Pernicious (B12-deficient) anemia. B12-deficiency anemia in children: symptoms, treatment, principles of nutrition

Vitamin B12 belongs to the cobalamins. Its intake into the body is provided by products of animal origin: meat, cheeses, milk, eggs. Plant foods do not contain it. A person's own reserves of vitamin B12 without external intake are enough to live up to 5 years. Due to the rich variety of foods containing vitamin B12, anemia rarely develops due to its insufficient intake with food. Usually due to B12- deficiency anemia has a problem with absorption or competitive use of vitamin cobalamin in helminthic infestations.

Important! Suspicious for B12 deficiency anemia should be young people who identify themselves as strict vegetarians.

Chronic deficiency of vitamin B12 leads to a persistent violation of the formation of thymidine. Pathological, megaloblastic hematopoiesis develops, in which red blood cells are enlarged.

Among patients suffering from B12 deficiency anemia, the majority are over 50 years of age. It is extremely rare to find vitamin deficiency in young people.
IN clinical picture B12 deficiency anemia has 3 main syndromes:

anemic;
gastrointestinal disorders;
neurological.

Anemia syndrome

Diagnostically, anemia syndrome is confirmed by the values of the following indicators:

Erythrocytes are oval, large - the volume is up to 150 with a normal 80-150 fl. Often, Jolly bodies are found, Cabot rings are the remains of nuclei.

Important! An early laboratory criterion for megaloblastic anemia is an increase in neutrophil segmentation. Significant is the detection of cells with 6 segments or 5% of cells with 5 segments.

Inferiority of erythrocytes naturally leads to oxygen deficiency in all tissues. But not all tissues are equally sensitive to hypoxia. epithelial tissue, muscles, neurons are among the most susceptible, therefore, in the first place, anemia is manifested by symptoms on their part. Among the complaints of patients non-specific prevail:

weakness with drowsiness during the day and insomnia at night;
rapid fatigue;
decrease in working capacity;
memory impairment;
headache;
muscle weakness.

The manifestations of muscle weakness include both rapid fatigue when walking, and difficulty in swallowing dry food, an endoscopic probe. This is important to consider when performing esophagogastroduodenoscopy in a patient with suspected anemia.

Decreased working capacity and memory impairment are directly related to cerebral hypoxia. Their aggravation is noted in the presence of another pathology from the central nervous system- encephalopathy. Significantly affects the symptoms of anemia and the severity of atherosclerotic changes in the vessels of the neck and brain - large plaques that narrow the lumen of the vessels worsen cognitive impairment. Tortuosity of blood vessels on the background of osteochondrosis cervical of the spine in patients of the elderly age group increases hypoxic headaches.

Anemia syndrome objectively

Among the examination data indicating vitamin B12 deficiency, it makes sense to distinguish two groups of symptoms:

Trophic - from the side of the epithelium and its appendages.
Compensatory - from the respiratory and cardiovascular systems.

A decrease in hemoglobin and anemic hypoxia, as expected, adversely affect the trophism of those tissues whose ability to regenerate is above average. These are the cells of the epithelium of the skin, its adnexal formations and the mucous membrane gastrointestinal tract. Hemoglobin deficiency leads to atrophic processes in these tissues.

Clinically it is:

cheilitis;
aphthous stomatitis;
glossitis;
gastritis;
rapid fragility of hair and nails;
dry skin;
pallor of the skin, mucous membranes.

Often you can notice a slight yellowness of the sclera. This is due to the faster destruction of large red blood cells in B12-deficient anemia.

Lack of oxygen causes compensatory hyperfunction of the heart and respiratory system. The manifestation of these symptoms is comparable both with the severity of anemia and with the age of the patient: the older the person, the less pronounced compensatory reactions:

heartbeat;
shortness of breath on exertion.

Objectively, you can identify:

deafness of heart tones,
tachycardia more than 90 per minute,
increase in pulse pressure due to a decrease in diastolic,
systolic murmur at the apex of the heart.

Older patients with a history of angina pectoris may report an increase in attacks of chest pain, worsening of dyspnea, edema, and, in general, progression of heart failure.

Younger patients, especially women, have excellent compensatory abilities and are often not even aware of a low hemoglobin level, because they do not feel any symptoms.

Gastrointestinal disorders

Atrophic changes in the organs of the gastrointestinal tract have already been partially addressed as part of the anemic syndrome. But, it would be more logical to talk about them separately, highlighting them as a specific syndrome of gastrointestinal disorders.

Hunter's glossitis is a manifestation of impaired trophism of the mucous membrane of the tongue. Bright red areas of inflammation over the entire upper surface of the tongue cause pain and a burning sensation, especially when in contact with acidic foods - fruits, juices. More often, the foci are located along the edges of the tongue and at the tip. In the most severe cases, the areas cover the entire organ - this phenomenon is called "scalded tongue" and, indeed, looks like a consequence of a severe thermal burn.

Similar inflamed areas can be found on the gums, cheeks, soft palate. Over time, the foci of inflammation will heal with the formation of a smooth surface. The papillae of the tongue atrophy, leaving a red, shiny, "varnished" tongue.

Important! This glossitis is quite typical for hemoglobin deficiency of any nature, so the detection of such changes in oral cavity should definitely refer a diagnostician to look for anemia.

Atrophic changes in the stomach in the clinic are manifested:

loss of appetite;
fast saturation;
feeling of heaviness after eating;
nausea;
belching.

FGDS with biopsy confirms the diagnosis of atrophy of the gastric mucosa.

Important! It is not uncommon for patients with B12 deficiency anemia to have mild enlargement of the liver and spleen. As a rule, these changes can be detected only when ultrasound examination And they don't cause discomfort.

neurological syndrome

Damage to the nervous system is very characteristic of vitamin B12 deficiency, although the mechanism is not completely clear. Possibly related to metabolic disorders fatty acids. With a lack of B12, propionic and methylmalonic acids accumulate, which are extremely toxic to the nervous system. In parallel with this, the results of a biopsy of nerve fibers showed that in B12-deficient anemia, pathological fatty acids are synthesized that differ from normal ones. Such organic matter do not lead to normal myelin synthesis, which means that the structure of the nerve fiber is disturbed.

Funicular myelosis, which develops with B12-deficiency anemia, is characterized by early and late symptoms. The early phenomena of polyneuritis include:

paresthesia;
violation of sensitivity;
feeling of coldness, "cotton legs", tingling of pins;
numbness in the limbs.

At further development diseases without external intake of vitamin B12, the symptoms are aggravated due to damage spinal cord:

gait disturbance, uncertainty when walking;
weakness in the limbs;
symptom of Lhermitte;
impaired hearing, vision, taste sensations;
violation of the functions of the pelvic organs.

An objective neurological examination reveals in a patient:

violation of sensitivity - pain, tactile, deep, vibration;
ataxia when walking;
sharp instability in the Romberg position;
revival, decrease or asymmetry of knee jerks;
stop clonus;
positive sign of Babinski.

Primarily, neurological disorders affect lower limbs. Hands are affected much less frequently and less pronounced. Sensory disorders progress from the loss of superficial - tactile, temperature, pain - to the disappearance of deep sensitivity - vibrational, muscular-articular feeling.

Lermitte's symptom, the essence of which is in sharp sharp shootings along the spine, occurs infrequently, but is extremely difficult and painful for patients.

Often, those groups of patients in whom it is precisely neurological disorders that come to the fore turn to a neurologist for the first time at the outpatient stage and may long time remain undiagnosed.

Important! Differential Diagnosis with folic acid deficiency anemia is carried out on the basis of determining the levels of cyanocobalamin and folic acid in the blood.

Today, thanks to good diagnostics and replacement therapy, we almost do not see the most severe forms of funicular myelosis: with complete areflexia and persistent paralysis.

Video - Vitamin B12 deficiency

(from Latin perniciosus - fatal, dangerous) or B12-deficiency anemia or megaloblastic anemia or Addison-Birmer disease or ( obsolete name) malignant anemia - a disease caused by impaired hematopoiesis due to a lack of vitamin B12 in the body. The bone marrow and tissues of the nervous system are especially sensitive to the deficiency of this vitamin.

In 1855, the English physician Thomas Addison, and then in 1872 in more detail the German physician Anton Birmer, described the disease, which they called malignant (pernicious) anemia. Soon the French physician Armand Trousseau suggested 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 a congenital inability of the stomach to secrete a 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 a weakening of 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, so anemia, and often come to the fore in the clinic. The main cause of megaloblastic anemia is cyanocobalamin or folic acid deficiency.

Symptoms:

B12 deficiency anemia develops relatively slowly and may be asymptomatic. Clinical signs anemias are nonspecific: weakness, fast fatiguability, heartbeat. Patients are pale, subicteric. There are signs - with areas of inflammation and atrophy of the papillae, varnished tongue, there may be an increase in the spleen and liver. Gastric secretion is sharply reduced. With fibrogastroscopy, the gastric mucosa is detected, which is also 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 basis of neurological manifestations is the demyelination of nerve fibers. Distal, peripheral polyneuropathy, sensitivity disorders, increased tendon reflexes are noted.

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

Causes of occurrence:

Various etiological factors can cause a deficiency of cyanocobalamin or folic acid (less often a 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 internal factor;
- pernicious anemia;
- ;
- damage to the epithelium of the stomach with 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 the application of the gastrointestinal anastomosis;
- diverticula of the jejunum;
- intestinal stasis or obstruction due to strictures;
- helminthic invasion;
- wide 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 due to the use of neomycin, colchicine.

The causes of folate deficiency can be:
1. Insufficient supply
- meager 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. Increasing demand
- pregnancy
- hemolytic anemia
- exfoliative and

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

Treatment:

For treatment appoint:

Complex therapeutic measures with B12 - deficiency anemia, it 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 provisions:
- an indispensable condition for the treatment of B12 - deficiency anemia with helminthic invasion is deworming (to expel a wide tapeworm, fenasal is prescribed according to a certain scheme or male fern extract).
- for organic bowel diseases and diarrhea, enzyme preparations (panzinorm, festal, pancreatin), as well as fixing agents (calcium carbonate in combination with dermatol) should be used.
- normalization of the intestinal flora is achieved by taking enzyme preparations(panzinorm, festal, pancreatin), as well as the selection of a diet that contributes to the elimination of putrefactive or fermentative syndromes.
- a balanced diet with a sufficient content of vitamins, protein, the unconditional prohibition of alcohol - an indispensable condition for the treatment of B12 and folate deficiency anemia.
- pathogenetic therapy is carried out with the help of parenteral administration vitamin B12 (cyanocobalamin), as well as the normalization of altered indicators of central hemodynamics and the neutralization of antibodies to gastromucoprotein ("intrinsic factor") or the gastromucoprotein + vitamin B12 complex (corticosteroid therapy).

Blood transfusions are carried out only with a significant decrease in hemoglobin and the manifestation of symptoms of a coma. It is recommended to enter erythrocyte mass in 250 - 300 ml (5 - 6 transfusions).

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

More often, cyanocobalamin is used in doses of 200-300 micrograms (gamma). This dose is used if there are no complications (funicular myelosis, coma). Now they use 500 micrograms daily. Enter 1-2 times a day. In the presence of complications 1000 micrograms. After 10 days, the dose is reduced. Injections continue for 10 days. Then, for 3 months, 300 micrograms are administered weekly. After that, for 6 months, 1 injection is made every 2 weeks.

The materials are published for review and are not a prescription for treatment! We recommend that you contact a hematologist at your healthcare facility!

B12 deficiency anemia is considered quite dangerous disease, as in the absence of appropriate measures can lead to a coma. It is important to notice the symptoms of the problem in time and establish its causes.

A disease such as B12-deficiency (pernicious) anemia is otherwise known as pernicious or malignant. The disease is very insidious and life-threatening if not treated on time. Consider this type of anemia in more detail.

Features of the disease

In the human body, a balance of vitamins, micro and macro elements must be maintained. With a deficiency of vitamin B12, anemia develops. B12 deficiency provokes disturbances in the synthesis of DNA and RNA, which is a direct threat to the vital organs. important functions. That is why this type of anemia is considered fatal.

It will be useful for you to learn also about that on our website.

Symptoms and types

In order to prevent the disastrous consequences of the disease, it is important to identify the lack of essential substances as early as possible. To do this, you need to know how B12-deficiency anemia manifests itself. Symptoms of the disease are similar to the traditional signs of anemia:

dizziness;
flashing before the eyes;
muscle weakness;
drowsiness or insomnia;
deterioration of the skin, nails, hair;
dyspnea;
crashes heart rate and pain in the sternum;
numbness of certain parts of the body;
pallor;
digestive disorders;
fainting.

Most hallmark is blanching of the skin, the acquisition of a painful shade, as well as changes in the oral cavity. The patient has a feeling of dryness and burning in the mouth, atrophy of the papillae of the tongue. The tongue itself takes on a bright red or crimson color, and its surface becomes "varnished" in appearance.

The characteristic symptom is glossitis.

In addition, there is a decrease in hemoglobin levels, which leads to intense oxygen starvation tissues, including the brain. This affects not only the well-being of the patient, but also on his mental activity. The changes affect the bone marrow, where red blood cells are synthesized.

Depending on the observed concentration of hemoglobin and the number of red blood cells, anemia can be of three degrees of severity:

light;
moderate;
heavy.

Important: in men, the level of hemoglobin is higher, therefore, with indicators of 110 g / l, you should be wary, while in women this is the norm.

There are also congenital and acquired forms of the disease. Congenital is observed in children born to a mother with anemia, when a woman is a vegetarian, as well as in the presence of pathologies of the systems responsible for the absorption of vitamin B12 and hematopoiesis.

Causes and consequences

Vitamin B12 is very important for the body, as it is involved in the process of RNA synthesis. If this process is disrupted, Negative influence spread throughout the body, and some organs may stop working properly.

Indicators	Iron- scarce	Hemo- lytic	Hypo- plastic	B12-deficient
Hemoglobin	↓	↓↓	↓↓	↓↓↓
red blood cells	↓	↓	↓↓	↓↓
Color indicator	↓	Norm	Norm
RBC diameter	↓	↓	Norm
Mean erythrocyte volume (MEV) (MCV)	Norm, ↓		Norm
Mean erythrocyte hemoglobin (MCH)(MSH)	↓		Norm
Mean erythrocyte hemoglobin concentration (MEH)(MCHC)	↓	Norm	Norm
Reticulocytes	Norm		↓↓↓	↓

Table: The main indicators of deviations from the norm at different forms anemia, including B12 (highlighted)

The main reason is the lack of vitamin B12, but it can be provoked by various factors.

To understand in which direction to move in the fight against anemia of this type, it is important to know what factors lead to a lack of such an important vitamin:

If you do not start treating anemia, the consequences can be extremely dangerous, because it is not without reason that this disease is called malignant. The following complications are possible:

tissue hypoxia and disruption internal organs;
changes bone marrow;
irreversible neurological disorders, in particular in the brain, such as funicular myelosis;
pernicious coma.

Diagnosis and treatment of B12 anemia

To establish a reliable diagnosis for B12-deficiency anemia, the patient must undergo a series of examinations. Modern diagnostics includes the following methods:

general and biochemical blood test;
Analysis of urine;
examination of bone marrow punctate;
analysis of the patient's symptoms and lifestyle in general.

Treatment is carried out comprehensively and in accordance with the severity of the situation. It is important to eliminate vitamin B12 deficiency and restore its normal perception by the body. To do this, you need to work on several fronts:

Diet. Foods rich in a deficient substance are introduced into the diet: eggs, meat, seafood, spinach, soybeans, beans, liver, dairy products.

In past years, anemia caused by vitamin B12 deficiency was called pernicious anemia or malignant anemia. For the first time, the English doctor Thomas Addison officially announced the disease. It happened back in 1855. Seventeen years later, the German scientist A. Birmer described B12-deficient anemia in much more detail. However, the discovery of this disorder belongs to the English doctor, so B12-deficiency anemia is rightly called Addison's disease. In some sources, you can also find the term "Addison-Birmer's disease."

In the 20s of the last century, a real breakthrough occurred in the treatment of this disorder. While earlier, the disease was considered incurable. The fact that you can get rid of B12-deficiency anemia was told to the world by doctors from America: George Will, William Murphy and George Minot. Moreover, for a cure, it will be necessary to eat raw liver. For their discovery in 1934, scientists received the Nobel Prize. They proved that B12 deficiency anemia develops in people whose stomach is not able to secrete substances that would help vitamin B12 be absorbed from food. IN modern medicine Megaloblastic anemia, which is characterized by a lack of cyanocobalamin (the name of vitamin B12), doctors call B12-deficiency anemia. In addition, B12-folate deficiency anemia is distinguished, which is accompanied by a deficiency of folic acid (vitamin B9).

B12-deficiency anemia manifests itself as a violation of the function of hematopoiesis, against the background of vitamin B12 deficiency, from which the nervous system and digestive organs suffer.

According to statistics, cyanocobalamin deficiency anemia occurs in 0.1% of people living worldwide. If we separately consider older citizens, then among them about 1% of the total number of pensioners are ill. Sometimes vitamin B12 deficiency develops during pregnancy and resolves on its own after childbirth.

B12 deficiency anemia in numbers and facts:

In people over the age of 70, in 10% of cases there is a lack of vitamin B12. However, not everyone develops symptoms of anemia.

No animal or plant on earth can produce vitamin B12 on its own.

Vitamin B12 is produced only by bacteria that are located in lower section intestines of animals and humans. Vitamin from this part of the intestine cannot get into the blood, since the absorption of all substances into the blood occurs in the small intestine.

The picture below shows blood in B12-deficiency anemia:

Vitamin B12 and folic acid deficiency: what is the danger

B12-deficiency anemia and its variety, accompanied by a lack of folic acid in the body, are megaloblastic anemias, which lead to a disruption in the production of DNA responsible for cell proliferation. With anemia, cells of the bone marrow, skin, and mucous membranes of the gastrointestinal tract suffer more than others.

The "affected" cells are hematopoietic cells. They are also called hematopoietic cells. If this process is disturbed, then the patient develops anemia. Often, in addition to anemia, which is accompanied by a drop in the level of red blood cells and hemoglobin in the blood, people develop a shortage of other blood cells: platelets, neutrophils, monocytes, reticulocytes.

All violations of the hematopoietic system have a close relationship with each other. The explanation for this is as follows:

In order for the body to form active folic acid, vitamin B12 is needed.

In turn, folic acid is needed for the production of thymidine - this is an important component of DNA. If there is not enough vitamin B12 in the body, then the synthesis of thymidine stops, which leads to the formation of defective DNA. It quickly collapses, and the cells of tissues and organs die.

If at least one of the links in this chain is broken, then blood cells and cells of the digestive tract will not be able to form normally.

Vitamin B12 is responsible for the breakdown and production of certain fatty acids. If it is deficient in the body, then this leads to the accumulation of methylmalonic acid, which is detrimental to neutrons. Its excess reduces the production of myelin, which is part of the myelin sheath that covers nerve fibers and is responsible for transmitting impulses through nerve cells.

Folic acid does not affect the breakdown of fatty acids, it is not required to provide normal operation nervous system. If a person suffering from vitamin B12 deficiency is prescribed folic acid, then for some time it will stimulate the production of red blood cells, but when it accumulates in the body in too much, this effect will end. Excess folic acid will stimulate vitamin B12 to start the process of erythropoiesis. Moreover, even that vitamin B12, which is intended for the breakdown of fatty acids, will be forced to work. Naturally, this will negatively affect the nerve fibers, the spinal cord (the processes of its degeneration will be launched), the functional sensitivity and motor function of the spinal cord will be disturbed, and combined sclerosis may develop.

So, low level vitamin B12 in the body entails a violation of the growth of blood cells and provokes the occurrence of anemia. Also, vitamin B12 deficiency negatively affects the functioning of the nervous system. Folic acid negatively affects the process of division of hemocytoblasts, but the human nervous system does not suffer.

What is the mechanism of development of B12 deficiency anemia?

So that vitamin B12 can be absorbed from food by the organs digestive system, it is necessary that he be "helped" by the internal factor of Castle, which is a special enzyme. This enzyme is produced by the lining of the stomach.

The process of absorption of vitamin B12 in the body occurs as follows:

Once in the stomach, vitamin B12 finds protein-R, combines with it and in such a bundle enters the duodenum. There, the vitamin will be affected by enzymes that break it down.

IN duodenum vitamin B12 detaches protein-R from itself and free state meets the internal factor of Castle, forming new complex.

This new complex travels to the small intestine, searches for receptors that respond to intrinsic factor, binds to it, and is absorbed into the bloodstream.

Once in the blood, vitamin B12 is attached to the transport protein (transcobalamin I and II) and sent to the organs that need it, or to the depot. The place of reserve is the liver and bone marrow.

If vitamin B12 does not combine with intrinsic factor in the duodenum, it will simply be brought out. Deficiency of the intrinsic factor will lead to the fact that 1% of vitamin B12 enters the bloodstream, and the rest of it simply disappears without benefiting the person.

Normally, a healthy person should receive 3-5 micrograms of vitamin B12. It should be at least 4 g in the reserve reserves of the body. Therefore, provided that vitamin B12 does not enter the body, or ceases to be absorbed by it, its acute deficiency will develop only after 4-6 years.

Folic acid reserves are designed for a shorter period, this vitamin will be completely removed from the body after 3-4 months. Therefore, if a woman has not previously suffered from a vitamin B12 deficiency, then during pregnancy, even with a lack of it, she is not at risk of anemia. While the level of folic acid can decrease significantly, especially if there were no reserves in the body, and the woman eats few raw vegetables and fruits. The development of folic acid deficiency anemia in this case is quite likely.

The source of vitamin B12 is animal products, and the body can “get” folic acid for itself from almost any food. However, vitamin B12 tolerates heat well, while folic acid is rapidly destroyed. It is enough to boil the product for 15 years so that vitamin B9 completely disappears from it.

Causes of vitamin B12 and folic acid deficiency

Vitamin B12 deficiency in the body can be caused by the following reasons:

Insufficient intake of vitamin B12 from food. Due to various circumstances, a person may not eat meat, liver, eggs, dairy products. Vitamin B12 deficiency is often seen in people who eat exclusively vegetable food. As a rule, when balanced diet at healthy person anemia with a lack of vitamin B12 does not develop.

Diseases in the body that are caused by vitamin B12 deficiency have several medical names:

Medical history

The history of the disease of this species goes back to 1855, when the British doctor Addison gave detailed explanation of this disease, and in 1872 the German doctor Birmer supplemented the description of this pathology, and after that the lack of vitamin B12 began to be characterized as anemia, which is malignant in nature.

At that time, there were no methods for correctly diagnosing pathology, as well as qualified treatment, so hemoglobin dropped to 30.0 g / l and below, a person fell into a coma, which led to death.

It was not until the 20th century, in 1926, that a discovery was made, which was evaluated by the Nobel paremia, that vitamin B12 deficiency anemia is the inability of the stomach organ to produce a specific enzyme that helps absorption this vitamin from the digestive system.

ICD code 10

By international classification diseases of the tenth revision of the ICD-10 - this pathology belongs to class D 51, "Vitamin-B12-deficiency anemia".

Megaloblastic type of anemia

Pernicious (with B12 deficiency) anemia refers to the megaloblastic form of anemia, and is rarely combined with another megaloblastic anemia - folate deficiency.

Megaloblastic anemia is a rather rare form of pathology in which there is a deviation from the normal absorption of the digestive system of folic acid, vitamin B12 and cyanocobalamin substances.

As a result, there is a lack of B vitamins in the body: B12 and B9.

Megaloblasts are modified red blood cells that are synthesized in DNA and RNA cells. Megaloblasts appear in bone marrow cells as a consequence of a deviation in the synthesis procedure. This manifests itself in morphological modifications of the composition of cells.

What do the 2 types of megaloblastic anemia have in common and how do they differ?

The B vitamins are in human body with products of animal origin. In the stomach, they bind to gastromucoprotein and are absorbed in the stomach. small intestine. For the normal functioning of the body, the daily dosage of vitamin B12 should be 7 mcg.

The supply of this vitamin is in the liver - no more than 5 mg. The body's need for folic acid- about 100 mcg per day. The supply of vitamin B9 is up to 10 mg.

Violations in the synthesis of DNA molecules lead to the inability of these bone marrow cells to rapidly divide.

These cells include:

The membranes of the mucous system;
Systems digestive tract;
bone marrow cells;
Skin cells.

Cells of the hematopoietic system (hematopoietic) are cells that multiply faster than others. Therefore, indicators (reduced levels of erythrocytes and low coefficient hemoglobin) in the hematopoietic system characterize the first manifestations of megaloblastic anemia.

With the manifestation of anemia, such signs of the hemolytic nature of anemia are often observed:

Pathology thrombocytopenia - a decrease in the index in the blood of platelets;
Neutropenia disease - a reduced rate of neutrophilic type leukocytes;
Blood pathology agranulocytosis - a decrease in the index of leukocytes;
The disease monocytosis is a decrease in the molecules of monocytes;
Decreased synthesis of reticulocytes.

The difference and relationship between folate deficiency B9 anemia and vitamin B deficiency - B12:

Vitamin B12 is involved in the synthesis of folic acid molecules. The acid is part of the thymidine molecule, which is a component of the DNA molecule. At well-coordinated work these components, and with their required amount for a biochemical reaction, normal formation of blood cells and cells occurs for the normal functioning of the digestive tract;
The functional duties of vitamin B12 are to help in the synthesis and breakdown of fatty acids in the body. With a deficiency of cyanocobalamin molecules, a violation occurs in a coordinated reaction, and methylmalonic acid is deposited, which has a detrimental effect on the atoms of neurons. There is also a decrease in the synthesis of myelin, which forms a sheath for the fibers of nerve cells.

Folic acid is not involved in the breakdown of fatty acids and is not involved in the formation of sheaths for nerve fibers.

With a deficiency of vitamin B12, the doctor prescribes taking drugs with folic acid, then it activates erythropoiesis, but only until given acid does not become abundant in the body.

With an overdose of folic acid, the following occurs:

Disorder in the nervous system;
Changes of a degenerative nature in the bone spinal cord;
Combined sclerosis with loss of motor functions;
Funicular type myelosis.

Symptoms of anemia

Symptoms of B12 deficiency anemia and folic acid (as well as its deficiency) are classified in the following areas in the manifestation of pathology:

Anemic syndrome in the hematopoietic system;
Gastroenterological symptoms - disorders in the digestive tract;
neurological nature;
Symptoms in violation of the structure of the brain.

The classification of the anemic direction is manifested in the following symptoms:

Severe circling of the head;
Weakness of the whole body;
state of fainting;
Rapid contraction of the heart muscle (sinus type of tachycardia);
Dyspnea;
Pain in the chest;
Noise in ears;
Uncertainty in the perception of objects from the organs of vision;
Yellow tint of the skin (hue gives high level bilirubin in the blood).

Gastroenterological symptoms:

Syndrome of a neurological nature:

Birmer anemia - Addison-Birmer disease;
Slight tingling in the fingers and toes;
Constant feeling of chills;
Unsteadiness in movement;
Numbness in the lower limbs;
Lethargy of the legs;
The sensitivity of the skin disappears;
Difficulties in movement.

Deviations in the brain of this type of anemia, as well as disorders in the spinal cord:

Lack of memory;
hallucinations;
Lost state;
overexcitation;
Feeling constantly irritated;
Coma state;
Muscle cramps.

With anemia, a lack of vitamin B12, as well as with iron deficiency anemia, there are signs of severe hypoxia in the body:

Forms of development

The pathogenesis of anemia with insufficient disappearance of molecules of B vitamins, namely B12 and B9, into the body, which affects the level of hemoglobin molecules, which is located in red blood cells and is responsible for delivering oxygen atoms to all cells of the human body.

Anemia is divided into forms according to the index of hemoglobin molecules in the blood plasma.

The lower the hemoglobin index, the more severe the course of deficient pathology:

Light stage of development and course - hemoglobin index from 90.0 to 110.0 grams per liter of biological fluid;
Moderate severity - hemoglobin index from 70.0 to 90.0 grams per liter of blood plasma;
The severe stage of the course of this pathology - the coefficient of red pigment does not exceed 70.0 and decreases even below this indicator.

Normative indicators of the amount of hemoglobin in the blood in men - 130.0 - 160.0 g / l.

In women, the standard is 120.0 - 135.0 g / l.

B12-deficient anemia in children

To the main types of etiology of anemia with a lack of this vitamin in childhood are:

Changes in the microflora of the baby;
Not enough of this vitamin in the body of a child;
The presence of worms in the body;
The Castle factor during the period of intensive growth of the child.

Clinical indicators and manifestations of this type of pathology are similar to the symptoms of an adult, but there are characteristic symptoms in the child's body:

Severe dental caries from a young age;
Persistent stomatitis that begins in infancy;
Changes in the eyeball;
Changes in the nail plate - the plate is weak, brittle;
Violation of attention and intelligence - reduced school performance.

In the transcripts of the results of the clinical laboratory, the following values are:

Low hemoglobin index;
Reduced number of erythrocyte molecules;
Chromaticity index increased - more than 1.5;
In the molecules of erythrocytes, Kebot rings, as well as Jolly bodies, are present in such an amount that they are determined by analysis;
Reticulocytes are increased;
The index of lymphocytes is increased;
Platelets, as well as leukocytes - in small quantities;
In biochemistry, megaloblasts were found as part of a bone marrow puncture.

To help laboratory parameters, to establish a diagnosis of B12 deficiency anemia, an instrumental method for diagnosing a child's body is used:

The treatment of anemia in a child with B12 deficiency is to saturate the cells of the body with these vitamins. Medication vitamin course 15 calendar days. A high-calorie diet is also prescribed, in which there are foods with vitamin B12 and folic acid.

To replenish vitamin molecules in the body, it is prescribed drug preparation Cyanocobalamin. Initial dosage this tool- this is from 30.0 mcg to 50.0 mcg, with daily intake. This drug administered orally by injection.

The dosage is calculated by the attending doctor individually. The drug course is carried out in children under the strict supervision of a specialized specialist.

After the end of the course of treatment for preventive purposes and as maintenance treatment, 100.0 - 250.0 mcg 2 times a month.

Normative indicators of vitamin cyanocobalamin in the child's body:

Etiology

Vitamin B12 benefits the body when it is absorbed in the intestines. For this absorption reaction to occur, an enzyme is needed that is produced by the internal parts of the stomach - the Castle enzyme.

Without the formation of an enzyme, the vitamin B12 molecule is excreted outside the body without entering it for biochemical processes, through feces.

With B12 deficiency anemia, the Castle enzyme is not synthesized in the stomach, so the vitamin that is ingested in food is also not absorbed through the intestines.

In liver cells there is a supply of vitamin B12 molecules, which, with reasonable use, can be enough for 5 calendar years. As a result, anemia occurs after a while, after the stomach has ceased to produce this factor.

Castle factor deficiency is main reason pathology of B12 deficiency anemia.

Causes

The lack of cyanocobalamin is caused by the following factors:

Low Vitamin B12 Foods (Main Cause). Cyanocobalamin is found in animal products. Vegetarianism is a major risk factor for dietary B12 deficiency;
Impaired function of the Castle factor. With atrophy of the cells of the mucous membranes, the functionality of the internal factor does not manifest itself, or it decreases. This reason atrophy is genetic, congenital, with gastritis of the stomach, when the stomach is exposed to toxic elements (intoxication of the body), as well as exposure to the antibody factor;
Absence or partial loss of receptors that are necessary for the factor. This pathology develops with Crohn's disease, with neoplasms in the small intestine (cancer), with tuberculosis disease, with intestinal infantilism, and also with enteritis in chronic stage course of pathology;
Absorption of B12 molecules by worms and pathogenic microorganisms . It is necessary to treat this pathology with therapy against competitors that absorb cyanocobalamin;
With pathology of the pancreas. With this pathology, there is a deviation in the breakdown of the protein protein, which is the connecting link of the factor with vitamin B12;
genetic hereditary congenital anomaly - this is a reduced indicator in the body of the synthesis of transcobalamin, which leads to a disruption in the transport of cyanocobalamin molecules to bone marrow cells.

For folic acid deficiency anemia, the etiology with food is not suitable, because vitamin B9 is present in every plant and animal product. This vitamin of group B does not need the help of a factor and is absorbed independently.

Folio deficiency problems begin when the following causes appear in the body:

Poor diet;
Small food intake;
Starvation;
Anorexia;
The elderly age of the patient, at this age there is a difficult digestibility of vitamins from food;
Reception of alcoholic beverages. At alcohol addiction, a person cannot eat fully;
Pathology in the intestines, which does not allow vitamins to be absorbed by the body;
Crohn's disease;
Pathology of celiac disease;
Malignant neoplasms in the intestines;
Increased need for vitamin B12 and folic acid in a woman during the prenatal formation of a baby. In pregnant women, dietary intake of these products should be increased to avoid fetal hypoxia;
Increased consumption of B9 in the pathology of psoriasis;
When taking anticonvulsants medications, vitamin B9 and B12 deficiency occurs.

When taking medication, there is a deficiency of vitamins

Diagnostics

When making this diagnosis - B12 deficiency anemia, the doctor first of all collects an anamnesis during the diagnosis - when and under what circumstances did the pronounced symptoms of anemia appear, with its weakness and manifestations of pathology in the process of digestion.

It is also necessary to find out if the patient has diseases that occur in the chronic stage, as well as to provide information about possible genetic hereditary congenital diseases.

After the anamnesis, the patient's skin is examined, the severe symptoms on the skin.

The doctor also measures the index blood pressure(with anemia, the pressure is lowered), as well as the heart pulse (often the pulse is rapid).

After this examination, based on external signs, appointed laboratory diagnostics(blood test), as well as a list of instrumental studies:

General blood analysis;
Biochemical analysis of blood composition;
Urine for general analysis;
Puncture of the bone marrow;
Electrocardiography (ECG);
Ultrasound of the liver and spleen;
Ultrasound of the intestine;
Ultrasound of the stomach.

When decrypting general analysis the whole picture of the blood is visible, the indicators of each element in its composition. By this analysis with vitamin B12 deficiency anemia, a decrease in erythrocyte molecules is seen, as well as a reduced synthesis of reticulocytes.

The level of red pigment (hemoglobin) is reduced, platelets are also reduced, which provokes hypoxia. Color increases with anemia and reaches more than 1.50 (at a rate of 0.860 - 1.050).

During the analysis, the presence of proteins in the urine, and the possible detection of concomitant pathologies, are observed.

Biochemistry is the most valuable analysis for detecting deviations in the structure and composition of the blood.

As part of biochemistry, the following indicators are detected in anemia B12 deficient:

Often elevated with anemia cholesterol index;
The presence of creatinine;
Glucose in the blood;
Uric acid;
Electrolyte indicators of calcium, potassium and sodium molecules;
Lactate dehydrogenase is an enzyme in the liver cells that promotes the absorption of iron by cells. Indicator of biological reactions for the synthesis of erythrocytes and hemoglobin;
B vitamins are reduced. The B12 index is low.

The blood hemogram shows the hematocrit number, the percentage of all types of leukocytes - the leukocyte formula is established.

Myelogram, or indicators of bone marrow puncture, determines the level of production of erythrocyte molecules, as well as megaloblasts in the blood, which confirms the megaloblastic nature of hematopoiesis in the human body.

Instrumental technique determines deviations from normative indicators the structure of internal organs, and also reveals violations in their functionality.

Therapy for B12 deficient anemia

Therapy for B12 deficiency anemia begins with treating the underlying cause of the deficiency, which is medical therapy for the destruction of helminths, normal and balanced nutrition, as well as surgical technique treatment of a malignant neoplasm.

For complex treatment anemia, the drug B12 is injected into the body at a dosage of 200.0 mcg - 250.0 mcg per day. The drug is administered by injection into muscle tissue, or by injection under skin covering human body.

If anemia has affected the centers of the nervous system, then the scheme drug therapy this is the first 3 calendar days dosage of vitamin 1000.0 mcg per day, and subsequent treatment according to the prescribed scheme. The treatment regimen, as well as the dosage of B12, is prescribed by the attending doctor and depends on the degree of deficiency in the body of vitamin B12, which caused anemia.

After stabilization of this vitamin in the body, in order to maintain it at a normal level, B12 preparation is used in the treatment at 100.0 mcg - 200.0 mcg 1 time in one calendar month.

Clinical guidelines for rapid replenishment of erythrocytes in the blood - the introduction of an intravenous erythrocyte mass, which can restore the destroyed balance in the composition of the blood plasma of the human body.

Complicated B12 deficiency anemia

If not taken emergency measures in treatment, the consequences of this type of anemia can be quite serious and pose a threat to the life of the patient:

Coma in which the patient does not respond to external stimuli. Coma can occur from cerebral hypoxia with anemia and can cause death;
Severe degree of anemia, which significantly worsens the condition of the body and triggers irreversible consequences in it. This degree occurs when the hemoglobin index is lower than 70.0 g/l;
Funicular myelosis- This is a lesion of the cells of the spinal cord, as well as the nerve endings of the peripheral parts of the body. The defeat of the connecting nerve fibers of the spinal cord with the centers of the brain, as well as with all the internal organs and systems of the body. With these disorders, the sensitivity of the limbs decreases, unsteadiness in movements appears, and the period of progression of myelosis - the sensitivity disappears altogether and the person is not capable of independent movement;
Destruction of the cells of internal organs, which subsequently leads to the non-functionality of this organ (the heart, liver and spleen cells, digestive tract, kidney cells, respiratory system are affected).

If healing process started too late, then complications in the nervous system cannot be restored. These destructions are irreversible.

Prevention

Prevention is mainly aimed at improving B12 intake through foods:

The use of animal products with a large amount of B12 in them;
Timely treatment of pathologies that can cause B12 deficiency and provoke anemia;
After surgical intervention on the organs of the digestive tract, take drugs to maintain the level of this vitamin.

Diet for this form of anemia

A balanced diet is especially necessary during the period of intrauterine development of the child, since the formation of the baby depends on the intake of vitamins in the body of a pregnant woman, as well as the occurrence of intrauterine pathologies that will be revealed after birth.

During pregnancy, the need for vitamin B12 increases by 50.0%.

products	amount of B12 in mcg
veal liver	60.0
Liver of a young piglet	30.0
chicken liver	16.0
mackerel fish	12.0
rabbit meat	4.30
veal	2.60
perch fish	2.40
· pork	2.0
· eggs	0.40
fat sour cream

With B12 deficiency anemia, a diet is used - table number 11. This diet should increase the content of protein and vitamin B12 in the body. The method of food preparation is conventional. You need to eat 5 times a day.

Energy value of diet number 11:

Proteins - 110.0 grams - 130.0 grams (60.0% animal origin, 40.0% vegetable);
Fats - 100.0 grams - 120.0 grams (80.0% - animals and only 20.0% vegetable);
Carbohydrates - 400.0 grams - 450.0 grams;
Salt - no more than 15.0 grams;
Purified water 1.5 liters.

foods useful for B12 deficiency anemia	prohibited products
calf, pork, chicken liver	· milk
· salo	muffin
· butter	confectionery products
mackerel fish	· tea
meat: veal, rabbit, pork	beverages containing caffeine
· eggs	· Coca Cola
fat sour cream	· alcoholic drinks
fat-free cottage cheese	Do not use vinegar in cooking
· hard cheese	sugary carbonated drinks
soft cheese
legumes: peas, lentils
vegetables: carrots, potatoes, cabbage, beets, tomatoes
fruits of all varieties
berries of all kinds
green vegetables are rich in iron
garden greenery
mineral water

Life prognosis for B12 deficiency anemia

Favorable prognosis	Unfavorable prognosis
with early treatment	with late therapy
· indicators in peripheral blood return to normal in 45 - 50 calendar days.	Pronounced anemia, which is difficult to treat.
Hemoglobin returns to normal within 30 - 60 calendar days.	Symptoms of damage to the centers of the nervous system, which is not restored.
B12 index is kept within the normative framework and anemia does not show its harmful effects on the body.	The body does not perceive drug B12, which is fraught with an anemic type of coma.
	With the genetic form of anemia, in most cases it is impossible to achieve a complete cure. Lifelong maintenance therapy in 70.0% of these patients.