Pernicious Anemia (Juvenile Pernicious Anemia; Congenital Pernicious Anemia)

Description

Pernicious anemia occurs when the body is unable to absorb vitamin B12 from food due to a lack of a protein called intrinsic factor, which is produced in the stomach. Intrinsic factor is necessary for the absorption of vitamin B12. Pernicious anemia is often associated with an autoimmune-mediated attack of gastric parietal cells and/or intrinsic factor. Anemia is the insufficient supply of oxygen to the body's cells by red blood cells. The earlier treatment for pernicious anemia begins, the better the result.

Causes of pernicious anemia

There are many possible reasons pernicious anemia. Some of them are listed below.

• Atrophic gastritis (inflammation of the stomach);
• Removal of all or part of the stomach;
• Reaction immune system(in the form of an attack) on:
  • Intrinsic factor is a protein necessary for the absorption of vitamin B12
  • Cells that produce internal factor and hydrochloric acid in the stomach;
• Genetic disorders.

Risk factors

Factors that increase the likelihood of developing pernicious anemia:

• Autoimmune disorders and other diseases such as:
  • Type 1 diabetes;
  • Addison's disease;
  • Graves' disease;
  • Myasthenia;
  • Secondary amenorrhea;
  • Hypoparathyroidism;
  • Hypopituitarism;
  • Testicular dysfunction;
  • Chronic thyroiditis;
  • Vitiligo;
  • Idiopathic adrenal insufficiency;
• Origin: Northern Europe and Scandinavia;
• Age: over 50 years old.

Symptoms of pernicious anemia

Symptoms of pernicious anemia may vary. Symptoms may change or worsen over time. These symptoms may be caused by other diseases. You must inform your doctor if any of them appear.

Symptoms may include:

• Tingling sensation in the legs or arms;
• Variable constipation and diarrhea;
• a burning sensation on the tongue or a sensitive red tongue;
• Significant weight loss;
• Inability to distinguish between yellow and blue colors;
• Fatigue;
• Pallor;
• Changed taste sensations;
• Depression;
• Impaired sense of balance, especially in the dark;
• Tinnitus;
• Chapped lips;
• Yellow skin;
• Fever;
• Inability to feel vibrations in the legs;
• Dizziness when moving from a sitting to a standing position;
• Cardiopalmus.

Diagnosis of pernicious anemia

Tests to diagnose pernicious anemia include:

• Complete blood count - counting the number of red and white blood cells in the blood;
• Vitamin B12 level test, which measures the amount of vitamin B12 in the blood;
• Measuring the amount of methylmalonic acid in the blood - this test shows whether there is a vitamin B12 deficiency;
• Homocysteine ​​level is a test that measures the amount of homocysteine ​​in the blood (homocysteine ​​is a component that is involved in the formation of protein). Homocysteine ​​levels will be elevated if there is a vitamin B12 deficiency, folic acid or vitamin B6;
• The Schilling test is a test that uses a harmless amount of radiation to assess vitamin B12 deficiency (rarely used);
• Measuring the amount of folic acid;
• Measuring the amount of a protein called intrinsic factor (Castle's factor) - usually done in the stomach;
• Coloring bone marrow Prussian blue is a test that shows whether iron deficiency exists.

Treatment of pernicious anemia

Treatment may include:

Vitamin B12 injections

Treatment consists of an intramuscular injection of vitamin B12. These injections are necessary because the intestines cannot absorb the required amount of vitamin B12 without the presence of intrinsic factor in the stomach.

Oral Vitamin B12

The procedure consists of taking high doses of vitamin B12 orally.

Intranasal vitamin B12

The doctor gives the patient vitamin B12 supplements, which are administered through the nose.

Oral intake of iron supplements

Prevention of pernicious anemia

To reduce your chance of developing pernicious anemia, you should take the following steps:

• Long-term overconsumption alcohol;
• Ask your doctor to test for iron deficiency;
• Get tested if the doctor suspects infection Helicobacter bacterium pylori.

Basic blood functions such as oxygen transport and nutrients to tissues, the removal of metabolic products is carried out thanks to red blood cells - erythrocytes. When the number of these cells in the blood decreases, it develops pathological condition- anemia. According to the mechanism of development of anemic syndrome, three main factors are distinguished - large blood loss, destruction of red blood cells during autoimmune diseases, and decreased production of red blood cells in the body.

Let's consider one of the infrequent forms of pathology that develops as a result of impaired blood formation - pernicious anemia.

Pernicious anemia - what is it?

Pernicious anemia, or Addison-Biermer disease, develops when the synthesis of red blood cells (erythrocytes) is impaired due to a lack of vitamin B12 in the body. Cobalamin (B12) deficiency occurs as a result of insufficient intake of this substance or the body's inability to absorb it.

This disease is characterized by a disruption in the maturation of red blood cells in the bone marrow; their synthesis is interrupted at the stage of megaloblasts - immature blood cells that are large in size and contain an increased amount of hemoglobin. Megaloblasts are unable to perform the transport function of blood and are soon destroyed when passing through the spleen, which is why the body's cells may experience oxygen starvation, as well as intoxication by products of its own decay.

In addition to the synthesis of red blood cells, cobalamin is involved in the oxidation fatty acids and utilization of their breakdown products; in a deficient state, this process is suspended and toxic substances accumulate in the body, destroying the sheath of nerve fibers. Addison-Beermer disease is the only anemia associated neurological symptoms and mental disorder.

Because of big size cell anemia is called megaloblastic, and an increased hemoglobin content, which gives the cells a bright color, indicates hyperchromic pathology.

Manifestations of anemic syndrome were first described in 1855 by Thomas Addison, who was unable to find out the causes of the disease. A little later, German doctor Anton Birmer studied the mechanism of development of anemia, giving it the name pernicious, which means “malignant”. In those days, malignant anemia was an incurable disease, over time leading to irreversible changes in the internal organs, nervous exhaustion and even to death. And only half a century later, a group of doctors made a discovery that was awarded Nobel Prize, they were able to cure anemia in dogs by adding raw liver to food, and later isolated a factor from the liver that eliminated anemia, which was called vitamin B12 or Castle's extrinsic factor.

The disease develops in 1% of people in the older age category. The risk group includes teenagers, athletes, and women in late pregnancy who need increased amounts of the vitamin. In children, pathology develops due to a hereditary predisposition to the disease, external factors Serious malnutrition may occur, as well as vegetarianism of the mother during the period of bearing the baby.

Causes of the disease and risk factors

Vitamin B12 is synthesized by a special strain of bacteria and can only be absorbed in the lower part of the small intestine. In herbivores and some bird species, the intestinal microflora is populated by bacteria that produce cobalamin, which allows them to replenish the substance on their own. In the human body, such bacteria inhabit only the large intestine, so the vitamin B12 they synthesize is excreted along with the feces.

For this reason, a person can only obtain B12 from animal products, since plant foods contain its inactive analogue. Most cobalamin is found in the kidneys and liver, a little less in meat and seafood, dairy products and eggs contain small amounts of the vitamin, but if they are consumed regularly, a deficiency of this nutrient can be avoided.

Once in the stomach, vitamin B12 forms a bond with protein molecules (gastromucoprotein), which is synthesized by special cells of the gastric epithelium. This protein is commonly called intrinsic Castle factor; it protects cobalamin from the damaging effects of an acidic environment. gastrointestinal tract. The breakdown of the protein-vitamin complex occurs in small intestine, in its lower section, here the vitamin is absorbed by the mucous membrane and enters directly into the blood.

Pernicious anemia develops when one of the links that ensures the supply, absorption or storage of the vitamin in the human body is excluded. These may be the following factors:

1. Insufficient intake or complete absence in the diet of foods containing vitamin B12. Since cobalamin can accumulate in the liver and other organs, its reserves in the body are impressive; they can last for a couple of years, provided that animal products are completely avoided.
2. Helminthic infestations. Infection with tapeworms that absorb vitamin B12.
3. Disruption of the gastric epithelial cells responsible for the synthesis of gastromucoprotein, due to which the vitamin is destroyed without reaching the intestines. Factors contributing to the development of this pathology may include:
   • taking medications that interfere with the fermentation of the stomach or changes in the cells of its mucous membrane;
   • autoimmune diseases in which cells that produce internal Castle factor are degenerated;
   • hereditary diseases, which are characterized by the absence of protective protein in the stomach or its slow synthesis;
   • gastritis or;
   • change in acidity gastric juice.
4. Spicy and chronic diseases intestines, in which the absorption of vitamin B12 is impaired, such as:
   • malignant neoplasms;
   • partial removal of the small intestine;
   • Crohn's disease;
   • intestinal dysbiosis;
   • Zollinger-Ellison syndrome.
5. Impaired storage of vitamin reserves in the liver when it is destroyed by cirrhosis.

Anemia can occur with increased consumption of the vitamin by the body during growth, significant strength loads, and multiple pregnancies. However, provided good nutrition and the absence of other factors that contribute to the aggravation of the pathology, B12-deficiency anemia can resolve itself.

What happens in the body when there is a lack of vitamin B12

Pernicious anemia has a gradual tendency to develop, manifesting itself initially as anemic syndrome and then disrupting the work nervous system And internal organs.

Long before the appearance of neurological disorders and signs of megaloblastic anemia, the patient complains of weakness, drowsiness, severe headaches, loss of appetite, and dizziness. Such symptoms indicate oxygen starvation of cells caused by impaired transport of hemoglobin by red blood cells. A decrease in blood viscosity leads to changes in its pressure, which is expressed in arrhythmia and tachycardia.

Since immature red blood cells (megaloblasts) have a short lifespan, their death and breakdown of hemoglobin in the liver and spleen leads to an increase in these organs and disruption of the functioning of these organs.

Over time, the skin and sclera of the eyes may become jaundiced due to incomplete removal of bilirubin by the liver, and the tissues of the tongue, accumulating hemoglobin, become inflamed. A characteristic feature Pernicious anemia is an enlarged tongue, scarlet in color with atrophied papillary epithelium, due to which the organ becomes smooth.

Progression of the disease leads to damage to the epithelium oral cavity and gastrointestinal tract, which is expressed in the following symptoms:

• stomatitis and burning sensation of the tongue;
• glossitis - inflammation of the tissues of the tongue;
• feeling after eating;
• chronic constipation;
• pain in the intestines.

When fatty acid metabolism is disturbed, toxic substances accumulate, destroying the fatty membrane of neurons in the brain and spinal cord. CNS lesions manifest themselves as follows:

• memory loss;
• disorientation;
• absent-mindedness;
• irritability.

The long-term course of B12 deficiency anemia syndrome can be manifested by behavioral disorders, inability to formulate and express thoughts, and memory loss. Since the ability to absorb the vitamin decreases with age, older people are most in need of additional sources of cyanocobalamin. The symptoms of Addison-Birmer disease are often confused with senile dementia, but curing the disease is so simple.

With degenerative damage to the spinal cord, funicular myelosis occurs, which is characterized by the following symptoms:

• numbness of the limbs, which is accompanied by tingling;
• convulsions;
• unsteady gait, stiffness and weakness in the legs;
• loss of sensation in the feet.

On late stages manifestations of the disease can be:

• urinary disturbance;
• sexual dysfunction in men;
• decreased hearing and vision;
• mental disorders;
• hallucinations;
• paresis and paralysis;
• amyotrophy.

Diagnosis and differential diagnosis

The diagnosis of pernicious anemia is made based on the following indications:

• collection of patient complaints, from which the doctor can determine the duration of the disease;
• a physical examination of the patient during which the doctor pays attention to changes in the epithelial covers of the tongue, skin tone, and decreased sensitivity of the extremities.
• lab tests.

Mandatory laboratory research if B12 deficiency anemia is suspected, the following are:

1. Clinical blood test. With cyanocobalamin deficiency, red blood cells have an increased size, pronounced color, and uneven shape. The values ​​of leukocytes, erythrocytes and platelets in the blood are reduced, while the values ​​of lymphocytes exceed the norm.
2. Immunological analysis for the presence of antibodies to intrinsic Castle factor in the blood.
3. Bone marrow analysis performed by puncture shows the megaloblastic type of hematopoiesis.
4. Urine and stool tests are necessary to determine the amount of vitamin B12 that is excreted from the body.
5. If the amount of cyanocobalamin is increased in the analysis, the Schilling test is performed to determine the cause of poor absorption of the substance.

Additional diagnostics can help determine the cause of anemia. Thus, gastroscopy allows you to determine the content of hydrochloric acid in the stomach, as well as the presence of antibodies that destroy stomach cells that synthesize protective protein. Additionally, a stool test is prescribed to check for the presence of helminthic infestations in the body. Studies of the stomach, intestines and liver are carried out if pathological diseases are suspected that have led to the development of anemia.

When making a diagnosis, Addison-Biermer disease is differentiated from erythromyelosis and folate deficiency anemia.

Treatment of Addison-Birmer disease

Treatment of pernicious anemia is carried out under the supervision of such specialists as a hematologist, gastroenterologist, and neurologist.

The main therapy consists of replenishing the deficiency of vitamin B12 in the body by administering it subcutaneously. At the same time, the gastrointestinal tract is treated, the microflora is normalized, and, if necessary, the elimination helminthic infestation. For autoimmune pathologies, glucocorticosteroids are administered simultaneously with synthetic vitamin preparations to neutralize antibodies to the intrinsic factor.

Drug treatment with drugs "Oxycobalamin" or "Cyanocobalamin", which are administered in the form of subcutaneous injections, takes place in two stages - saturation and maintenance. During an exacerbation, the patient is administered the drug daily; the dosage and duration of the course depend on the age and severity of anemia. After vitamin B12 levels have returned to normal, maintenance therapy is carried out, which consists of administering the drug once every two weeks.

In parallel with this, diet therapy is used, which consists of correcting the patient’s diet. IN daily diet introduce foods rich in vitamin B12, such as beef, pork and chicken liver, seafood, mackerel, sardines, dairy products.

Deadlines full recovery hematopoiesis depend on the initial severity of anemia. Improvement occurs 2–3 months after the start of therapy.

Treatment prognosis and possible complications

At timely treatment the symptoms of the pathology are gradually eliminated, the skin acquires a natural shade after 2 weeks, after the normal red blood cells are restored, digestive problems disappear, and stool returns to normal. Neurological disorders are gradually smoothed out, tissue sensitivity is normalized, gait is restored, neuropathy and memory loss disappear.

Unfortunately, when the stage is too advanced, atrophied optic nerves, as well as leg muscles, cannot be restored. In very rare cases, after recovery, patients experience toxic goiter and myxedema.

If anemia occurs during pregnancy, vitamin B12 deficiency leads to placental abruption and premature birth. Insufficient oxygen supply to the fetus causes hypoxia (oxygen starvation), which affects the growth and development of the child.

In children with a hereditary vitamin B12 absorption disorder, anemia can manifest itself in enlarged internal organs (liver and spleen), decreased appetite, and developmental delays. The cause of cyanocobalamin deficiency in babies may be the mother's vegetarianism during breastfeeding.

Prevention

To prevent the development of the disease, you should properly organize your diet by including animal products rich in vitamin B12. Fatty foods should be limited, as it slows down the processes of hematopoiesis. You should also not abuse medications that inhibit the production of hydrochloric acid in gastric juice and can cause the destruction of the vitamin.

At chronic diseases stomach and liver, you should regularly undergo a blood test to check the vitamin content in the body.

Elderly people need to take vitamin B12 as part of a multivitamin complex, or take injections medicinal product for preventive purposes.

Pernicious anemia - serious illness, which can lead to irreversible changes in the body and even disability. Before the discovery of vitamin B12 and Castle factor, the pathology was considered incurable and caused a slow decline ending fatal. Nowadays, the disease is very rare and occurs mainly due to impaired absorption of vitamin concomitant diseases Gastrointestinal tract. However, people who practice veganism (strict vegetarianism), as well as those who practice therapeutic fasting, put themselves at risk of developing B12-deficiency anemia.

My name is Elena. Medicine is my calling, but it so happened that I was unable to realize my desire to help people. But, I am the mother of three beautiful children, and writing articles on medical topics has become my hobby. I want to believe that my texts are understandable and useful to the reader.

Pernicious anemia (B12 deficiency, megaloblastic or Addison-Biermer disease) is a disease of the blood system characterized by a decrease in hemoglobin and the number of red blood cells, resulting from a lack of vitamin B12 (cyanocobalamin) and affecting the digestive, nervous and hematopoietic systems.

What happens with pernicious anemia?

Normally, vitamin B12 is absorbed in the stomach when it is separated from proteins supplied with food (meat, fermented milk products). This breakdown requires enzymes from gastric juice and the specific intrinsic factor of Castle, which simultaneously serves as a carrier protein for vitamin B12. Only in the presence of this factor is the vitamin absorbed into the bloodstream; in its absence, cyanocobalamin enters the large intestine and is excreted from the body along with feces.

Vitamin deficiency does not manifest itself clinically immediately, since it is synthesized in the liver and for some time (about 2 - 4 years) compensation for hypovitaminosis occurs. Castle factor is produced by specific parietal cells of the gastric mucosa; when they are damaged or destroyed, the risk of pernicious anemia increases.

Possible causes of pernicious anemia

How does pernicious anemia manifest?

Pernicious anemia is a polysyndromic disease, that is, it manifests itself in many symptoms. Vitamin B12 is involved in the formation of blood cells, metabolic processes occurring in the nervous system. Therefore, a deficiency of this vitamin is primarily manifested by symptoms in the blood system, gastrointestinal tract and nervous system.

1. Anemic syndrome. With a lack of cyanocobalamin, the formation of normal red blood cells is disrupted, they stop carrying oxygen to tissues and organs. This causes weakness, pallor skin, fast fatiguability, tachycardia (increased heart rate), shortness of breath and dizziness. Sometimes a low-grade fever may occur - an increase in body temperature to low numbers (not higher than 38 degrees).
2. Gastroenterological syndrome - manifestations from the organs digestive system. There is a decrease in appetite, stool disturbances (constipation or diarrhea), and an increase in liver size (hepatomegaly). Characteristic changes in the language. They appear in the form inflammatory reactions mucous membrane of the tongue (glossitis) or corners of the lips (angulitis), in the form of burning and pain in language. Also specific symptom there will be a “varnished tongue” - this smooth tongue raspberry color. In the stomach, atrophy of the mucous membrane and development will occur atrophic gastritis with a decrease in secretory functions.


3. Neurological syndrome is a manifestation of the nervous system. They arise as a result of disturbances in fat metabolism and the formation of toxic acids that damage nerve cells. There is also a disruption in the synthesis of myelin, which is necessary for the formation of the protective sheath of the nerves. The syndrome manifests itself in the form of numbness of the limbs, gait disturbances and fine motor skills, muscle stiffness. Also, as a result of relaxation of the sphincters, enuresis (urinary incontinence) and encopresis (fecal incontinence) can occur. Mental symptoms such as insomnia, depression, psychosis or hallucinations may occur.
4. Hematological syndrome - blood symptoms. It appears in the results of a blood test in the form of progressive anemia (decrease in hemoglobin and red blood cells), leukopenia (decrease in the number of white blood cells), and the appearance of atypical red blood cells - megaloblastic forms.

Etiology

Three factors are involved in the development: PAa) family predisposition, b) severe atrophic gastritis, c) connection with autoimmune processes.

In the UK, a family predisposition to PA was noted in 19% of patients, and in Denmark - in 30%. The average age of patients was 51 years in the group with a family predisposition and 66 years in the group without a family predisposition. Identical twins developed PA at approximately the same time. Research by Callender, Denborough (1957)

It showed that 25% of relatives of patients with PA suffer from achlorhydria, and a third of relatives with achlorhydria (8% of the total) have a reduced level of vitamin B12 in the serum and its absorption is impaired. There is a connection between blood type A, on the one hand, and PA and stomach cancer, on the other, there is no clear connection with the HLA system.

More than 100 years have passed since Fenwick (1870) discovered atrophy of the gastric mucosa and cessation of pepsinogen production in patients with PA. Achlorhydria and the virtual absence of intrinsic factor in gastric juice are characteristic of all patients. Both substances are produced by the parietal cells of the stomach. Mucosal atrophy affects the proximal two-thirds of the stomach. Most or all of the secreting cells die and are replaced by mucus-forming cells, sometimes intestinal type. Lymphocytic and plasmacytic infiltration is observed. This picture, however, is characteristic not only of PA. It is also found in simple atrophic gastritis in patients without hematological abnormalities, and they do not develop PA even after 20 years of observation.

Third etiological factor represented by the immune component. Two types of autoantibodies have been found in patients with PA:

to parietal cells and intrinsic factor.

Using immunofluorescence, antibodies that react with gastric parietal cells are detected in the serum of 80-90% of patients with PA.

The same antibodies are present in the serum of 5-10% of healthy individuals. In elderly women, the frequency of detection of antibodies to gastric parietal cells reaches 16%. Microscopic examination of biopsies of the gastric mucosa reveals gastritis in almost all individuals who have antibodies to gastric parietal cells in their serum. Administration of antibodies to gastric parietal cells to rats leads to the development of moderate atrophic changes, a significant decrease in the secretion of acid and intrinsic factor. These antibodies obviously play important role in the development of atrophy of the gastric mucosa.

Antibodies to intrinsic factor are present in the serum of 57% of patients with PsA and are rarely found in individuals who do not suffer from this disease. When administered orally, antibodies to intrinsic factor inhibit the absorption of vitamin B12 due to their combination with intrinsic factor, which prevents the latter from binding to vitamin B!2.

IgG. In some patients, antibodies are present only in gastric juice. Based on data on the detection of antibodies in both serum and gastric juice, we can conclude that such antibodies to the internal factor are detected in approximately 76% of patients.

Another form of immune response to intrinsic factor is cellular immunity, detected in tests of inhibition of leukocyte migration or blast transformation of lymphocytes. Cellular immunity found in 86% of patients. If we combine the results of all tests, i.e. data on the presence of humoral antibodies in serum, in gastric secretions, immune complexes in gastric secretions and

Pernicious anemia is anemia that occurs due to a lack of important vitamin like B12. The deficiency itself can be caused by the fact that a person does not eat properly or his body has simply lost the ability to absorb it. Often this disease is inherited.

It is worth recalling that anemia is nothing more than a disease that is associated with a lack of red blood cells (erythrocytes). With it, the blood becomes unable to deliver as much oxygen to the tissue cells as they need. The consequences of anemia vary. The main and universal, perhaps, is chronic fatigue.

Pernicious anemia can cause cells to simply stop dividing or become really large so that they cannot leave the bone marrow.

Vitamin B12 is in our body for the reason that it is responsible for the formation of red blood cells. It also has a beneficial effect on the functioning of the nervous system. Typically, a person gets it from meat, fish, eggs and various dairy products. It is not uncommon for the body to lack it, not for the reason that a person does not consume the necessary foods, but because the stomach lacks protein, without which B12 cannot be absorbed.

By the way, an interesting fact is that pernicious anemia often torments those who have chosen the wrong diet to combat excess weight. I think everyone understands what we are talking about.

Pernicious anemia: symptoms

It develops very slowly, and its first symptoms usually appear when the human body is weakened (for example, after suffering infectious disease). People from thirty-five to sixty years of age are most susceptible to it. Gender doesn't matter.

The symptoms can be identified as follows:

- burning tongue;

- the patient constantly feels tingling in his fingers;

- chronic fatigue;

- muscle pain appears;

- appetite decreases;

- appears, diarrhea, vomiting, belching. Flatulence is also quite possible;

- the skin loses sensitivity.

It is also worth mentioning that the tongue turns bright red.

This disease always progresses in the spring.

Pernicious anemia may well lead to pathology of the nervous system, heart and much more. All this means that treatment should begin immediately after the disease has been diagnosed. The diagnosis is usually made by the doctor after listening to all the patient’s complaints and checking the test results. Anemia is not always difficult to detect early stages, which means from your attending physicians in in this case a lot depends.

Pernicious anemia: treatment and prevention of the disease

All treatment usually comes down to the fact that the patient is given B12 in certain doses. Unfortunately, some people will have to take it for the rest of their days on earth.

During treatment, doctors try to make up for the deficiency the right vitamin, eliminate the consequences of this disease, as well as eliminate the cause (if pernicious anemia was not caused by poor diet).

I would like to note that vitamin B12 can be injected with a syringe or taken in tablet form. In mild cases, just a few days after starting treatment, the first improvements will appear, and after one or two weeks the person will forget that he had this illness.

Regarding prevention, it is worth saying that you need to eat right, and not haphazardly. Diet is a good thing, however, you should not take it from a source that raises at least some doubt. Ask your friends, consult a nutritionist - there is no need to rush, since it is much easier to undermine your health than to restore it.

Of course, you also need to use all kinds of vitamin complexes, which contain a lot of B12.

Pernicious anemia is a disease that begins to manifest itself years after its onset. During this time, irreversible changes occur in the human body in the gastrointestinal tract, nervous system and bone marrow. This leads to the development of many symptoms and their complications. This is why this type of anemia needs to be diagnosed and treated as early as possible. Knowing the first symptoms and causes of the disease can help prevent complications.

Pernicious anemia (B12 deficiency, megaloblastic or Addison-Biermer disease) is a disease of the blood system characterized by a decrease in hemoglobin and the number of red blood cells, resulting from a lack of vitamin B12 (cyanocobalamin) and affecting the digestive, nervous and hematopoietic systems.

What happens with pernicious anemia?

Normally, vitamin B12 is absorbed in the stomach when it is separated from proteins supplied with food (meat, dairy products). This breakdown requires enzymes from gastric juice and the specific intrinsic factor of Castle, which simultaneously serves as a carrier protein for vitamin B12. Only in the presence of this factor is the vitamin absorbed into the bloodstream; in its absence, cyanocobalamin enters the large intestine and is excreted from the body along with feces.

Vitamin deficiency does not manifest itself clinically immediately, since it is synthesized in the liver and for some time (about 2 - 4 years) compensation for hypovitaminosis occurs. Castle factor is produced by specific parietal cells of the gastric mucosa; when they are damaged or destroyed, the risk of pernicious anemia increases.

Possible causes of pernicious anemia

How does pernicious anemia manifest?

Pernicious anemia is a polysyndromic disease, that is, it manifests itself in many symptoms. Vitamin B12 is involved in the formation of blood cells and in metabolic processes occurring in the nervous system. Therefore, a deficiency of this vitamin is primarily manifested by symptoms in the blood system, gastrointestinal tract and nervous system.

1. Anemic syndrome. With a lack of cyanocobalamin, the formation of normal red blood cells is disrupted, they stop carrying oxygen to tissues and organs. This causes weakness, pale skin, fatigue, tachycardia (increased heart rate), shortness of breath and dizziness. Sometimes a low-grade fever may occur - an increase in body temperature to low numbers (not higher than 38 degrees).
2. Gastroenterological syndrome – manifestations of the digestive system. There is a decrease in appetite, stool disturbances (constipation or diarrhea), and an increase in liver size (hepatomegaly). Characteristic changes in the language. They manifest themselves in the form of inflammatory reactions of the mucous membrane of the tongue (glossitis) or the corners of the lips (angulitis), in the form of burning and pain in the tongue. Also a specific symptom will be a “varnished tongue” - this is a smooth, crimson-colored tongue. In the stomach, atrophy of the mucous membrane and the development of atrophic gastritis with a decrease in secretory functions will occur.
3. Neurological syndrome is a manifestation of the nervous system. They arise as a result of disturbances in fat metabolism and the formation of toxic acids that damage nerve cells. There is also a disruption in the synthesis of myelin, which is necessary for the formation of the protective sheath of the nerves. The syndrome manifests itself in the form of numbness of the limbs, impaired gait and fine motor skills, and muscle stiffness. Also, as a result of relaxation of the sphincters, enuresis (urinary incontinence) and encopresis (fecal incontinence) can occur. Mental symptoms such as insomnia, depression, psychosis or hallucinations may occur.
4. Hematological syndrome - blood symptoms. It appears in the results of a blood test in the form of progressive anemia (decrease in hemoglobin and red blood cells), leukopenia (decrease in the number of white blood cells), and the appearance of atypical red blood cells - megaloblastic forms.