other organs due to impaired production of red blood cells (anemia). In sports, this leads to decreased performance

    3 Tingling sensation in arms and legs

    One of the serious side effects of vitamin B12 deficiency is damage nerve cells .

    This happens over time and is due to the fact that Vitamin B12 is necessary to create a protective sheath for nerve cells, which is called myelin 5.

    A sign that damage has occurred is paresthesia or a tingling sensation in the extremities (arms and legs).

    Such a violation nervous function Vitamin B12 deficiency very often occurs against the background of the anemia described above. But not always.

    One study of physicians found that 28% of patients with B12 deficiency had neurological symptoms and no anemia 6 .

    This suggests that the presence of one symptom (anemia or tingling in the fingers) is not a sufficient basis for diagnosing vitamin B12 deficiency.

    Vitamin B12 plays an important role in creating the protective sheath of nerve cells - myelin; Deficiency of this vitamin leads to nerve damage, which is accompanied by a tingling sensation in the limbs

    4 Impaired coordination

    If vitamin B12 deficiency is not recognized and treated early, ongoing damage to the nervous system can lead to impaired motor function.

    In particular, it can affect coordination, increasing the risk of falling. This symptom is especially common in older people 7 and often in young people 8 and vegetarians with severe vitamin B12 deficiency.

    Diagnosis and treatment improves mobility.

    Chronic vitamin B12 deficiency can lead to poor coordination and falls

    5 Tongue inflammation and oral cancer

    Inflammation of the tongue or glossitis manifests itself in a change in its color, shape and the appearance of a feeling of pain. It becomes redder than usual and swells, and the surface becomes smooth as the small bumps containing taste buds disappear.

    Such changes cannot but affect the ability to speak and eat.

    Scientists say that an inflamed and swollen tongue with elongated lesions on its surface - one of early signs vitamin B12 deficiency 9,10 .

    Sometimes vitamin B12 deficiency can lead to the development of tongue cancer, tingling, burning and itching sensations in the tongue 9 .

    One of early symptom Vitamin B12 deficiency is a red, swollen tongue with elongated swellings on the surface

    6 Shortness of breath and dizziness

    Anemia due to vitamin B12 deficiency leads to shallow rapid breathing and dizziness, especially during moments of physical stress.

    This is a consequence of poor oxygen supply to the organs: when the transport function of the blood is disrupted, the body tries to meet the constant need for it by pushing a larger volume of air through the lungs, increasing the breathing rate.

    However, shortness of breath and dizziness do not always indicate a lack of vitamin B12: this symptom can have a huge number of other causes.

    Anemia, which develops with vitamin B12 deficiency, often leads to shortness of breath and dizziness, as the cells do not receive enough oxygen.

    7 Deterioration of vision

    Another symptom of vitamin B12 deficiency is blurred vision.

    This happens because the optic nerve is damaged, through which signals are transmitted from the retina to the brain 11,12. In medical language this condition is called optical neuropathy.

    Despite the seriousness this symptom reversible if you start taking vitamin B12.

    Chronic vitamin B12 deficiency may impair vision due to damage to the optic nerve.

    8 Bad mood

    Very often, people with vitamin B12 deficiency complain of worsening mood.

    Low levels of this vitamin are associated with psychological and mental disorders such as depression and dementia 13,14 .

    This is a consequence of an increase in the level of the amino acid homocysteine, which occurs when the concentration of vitamin B12 decreases, which, according to scientists, can lead to brain damage And disrupt the propagation of nerve impulses from the brain and into it 15.

    Supplementation with vitamin B12 may improve this symptom 16 .

    But here too, it is important to understand that mood changes, depression and dementia can occur for many other reasons. Therefore, taking vitamin B12 to treat them may not give any result.

    Sometimes vitamin B12 deficiency is accompanied by worsening mood, depression and decreased mental function, in particular dementia

    9 Increase in temperature

    In rare cases, a lack of vitamin B12 may be accompanied by a fever.

    It is not entirely clear why this happens, however, doctors have recorded several cases where in patients with B12 deficiency, the body temperature returned to normal after taking it additionally 17 .

    Sometimes one of the symptoms of vitamin B12 deficiency can be an increase in body temperature

    Treatment of vitamin B12 deficiency

    Injections

    To treat vitamin B12 deficiency, doctors often prescribe intramuscular injections (shots) hydroxocobalamin or cyanocobalamin.

    This is the most effective method treatment.

    From a safety point of view, injections do not have serious side effects. IN in rare cases noted allergic reaction 18,19 .

    Food

    Vitamin B12 is found in animal products and foods fortified with it. In order to make up for its deficiency or avoid it, you just need to regularly include them in your diet.

    Most often, they are enriched with breakfast cereals and plant-based milks (soy, rice, almond). Read the description on the labels.

    List of foods containing vitamin B12 large quantities 22:

    • liver: 1/3 cup (~75 g) provides approximately 881% of daily needs;
    • beef kidneys: 1/3 cup (~75 g) provides approximately 331% of daily needs;
    • trout
    • canned salmon: 1/3 cup (~75 g) provides approximately 61% of daily needs;
    • Ground beef: 1/3 cup (~75 g) provides approximately 40% of daily needs;
    • eggs: 2 large eggs provide approximately 25% of daily needs;
    • milk: 1 cup (250 ml) 20% daily requirement;
    • chicken: 1/3 cup (75 g) 3% daily requirement.

    As you can see, in the list - only animal products. This means that providing the required amount of vitamin B12 for individuals following a strict vegetarian diet(for vegans and raw foodists), it’s quite difficult.

    Therefore, to avoid and treat vitamin B12 deficiency, it is recommended that all individuals at risk take it as a dietary supplement.

    Pills

    Scientific research confirms that oral medications vitamin B12 (tablets) are no less effective in treating its deficiency than injections 20,21.

    However, many doctors prefer injections, considering them more effective.

    To prevent and treat vitamin B12 deficiency, injections, oral medications (tablets) and foods rich in vitamin B12 are recommended. Scientists say injections and oral medications are equally effective

    Afterword

    Vitamin B12 deficiency is very common in the world and can manifest itself multiple symptoms, which makes accurate diagnosis difficult. Among them are poverty and yellowness of the skin, impaired vision and coordination, tingling sensation in the limbs, blurred vision and others.

    Elderly people and strict vegetarians who do not eat animal products are at particular risk of deficiency.

    In most cases, simply taking a vitamin B12 supplement by those at risk can be an effective preventive measure to avoid serious consequences.

    Scientific references

    1 Herrmann W, Obeid R. Cobalamin deficiency. Subcell Biochem. 2012;56:301-22.
    2 Morris MS, Jacques PF. Folate and vitamin B-12 status in relation to anemia, macrocytosis, and cognitive impairment in older Americans in the age of folic acid fortification Am J Clin Nutr. 2007 Jan;85(1):193-200.
    3 Green R, Datta Mitra A. Megaloblastic Anemias: Nutritional and Other Causes. Med Clin North Am. 2017 Mar;101(2):297-317
    4 Dusol M Jr, Schiff ER. Clinical approach to jaundice. Postgrad Med. 1975 Jan;57(1):118-24.
    5 Briani C, Dalla Torre C. Cobalamin deficiency: clinical picture and radiological findings. Nutrients. 2013 Nov 15;5(11):4521-39
    6 Lindenbaum J, Healton EB. Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocytosis. N Engl J Med. 1988 Jun 30;318(26):1720-8.
    7 Clarke R, Grimley Evans J. Vitamin B12 and folate deficiency in later life. Age Aging. 2004 Jan;33(1):34-41.
    8 Crawford JR, Say D. Vitamin B12 deficiency presenting as acute ataxia. BMJ Case Rep. 2013 Mar 26;2013
    9 Graells J, Ojeda RM. Glossitis with linear lesions: an early sign of vitamin B12 deficiency. J Am Acad Dermatol. 2009 Mar;60(3):498-500
    10 Petavy-Catala C, Fontès V. . Ann Dermatol Venereol. 2003 Feb;130(2 Pt 1):191-4.
    11 Ralapanawa DM, Jayawickreme KP. B12 deficiency with neurological manifestations in the absence of anemia. BMC Res Notes. 2015 Sep 18;8:458
    12 Azenha C, Costa JF. You are what you eat: ophthalmological manifestations of severe B12 deficiency. BMJ Case Rep. 2017 May 6;2017.
    13 Almeida OP, Ford AH. Systematic review and meta-analysis of randomized placebo-controlled trials of folate and vitamin B12 for depression. Int Psychogeriatr. 2015 May;27(5):727-37.
    14 Malouf R, Areosa Sastre A. Vitamin B12 for cognition. Cochrane Database Syst Rev. 2003 (3)
    15 Bhatia P, Singh N. Homocysteine ​​excess: delineating the possible mechanism of neurotoxicity and depression. Fundam Clin Pharmacol. 2015 Dec;29(6):522-8
    16 Reid SD. Pseudodementia in a twenty-one-year-old with bipolar disorder and vitamin B12 and folate deficiency. West Indian Med J 2000 Dec;49(4):347-8.
    17 Manuel K, Padhi S, G"boy Varghese R. Pyrexia in a patient with megaloblastic anemia: a case report and literature review. Iran J Med Sci. 2013 Jun;38(2 Suppl):198-201.
    18 J James and R P Warin. Sensitivity to cyanocobalamin and hydroxocobalamin. Br Med J 1971 May 1; 2(5756): 262.
    19 Bilwani F1, Adil SN. Anaphylactic reaction after intramuscular injection of cyanocobalamin (vitamin B12): a case report. J Pak Med Assoc. 2005 May;55(5):217-9.
    20 L Masucci and R Goeree. Vitamin B12 Intramuscular Injections Versus Oral Supplements. Ont Health Technol Assess Ser. 2013; 13(24): 1–24.
    21 Kolber MR, Houle SK. Oral vitamin B12: a cost-effective alternative. Can Fam Physician. 2014 Feb;60(2):111-2.
    22 https://www.healthline.com/nutrition/vitamin-b12-injections#section6



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