Addison-Birmer disease (malignant anemia, pernicious anemia, B12 deficiency anemia). Pernicious anemia (Addison-Birmer disease, B12 deficiency anemia) The most reliable sign confirming the diagnosis of pernicious anemia

This leads to impaired absorption of vitamin B12, which is necessary for normal hematopoiesis, and the development of pathological megaloblastic hematopoiesis, resulting in anemia of the “pernicious” type. People over the age of 50 get sick.

Disorders of the cardiovascular, nervous, digestive and hematopoietic systems are characteristic. Complaints of patients are diverse: general weakness, shortness of breath, palpitations, pain in the region of the heart, swelling of the legs, crawling sensation in the hands and feet, gait disorder, burning pain in the tongue, periodic diarrhea. The appearance of the patient is characterized by pale skin with a lemon-yellow tint. The sclera are subicteric. The patients are not exhausted. In the study of the cardiovascular system, anemic noises are typical, associated with a decrease in blood viscosity and an acceleration of blood flow. On the part of the digestive organs, the so-called hunter's glossitis (the tongue is bright red, the papillae are smoothed), histamine-resistant achilia (lack of free hydrochloric acid and pepsin in the gastric contents) are found. The liver and spleen are enlarged. With a significant decrease in the number of red blood cells (below 2 million), a fever of the wrong type is observed. Changes in the nervous system are associated with degeneration and sclerosis of the posterior and lateral columns of the spinal cord (funicular myelosis).

Blood picture: hyperchromic type anemia, macrocytes, megalocytes, erythrocytes with Jolly bodies, Cabot rings, leukopenia, thrombocytopenia (during an exacerbation).

Treatment is carried out with vitamin B12-100-200 mcg intramuscularly daily or every other day until remission occurs. In the event of an anemic coma - urgent hospitalization, blood transfusion, preferably erythrocyte mass (150-200 ml). Maintenance therapy with vitamin B12 is necessary to prevent relapse. Systematic monitoring of the composition of the blood in people with persistent achilia, as well as those who underwent gastric resection, is shown. Patients suffering from pernicious anemia should be under dispensary observation (possible occurrence of stomach cancer).

1. Pernicious anemia (synonym: pernicious anemia, Addison-Birmer disease). Etiology and pathogenesis. Currently, pernicious-anemic syndrome is considered as a manifestation of B12-avitaminosis, and Addison-Birmer disease is considered as endogenous B12-avitaminosis due to atrophy of the fundic glands that produce gastromucoprotein, resulting in impaired absorption of vitamin B1a, which is necessary for normal, normoblastic, hematopoiesis, and pathological, megaloblastic, hematopoiesis develops, leading to anemia of the "pernicious" type.

Clinical picture (symptoms and signs). Persons aged 40 45 are ill more senior. Characterized by violations of the cardiovascular, nervous, digestive and hematopoietic systems. Complaints of patients are diverse: general weakness, shortness of breath, palpitations, pain in the region of the heart, swelling of the legs, dizziness, crawling in the hands and feet, gait disorder, burning pain in the tongue and esophagus, periodic diarrhea. The appearance of the patient is characterized by pale skin with a lemon-yellow tint. The sclera are subicteric. The patients are not exhausted. The face is puffy, swelling in the ankles and feet. Edema can reach high degrees and be accompanied by ascites, hydrothorax. On the part of the cardiovascular system - the appearance of systolic murmur at all openings of the heart and the noise of the "top" on the bulb of the jugular vein, which is associated with a decrease in blood viscosity and an acceleration of blood flow; possible anoxemic angina pectoris. With prolonged anemia, fatty degeneration of organs develops, including the heart (“tiger heart”), as a result of persistent anoxemia. On the part of the digestive organs - the so-called hunter's (gunter's) glossitis, the tongue is clean, bright red, devoid of papillae. Analysis of gastric juice, as a rule, reveals histamine-resistant achilia. Periodic diarrhea is a consequence of enteritis. The liver is enlarged, soft; in some cases - a slight increase in the spleen. With a significant drop in the number of red blood cells (below), there is a fever of the wrong type. Changes in the nervous system are associated with degeneration and sclerosis of the posterior and lateral columns of the spinal cord (funicular myelosis). The clinical picture of the nervous syndrome consists of combinations of spastic spinal paralysis and tabic symptoms (the so-called pseudotabes): spastic paraparesis with increased and pathological reflexes, clonuses, crawling, numbness of the extremities, girdle pain, violation of vibrational and deep sensitivity, sensory ataxia and dysfunction pelvic organs; less often - bulbar phenomena.

Blood picture. The most characteristic symptom is anemia of the hyperchromic type. The morphological substrate of hyperchromia is large, hemoglobin-rich erythrocytes - macrocytes and megalocytes (the latter reach 12-14 microns or more). With an exacerbation of the disease, the number of reticulocytes in the blood decreases sharply. The appearance of a large number of reticulocytes portends a close remission.

An exacerbation of the disease is characterized by the appearance of degenerative forms of erythrocytes [poikilocytes, schizocytes, basophilic punctured erythrocytes, erythrocytes with Jolly bodies and Cabot rings (printing table, Fig. 3)], individual megaloblasts (printing table, Fig. 5). Changes in white blood are characterized by leukopenia due to a decrease in the number of cells of bone marrow origin - granulocytes. Among the cells of the neutrophilic series, giant, polysegmentonuclear neutrophils are found. Along with the shift of neutrophils to the right, there is a shift to the left with the appearance of young forms and even myelocytes. The number of platelets during the period of exacerbation is significantly reduced (to or less), however, thrombocytopenia, as a rule, is not accompanied by hemorrhagic phenomena.

Bone marrow hematopoiesis during the period of exacerbation of pernicious anemia occurs according to the megaloblastic type. Megaloblasts are a morphological expression of a kind of "dystrophy" of bone marrow cells in conditions of insufficient supply of a specific factor - vitamin B12. Under the influence of specific therapy, normoblastic hematopoiesis is restored (printing table, Fig. 6).

Symptoms of the disease develop gradually. For many years before the disease, gastric achilia is detected. At the beginning of the disease, general weakness is noted; patients complain of dizziness, palpitations at the slightest physical exertion. Then the dyspeptic phenomena, paresthesias join; patients go to the doctor, being already in a state of significant anemization. The course of the disease is characterized by cyclicity - a change in periods of improvement and deterioration. In the absence of proper treatment, relapses become longer and more severe. Before the introduction of liver therapy into practice, the disease fully justified its name "fatal" (pernicious). During the period of severe relapse - the sharpest anemization and the rapid progression of all the symptoms of the disease - a life-threatening coma (coma perniciosum) may develop.

Pathological anatomy. An autopsy of a person who died from pernicious anemia reveals a sharp anemia of all organs, with the exception of the red bone marrow; the latter, being in a state of hyperplasia, fills the diaphysis of the bones (printing table, Fig. 7). There is fatty infiltration of the myocardium ("tiger heart"), kidneys, liver; in the liver, spleen, bone marrow, lymph nodes - hemosiderosis (printing table, Fig. 8). Changes in the digestive organs are characteristic: the papillae of the tongue are atrophic, atrophy of the gastric mucosa and its glands - anadenia. In the posterior and lateral columns of the spinal cord, very characteristic degenerative changes are noted, referred to as combined sclerosis, or funicular myelosis.

Rice. 3. Blood in anemia: 1 - 4 - erythrocytes of the last stage of normal hematopoiesis (the transformation of an erythroblast into an erythrocyte); 5-9 - disintegration of the nucleus with the formation of Jolly bodies in basophilic punctured (5, 6) and polychromatophilic (7 - 9) erythrocytes; 10 and 11 - Jolly bodies in orthochromic erythrocytes; 12 - chromatin dust particles in erythrocytes; 13 - 16 - Kebot rings in basophilic punctured (13, 14) and orthochromic (15, 16) erythrocytes (pernicious anemia); 17 - 23 - basophilic punctured erythrocytes in lead anemia; 24 and 25 - polychromatophilic erythrocytes (microcyte and macrocyte); megalocyte (26) and poikilocyte (27) in pernicious anemia; 28 - normocyte; 29 - microcytes.

Rice. 5. Blood in pernicious anemia (severe relapse): orthochromic (1) and polychromatophilic (2) megalocytes, erythrocytes with Cabot rings (3), Jolly bodies (4) with basophilic puncture (5), megaloblasts (6), polysegmentonuclear neutrophil ( 7), anisocytosis and poikilocytosis (8).

Rice. 6. Bone marrow in pernicious anemia (initial remission 24 hours after the administration of 30 µg of vitamin B12): 1 - normoblasts; 2 - metamyelocytes; 3 - stab neutrophil; 4 - erythrocyte.

Rice. 7. Myeloid hyperplasia of the bone marrow in malignant anemia.

Rice. 8. Hemosiderin pigmentation of the periphery of the hepatic lobules in pernicious anemia (reaction to Prussian blue).

Treatment. Since the 1920s, raw liver, especially lean veal liver, passed through a meat grinder (200 g per day) has been used with great success for the treatment of malignant anemia. A great achievement in the treatment of pernicious anemia was the manufacture of liver extracts, especially for parenteral administration (campolone, antianemin). The specificity of the action of hepatic drugs in pernicious anemia is due to their content of vitamin B12, which stimulates the normal maturation of erythroblasts in the bone marrow.

The greatest effect is achieved with the parenteral use of vitamin B12. The daily dose of vitamin B2 is 50-100 mcg. The drug is administered intramuscularly, depending on the patient's condition - daily or every 1-2 days. Oral use of vitamin B12 is effective only in combination with the simultaneous intake of an internal anti-anemic factor (gastromucoprotein). At present, favorable results have been obtained from the treatment of patients with pernicious anemia by internal use of the drug mucovit (available as a dragee) containing vitamin B12 (200-500 mcg) in combination with gastromucoprotein (0.2). Mucovit is prescribed 3-6 tablets per day daily until the onset of a reticulocyte crisis and then 1-2 times a day until the onset of hematological remission.

The immediate effect of antianemic therapy in terms of blood replenishment with newly formed erythrocytes begins to affect the rise of reticulocytes to 20-30% or more from the 5-6th day of treatment (“reticulocyte crisis”). Following the reticulocyte crisis, the amount of hemoglobin and erythrocytes begins to increase, which after 3-4 weeks reaches a normal level.

Folic acid, administered orally or parenterally at a dose of 30-60 mg or more (up to 120-150 mg) per day, causes a rapid onset of remission, but does not prevent the development of funicular myelosis. With funicular myelosis, vitamin B12 is used intramuscularly in large doses of 200-400 micrograms, in severe cases, 500-000 (!) micrograms per day] until complete clinical remission is achieved. The total dose of vitamin B12 during a 3-4-week course of anemia treatment is 500-1000 mcg, with funicular myelosis - up to 5000 mcg and above.

The effectiveness of vitamin B12 therapy has a known limit, upon reaching which the growth of quantitative blood parameters stops and anemia acquires a hypochromic character; during this period of the disease, it is advisable to use treatment with iron preparations (2-3 g per day, washed down with diluted hydrochloric acid).

The question of the use of blood transfusions in pernicious anemia in each case is decided according to indications. An unconditional indication is a pernicious coma, which poses a threat to life due to increasing hypoxemia. Repeated blood transfusions or (better) erythrocyte mass (250-300 ml each) often save the lives of patients until the moment when the therapeutic effect of vitamin B12 manifests itself.

Prevention. The minimum daily human requirement for vitamin B12 is 3-5 mcg, therefore, in order to prevent the recurrence of pernicious anemia, it can be recommended to inject 100-200 mcg of vitamin B12 2 times a month, and in spring and autumn (when relapses occur more often) - once a week or 10 days. It is necessary to systematically monitor the composition of the blood in persons who have undergone an extensive resection of the stomach, as well as those who have persistent achilia of the stomach, provide them with a complete diet, and, if necessary, apply early antianemic treatment. It should be remembered that pernicious anemia can be an early symptom of stomach cancer. In general, it is known that patients with stomach achylia and especially pernicious anemia more often than others develop stomach cancer. Therefore, all patients with pernicious anemia should be under dispensary observation and annually undergo a control x-ray examination of the stomach.

pernicious anemia

Pernicious anemia (malignant anemia, Addison-Birmer disease) was first described by Addison and Birmer (1855-1871). Pernicious anemia was considered incurable until 1926, but then became curable, and therefore not "malignant".

It was once believed that the root cause of this disease is intoxication. However, the source of intoxication remained unknown; for differential diagnosis, they relied on the most characteristic moments of the clinic and pathological anatomy of the disease.

Some attached great importance to the state of the bone marrow in malignant anemia, such as Ehrlich, who called this state "return to the embryonic state." Others attached particular importance to the increased activity of the blood-destroying system (based on the determination of the daily amount of urobilin in feces and bilirubin in bile).

It seemed to many that the spleen was significantly interested in the pathogenesis of the disease, although it was not always enlarged. Evidence of the involvement of the spleen in the pathogenesis of the disease were prolonged remissions that occurred after splenectomy. At the same time, Decastello attributed the positive effect of splenectomy to the loss of physiological hemolysis; others argued that the function of an organ with increased hemolytic activity falls out, others believed that during splenectomy, an organ that inhibits the erythropoietic activity of the bone marrow is removed.

The onset of remission and after other methods of treatment, as well as the return of the disease and after splenectomy proved that not only hemolysis is to blame for the pathogenesis of malignant anemia.

Currently, the cause of Addison-Birmer disease is considered to be a lack of hematopoietic vitamin B12 and folic acid. The insufficiency of this vitamin develops on the basis of functional or anatomical disorders of the fundic glands of the stomach of a neurotrophic nature; the same avitaminosis also occurs with Achilles gastritis (syphilis, polyposis or gastric cancer) or agastria (gastrectomy or exclusion of the stomach by other operations), with helminthic invasion (wide tapeworm), pregnancy, sprue (prolonged enteritis), with resection or exclusion of the small intestine. All these are secondary forms; in some of them, the disease proceeds without nervous phenomena, achilia, and is cured with the elimination of the etiological factor. And, finally, vitamin deficiency B12 may be of exogenous origin - a lack of vitamin B12 in food. Pathogenetically, we are talking about a violation of bone marrow hematopoiesis (violation of the maturation of the formed elements of the erythroid germ by the type of return to embryonic hematopoiesis).

The hemolysis that accompanies this form of anemia does not put it among hemolytic anemias, since we are talking about the destruction of red blood cells in the bone marrow itself due to impaired hematopoiesis.

Symptoms of pernicious anemia

The disease affects people over the age of 40 years (before 25 years of age is exceptionally rare), equally often men and women. It all starts with achilia and changes in the nervous system. There is weakness, dizziness, and then signs of anemia - shortness of breath, palpitations with slight physical exertion. Simultaneously with anemia, glossitis occurs (pain and burning in the tongue) - a pathognomonic symptom of pernicious anemia. In the future, inflammation is replaced by atrophy of the papillae and the tongue becomes as if varnished.

Patients are pale, with a lemon-yellow skin tone. There is some puffiness of the face, swelling of the feet and a tendency to obesity. The liver is enlarged, the spleen is not. If occasionally the spleen is enlarged, then this should by no means be considered an indication for splenectomy, as was the case in the period before the 20s of our century due to misconceptions about the essence of the disease.

The course of pernicious anemia is cyclic - deterioration is replaced by remissions, which can occur spontaneously even after very prolonged deterioration. During deterioration, hyperchromic anemia is especially pronounced due to hemoglobin-rich macrocytes-megalocytes (a product of megaloblastic hematopoiesis) without central enlightenment; few polychromatophiles and reticulocytes (their appearance heralds remission).

Until now, hyperchromic anemia with phenomena of the embryonic type of hematopoiesis (megaloblasts from megaloblasts) is the main characteristic feature that distinguishes true pernicious anemia from other anemias. Otherwise, the blood picture is characterized by a significant decrease in the number of red blood cells, a decrease in hemoglobin, aniso- and poikilocytosis; erythro- and normoblasts by no means represent the characteristic features of a blood smear and are found in significant numbers only on the eve of remissions. As a rule, there is also leukopenia with relative lymphocytosis; among neutrophils there are hypersegmented forms; sometimes myelocytes are found (a sign of particular irritation of the bone marrow). There are always few platelets. The blood serum is dark yellow, especially at the moments of deterioration (hemolysis phenomena); in parallel with bilirubinemia, urobilinuria is observed. These phenomena are directly dependent on the severity of pernicious anemia, so they may be completely absent during the period of remission. Significant deterioration can be combined with the phenomena of hemorrhagic diathesis. Malnutrition of the heart muscle (due to hypoxia associated with anemia) affects the negative T wave on the electrocardiogram.

In the pathoanatomical picture, along with severe anemia of all internal organs, degenerative fatty infiltration and siderosis (deposition of iron-containing pigment), especially a lot of iron is found in the liver, spleen, bone marrow, and lymph nodes. In the spleen, iron is found mainly intracellularly, and this distinguishes pernicious anemia from aplastic anemia, in which siderosis is extracellular. Intracellular hemolysis is a normal type of hemolysis that maintains the balance of iron metabolism in the body, while extracellular hemolysis disrupts it. That is why with pernicious anemia there is hyperchromemia, and with aplastic - hypochromemia.

Pathological changes in the spleen in pernicious anemia appear already and macroscopically in the form of a particularly strong overflow with blood; in the histological picture, there is a significant overflow of the spleen pulp with erythrocytes located more around the trabeculae and follicles; the latter are almost always preserved, and in some cases their number is even increased. Sometimes there is extramedullary hematopoiesis in the form of the appearance of scattered myeloid foci located near the adventitia of the vessels. According to some, there are also vascular changes, especially in the form of thickening of the walls of the central arteries and the deposition of hyaline in the intima. Hyaline degeneration of the small vessels of the spleen is a very common occurrence in persons aged between 10 and 40 years, and even more often in the elderly. At the same time, the whole intima is reborn in small vessels.

Other changes in the hematopoietic system include the appearance of red bone marrow in long tubular bones and the presence of a large number of megaloblasts in the microscopic picture of the bone marrow; in the lymph nodes and in the liver, extramedullary hematopoiesis is also sometimes observed.

Along with the hematopoietic system, there are changes in the digestive tract; they are reduced to inflammation and atrophy of the mucous membrane of the stomach and intestines. Changes in the adrenal glands are found in the form of a decrease in lipoids and chromaffin substance.

Anemia agastric - anemia due to loss of antianemic function of the stomach (after removal of the stomach or with some of its diseases). Anemia develops according to the type of pernicious anemia, but more often according to the type of Achilles chloranemia. Fears that gastric resection supposedly always entails such anemia are exaggerated. Severe anemia of the malignant type sometimes occurs only after total gastrectomy (about 8%); treatment in these cases is not unsuccessful, and postponing surgery to prevent anemia is dangerous from an oncological point of view. Conventional resection of the stomach, especially with peptic ulcer, is sometimes accompanied (15-20% of cases) by a slight anemia of the chloranemic order, which responds well to iron treatment.

Treatment of pernicious anemia

Currently, pernicious anemia is cured by organo- and vitamin therapy. Recommended raw veal liver (passed through a meat grinder) twice a day, 100 g (drink with diluted hydrochloric acid - 25 drops in half a glass of water) 2 hours before the usual meal for 5-6 weeks. Liver extracts for internal use and parenterally. The effectiveness of all the above methods of treatment depends on the content of hematopoietic vitamin B12 in them. Liver extract has been successfully used recently.

To prevent the recurrence of pernicious anemia, liver therapy (liver extract or liver itself, as indicated above) should be performed regularly every other day. Recently, antianemin (liver concentrate in combination with cobalt) has been successfully used in the form of injections into muscles, 2-4 ml daily. You can also use the intramuscular injection of pure (crystalline) vitamin B12 at 15-30 mcg.

In functional myelosis, raw liver (rich in vitamins B1 and B12) is most effective.

Anemia of pregnancy is cured by vigorous parenteral hepatic therapy, campolone (termination of pregnancy is allowed only in case of ineffective treatment).

Attempts by surgeons to influence pernicious anemia by a combined intervention in the form of removal of the spleen and simultaneous transplantation of the adrenal gland (the latter event was based on changes in the adrenal glands of patients) were also unsuccessful.

Prognosis for pernicious anemia

The prognosis is favorable. With systematic treatment, remission lasts for years. Even better is the prediction when the cause of the disease is syphilis and broad tapeworm, the expulsion of the latter or a specific anti-syphilitic treatment leads to a complete recovery.

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Anemia in cancer

In more than 1/3 of cancer patients, a drop in hemoglobin levels is observed. Cancer anemia is measured by the level of oxygen saturation in the blood, which in this case drops to less than 12 g/dL. This condition of the body is also often observed in patients who have undergone chemotherapy.

Lack of oxygen in the circulatory system adversely affects the general condition of the patient and worsens the prognosis of the disease.

Causes of anemia in cancer

The etiology of this pathology is associated with three main factors:

1. Slowing down the production of red blood cells.
2. Accelerated destruction of blood cells.
3. The occurrence of internal bleeding.

In some clinical cases, the anemic state of the body is a consequence of chemotherapy or radiation exposure. This type of anti-cancer treatment negatively affects the processes of hematopoiesis. For example, platinum-containing drugs reduce the amount of erythropoietin in the kidneys. This substance is a kidney hormone that stimulates the formation of red blood cells.

Determining the exact cause of this pathology is necessary for an adequate selection of a method for treating a malignant neoplasm.

The first signs and symptoms of cancerous anemia

The first symptoms of the disease are considered to be a sharp pallor of the skin and a violation of the digestive function. Most patients lose their appetite and experience chronic nausea and vomiting.

The progression of the underlying cancer is accompanied by a gradual deterioration in general well-being. Patients report constant malaise, muscle weakness, fatigue and loss of efficiency.

Cancer anemia is diagnosed on the basis of a detailed blood test. A quantitative study of the circulatory system is recommended several times during the course of treatment. This allows specialists to assess the dynamics of the development of pathology.

Treatment of anemia in cancer patients

For the treatment of anemic blood damage, doctors use the following methods:

Red blood cell transfusion:

The undoubted advantage of intravenous administration of erythrocyte preparations is the rapid restoration of normal hemoglobin values. At the same time, this technique has a short-term therapeutic effect. Many experts do not recommend prescribing transfusion to cancer patients from the first days of anemia. In the initial period, the patient's body independently copes with the insufficiency of red blood cells. Compensation is achieved by changing blood viscosity and oxygen uptake.

Blood transfusion is mainly carried out in the presence of a bright clinical picture of oxygen starvation.

Also, cancer patients should take into account that science has not proven a direct relationship between life expectancy, tumor recurrence and red blood cell transfusion.

Stimulation of the production of red blood cells:

Many clinical studies indicate the high effectiveness of erythropoietin hormonal preparations. In many cases, this treatment option can replace systemic blood transfusion. Particular attention should be paid to patients with chronic renal failure. For these patients, there is an increased risk of premature death.

The use of iron preparations:

Iron deficiency is observed in approximately 60% of cancer patients. Causes of iron deficiency can be:

• chronic internal bleeding;
• surgical interventions on the organs of the gastrointestinal tract;
• cancerous anorexia.

What are the consequences of anemia in cancer?

Many doctors believe that an anemic condition accompanies the course of all oncological diseases to one degree or another. The danger of erythrocyte deficiency lies in the development of oxygen starvation of all tissues and body systems. Also, this disease, as a rule, aggravates chemotherapy and radiation therapy.

Forecast

The consequences of the disease depend on the stage of primary diagnosis of the tumor process. Erythrocyte insufficiency, which is detected in the early stages of oncology, has a favorable prognosis. A positive outcome in this case is due to the high probability of a complete cure of the primary cancer focus.

Anemia in cancer with a negative prognosis is observed in patients with malignant neoplasms of 3-4 stages of development. At this stage, tumors cause cancer intoxication, the formation of metastases and death.

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Anemia malignant

Pernicious Anemia (Juvenile Pernicious Anemia; Congenital Pernicious Anemia)

Description

Pernicious anemia develops 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 essential for the absorption of vitamin B12. Pernicious anemia is often associated with autoimmune-mediated attack of gastric parietal cells and/or intrinsic factor. Anemia is the insufficient supply of red blood cells with oxygen to the cells of the body. The sooner treatment for pernicious anemia is started, the better the outcome.

Causes of pernicious anemia

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

• Atrophic gastritis (inflammation of the stomach);
• Removal of all or part of the stomach;
• The reaction of the immune system (in the form of an attack) to:
  • Intrinsic factor - a protein required for the absorption of vitamin B12
  • Cells that produce intrinsic 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 insufficiency of the adrenal cortex;
• Origin: Northern Europe and Scandinavia;
• Age: over 50 years old.

Symptoms of pernicious anemia

Symptoms of pernicious anemia can vary. Symptoms may change or worsen over time. These symptoms may be caused by other diseases. It is necessary to inform the doctor if any of them appear.

Symptoms may include:

• tingling sensation in the legs or arms;
• Intermittent constipation and diarrhea;
• burning sensation on the tongue or sensitive red tongue;
• Significant weight loss;
• Inability to distinguish between yellow and blue;
• Fatigue;
• Pallor;
• Altered taste sensations;
• Depression;
• Violation of the sense of balance, especially at night;
• Tinnitus;
• Chapped lips;
• Yellow skin;
• Fever;
• Inability to feel vibrations in the legs;
• Vertigo 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 test, which measures the amount of vitamin B12 in the blood
• Measuring the amount of methylmalonic acid in the blood - this test shows if there is a vitamin B12 deficiency;
• Homocysteine ​​level - a test that measures the amount of homocysteine ​​in the blood (homocysteine ​​is a component that is involved in protein formation). Homocysteine ​​levels will be elevated if there is a deficiency of vitamin B12, folic acid, or vitamin B6;
• Schilling test - a test that uses a harmless amount of radiation to assess vitamin B12 deficiency (rarely used);
• Measuring the amount of folic acid;
• Measurement of the amount of a protein called intrinsic factor (Castle factor) - usually done in the stomach;
• Bone marrow staining with Prussian blue is a test that shows if there is an iron deficiency.

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 in taking increased doses of vitamin B12 orally.

Intranasal vitamin B12

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

Oral iron supplements

Prevention of pernicious anemia

To reduce the chance of developing pernicious anemia, the following steps should be taken:

• Long-term excessive alcohol consumption should be avoided;
• Ask your doctor to test for iron deficiency;
• Get tested if your doctor suspects Helicobacter pylori infection.

pernicious anemia

Pernicious anemia is a violation of the red germ of hematopoiesis, due to a lack of cyanocobalamin (vitamin B12) in the body. With B12-deficiency anemia, circulatory-hypoxic (pallor, tachycardia, shortness of breath), gastroenterological (glossitis, stomatitis, hepatomegaly, gastroenterocolitis) and neurological syndromes (impaired sensitivity, polyneuritis, ataxia) develop. Confirmation of pernicious anemia is based on the results of laboratory tests (clinical and biochemical blood tests, bone marrow punctate). Treatment of pernicious anemia includes a balanced diet, intramuscular injection of cyanocobalamin.

pernicious anemia

Pernicious anemia is a type of megaloblastic deficiency anemia that develops with insufficient endogenous intake or absorption of vitamin B12 in the body. "Pernicious" in Latin means "dangerous, disastrous"; in the domestic tradition, such anemia used to be called "malignant anemia". In modern hematology, pernicious anemia is also synonymous with B12-deficiency anemia, Addison-Birmer disease. The disease occurs more often in older people, somewhat more often in women. The prevalence of pernicious anemia is 1%; however, about 10% of older people over the age of 70 suffer from vitamin B12 deficiency.

Causes of pernicious anemia

The daily human need for vitamin B12 is 1-5 micrograms. It is satisfied by the intake of the vitamin with food (meat, dairy products). In the stomach, under the action of enzymes, vitamin B12 is separated from dietary protein, but for absorption and absorption into the blood, it must combine with a glycoprotein (Castle factor) or other binding factors. The absorption of cyanocobalamin into the bloodstream occurs in the middle and lower parts of the ileum. The subsequent transport of vitamin B12 to tissues and hematopoietic cells is carried out by blood plasma proteins - transcobalamins 1, 2, 3.

The development of B12-deficiency anemia can be associated with two groups of factors: alimentary and endogenous. Nutritional causes are due to insufficient intake of vitamin B12 with food. This can occur with fasting, vegetarianism, and diets that exclude animal protein.

Under endogenous causes is meant a violation of the absorption of cyanocobalamin due to a deficiency of the internal factor of Castle with its sufficient intake from the outside. Such a mechanism for the development of pernicious anemia occurs in atrophic gastritis, a condition after gastrectomy, the formation of antibodies to the intrinsic factor of Castle or parietal cells of the stomach, and congenital absence of the factor.

Violation of the absorption of cyanocobalamin in the intestine can be observed in enteritis, chronic pancreatitis, celiac disease, Crohn's disease, diverticula of the small intestine, tumors of the jejunum (carcinoma, lymphoma). Increased consumption of cyanocobalamin may be associated with helminthiases, in particular, diphyllobothriasis. There are genetic forms of pernicious anemia.

Absorption of vitamin B12 is impaired in patients who underwent resection of the small intestine with the imposition of a gastrointestinal anastomosis. Pernicious anemia may be associated with chronic alcoholism, the use of certain drugs (colchicine, neomycin, oral contraceptives, etc.). Since the liver contains a sufficient reserve of cyanocobalamin (2.0-5.0 mg), pernicious anemia develops, as a rule, only 4-6 years after the violation of the intake or absorption of vitamin B12.

In conditions of vitamin B12 deficiency, there is a deficiency of its coenzyme forms - methylcobalamin (participates in the normal course of erythropoiesis processes) and 5-deoxyadenosylcobalamin (participates in metabolic processes occurring in the central nervous system and peripheral nervous system). The lack of methylcobalamin disrupts the synthesis of essential amino acids and nucleic acids, which leads to a disorder in the formation and maturation of red blood cells (megaloblastic type of hematopoiesis). They take the form of megaloblasts and megalocytes, which do not perform an oxygen transport function and are rapidly destroyed. In this regard, the number of erythrocytes in the peripheral blood is significantly reduced, which leads to the development of anemic syndrome.

On the other hand, with a deficiency of the coenzyme 5-deoxyadenosylcobalamin, the metabolism of fatty acids is disturbed, as a result of which toxic methylmalonic and propionic acids accumulate, which have a direct damaging effect on the neurons of the brain and spinal cord. In addition, myelin synthesis is disrupted, which is accompanied by degeneration of the myelin layer of nerve fibers - this is due to damage to the nervous system in pernicious anemia.

Symptoms of pernicious anemia

The severity of pernicious anemia is determined by the severity of circulatory-hypoxic (anemic), gastroenterological, neurological and hematological syndromes. Signs of an anemic syndrome are nonspecific and are a reflection of a violation of the oxygen transport function of erythrocytes. They are represented by weakness, decreased endurance, tachycardia and palpitations, dizziness and shortness of breath when moving, low-grade fever. On auscultation of the heart, a whirlpool or systolic (anemic) murmur may be heard. Outwardly, there is pallor of the skin with a subicteric shade, puffiness of the face. A long "experience" of pernicious anemia can lead to the development of myocardial dystrophy and heart failure.

Gastroenterological manifestations of B12-deficiency anemia are decreased appetite, stool instability, hepatomegaly (fatty liver). The classic symptom found in pernicious anemia is a raspberry-colored “varnished” tongue. The phenomena of angular stomatitis and glossitis, burning and pain in the tongue are characteristic. During gastroscopy, atrophic changes in the gastric mucosa are detected, which are confirmed by endoscopic biopsy. Gastric secretion is sharply reduced.

Neurological manifestations of pernicious anemia are caused by damage to neurons and pathways. Patients indicate numbness and stiffness of the limbs, muscle weakness, impaired gait. Possible incontinence of urine and feces, the occurrence of persistent paraparesis of the lower extremities. Examination by a neurologist reveals a violation of sensitivity (pain, tactile, vibration), increased tendon reflexes, symptoms of Romberg and Babinsky, signs of peripheral polyneuropathy and funicular myelosis. With B12-deficiency anemia, mental disorders can develop - insomnia, depression, psychosis, hallucinations, dementia.

Diagnosis of pernicious anemia

In addition to a hematologist, a gastroenterologist and a neurologist should be involved in the diagnosis of pernicious anemia. Vitamin B12 deficiency (less than 100 pg / ml at normepg / ml) is established during a biochemical blood test; it is possible to detect antibodies to the parietal cells of the stomach and to the internal factor of the Castle. For a complete blood count, pancytopenia (leukopenia, anemia, thrombocytopenia) is typical. Microscopy of a peripheral blood smear reveals megalocytes, Jolly and Cabot bodies. Examination of feces (coprogram, analysis for eggs of worms) can reveal steatorrhea, fragments or eggs of a wide tapeworm in diphyllobothriasis.

The Schilling test allows you to determine the malabsorption of cyanocobalamin (by urinary excretion of radioactively labeled vitamin B12 taken orally). Bone marrow puncture and myelogram results reflect an increase in the number of megaloblasts characteristic of pernicious anemia.

To determine the causes of impaired absorption of vitamin B12 in the gastrointestinal tract, FGDS, radiography of the stomach, and irrigography are performed. In the diagnosis of concomitant disorders, ECG, ultrasound of the abdominal organs, electroencephalography, MRI of the brain, etc. are informative. B12-deficiency anemia must be distinguished from folic acid deficiency, hemolytic and iron deficiency anemia.

Treatment of pernicious anemia

Establishing a diagnosis of pernicious anemia means that the patient will need lifelong pathogenetic treatment with vitamin B12. In addition, regular (every 5 years) gastroscopy is indicated to exclude the development of gastric cancer.

In order to compensate for the deficiency of cyanocobalamin, intramuscular injections of vitamin B12 are prescribed. Correction of the conditions that led to B12-deficiency anemia (deworming, taking enzyme preparations, surgical treatment) is required, and with the alimentary nature of the disease, a diet with a high content of animal protein. In case of violation of the production of the intrinsic factor of Castle, glucocorticoids are prescribed. Blood transfusions are used only for severe anemia or signs of anemic coma.

Against the background of therapy for pernicious anemia, blood counts usually normalize after 1.5-2 months. The neurological manifestations persist the longest (up to 6 months), and with late treatment they become irreversible.

Prevention of pernicious anemia

The first step towards preventing pernicious anemia should be a nutritious diet that provides sufficient intake of vitamin B12 (meat, eggs, liver, fish, dairy products, soy). Timely therapy of pathologies of the gastrointestinal tract that violates the absorption of the vitamin is necessary. After surgical interventions (resection of the stomach or intestines), it is necessary to conduct maintenance courses of vitamin therapy.

Patients with B12-deficiency anemia are at risk for the development of diffuse toxic goiter and myxedema, as well as stomach cancer, therefore, they need to be monitored by an endocrinologist and gastroenterologist.

Pernicious anemia
Chronic diseases / anemia due to insufficient absorption of vitamin B 12

It occurs in adults as a result of gastric atrophy (cannot absorb vitamin B12). The wall cells in the stomach that produce the intrinsic factor necessary for the absorption of vitamin B12 and, if destroyed, lead to a lack of this very important vitamin.

The name of pernicious anemia has remained since the time when this type of anemia was fatal and has retained the name for historical reasons.

Due to lack of vitamin B12 can cause a number of diseases and conditions, but anemia only includes those caused by atrophic gastritis and loss of parietal cell function.
Dr. Addison first described the disease and before 1920 people died from this disease one to three years after diagnosis. Doctors have investigated this anemia so that patients consume more raw liver and juice in large quantities. And so they deservedly received the Nobel Prize in 1934, incurable diseases!

We are very grateful for the progress, as well as the fact that we do not eat raw liver, but have solved the lack of this vitamin with pills or injections!
Vitamin B 12 cannot be created/synthesized by the human or animal body in such a way that it must be supplied with food. It is essential for the proper functioning of the brain and nervous system, it is involved in the metabolism of every cell in the body.

Most people get their vitamin B12 from meat (especially liver), fish, shellfish, and dairy products.

The genetic variant of pernicious anemia is an autoimmune disease, with a definitive genetic predisposition. Antibodies are found in 90% of people with pernicious anemia, and currently only 5% of people in the general population.
Classic pernicious anemia caused by a lack of intrinsic factors synthesized in the parietal cells of the stomach, not absorption of vitamin B12, the result: megaloblastic anemia.
Any disease or condition can lead to vitamin B12 deficiency malabsorption and anemia is observed (although not always), a neurological condition.

Periodicity:
The most widespread in the North European population. English, Scandinavian, Irish, Scottish, aged 40-70 years of age.

Problem:
weight loss, fever
Anemia is quite tolerable, even when hemoglobin is very low (40-50), MCV (mean corpuscular volume) is high: more than 100 UGL
About 50% of patients have a very smooth tongue, without papillae (glositis)
Changes in character and personality
Disrupted thyroid function
Diarrhea
Paresthesias: tingling in the arms/legs
The most difficult: neurological disorders: balance problems, gait problems, muscle weakness. In an elderly person with signs of dementia, a lack of vitamin B12 is detected and memory problems, hallucinations, and irritability may occur.

Diagnosis:

Laboratory tests: complete blood count, peripheral blood, levels of vitamin B12, folic acid, methylmalonic acid and homocysteine ​​in the blood
testing the patient's ability to absorb vitamin B12.

Presence of antibodies and intrinsic factors in the blood.

THERAPY:
As you probably guessed, the therapy is to replace vitamin B12. Vitamin B12 does not exist in nature, but is synthesized and applied to patients in the form of tablets, transdermal, nasal or injection (IM, subcutaneous).
Today there are pills that contain high doses of vitamin B12: 500-1000 mcg, so that there is a sufficient amount of vitamin B12 cells in the body.

Is there any doubt, anyway, to provide replacement therapy in the form of injections!
Famous people with pernicious anemia
Alexander Graham Bell
Annie Oakley: 1925. died of pernicious anemia at age 65

Health

Pernicious anemia is a condition in which a sick person's body is no longer able to produce the required amount of healthy red blood cells due to a deficiency of vitamin B12 (a nutrient found in certain foods).

For example, people who suffer from pernicious anemia are unable to absorb enough vitamin B12 due to a lack of so-called intrinsic factor (a protein produced in the stomach).

However, other causes and conditions can also lead to vitamin B12 deficiency.

Causes of pernicious anemia and risk factors

-- One of the most common causes is a lack of "intrinsic factor" in the stomach, which causes the body to become unable to absorb enough vitamin B12.

-- Some cases of pernicious anemia are due to the presence of harmful bacteria in the small intestine, which in turn causes the small intestine to not absorb vitamin B12 properly; interfere with the absorption of vitamin B12 and some diseases, taking certain medications, surgery to partially or completely remove the small intestine, as well as teniidosis (the presence of worms of a certain group).

-- Another reason why the human body may not receive adequate amounts of vitamin B12, resulting in pernicious anemia, is the lack of this vitamin in the patient's diet.

There are also several risk factors that increase the risk of pernicious anemia:

-- Having a family history of the condition (family history).

-- If there was an operation to partially or completely remove the stomach.

-- If there are some autoimmune diseases that affect the endocrine glands (for example, chronic insufficiency of the adrenal cortex (Addison's disease), type 1 diabetes, Graves' disease and vitiligo).

-- If there was surgery to partially or completely remove the small intestine.

-- In the presence of certain gastrointestinal diseases or disorders that do not allow the patient's body to properly absorb vitamin B12.

-- If certain medications are taken, one of the side effects of which is also that the body temporarily stops absorbing vitamin B12 properly.

-- If the patient follows a strict vegetarian diet, not allowing himself a single gram of meat and dairy products and refusing to take vitamin B12 supplements. Very often, poor nutrition in general is a risk factor.

Symptoms and treatment of pernicious anemia

In addition to the symptoms that are characteristic of all types of anemia (fatigue, dizziness, and so on), vitamin B12 deficiency is accompanied by characteristic serious signs:

-- Nerve damage.

-- Neurological problems such as confusion, dementia, depression and memory loss.

-- Symptoms related to the gastrointestinal tract, including nausea and vomiting, heartburn, bloating and gas, constipation or diarrhea, loss of appetite and weight loss.

-- Enlargement of the liver.

-- Swelling of the tongue, which loses its roughness and becomes smooth.

-- Infants who suffer from vitamin B12 deficiency may show poor reflexes, inappropriate body movements, and facial twitching.

Interventions for the treatment of pernicious anemia usually include the replacement of vitamin B12 that is not being received by the body.

Treatment can be highly successful, but requires a long period of time and sometimes lasts throughout the life of the patient.

Pernicious anemia (B12-deficiency anemia) is a disease that is caused by impaired hematopoiesis (formation of blood cells), which develops as a result of a lack of vitamin B12 in the body.

Symptoms of pernicious anemia

Anemia develops rather slowly and has no specific symptoms in the initial period. Patients complain of weakness, fatigue, shortness of breath and increased heart rate during exercise, as well as dizziness.

With severe anemia, the skin becomes pale icteric, yellowness of the sclera appears. Some patients are concerned about pain in the tongue and impaired swallowing associated with the development of glossitis (inflammation of the tongue), it is also possible to enlarge the spleen, and sometimes the liver.

Pernicious anemia is characterized by damage to the nervous system called funicular myelosis. Its first symptom is sensory disturbance with constant pain in the limbs, resembling tingling, crawling, and numbness. Patients are concerned about pronounced muscle weakness, as a result of which the gait is disturbed, muscle atrophy may develop.

If the disease is not treated, then the spinal cord is affected. First of all, there is a symmetrical lesion of the lower extremities, a violation of surface and pain sensitivity. The lesion has an ascending character and can spread to the abdomen and above. There is a violation of vibrational and deep sensitivity, hearing and smell. Perhaps the occurrence of mental disorders, the appearance of auditory and visual hallucinations, delusions, as well as memory impairment.

In the most severe cases, patients experience exhaustion, inhibition of reflexes and paralysis of the lower extremities.

Causes of pernicious anemia

Most often, this form of anemia develops when malabsorption of cyanocobalamin (vitamin B12) and folic acid in the stomach is impaired. This is due to congenital and acquired diseases of the gastrointestinal tract, such as Crohn's disease, celiac disease and Sprue, malabsorption (lack of absorption of nutrients in the intestine), intestinal lymphoma. Very often, patients have a violation of the production of the internal factor of Castle, which is necessary for the absorption of cyanocobalamin.

The reasons for the development of pernicious anemia can be: a lack of vitamin B12 intake from food as a result of vegetarianism or an unbalanced diet, alcoholism, parenteral nutrition and anorexia of a neuropsychic nature.

It is also not uncommon for pregnant and lactating women and people suffering from psoriasis and exfoliative dermatitis to develop anemia, since they have an increased need for vitamin B12.

Pernicious anemia during pregnancy

Pernicious anemia can develop with insufficient intake of cyanocobalamin and folic acid into the body of a pregnant woman.

The disease can begin in the second half of pregnancy, it leads to a sharp decrease in the production of red blood cells by the bone marrow, while the hemoglobin content in them is normal or even increased. These changes are reflected in the results of a clinical blood test, so it is important to do blood tests prescribed by a doctor in a timely manner.

Pernicious anemia develops in pregnant women slowly, pale skin appears, women complain of weakness and fatigue, which gives the doctor the opportunity to suspect anemia. Later, digestive disorders may join. Damage to the nervous system is extremely rare, possibly a slight decrease in sensitivity in the extremities.

B12-deficiency anemia in pregnant women should be treated because the presence of this disease increases the risk of placental abruption, preterm labor and stillbirth. Treatment is carried out according to the general scheme, and after childbirth, recovery usually occurs.

Pernicious anemia in children

Most often, pernicious anemia affects children who have hereditary disorders in the gastrointestinal tract, as a result of which the absorption of vitamin B12 is impaired. It is extremely rare, but still there are cases of anemia in children as a result of insufficient intake of vitamins from food (breastfeeding by a vegetarian mother, unbalanced nutrition).

In children with hereditary disorders, anemia develops as early as three months of age, but symptoms may appear only by the third year of life.

When examining such children, attention is drawn to dryness and peeling of the skin, as well as their lemon shade, glossitis and enlargement of the spleen. Patients' appetite is reduced, digestive disorders are observed. Children get sick quite often. In severe cases, a lag in physical development is possible.

Treatment of pernicious anemia

Pernicious anemia responds well to treatment, which should first of all be aimed at eliminating the factor that caused the disease. It is necessary to cure diseases of the gastrointestinal tract and balance nutrition.

In order to normalize hematopoiesis in the bone marrow, replacement therapy is used, which consists in the intravenous administration of vitamin B12. Already after the first injections of the drug, patients notice a significant improvement in well-being, and blood test results are normalized. The course of treatment can last a month or more, depending on the severity of anemia and the intermediate results of treatment.

To achieve a stable remission of the disease, it is necessary to continue therapy for six months. Patients are given weekly administration of cyanocobalamin for 2 months, then injections of the drug are performed 1 time in 2 weeks.

The appointment of iron-containing drugs for this form of anemia is not advisable.

Nutrition for pernicious anemia

Patients with pernicious anemia require a balanced diet containing sufficient amounts of proteins and vitamins. It is necessary to eat beef (especially tongue and heart), rabbit meat, eggs, seafood (octopus, eel, sea bass, cod mackerel, etc.), dairy products, peas, legumes. Fats should be limited because they slow down the processes of hematopoiesis in the bone marrow.

With pernicious anemia, the process of the red germ of hematopoiesis is disrupted. Irreversible phenomena occur in the body associated with a lack of vitamin B12. At the same time, there are deviations from various body systems.

Including the systems undergoing a pathological process include digestive pathology. That is, damage to the digestive system. The functioning of the stomach and liver is disturbed. From the side of the nervous system, pathological phenomena are also observed.

Some sources describe this disease as a malignant pathology. In this case, the name of this anemia matters. Modern hematology has developed certain therapeutic measures aimed at curing this disease.

What it is?

Pernicious anemia is a serious pathology associated with the development of anemia. As mentioned above, in some cases it is considered the most formidable disease. It is known that the lack of B 12 is replenished as a result of the use of products containing these vitamins.

Of great importance in the process of assimilation of the vitamin is the lifestyle of a person. People who lead a lifestyle associated with starvation are most susceptible to pernicious. Therefore, appropriate treatment is required.

Much depends on the accompanying pathology. In some cases, the disease occurs as a result of pathological processes. It is known that disorders in the digestive system can often lead to other diseases. After all, the direct absorption of vitamins into the human body occurs due to the proper functioning of internal organs.

The reasons

What are the main causes of pernicious anemia? The main etiology of the disease is associated with the influence of internal factors. There is also an alimentary way of intake of vitamins B 12 in the human body. Therefore, the causes of the disease are associated with the presence of adverse factors.

What exactly are the diseases that lead to pernicious anemia? Most often, the etiology of pernicious anemia is associated with the following pathological factors:

• atrophic gastritis;
• impact of medical interventions (gastrectomy);
• internal factor of Castle.

Of great importance in the etiology of the disease is enteritis, chronic pancreatitis, Crohn's disease. Tumor formations in the intestine also play a role. Often the causes of pernicious anemia are.

Pernicious anemia is caused by alcohol intoxication. Or the effects of drugs. What drugs cause pernicious anemia?

• colchicine;
• neomycin;
• contraceptives.

Symptoms

Pernicious anemia is predominantly manifested by the presence of symptoms characteristic of anemia. It is known that anemia is characterized by weakness, decreased performance and dizziness. The following symptoms are also distinguished:

• cardiopalmus;
• shortness of breath (with physical activity);
• heart murmurs.

External symptoms of the disease are also noted. Which is the pallor of the skin, puffiness of the face. Complications of these conditions are not uncommon. Myocarditis occurs.

In some cases, heart failure may develop. On the part of the digestive system, there is a decrease in appetite. In most cases, dyspepsia can be observed. It is expressed in the phenomena of loose stools.

Pernicious anemia is characterized by enlargement of the liver. This is the most powerful argument for the development of anemia associated with a lack of vitamin B 12. The tongue in this disease has a crimson color.

Often the oral mucosa suffers. At the same time, stomatitis, glossitis and other pathologies are noted. The patient feels a burning sensation in the tongue. That is why the appetite is sharply reduced.

Gastritis with low acidity may be detected. As you know, gastritis with high acidity is most conducive to stomach ulcers. It is the most serious pathological condition.

From the side of the nervous system, neuronal damage is possible. It is the body's network of nerve cells. In this case, the following symptoms are noted:

• numbness and stiffness of the limbs;
• muscle weakness;
• gait disturbance.

The patient may experience incontinence. And incontinence of urine and feces. Sensitivity is broken. The patient, especially in old age, notes:

• insomnia;
• depression
• hallucinations.

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Diagnostics

Of great importance in the diagnosis of pernicious anemia is the collection of anamnesis. Anamnesis involves the collection of the necessary information. This information relates to the possible causes of the disease. The clinical picture is established.

Diagnosis consists in an objective examination of the patient. At the same time, there are complaints from the patient. There are also signs of anemia. A biochemical study is also used.

It involves the detection of antibodies to the cells of the stomach. This includes the Castle factor. The method of general blood analysis is mainly used. It shows the following trend:

• leukopenia;
• anemia;
• thrombocytopenia.

Of great importance in the diagnosis of the disease is the analysis of feces. In this case, the coprogram plays the role. Directly for the study of pathologies of the gastrointestinal tract. In the presence of helminths, feces on the worm egg are widely used.

If the cause is the pathology of the digestive system, then the Schilling test can be used in the diagnosis of the disease. This test allows you to determine the violation of absorption, directly of vitamin B 12. If tumor formations are involved in the pathological process, then additional studies are carried out.

Additional methods for diagnosing pernicious anemia include a bone marrow biopsy. This allows you to determine the increase in the number of megaloblasts. The FGDS method is widely used. In some cases, x-rays of the stomach are performed.

Diagnosis is also aimed at identifying cardiac pathologies. Therefore, electrocardiography, ultrasound examination of the abdominal organs is used. An MRI of the brain may be required.

Prevention

Preventive measures are aimed at filling the deficiency of vitamin B 12. Therefore, preference is given to the use of proper nutrition. Nutrition should not only be balanced, but also contain vitamins necessary for the body.

What products should be preferred? Foods containing vitamin B 12 include:

• meat;
• eggs;
• liver;
• fish;
• dairy.

An obligatory condition in the prevention of the disease is the treatment of the underlying disease. Mostly diseases of the gastrointestinal tract. It is also necessary to avoid exposure to adverse factors. For example, alcohol intoxication should be excluded.

It is bad habits that can provoke pernicious anemia. Including the use of drugs. Drug intoxication should be limited.

If surgical manipulations were performed, then it is advisable to carry out restorative treatment. In this case, the treatment will be aimed at restoring the human body. Vitamins contribute not only to strengthening the immune system, but also to the absorption of necessary substances.

Expert advice is of great importance. These specialists include a gastroenterologist and an endocrinologist. Often, patients are registered with these specialists.

In the treatment of pernicious anemia, great importance is given to the elimination of vitamin B12 deficiency. This means that it is directly replenished for the patient's body. However, this therapy can be carried out for life.

It is also necessary to check the stomach. This event is associated with the use of gastroscopy. This allows you to identify a tumor of the stomach. What is a common complication of this disease. Or the most significant reason for its development.

The introduction of vitamin B 12 is advisable to produce intramuscularly. The condition of the patient is also directly corrected. In this case, the following actions are relevant:

• elimination of helminths;
• intake of enzymes;
• surgical intervention.

Surgical intervention is advisable to carry out with the aim of direct removal of malignant neoplasms. Including tumors of the stomach and intestines. Nutritional modification includes a diet containing animal protein.

If the patient's condition is preceded by an anemic coma. What is also a frequent complication, you should resort to blood transfusion. That is, apply the methods of blood transfusion.

In adults

Pernicious anemia in adults can be observed in some cases. This is primarily due to various pathologies. This is especially true in old age. Anemia after seventy years is the most dangerous.

Pernicious anemia develops in the category of forty years and above. Naturally, the older the patient, the more serious the course of the disease. In addition, anemia does not develop immediately. Usually after a certain period of time.

This period of time can be quite long. Make a time period of four years. The course of the disease in the elderly is quite severe. First of all, this is due to the following factors:

• the presence of neurological disorders for a long time;
• lifelong use of drugs;
• occurrence of complications.

Adults have to live with drugs. Moreover, these drugs should directly restore the deficiency of vitamin B 12. If the cause of the vitamin deficiency is a tumor, then an adult is most susceptible to complications.

Symptoms of pernicious anemia in adults are as follows:

• decrease in working capacity;
• lethargy;
• dizziness;
• insomnia.

A significant symptom of the disease in adults is insomnia. At the same time, a person is excited, frequent lack of sleep affects his ability to work. After all, the phenomena of pernicious anemia are not uncommon in people of the middle age category.

Oddly enough, women are susceptible to the disease. Men get pernicious anemia less often. Therefore, it is necessary to clearly establish the possible causes of this pathology. Causes of illness in adults include:

• pathology of internal organs;
• malignant neoplasms;
• medicinal substances;
• body intoxication.

In children

Pernicious anemia in children is manifested by the presence of severe symptoms. Children with anemia lag behind in development. They are the most susceptible to various diseases. Often anemia in children is caused by the following factors:

• severe pregnancy;
• maternal infections;
• prematurity

There are genetic diseases. Usually, diseases associated with the circulatory system contribute to the development of anemia. For example, hemophilia. That is a direct violation of blood clotting.

What are the main symptoms of the disease in a child? The main clinical signs include:

• fragility of nails;
• pale skin;
• weakness;
• dizziness.

In severe cases, children develop stomatitis. Children with pernicious anemia are at risk for respiratory pathology. More often they get bronchitis and pneumonia. In young children, tearfulness and exhaustion are noted.

In children, tachycardia is often detected. Blood pressure may decrease. Up to the development of collapse. The child may faint. For infants, pernicious anemia has the following symptoms:

• regurgitation is frequent;
• vomiting after feeding;
• flatulence;
• decreased appetite.

Forecast

With pernicious anemia, the prognosis largely depends on the presence of complications. The prognosis is best if timely treatment is carried out. If the treatment is late, then the prognosis is the worst.

Much depends on the presence of the underlying disease. With malignant pathology, the prognosis is unfavorable. In the presence of cardiac abnormalities, the prognosis is also the worst.

The disease is quite long. The prognosis will directly depend on the condition of the patient. Also from the course of the underlying disease. And of course, from the availability of adequate therapy.

Exodus

Fatal outcome in pernicious anemia is possible if there is a malignant tumor. Even in the presence of long-term medical therapy, the outcome will depend on further actions. The outcome is favorable if the patient follows some recommendations.

First of all, the outcome will depend on the correction of lifestyle and nutrition. Especially in the presence of an intoxication factor and alimentary etiology. In people over the age of seventy, the outcome is often unfavorable.

Recovery is possible. But treatment therapy is quite long. May vary from several years. Moreover, the outcome in this case may be associated with life-long intake of this vitamin.

Lifespan

In the treatment of pernicious anemia, consultation and supervision of specialists is of great importance. In some cases, the further course of the disease depends on this. And also longevity.

If the disease was eliminated in a timely manner, then life expectancy increases. If the diagnosis is late, which can be often, then the disease ends with a decrease in the quality of life. The patient may be suffering from heart failure.

With heart failure, the course of the disease is aggravated. And the presence of an anemic coma worsens the quality of life, reduces its duration. Urgent action must be taken.