home Auditorium 8 B12 anemia symptoms. Treatment of b12 deficiency anemia. Disease severity

B12 anemia symptoms. Treatment of b12 deficiency anemia. Disease severity

Vitamin B12 belongs to cobalamins. Its intake into the body is ensured 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 supply are enough to live up to 5 years. Due to the rich variety of foods containing vitamin B12, anemia rarely develops due to insufficient intake from food. Typically, B12 deficiency anemia is caused by an absorption problem or competitive use of the vitamin cobalamin during helminthic infestations.

Important! Young people who consider themselves strict vegetarians should be suspicious of B12 deficiency anemia.

Chronic deficiency of vitamin B12 leads to persistent disruption of thymidine formation. Pathological, megaloblastic hematopoiesis develops, in which red blood cells are increased in size.

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 the clinical picture of B12-deficiency anemia, there are 3 main syndromes:

anemic;
gastrointestinal disorders;
neurological.

Anemic syndrome

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

Red blood cells are oval, large - volume up to 150 with a normal volume of 80-150 fl. Jolly bodies and Cabot rings are often found - remnants of nuclei.

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

Inferiority of red blood cells 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, first of all, anemia manifests itself as symptoms on their part. Among the patients' complaints, nonspecific ones predominate:

weakness with drowsiness during the day and insomnia at night;
rapid fatigue;
decreased ability to work;
memory impairment;
headache;
muscle weakness.

To manifestations muscle weakness This includes both rapid fatigue when walking and difficulty swallowing dry food and an endoscopic probe. This is important to consider when performing esophagogastroduodenoscopy on a patient with suspected anemia.

Decreased work capacity and memory impairment are directly related to brain hypoxia. Their aggravation is noted in the presence of other 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 blood vessels worsen cognitive disorders. Vascular tortuosity due to osteochondrosis cervical spine spine in elderly patients age group increases hypoxic headaches.

Anemic syndrome objectively

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

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

A decrease in hemoglobin and anemic hypoxia, as expected, have an adverse effect on the trophism of those tissues whose ability to regenerate is above average. These are epithelial cells of the skin, its adnexal structures and the mucous membrane of the gastrointestinal tract. Hemoglobin deficiency leads to atrophic processes in these tissues.

Clinically it is:

You can often notice a slight yellowing of the sclera. This is due to the faster destruction of large red blood cells in B12 deficiency anemia.

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

heartbeat;
shortness of breath on exertion.

Objectively it is possible to identify:

dullness of heart sounds,
tachycardia more than 90 per minute,
promotion 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 increased attacks of chest pain, worsening shortness of breath, swelling and, in general, progression of heart failure.

Younger patients, especially women, have excellent compensatory capabilities and often do not even realize that they have low hemoglobin levels because they do not experience any symptoms.

Gastrointestinal disorders

Atrophic changes in the gastrointestinal tract have already been partially affected 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 tongue mucosa. Bright red areas of inflammation along the entire upper surface of the tongue cause pain and a burning sensation, especially when in contact with acidic foods– fruits, juices. Most often, the lesions are located along the edges of the tongue and at the tip. In the most severe cases 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, and soft palate. Over time, the foci of inflammation will heal with the formation of a smoothed surface. The tongue papillae atrophy, leaving a red, shiny, “varnished” tongue.

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

Atrophic changes in the stomach in the clinic are manifested:

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

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

Important! Often, patients with B12 deficiency anemia have a slight enlargement of the liver and spleen. As a rule, these changes can only be detected by ultrasound examination and they do not cause discomfort.

Neurological syndrome

Damage to the nervous system is very typical for vitamin B12 deficiency, although the mechanism is not completely clear. There is probably a connection with impaired fatty acid metabolism. 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-deficiency anemia, pathological fatty acids are synthesized that differ from normal ones. Such organic substances do not lead to normal myelin synthesis, which means the structure of the nerve fiber is disrupted.

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

paresthesia;
sensory disturbance;
feeling of cold, “cotton legs”, tingling pins;
numbness in the limbs.

With further development of the disease without external supply of vitamin B12, the symptoms worsen due to damage spinal cord:

gait disturbance, uncertainty when walking;
weakness in the limbs;
Lhermitte's sign;
hearing impairment, vision impairment, taste sensations;
dysfunction of the pelvic organs.

An objective neurological examination reveals in the patient:

disturbance of sensitivity - pain, tactile, deep, vibration;
ataxia when walking;
sharp instability in the Romberg position;
increased, decreased, or asymmetry of knee reflexes;
stop clonus;
positive Babinski sign.

First of all, neurological disorders affect the lower extremities. Hands are affected much less frequently and less severely. Sensory disorders progress from the loss of superficial - tactile, temperature, pain - to the disappearance of deep sensitivity - vibration, muscle-articular feeling.

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

Often, those groups of patients in whom neurological disorders come to the fore first turn to a neurologist on an outpatient basis and may long time remain without a diagnosis.

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

Today, thanks to good diagnostics and replacement therapy, we almost never see the most severe forms of funicular myelosis: with complete areflexia and persistent paralysis.

Video - Vitamin B12 deficiency

Candidate of Medical Sciences, Associate Professor V.A. Tkachev

IN 12 -DEFICIENCY ANEMIA

IN 12 -deficiency anemia is a severe progressive anemia that occurs when the absorption of vitamin B12 supplied with food is impaired, due to reduced (or absent) secretion of internal gastric factor.

The nomenclature of the name of this disease is different, and it is often referred to in the literature as pernicious anemia (perniciosa - fatal), malignant disease Addison-Birmer (by the name of the authors), as well as megaloblastic anemia (by the type of hematopoiesis).

People over 40 years of age are affected. Women are susceptible to this disease twice as often as men and, above all, over the age of 50–60 years. There are known cases of B 12 deficiency anemia in children fed goat milk or powdered milk formulas. The incidence ranges from 20 to 60 cases per 10,000 population.

Historical reference. The first description of this disease was made by Coombs in 1822 and called it severe primary anemia. In 1855, physician Addison described this suffering under the name "idiopathic anemia." In 1872, Birmer published the results of an observation of a group of patients suffering from progressive pernicious anemia. However, the possibility of curing this disease arose only in 1926, when Minot and Murphy discovered a pronounced healing effect from the purpose of raw liver.

Three years later, the American physiologist Castle showed that raw meat, liver, yeast treated with gastric juice healthy person, have the property of causing remission in a patient with pernicious anemia. Castle's research formed the basis of the concept according to which, as a result of the interaction of two factors - external, contained in raw meat, raw liver, yeast, and internal, produced by the gastric mucosa, an anti-anemic compound is created, which ensures the physiological maturation of bone marrow cells.

The nature of the external factor has been established - it is cyanocobalamin (vitamin B 12 ) . Vitamin B 12, according to the body's needs, is used not only for hematopoiesis in the bone marrow, but also for the normal functioning of nervous tissue and digestive organs.

A complex compound consisting of peptides (appearing during the conversion of pepsinogen to pepsin) and mucoids (secreted by accessory cells of the gastric mucosa) was named gastromucoprotein or intrinsic Castle factor. The role of the internal factor (gastromucoprotein) is to form a complex with vitamin B 12, which ensures the transport of cyanocobalamin through the intestines and prevents its decay and inactivation. Resorption (absorption) of vitamin B 12 occurs in the ileum. Its further entry into the portal bloodstream is carried out with the help of protein carriers: transcobalamin-1 (-globulin) and transcobalamin-2 (-globulin), which form a protein-B 12 vitamin complex that can be deposited in the liver.

Etiology. The leading factor in the etiology of the disease is endogenous vitamin B deficiency 12 , arising as a result of a violation of its absorption due to the cessation of secretion of the internal factor (gastromucoprotein).

Malabsorption of B 12 may occur as a result of damage to the gastrointestinal tract by inflammatory or malignant process, after subtotal or total removal of the stomach, after extensive resection of part small intestine . IN in rare cases Pernicious anemia develops with normal secretion of intrinsic gastric factor and is caused by congenital absence of transcobalamin-2, with which vitamin B 12 binds and is delivered to the liver, or as a result absence of a protein acceptor in the intestine(perceiving) vitamin B 12, necessary for the entry of cyanocobalamin from the intestine into the bloodstream. In some cases there is genetic development factor In 12-deficiency anemia due to a congenital disorder in the production of gastric factor or the presence of antibodies against parietal cells.

The following factors can also lead to B 12 deficiency anemia:

impaired absorption of B 12 in the small intestine as a result chronic enteritis or celiac enteropathy;

competitive absorption of vitamin B 12 in the small intestine wide tapeworm or microorganisms;

complete exclusion of food of animal origin;

long-term decreased exocrine activity of the pancreas, the consequence of which is a violation of the breakdown of protein R, without which vitamin B 12 cannot contact mucopolysaccharide;

long-term appointment some medications: methotrexate, sulfasalazine, triamterene, 6-mercaptopurine, azathioprine, acyclovir, fluorouracil, cytosar, phenobarbital, etc.

Pathogenesis. Hematopoietic disorders with B 12 deficiency anemia are characterized by megaloblastic type for all three blood lineages: erythroid, granulocytic and megakaryocytic. There is ineffectiveness of red hematopoiesis: impaired differentiation of erythroid cells and the appearance of abnormal cells such as promegaloblasts, megaloblasts (large cells with basophilic cytoplasm and a nucleus containing nucleoli).

As a result of defective metabolism of folic acid (due to B12 deficiency), which is involved in the formation of DNA, cell division is disrupted. The consequence of this is pronounced intramedullary death of erythroid elements and a decrease in the number of erythrocytes in the periphery.

Due to the failure of the cellular elements of the blood, it is strengthened hemolysis, which is manifested by hyperbilirubinemia, urobilinuria, and an increase in stercobilin in the feces.

Pathological changes are characterized by general anemia, yellowness of the skin and mucous membranes, fatty degeneration of the myocardium, liver, and kidneys. The bone marrow is juicy and crimson in color due to hyperplasia.

On the part of the digestive organs, atrophic changes in the papillae of the tongue (their smoothness), inflammatory changes (glossitis), aphthous rashes, cracks (Gunter's glossitis), as well as atrophy of the mucous membrane of the cheeks, palate, pharynx, and esophagus are detected. The greatest atrophy is recorded in the stomach, which is characterized by thinning of its walls and the formation of polyps. The intestinal mucosa is also atrophied. The spleen is usually normal sizes or increased.

Hepatomegaly is not expressed. Hemosiderosis is detected in the liver, spleen, kidneys (rusty tint on the section) as a result of hemolysis of red blood cells.

Dystrophic changes are observed in the nerve fibers of the tongue (nerve plexuses of Meissner and Auerbach), as well as in the posterior columns of the spinal cord (focal swelling with disintegration of myelin nerve fibers).

Clinical manifestations In 12-deficiency anemia, they often develop gradually: weakness, malaise, dizziness, dyspeptic disorders, tinnitus, and a tendency to obesity increase. Rarely, the disease begins acutely, with a rise in body temperature to 38 C and severe weakness.

Anemic syndrome characterized by lethargy, pallor of the skin with a lemon-yellow tint, and sometimes (in 12% of patients) subicteric sclera. In the peripheral blood, anemia is recorded, more often (58%) severe, with an increase in the color index to 1.4, a decrease in reticulocytes to 0.5 - 1.0% (in a third of patients - reticulocytosis), poikilocytosis and the presence of Jolly bodies and Cabot rings in red blood cells. Leukopenia, lymphocytosis, but thrombocytopenia are often detected.

In the bone marrow, signs of the megaloblastic type of hematopoiesis are determined.

Gastric dyspepsia syndrome(37.% of observations) is manifested by belching, nausea, loss of taste, decreased appetite up to aversion to food, heaviness in the epigastrium, sometimes dysphagia, a burning sensation of the tongue and oral mucosa. EGDS reveals atrophic changes in the mucous membrane of the esophagus and stomach.

Intestinal dyspepsia syndrome characterized by unstable stools and weight loss.

Glossitis manifested by the presence of a “scalded” (red) or “varnished” tongue with cracks. Pain in the tongue is observed in 30% of patients with B 12 deficiency anemia.

Jaundice syndrome occurs in 50% of patients and is manifested by subicteric sclera and hyperbilirubinemia.

Funicular myelosis syndrome(sensory ataxia - impaired coordination of movements) is observed in patients with B 12 -deficiency anemia in 11% of cases and develops as a result of impaired proprioceptive sensitivity due to atrophic processes in hind horns spinal cord. There may be other symptoms of damage to the nervous system: paresthesia, dysfunction of the pelvic organs, decreased reflexes.

Intercostal neuralgia syndrome occurs significantly more often (up to 30% of cases) than signs of funicular myelosis, manifests itself as neuralgic pain along the intercostal spaces and is also caused by functional insufficiency of the nerve tissue of the conductors.

Some patients experience damage to the cranial nerves (visual, auditory, olfactory), and the presence of symptoms of spinal paralysis (spastic paraparesis with increased reflexes and clonus). Central scotoma (visual field defect) with loss of vision may be detected.

Changes from the side central nervous system may appear psychomotor agitation syndrome(manic state with euphoria or depression syndrome with impaired memory and criticism - megaloblastic dementia).

Cardiac syndrome(in 15–20% of cases) is characterized by shortness of breath, palpitations, pain in the heart area, myocardial dystrophy. On auscultation of the heart, a functional anemic murmur is heard. The ECG shows a decrease in ST and an expansion of the ventricular complex.

Edema syndrome occurs in B12-deficiency anemia in 80% of cases and is manifested by peripheral edema, which can reach the degree of anasarca, as a result of circulatory failure.

Liver enlargement ( hepatomegaly syndrome) occurs in 22% of patients, enlarged spleen ( splenomegaly syndrome) in 10% of cases.

With untreated B 12 deficiency anemia may develop pernicious coma syndrome, manifested by cerebral ischemia, loss of consciousness, areflexia, drop in body temperature, decrease in blood pressure, vomiting, involuntary urination.

With the aim of diagnosis of the disease a thorough hematological examination is carried out, including the study peripheral blood pictures, sternal punctate and serum factors involved in hematopoiesis. An accurate diagnosis is very important because... these patients in some cases require lifelong treatment.

Hypersegmentation of neutrophils(more than five nuclear lobes) of peripheral blood is the first hematological pathology in megaloblastic status. In a healthy person, up to 2% of hypersegmented neutrophils can circulate in the blood. In patients with megaloblastic anemia, the number of hypersegmented neutrophils exceeds 5%.

Bone marrow hematopoiesis is characterized by megaloblastic type, which is characterized by irritation of the red sprout and the appearance of megaloblasts. The bone marrow is hypercellular due to an increase in the number of nucleated red cells. As a result of impaired cell division, erythroid cells become very large ( megaloblasts). They are characterized by their large size, delicate structure and unusual arrangement of chromatin in the nucleus, asynchronous differentiation of the nucleus and cytoplasm.

In blood serum in patients with B 12 deficiency anemia increased concentration of bilirubin, iron, ferritin(iron-containing liver protein). Serum lactate dehydrogenase (LDH) activity is significantly increased and increases as the disease progresses. Level serum cyanocobalamin usually low, but may be normal.

Differential diagnosis held with folate deficiency anemia. Folic acid deficiency is usually observed in more at a young age, is not accompanied by atrophic changes in the gastric mucosa and neurological symptoms.

To exclude folate-deficiency anemia, a Schilling test is performed: vitamin B 12 is administered parenterally, which is determined in the urine in minimal quantities in case of B 12-deficiency anemia and in large quantities in case of folate deficiency anemia. It is important to consider that the administration of folic acid to patients with B12-deficiency anemia quickly contributes to the development of funicular myelosis.

It should be remembered that symptomatic megaloblastic anemia is caused by tumors of the stomach, small intestine and cecum, as well as helminthic infestation (helminthic B 12 deficiency anemia), which must be excluded when verifying the diagnosis.

It is necessary to differentiate with erythromyelosis(initial forms of manifestation of leukemia), which are accompanied by anemia occurring with increased content in the blood of vitamin B 12 and resistant to treatment with cyanocobalamin.

When carrying out differential diagnosis of B 12 deficiency anemia, it is necessary to establish its causes.

Treatment 12-deficiency anemia includes parenteral administration of vitamin B 12 or hydroxycobalamin (a metabolite of cyanocobalamin) in doses that ensure the satisfaction of daily requirements and doubling of depot reserves. Vitamin B 12 is administered 1000 mcg intramuscularly daily for two weeks, then once a week until hemoglobin levels normalize, after which they switch to administration once a month throughout life.

Oxycobalamin By pharmacological properties is close to cyanocobalamin, but compared with the latter it is quickly converted into an active coenzyme form in the body and remains in the blood longer. Oxycobalamin is administered at a dose of 500–1000 mcg every other day or daily. In the presence of neurological symptoms, it is necessary to administer the drug at a dose of 1000 mcg every two weeks for six months.

For funicular myelosis, massive doses of cyanocobalamin are prescribed, 1000 mcg daily for 7–10 days, then twice a week until neurological signs disappear.

Initiation of cobalamin therapy quickly improves the well-being of patients. Bone marrow erythropoiesis transforms from megaloblastic to normoblastic within 12 hours after administration of vitamin B12. Therefore, the administration of vitamin B 12 in a comatose state is an emergency measure. Reticulocytosis appears on days 3–5, its peak (reticulocytic crisis) is most pronounced on days 4–10. Hemoglobin concentration normalizes after 1–2 months. Hypersegmentation of neutrophils persists for up to 10–14 days.

Red blood cell transfusions indicated for the urgent elimination of symptoms of hypoxia.

After cobalamin therapy, it may develop severe hypokalemia. Therefore, during treatment with vitamin B 12, it is necessary to carefully monitor the potassium content in the blood and, if necessary, carry out replacement therapy.

Treatment with cobalamin should be prescribed to all patients after total gastrectomy. To prevent exacerbation, vitamin B 12 is administered once every two weeks, 100–200 mcg.

Clinical examination. Patients with B 12 deficiency anemia are subject to dispensary observation, during which the condition of peripheral blood is monitored 1-2 times a year, as well as treatment of diseases and conditions that led to the development of this type of anemia.

There are different regimens for maintenance therapy with cobalamins. Upon appointment cyanocobalamin Lifelong annual preventive three-week courses of 400-500 mcg every other day or monthly administration of 500-1000 mcg of the drug are recommended. Hydroxycobalamin It is recommended to take annual preventive courses of one injection per week (1 mg) for 2 months.

Cyanocobalamin deficiency in the body can occur as a result of the influence of many endogenous and exogenous factors:

External clinical signs of this type of anemia may not appear for a long time. Patients may complain of symptoms characteristic of many conditions and diseases, such as weakness, dizziness, tinnitus, increased fatigue, and decreased exercise tolerance.

Later, symptoms from the digestive system appear. Patients develop stomatitis and glossitis. Atrophy of the papillae of the tongue occurs, as a result of which its surface is smoothed, becomes shiny (“varnished”), and it acquires a bright red or even crimson color. This is one of the most specific signs pernicious anemia. It is also possible to develop gastroenterocolitis; patients may complain of nausea, vomiting, changes in taste preferences, abdominal pain, flatulence, constipation or diarrhea. In some cases, an increase in the size of the liver and spleen is observed.

At the same time, neurological symptoms appear; with cyanocobalamin deficiency, the peripheral nervous system is primarily affected. Patients feel weakness and numbness in the limbs, “crawling goosebumps”, as a result of which the fine motor skills, the gait becomes unsteady. With a further increase in vitamin B12 deficiency, disorders occur in the spinal cord and brain; patients may experience severe headaches, cramps in the limbs, color vision is impaired, and hallucinations and delusions may occur.

You can learn how to recognize a deficiency of vitamin B12 in the body from the popular TV show:

Treatment of pernicious anemia

Before starting treatment, it is necessary to identify the cause of vitamin B12 deficiency, since one of the conditions for successful treatment is the elimination of the factors that led to the development of anemia. If there is a helminthic infestation, you must contact an infectious disease specialist and undergo deworming. In cases where patients have structural changes organs of the digestive system or diseases in which the absorption of nutrients is impaired, treatment by a gastroenterologist is necessary.

Treatment of B12-deficiency anemia is carried out using cyanocobalamin injections, most often the drug is administered intramuscularly. Pathogenetic therapy begins only after examination and confirmation of the diagnosis, since even one injection of a vitamin can affect the result of a blood test.

Treatment regimens are selected individually by a hematologist. For B12-deficiency anemia without damage to the nervous system, doses of cyanocobalamin up to 500 mcg are used for treatment, usually injections are performed every other day or daily for 7-10 days. If the patient has neurological symptoms, higher doses of cyanocobalamin are used for treatment, daily dose can reach 1000 mcg. Then the administration of the drug continues in a maintenance dose once a week for a month. If further prevention of the development of B12-deficiency anemia is necessary, patients are given one injection of the vitamin once a month, the duration of treatment is determined by the doctor.

Diet plays an important role in restoring the body; patients need a complete diet rich in vitamins, foods that irritate the mucous membrane of the digestive system are excluded, and it is also necessary to completely abstain from alcohol.

The restoration of normal blood counts occurs within several months; the condition of patients improves quite quickly during therapy, but neurological symptoms can persist for up to six months.

Prevention of B12 deficiency anemia

The development of pernicious anemia in healthy people is possible only with an unbalanced diet or prolonged fasting, therefore the most effective preventive measure is good nutrition, rich in vitamins and other nutrients. The main source of vitamin B12 is food of animal origin:

offal (beef, pork, chicken liver, heart, kidneys, etc.);
fish, seafood;
meat (beef, rabbit, lamb, pork, etc.);
egg yolk;
cheeses;
dairy products.

Recent research shows that products plant origin Cyanocobalamin is not found and can be obtained in small quantities from yeast, yeast extract and mushrooms. Therefore, strict vegetarians are recommended to take vitamin supplements constantly or in courses to prevent pernicious anemia.

People suffering from diseases in which the absorption of vitamins is impaired may be prescribed continuous preventive therapy, once a month or less often parenteral administration of a maintenance dose of the vitamin is performed. This will allow you to regularly replenish cyanocobalamin reserves in the body and prevent the development of anemia.

Identification and treatment of patients with diphyllobothriasis (a type of helminthiasis), as well as its prevention among workers in the fishing industry and people involved in food preparation, is also a means of preventing B12-deficiency anemia.

Which doctor should I contact?

At the onset of the disease, the symptoms of B12 deficiency anemia are nonspecific, so if unexplained weakness appears, feeling unwell you need to see a therapist. Anemia can be suspected by a general blood test. The patient is subsequently treated by a hematologist. In case of damage to the stomach and intestines, an examination is carried out by a gastroenterologist, in case of pathology of the nervous system - by a neurologist, in case of stomatitis and glossitis - by a dentist. If the cause of the disease is infection with worms, you need to consult an infectious disease specialist. Pick up proper nutrition A nutritionist will help.

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b12 deficiency anemia, treatment, symptoms

Insufficient intake of vitamin B 12 into the body over time can lead to impaired hematopoiesis or a pathology called b 12 deficiency anemia. Clinically, symptoms of anemia appear against the background of a decrease in the level of red blood cells and hemoglobin in the blood. Often the disease occurs in a combined form, when the body experiences an incomplete supply of two vitamins at once - B6 and B12, leading to the development of additional folate deficiency anemia, impaired proliferation and fast growth cells of the bone marrow, gastrointestinal tract, skin.

Such disturbances in the body can be caused by the following factors:

poor consumption of folic acid together with foods;
impaired absorption of vitamins or increased excretion from the body;
inadequate, meager nutrition, deliberate refusal to eat against the background of anorexia nervosa;
disorders in the digestive system and intestines;
dysbacteriosis;
long-term use of a number of medications (antibiotics, anticonvulsants);
alcohol abuse;
severe and prolonged intoxication of the body;
the onset of pregnancy against the background of restructuring of all functions;
Crohn's disease;
syndrome of impaired intestinal absorption;
development of malignant neoplasm;
hereditary factor due to a violation of the transport of cyanocobalamin into the bone marrow;
damage to the gastrointestinal tract by microorganisms, helminths, worms and flatworms, their increased reproduction and absorption of vitamin B12;
vegetarianism, deliberate fasting, non-eating meat, leading to nutritional deficiency;
liver and kidney diseases;
insufficient interaction of proteins in the blood with vitamins;
the development of a malignant tumor, leading to the rapid destruction of red blood cells (erythrocytes).

With folate deficiency anemia, folic acid ceases to be converted into a substance necessary to participate in the synthesis of the main components of DNA. The hematopoietic system as a whole is disrupted, red blood cells are destroyed and begin to divide pathological cells, toxic substances and fatty acids gradually accumulate in nerve fibers, but with a modified structure. Cells of the spinal cord and nervous system are affected, and patients exhibit neurological signs.

How does b12 deficiency anemia manifest?

Clinical manifestations of anemia may be absent for a long time. Pathology develops slowly. Primary signs not specific and can be easily confused with other diseases.

With anemia, damage to the digestive system is observed, leading to:

distortion of taste;
pain in the epigastric region of the gastrointestinal tract after eating;
indigestion;
departure unpleasant odor from mouth;
decreased appetite.

In case of damage to the nervous system, advanced cases of anemia contribute to:

disturbances in defecation and urinary passage;
decreased sensitivity in fingers;
the appearance of tingling, numbness in different parts of the body;
impaired formation of blood cells, leading to dizziness, yellowing of the skin, pain in the heart, increased heart rate, the appearance of spots before the eyes, and pre-fainting.

With b 12 deficiency anemia, the symptoms directly depend on the duration and severity of the disease. A lack of vitamin B12 negatively affects the digestive and nervous system. Present:

gastroenterological syndrome with dysfunction of the gastrointestinal mucosa;
circular hypoxic syndrome with insufficient oxygen supply, lack of supply to tissues and organs;
neuropsychiatric syndrome against the background of insufficient development of the myelin sheath of nerve fibers, when signs of anemia are evident: shortness of breath, attacks of tachycardia, pallor and yellowing of the integument, the appearance of age spots, belching, heartburn, lack of appetite, stool disturbances, loss of coordination of movements, paranoia, delirium.

On a note! All signs of anemia are not specific, so doctors must take into account blood counts when making a diagnosis.

The condition is especially dangerous when the psyche is disturbed. Patients begin to suffer from psychosis, hallucinations, depression, seizures, and insomnia.

B 12 deficiency and folate deficiency anemia, similarities and differences

The code for B12 deficiency anemia is ICD10, when the body lacks vitamin B12; for folate deficiency anemia, there is an additional deficiency of vitamin B9. Both types of anemia belong to the group - megaloblastic anemia, when DNA production is reduced and cells quickly divide with impaired proliferation.

Folate deficiency anemia is considered a hematological disease. Folic acid stops entering the body, leading to disruptions in the functions and systems of the body, affecting the hematopoietic system. There is a slow formation of red blood cells and the process can lead to irreparable consequences.

In addition to the reduced level of red blood cells in the blood, the patient clearly has hematological pathology. The platelet count is low, there are signs of agranulocytosis and thrombocytopenia.

Vitamin B12 takes an active part in the formation of good blood cells, in particular, it activates the production of folic acid, which is necessary for the production of thymidine. Thanks to vitamin B12, the body synthesizes and breaks down fatty acids. His own deficiency violates this process. Methylmalonic acid accumulates, leading to a decrease in the production of myelin, which forms the myelin sheath.

Folic acid does not lead to the breakdown of fatty acids and damage to the nervous system. However, it stimulates erythropoiesis and forces vitamin B12, which is necessary for the breakdown of fatty acids, to act. With a deficiency of folic acid, hematopoietic cells begin to rapidly divide, paralyzing the nervous system. The supply of vitamin B12, even if not supplied to the body, will last for about 6 years, and folic acid will be completely eliminated from the body after 4 months.

Often it is women who experience a lack of these vitamins during pregnancy. If a lack of vitamin B12 does not lead to disastrous consequences, as long as the level remains normal. The lack of folic acid and the lack of vegetables in the body, raw meat will ultimately lead to the development of b 12 folate deficiency anemia or a deficiency state.

On a note! Folic acid resists boiling and is completely destroyed after 15 minutes. While cyanocobalamin or vitamin B12 is retained in full when entering the body even after careful heat treatment products.

Diagnostics

Diagnostics is complex. To identify b 12 deficiency anemia, patients undergo a blood test for signs of thrombocytopenia and leukopenia, when the number of reticulocytes, hemoglobin, and red blood cells in the blood is reduced, and the color indicator, on the contrary, is increased:

smear by staining, when with anemia the picture is typical: red blood cells are normal, macrocytes acquire an oval shape;
bone marrow puncture for suspected leukemia, hypoplastic and aplastic condition, hemolytic anemia;
examination of the skin, when anemia leads to pallor, a smooth surface and a crimson color on the tongue, rapid pulsation, and decreased blood pressure;
urine ( general analysis) in order to identify other concomitant diseases;
blood test for biochemistry to detect the level of cholesterol, creatinine, urea, electrolytes in order to identify the affected internal organ;
ECG to determine the degree of heart rhythm disturbances and increased heart rate.

Patients are required to consult a therapist.

Treatment of deficiency anemia

For b 12 deficiency anemia, treatment is medicinal by administration of vitamin B12 in increased doses to completely eliminate signs of anemia. The main thing when carrying out therapy:

saturate the body with vitamin B12;
prevent further development of anemia.

Cyanocobalamin is prescribed at a dose of up to 300 mcg 2 times a day. In complicated cases - up to 1000 mcg per day. Once diagnosed, patients must continue to receive supportive care.

During treatment, it is important to take measures to restore the functions of the hematopoietic, digestive, and nervous systems. During treatment with medications, the patient must be under the supervision of specialists and donate blood in a laboratory at least twice a week. After blood counts in the periphery are brought back to normal, the manifestations of neuralgia are alleviated, the restoration of the gastrointestinal tract and digestive system as a whole is transferred to support. A blood test is carried out at least once a month.

The applicable method is blood transfusion. It is often prescribed to patients diagnosed with severe anemia and a hemoglobin level not exceeding 70 g/l. In an anemic coma, the patient may lose consciousness. The B12 drug is administered intramuscularly in increased doses until the threatening risks to the patient’s life are eliminated.

It is equally important for patients to adjust their diet, diversify the menu with foods high in vitamin B12 (meat, offal, corn, chicken liver, mackerel, greens, salads, plum juice, fresh cabbage, cheeses). Patients are prescribed a varied and nutritious diet.

Forecast

The sooner B 12 deficiency anemia is identified and an adequate treatment course is carried out, the more realistic and favorable the prognosis and return to normal health will be. to the usual way life.

The prognosis is more unfavorable if you visit doctors late or if hereditary form anemia, the appearance of signs of central nervous system damage. Patients will have to be treated for the rest of their lives. Otherwise, a severe course of b12 deficiency anemia can lead to death.

It is worth understanding that anemia is an insidious condition, but not life-threatening when contacting doctors for early and conducting a treatment course. A great danger is posed by impaired oxygen delivery to the brain, loss of consciousness and anemic coma, when treatment can no longer be done without transfusion of donor red blood cells by administering vitamin B12 intramuscularly. The transfusion must be carried out as quickly as possible, to eliminate the threatening factors for the life and condition of the patient.

When diagnosing anemia during pregnancy in women, it is important to support not only the woman’s body, but also the child, therefore the daily dose of vitamin B12 increases immediately by 50%, with multiple pregnancy by 75%. Cobalamin reserves in the body are significantly depleted during frequent pregnancy and liver diseases. Women are prescribed an enhanced diet with a high intake of vitamin B12 along with food.

Prevention for β12 deficiency anemia clinical guidelines are as follows:

sufficient consumption of foods with vitamin B12 (milk, liver, red meat);
timely removal of helminthic infestations and roundworms from the body;
conducting maintenance therapy after major intestinal surgery.

Vitamin B12 is administered to the body in increased doses.

/ Internal diseases / For medical clinics / Lectures / SELECTED lectures (c) Matrix. Neo/B12 DEFICIENCY ANEMIA

Candidate of Medical Sciences, Associate Professor V.A. Tkachev

The nomenclature of the name of this disease is different, and it is often referred to in the literature as pernicious anemia (perniciosa - fatal), malignant Addison-Biermer disease (by the name of the authors), as well as megaloblastic anemia (by the type of hematopoiesis).

Historical reference. The first description of this disease was made by Coombs in 1822 and called it severe primary anemia. In 1855, physician Addison described this suffering under the name "idiopathic anemia." In 1872, Birmer published the results of an observation of a group of patients suffering from progressive pernicious anemia. However, the possibility of curing this disease appeared only in 1926, when Minot and Murphy discovered a pronounced therapeutic effect from the administration of raw liver.

Three years later, the American physiologist Castle showed that raw meat, liver, and yeast, treated with the gastric juice of a healthy person, have the property of causing remission in a patient with pernicious anemia. Castle's research formed the basis of the concept according to which, as a result of the interaction of two factors - external, contained in raw meat, raw liver, yeast, and internal, produced by the gastric mucosa, an anti-anemic compound is created, which ensures the physiological maturation of bone marrow cells.

Nature external factor was installed - it is cyanocobalamin (vitamin B 12 ) . Vitamin B 12, according to the body's needs, is used not only for hematopoiesis in the bone marrow, but also for the normal functioning of nervous tissue and digestive organs.

Etiology. The leading factor in the etiology of the disease is endogenous vitamin B deficiency 12 , arising as a result of a violation of its absorption due to the cessation of secretion of the internal factor (gastromucoprotein).

Malabsorption of B 12 can occur as a result of damage to the gastrointestinal tract by an inflammatory or malignant process, after subtotal or total removal of the stomach, after extensive resection of part of the small intestine. In rare cases, pernicious anemia develops with normal secretion of intrinsic gastric factor and is caused by congenital absence of transcobalamin-2, with which vitamin B 12 binds and is delivered to the liver, or as a result absence of a protein acceptor in the intestine(perceiving) vitamin B 12, necessary for the entry of cyanocobalamin from the intestine into the bloodstream. In some cases there is genetic development factor In 12-deficiency anemia due to a congenital disorder in the production of gastric factor or the presence of antibodies against parietal cells.

The following factors can also lead to B 12 deficiency anemia:

impaired absorption of B 12 in the small intestine as a result chronic enteritis or celiac enteropathy;

competitive absorption of vitamin B 12 in the small intestine wide tapeworm or microorganisms;

complete exclusion of food of animal origin;

long-term decreased exocrine activity of the pancreas, the consequence of which is a violation of the breakdown of protein R, without which vitamin B 12 cannot contact mucopolysaccharide;

long-term appointment some medications: methotrexate, sulfasalazine, triamterene, 6-mercaptopurine, azathioprine, acyclovir, fluorouracil, cytosar, phenobarbital, etc.

Pathogenesis. Hematopoietic disorders with B 12 deficiency anemia are characterized by megaloblastic type for all three blood lineages: erythroid, granulocytic and megakaryocytic. There is ineffectiveness of red hematopoiesis: impaired differentiation of erythroid cells and the appearance of abnormal cells such as promegaloblasts, megaloblasts (large cells with basophilic cytoplasm and a nucleus containing nucleoli).

Due to the failure of the cellular elements of the blood, it is strengthened hemolysis, which is manifested by hyperbilirubinemia, urobilinuria, and an increase in stercobilin in the feces.

Pathological changes are characterized by general anemia, yellowness of the skin and mucous membranes, fatty degeneration of the myocardium, liver, and kidneys. The bone marrow is juicy and crimson in color due to hyperplasia.

Hepatomegaly is not expressed. Hemosiderosis is detected in the liver, spleen, kidneys (rusty tint on the section) as a result of hemolysis of red blood cells.

Dystrophic changes are observed in the nerve fibers of the tongue (nerve plexuses of Meissner and Auerbach), as well as in the posterior columns of the spinal cord (focal swelling with disintegration of myelin nerve fibers).

Clinical manifestations of 12-deficiency anemia often develop gradually: weakness, malaise, dizziness, dyspeptic disorders, tinnitus, and a tendency to obesity increase. Rarely, the disease begins acutely, with a rise in body temperature to 38 C and severe weakness.

In the bone marrow, signs of the megaloblastic type of hematopoiesis are determined.

Intestinal dyspepsia syndrome characterized by unstable stools and weight loss.

Glossitis manifested by the presence of a “scalded” (red) or “varnished” tongue with cracks. Pain in the tongue is observed in 30% of patients with B 12 deficiency anemia.

Jaundice syndrome occurs in 50% of patients and is manifested by subicteric sclera and hyperbilirubinemia.

Funicular myelosis syndrome(sensory ataxia - impaired coordination of movements) is observed in patients with B12-deficiency anemia in 11% of cases and develops as a result of impaired proprioceptive sensitivity due to atrophic processes in the dorsal horns of the spinal cord. There may be other symptoms of damage to the nervous system: paresthesia, dysfunction of the pelvic organs, decreased reflexes.

Edema syndrome occurs in B12-deficiency anemia in 80% of cases and is manifested by peripheral edema, which can reach the degree of anasarca, as a result of circulatory failure.

Liver enlargement ( hepatomegaly syndrome) occurs in 22% of patients, enlarged spleen ( splenomegaly syndrome) in 10% of cases.

In order to diagnose the disease, a thorough hematological study is carried out, including the study peripheral blood pictures, sternal punctate and serum factors involved in hematopoiesis. Accurate diagnosis very important, because these patients in some cases require lifelong treatment.

Differential diagnosis is carried out with folate deficiency anemia. Folic acid deficiency is usually observed at a younger age and is not accompanied by atrophic changes in the gastric mucosa and neurological symptoms.

It should be remembered that symptomatic megaloblastic anemia is caused by tumors of the stomach, small intestine and cecum, as well as helminthic infestation(helminthic B 12 deficiency anemia), which must be excluded when verifying the diagnosis.

It is necessary to differentiate with erythromyelosis(initial forms of leukemia), which are accompanied by anemia, which occurs with an increased level of vitamin B 12 in the blood and is resistant to treatment with cyanocobalamin.

When carrying out differential diagnosis of B 12 deficiency anemia, it is necessary to establish its causes.

Treatment for B 12 deficiency anemia includes parenteral administration of vitamin B 12 or hydroxycobalamin (a metabolite of cyanocobalamin) in doses that ensure the satisfaction of daily requirements and doubling of depot reserves. Vitamin B 12 is administered 1000 mcg intramuscularly daily for two weeks, then once a week until hemoglobin levels normalize, after which they switch to administration once a month throughout life.

Oxycobalamin Its pharmacological properties are similar to cyanocobalamin, but compared with the latter it is quickly converted into an active coenzyme form in the body and remains in the blood longer. Oxycobalamin is administered at a dose of 500–1000 mcg every other day or daily. In the presence of neurological symptoms, it is necessary to administer the drug at a dose of 1000 mcg every two weeks for six months.

For funicular myelosis, massive doses of cyanocobalamin are prescribed, 1000 mcg daily for 7–10 days, then twice a week until neurological signs disappear.

Red blood cell transfusions indicated for the urgent elimination of symptoms of hypoxia.

Treatment with cobalamin should be prescribed to all patients after total gastrectomy. To prevent exacerbation, vitamin B 12 is administered once every two weeks, 100–200 mcg.

Clinical examination. Patients with B 12 deficiency anemia are subject to dispensary observation, during which the condition of peripheral blood is monitored 1-2 times a year, as well as treatment of diseases and conditions that led to the development of this type of anemia.

There are different regimens for maintenance therapy with cobalamins. Upon appointment cyanocobalamin Lifelong annual preventive three-week courses of injections every other day or monthly administration of one kilogram of the drug are recommended. Hydroxycobalamin It is recommended to take annual preventive courses of one injection per week (1 mg) for 2 months.

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B12 deficiency anemia: causes, symptoms and treatment

B12 deficiency anemia is a disease characterized by impaired hematopoiesis and caused by a deficiency of vitamin B12 in the human body. This pathology It 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.

Naturally, impaired intestinal absorption of vitamin B12 will also occur after removal of part of the stomach and small intestine for medical reasons.

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

Please note: B12 deficiency anemia often develops in vegans who do not consume animal foods. The fact is that plant foods do not contain this vitamin, so vegans should consume foods artificially enriched with B12, as well as special vitamin complexes. For more information about the importance of vitamin B12 in a vegan diet and sources of this vitamin, read the article “Vitamin B12 in a vegan diet: why is it important?”.

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 initial stages characterized by weakness increased fatigue and drowsiness - completely nonspecific symptoms.

The main clinical manifestations of B12 deficiency anemia include:

Impaired blood cell formation. This is manifested by dizziness and frequent fainting, pallor and yellowness of the mucous membranes/skin, exercise intolerance, pain in the heart, 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 medical attention. 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.
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;
- pain in the epigastric region after eating;
- frequent infections in the oral cavity.
Damage to the nervous system. They usually only appear when neglected form B12 deficiency anemia and are:
- sensory disturbances in the fingers and wrists;
- paresthesia – numbness, “tingling” in certain places of the body;
- decreased muscle strength;
- problems with urination and bowel movements.

The most dangerous manifestation of B12 deficiency anemia is mental disorders, as evidenced by psychosis, depression, hallucinations, convulsions, and insomnia.

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 performing a general clinical and biochemical analysis in laboratory conditions;
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 prescribing such treatment are a confirmed diagnosis of B12 deficiency anemia and a pronounced clinical picture of 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 injection of kg of vitamin B12 once a day. Duration drug treatment is at least 6 weeks, then doctors transfer the patient to maintenance therapy - the dosage in this case will be 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 there is complete normalization of peripheral blood parameters, weakening neurological manifestations, 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. Since this method is considered quite difficult and even dangerous in some sense, it is used only if the patient’s life is in direct danger due to the development of β12 deficiency anemia. Unconditional indications for blood transfusion:

severe anemia, when the patient's hemoglobin level is less than 70 g/l;
anemic coma, manifested by loss of consciousness.

Since blood transfusion is prescribed only with a confirmed diagnosis, intramuscular administration of vitamin B12 is also prescribed simultaneously with this procedure. 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 at an early stage of its development, treatment was immediately prescribed and is being carried out, and normalization of peripheral blood counts 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 most early signs condition in question, the doctor will be able to quickly establish the cause of the disease and carry out effective treatment.

Tsygankova Yana Aleksandrovna, medical observer, therapist of the highest qualification category

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B12 folate deficiency anemia (pernicious, megaloblastic) is a disease accompanied by pathological abnormalities in the processes of hematopoiesis. The condition is caused by a lack of vitamin B12 (cobalamin). It is expressed in a significant lack of red blood cells (erythrocytes), iron-containing protein, damage to the central nervous system and gastrointestinal tract. The disease is diagnosed relatively rarely and is most often detected in older people. Occurs in pregnant women. Goes away on its own after delivery.

B12 deficiency anemia is included in the group of megaloblastic conditions. It is typically characterized by a decrease in hemoglobin and red blood cell volume due to insufficient intake and rapid consumption of vitamin B12 and folic acid.

A deficiency of chemical compounds provokes bone marrow damage. The pathological process involves nerve tissue. The disease is dangerous not only due to hypoxia of organ tissues. It can cause severe lesions brain.

The pathology was first diagnosed by the English physician Thomas Addison. But the name is given by the last name German doctor Anton Birmer, who described clinical symptoms condition.

Deficiency of B12 and folic acid provokes serious deviations in the process of DNA formation, which causes disturbances in the production of red hematopoietic cells. The condition is accompanied by signs of impaired erythrogenesis: a decrease in the number of red blood cells and hemoglobin is detected diagnostically. This type anemia is often accompanied by the development of thrombocytopenia and neutropenia.

Causes of B12 folate deficiency anemia

The causes of B12 deficiency anemia are varied. These are:

lack of incoming vitamins;
malabsorption syndrome;
increased consumption of existing cobalamin reserves;
hereditary pathologies, characterized by disturbances in B12 metabolic processes.

The body is not adapted to independently produce cobalamin. Replenishment of reserves occurs due to its intake along with food. The main source is meat, fish products, dairy products.

Cooking foods by heat treatment partially destroys vitamin B12 and this must also be taken into account when creating a diet. The cause of the deficiency is adherence to the principles of vegetarianism and abuse of alcohol-containing drinks.

Castle factor is a prerequisite for the full absorption of cobalamin. Otherwise, the absorption of folic acid becomes impossible; it is excreted along with the feces.

The following pathologies can provoke a lack of intrinsic factor Castle.

Diseases of the gastrointestinal tract, in particular, inflammation of the mucous membrane of the gastric pouch, which occurs in an atrophic and autoimmune form. In the first case, a decrease in its size and a violation of functionality, in the second, a violation of immune function occurs.
Malignant formation of the stomach.
Removal of the stomach (gastrectomy).
Congenital deficiency of Castle factor. It is caused by a gene defect, which contributes to the disruption of secretion production by gastric cells.

The absorption of the vitamin occurs through the mucous membranes of the small intestine. The following pathologies can cause disruption:

Active consumption of cobalamin occurs in the following cases:

during pregnancy;
with hyperthyroidism ( increased activity thyroid gland);
due to the presence of malignant tumors.

Hereditary pathologies can disrupt metabolic processes, in particular, hereditary deficiency of transcobalamin II, Imerslund-Gresbeck syndrome and others.

Pathogenesis

Vitamin B12 can only be obtained from protein foods. Combining with the intrinsic factor of Castle in the gastric pouch, entering the intestine, it is successfully absorbed by the mucous membrane thin section Gastrointestinal tract. If its absorption is impaired, B12 deficiency anemia is formed, since the intestinal tract breaks down the food bolus and removes the vitamin along with feces.

The condition causes dysfunction of hematopoiesis, characterized by a drop in the number of red blood cells and hemoglobin. Vitamin B12 is transported to the bone marrow, where it is involved in the process of creating red blood cells. With its deficiency, there is a lack of red blood cells.

With the development of megaloblastic anemia, significant disturbances in hematopoiesis are observed, which is accompanied by characteristic changes in the structure of red and white blood cells. The type of hematopoiesis changes (a normoblastic increase in reticulocytes is characteristic of a completely healthy person). Bone marrow cells have a young nucleus combined with old cytoplasm. Registered a large number of basophilic megaloblasts.

Symptoms of b12 deficiency anemia

Symptoms of B12 deficiency anemia can appear several years after the formation of the pathological condition. The disease progresses slowly and among its first signs it is worth highlighting:

weakness;
fatigue.

As the situation destabilizes, a characteristic clinical picture forms. The main symptoms include:

disturbances in the process of erythropoiesis;
gastrointestinal tract damage;
deviations in the functioning of the central and peripheral nervous system.

Disorders of the erythropoiesis process

B12-folate deficiency anemia is characterized by a decrease in the level of red blood cells. The following are typical signs of hematopoietic disorders.

Paleness, yellowness of the skin, mucous membranes - the condition develops slowly, over several months, due to a lack of hemoglobin and an increased content of bilirubin.
Tachycardia is caused by organ hypoxia.
Heart pain caused by active work of the myocardium due to lack of oxygen.
Negative reaction to physical exercise– fatigue, dizziness, etc.;
Dizziness, regular fainting - provoked oxygen starvation brain;
Flickering of flies in the field of view;
An increase in the size of the spleen, caused by blockage of the capillaries of the organ with large red blood cells.

During the disease, chronic cor pulmonale can be diagnosed – complex hemodynamic disorder. Rarely seen.

Gastrointestinal lesions

Disorders of the digestive system are one of the early symptoms of an anemic condition. The signs can be read below.

Digestive difficulties caused by a lack of digestive juices and enzymes.
Stool disorders - alternating constipation with diarrhea is observed.
Decreased appetite - due to decreased secretion gastric juice due to the formation atrophic gastritis.
Weight loss - caused by the development of partial/complete anorexia and disturbances in the digestion of food coma.
Changing the shape and color of the tongue - it gets a bright crimson hue and becomes completely smooth.
Impaired taste perception.
Regular inflammation of the oral mucosa - stomatitis, glossitis, gingivitis.
Soreness and a burning sensation in the mouth are caused by damage to the nerve endings.
Abdominal pain that occurs after eating.
Intestinal diseases (celiac disease).

Symptoms are nonspecific and can accompany other pathologies.

Deviations in the functioning of the nervous system

Lesions of the central nervous system are explained by the direct participation of cobalamin in the production of myelin sheaths. Process disruption provokes the development of neurological symptoms.

The brain is affected, clinical manifestations will be as follows:

Sensitivity disorder – formed in any part of the body;
paresthesia (pins and needles);
lack of coordination in muscle function - manifests itself in loss of balance, clumsiness, etc.;
decrease in muscle strength – expressed as atrophy of the muscular corset;
problems with bowel movements and Bladder– manifested by delay or incontinence;
mental disorders - insomnia, depressive states, severe psychosis, hallucinations.

Neurological symptoms develop sequentially. The legs are the first to be affected, followed by the abdomen and body, followed by the fingers, neck, face and head. Mental disorders are the most recent to develop.

B12 deficiency anemia for a child - in children and adults it is accompanied by the same symptoms - is especially dangerous.

Diagnostics

Diagnosis of B12 deficiency anemia includes the following measures.

Collection of complaints.
Physical examination.
Blood analysis. A decrease in the number of reticulocytes and red blood cells (erythrocytes) is detected. The pathology is accompanied by anemia.
Urine examination.
Biochemistry of blood. Helps determine cholesterol, glucose, uric acid, creatine, etc. Elevated levels of bilirubin are typical for the disease.
Bone marrow analysis. The study of punctate makes it possible to obtain reliable signs diseases: accelerated formation of red blood cells, megaloblastic type of hematopoiesis.
ECG. Determines the frequency of myocardial contractions.

When diagnosing B12-deficiency anemia, the patient, if necessary, is prescribed a consultation with a doctor general practice.

Treatment of B12 deficiency anemia involves a combined approach, since doctors need to restore the functionality of three systems at once.

Drug treatment of b12-deficiency anemia involves the patient obtaining the deficient vitamin artificially. The indication for vitamin B12 therapy is a confirmed diagnosis and the presence of a clear clinical picture anemic condition.

Cobalamin is preferably administered intramuscularly, but it can be taken in tablet form. The last option is used if there is a proven lack of an element due to poor nutrition.

The B12 treatment regimen is selected individually. At the beginning, it is 500.0 - 1000.0 mg, administered intramuscularly once a day. Then the doses of vitamin B12 for anemia are revised.

The total duration of treatment reaches 6 weeks. After this, the patient receives a maintenance dose. He will receive 200–400 mg of the drug (two to four injections per month). Sometimes throughout your entire life.

When taking cobalamin, it is necessary to monitor the effectiveness of the treatment protocol. To do this, the patient must donate blood two to four times a week to check the effectiveness and correction of therapy. After the indicators are restored, a transfer to maintenance therapy is performed. Blood donation is performed only once a month.

When diagnosing cyanocobalamin deficiency, blood transfusion is practiced. But it is preferable to transfuse red blood cells. The technique is implemented only in cases of severe anemia, an existing threat to human life.

The indication is a decrease in hemoglobin level below 70 g/l. Blood transfusion is practiced when there are symptoms of a precomatous state or when the patient falls into an anemic coma. Once the condition has stabilized, the transfusions are stopped.

An important stage of therapy is the correction of the current diet. Cobalamin deficiency in the initial stages of development can be successfully treated by following the principles dietary nutrition. The daily menu should include:

These products contain a large percentage of folic acid, vitamin B12.

Compilation diet menu when diagnosing an anemic condition, a specialist should deal with it, based on the current symptoms and existing health problems. The body's susceptibility to various food groups is taken into account.

Prevention of b12 deficiency anemia

Prevention of β12-deficiency anemia includes several measures.

Inclusion in the diet of foods containing large amounts of cobalamin.
Timely treatment of pathologies that contribute to the formation of an anemic state, in particular, helminthic infestations.
Prescription of maintenance dosages of cobalamin during postoperative period regarding gastric/intestinal resection.

If a vitamin B12 deficiency is detected, it is extremely important to follow all the recommendations of the treating doctor. With early diagnosis of anemic pathology and timely treatment, the prognosis for the outcome of the disease is favorable. Stabilization of the condition is observed a month after the start of therapy.

Due to a decrease in oxygen delivery (due to a decrease in the number of red blood cells and hemoglobin), tissues experience hypoxia. First of all, this concerns the brain. The patient complains of dizziness. Fainting and darkening of the eyes are possible. Performance decreases, attention and concentration are lost. The patient gets tired quickly at work and needs rest more often.

Mental disorders are typical both at the onset of the disease and during severe long-term anemia. Irritability or apathy appears. The disorders are of a mild neurotic nature. Some suffer from hypochondria. Aggression is not typical.

Manifestations from the digestive tract

The cells lining the internal organs divide and mature quite quickly. Vitamin B12 is involved in these processes as a cofactor of enzymatic reactions and a substrate of basic biochemical reactions. Therefore, a deficiency of cyanocobalamin will affect the condition of the gastrointestinal tract.

The tongue with anemia has a characteristic appearance. It is smooth, the papillae are not visualized. The color becomes crimson. Taste sensitivity is lost. Ulcers or aphthae are possible on the mucous membrane of the tongue due to the addition of a secondary bacterial or fungal infection.

Stomach pain, heaviness in the epigastrium, belching of air are manifestations of atrophic gastritis, which often accompanies anemia associated with a lack of cyanocobalamin. The appearance of symptoms is clearly associated with food intake.

Abnormal stool – common symptom with anemia. This is usually diarrhea. For older patients, alternating constipation and diarrhea is more typical. Possible bloating due to the accumulation of gases in the intestines.

Decreased appetite and aversion to certain types of food are an unfavorable sign. He talks about the presence of anemia, which is most likely associated with a tumor. Losing weight in this case should alert both the doctor and the patient even more.

Diagnosis of B12 deficiency anemia

Anemia is determined by analyzing blood components

The first thing to start with diagnostic examination, this is a blood test. It must be expanded. Close attention is paid to red blood indicators. In particular, these are:

Hemoglobin
Color and volume indicators

The hemoglobin norm varies from 110 to 130 g/l in women, 120-140 g/l in men. If the level decreases below these thresholds, anemia is diagnosed. Next, other indicators are assessed to differentiate the syndrome and prescribe adequate treatment.

Vitamin B12 deficiency is accompanied by the appearance in the blood of megaloblasts - red blood cells with a large nucleus and high content hemoglobin inside. But the red blood cells themselves are few. This picture is typical for the so-called megaloblastic type of hematopoiesis. Anemia is called macrocytic. When large red blood cells are detected in the blood, B12 deficiency is first ruled out.

With anemia associated with a decrease in cyanocobalamin, the average volume of red blood cells increases. It exceeds 100 femtoliters. The average hemoglobin content in an erythrocyte also increases (more than 35 pg), as well as the average hemoglobin concentration in an erythrocyte (more than 38 g/dL). Laboratory doctors note the appearance of red blood cells with nuclear remains, which they also call Cabot rings and Jolly bodies.

The last stage of diagnosis is a consultation with a hematologist. This specialist performs a bone marrow tap to rule out tumor diseases hematopoietic tissue.

Treatment of B12 deficiency anemia

B12 deficiency anemia is treated with intramuscular injections vitamin B12 analogues

The drugs are prescribed by a hematologist, because only this specialist has the right to make a diagnosis. Treatment is carried out according to the principle of replacement therapy - synthetic analogues of vitamin B12 are used.

The average dose of the drug ranges from 200 to 500 mcg, depending on the severity of clinical manifestations. For children, the amount of vitamin is calculated taking into account age and weight.

The drug is administered intramuscularly once a day. Beginner course– 7 injections. The next stage is intramuscular administration of the same dose, but every other day for a week. Then, for 3 months, the patient is injected with vitamin B12 into the muscle once a week.

If hemoglobin returns to normal, this does not mean that the treatment is over. – chronic illness. By modern recommendations When remission is achieved, the drug should be administered at an average therapeutic dose once a month.

Monitoring treatment effectiveness

This is already done by a therapist or general practitioner. On days 4, 9 and 14 after the start of therapy, a general blood test is prescribed with a mandatory count of reticulocytes (young forms of red blood cells). On day 4, their number should increase, reach a maximum on day 9 and return to normal by the second week of treatment.

The final normalization of hemoglobin levels should occur at 4 or 6 weeks after therapy. This depends on the initial severity of the anemia, the adequacy of treatment and other factors.

Diet for B12 deficiency anemia

Use sea fish useful for preventing vitamin B12 deficiency

Treatment based solely on following dietary recommendations will not lead to a cure in any case. After all, the vitamin content in food is low, and cyanocobalamin is not completely absorbed.

However, you should include nutrients containing increased amounts of vitamin B12 in your daily diet.

These include:

Rabbit meat
Pork liver
Beef meat
Sea fish
Poultry meat and liver

In the presence of atrophic gastritis, it is necessary to stimulate the secretion of gastric juice. To do this, half an hour before meals you should take foods rich in organic acids. These include dairy and fermented milk products. This maneuver will allow vitamin B12 to be better absorbed in the gastric mucosa.

Complications and consequences of B12 deficiency anemia

As a complication of B12 deficiency anemia, swelling of the legs increases

Cyanocobalamin is involved in nerve conduction, as it is part of myelin fibers. The lack of this substrate affects the function of the nervous system.

The patient is concerned about sensory disturbances. This may be a sensation of “pins and needles” crawling across the body, numbness in the fingers or toes. Impaired temperature sensitivity is typical for some elderly patients. The limbs feel cold, although they are warm to the touch, and the blood flow is preserved.

Muscle strength decreases. There may be weakness in the arms or legs. This reduces the patient’s performance and affects his daily activities.

Neurological complications appear in a patient with anemia in a clear sequence. First, the lower limbs are affected symmetrically, then pathological process The torso is involved, and ultimately the arms and neck are affected. The head area is usually intact.

The function of the sphincters is impaired. Their locking mechanism is weakened. Patients may experience involuntary urination, bowel movement. For young patients this serious problem, including psychological.

With severe anemia, the patient begins to experience insomnia. At first it is presomnic in nature (difficulty falling asleep), and then intrasomnic ( frequent awakenings). Depressive disorders may occur, which are layered with hypochondria and preoccupation with one’s complaints and feelings.

Psychoproduction occurs extremely rarely and indicates an unfavorable prognosis of the disease. Convulsions, hallucinations, and psychotic reactions are characteristic.

Complications of anemia include decompensation of cardiac function. Increases in severity and makes breathing difficult. at the same time unstable.

Prognosis for B12 deficiency anemia

The disease is chronic. This means that it requires permanent treatment and monitoring the patient’s condition, tracking changes in the blood. The more carefully this work is carried out by the doctor, the more diligent the patient himself is, the greater the chances for stable remission and reversibility of the changes that occur.

Congenital forms, severe forms, as well as the presence of neurological manifestations have an unfavorable prognosis.

Timely detection of the disease and its causes allows you to live long and maintain quality of life and ability to work. Neglecting the doctor’s recommendations will one day result in decompensation of the condition.

In the following video, see the dangers of vitamin B12 deficiency:

The detection of anemia syndrome associated with a lack of vitamin B12 is the reason for a series of examinations. Ultimately, the cause should be treated and the deficiency of cyanocobalamin should be replenished by injection according to a lifelong regimen. The treatment is carried out by a hematologist, and monitoring the patient’s condition rests on the shoulders of the local doctor.