Malignant anemia, anemia. Pernicious anemia prognosis Pernicious anemia

B12 deficiency anemia

A disease like pernicious anemia is very similar to ordinary anemia caused by a lack of vitamin B12. Both diseases are characterized by neurological manifestations and a megaloblastic hematopoietic process.

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perniciosus - disastrous, dangerous) or B12-deficiency anemia or megaloblastic anemia or Addison-Birmer disease or (outdated name) malignant anemia is a disease caused by impaired hematopoiesis due to a lack of vitamin B12 in the body.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

The specificity of this disease is the mandatory presence of three component causes:

• aggravated stage of atrophic gastritis;
• deficiency of vitamin B12, resulting from difficulty in absorption, regardless of the quantitative composition in food;
• transformation of hematopoiesis to the megaloblastic type, which is typical for embryonic development human body.

The second name for this pathology is pernicious or substandard anemia, which occurs in 1-2%, mainly after the age of sixty. Women are more often affected by this disease than men. In cases where there is a genetic predisposition, people in young and middle age can get sick.

Causes of pernicious anemia

The first description of the symptoms and causes of pernicious anemia was presented in the second half of the nineteenth century by the English physician Addison, and the second version was described by Birmer thirteen years later. The opinions of both doctors were that the disease could not be cured, since the main causes had not been identified.

In 1870, the relationship between anemia and atrophy of the gastric mucosa and interruption of the production of pesinogen was proven.

Subsequent studies of the disease made it possible to determine the characteristic features and degree of modifications in the stomach. It turned out that necrosis of parietal cells occurs in most of the mucosa and along with this, the ability to produce the enzyme is lost. Dead cells are replaced by others, similar to intestinal ones in the production of mucus.

Walls digestive organ infiltrated by lymphocytes and plasma. Such changes occur not only with pernicious anemia, but also with atrophic gastritis, and even with a long course of the disease, anemia is not observed.

Studies have shown that for the disease pernicious anemia to occur, the presence of two more factors is also necessary:

• Genetic predisposition.
• Autoimmune condition of the body.

The effect of immunity was proven by immunofluorescence of 2 types of antibodies in the blood serum of patients:

1. in 90% of patients to parietal cells;
2. in 57% of patients to the internal factor that produces the enzyme.

Basically, antibodies are also detected in gastric juice, which inhibit the absorption of vitamin B12.

Modern knowledge about immunity makes it possible to obtain a more complete picture of the causes of the disease. The genetic factor is confirmed by the presence of antibodies in healthy relatives. When the functioning of the immune system is impaired, antibodies appear against cells in the pancreas and thyroid gland, as well as the adrenal glands.

It has not yet been clarified which manifestation is primary, a disease of the digestive organ or autoimmune processes. Both symptoms are enhanced by each other and make it difficult to restore the mucous membrane.

The onset of vitamin B12 deficiency occurs gradually as parietal cells shrink. In some cases, signs of anemia appear after five or more years.

The clinical picture of Addison-Birmer disease is the manifestation common symptoms anemia in combination with digestive and neurological disorders. These signs include:

• severe fatigue, lethargy;
• feeling of heaviness after eating in the epigastric area;
• pain in the mouth and tongue;
• numb feeling skin lower and upper limbs;
• slight weight loss, but mostly a tendency to gain weight;
• in the acute period, intestinal dysfunction and change in stool color are likely;
• increase in body temperature due to the accelerated breakdown of red blood cells.

There may also be other symptoms, but they are rare. These include:

1. deterioration of potency in men and urination problems;
2. change in gait;
3. visual dysfunction.

With damage to the visual, olfactory and auditory senses nerve fibers There is impairment of vision, smell and hearing. Very rarely recorded mental disorders and hallucinations.

Diagnosis of B12 deficiency anemia

At a doctor’s appointment with a patient, after a thorough diagnosis of B12 deficiency anemia, the following may be discovered:

• pale skin;
• swelling of the face;
• brown dark spots in the area of ​​the nose and cheekbones;
• insignificance of scleral hysteria.

Examination of the oral cavity reveals following symptoms:

1. V initial stage the disease causes painful damage in the form of cracks;
2. the occurrence of an inflammatory process with ulcers on the gums and mucous membranes, and then spreading to the pharynx and esophagus;
3. in the acute period of the disease, the tongue acquires a scarlet color due to atrophy and swelling of the folds.

When palpating the abdomen, the soft part of the liver is determined with an increase in size. Changes in the spleen occur extremely rarely.

Which additional examination necessary?

The diversity of the disease requires confirmation of the diagnosis by various specialists:

1. An examination by a neurologist helps establish lost sensation in the legs and arms, impaired motor functions, which indicate damage to the myelin sheaths in the spinal cord.
2. To exclude the possibility of the formation of a low-quality formation, it is necessary to perform endoscopy of the stomach. The presence of atrophic gastritis is characterized by the appearance of shiny zones where cell death occurs.
3. Fluoroscopy shows increased evacuation and alignment of mucosal folds.
4. To prove the low absorption of vitamin B12 in the stomach, a Schilling diagnosis is made, in which the amount of the isolated element is determined after administration. The consistency of the reduction in blood and urine levels is also checked. A low rate indicates a large number of antibodies in the gastric juice.
   5. When researching gastric juice a low saturation of hydrochloric acid or its complete absence and a large volume of mucus are detected.
   6. Histology of the mucosa shows thinning and disappearance of the glandular epithelium. Pernicious anemia is characterized by a lack of gastromucoprotein and acid secretion.
   7. The cardiogram reveals oxygen starvation of the myocardium. The presence of tachycardia contributes to the development of arrhythmia, ischemia and early cardiosclerosis.

Blood picture with vitamin B 12 deficiency

Vitamin B12 deficiency can lead to impaired hematopoiesis in the bone marrow. There is a decrease in hemoglobin, while the number of red blood cells drops even more.

Peripheral blood analysis reveals the presence of large cells, megalocytes and macrocytes, which are twice the size of a red blood cell. The appearance of cells with an altered structure and remnants of nuclei is likely.

Changes in the following indicators are also observed:

• the quantitative composition of reticulocytes decreases;
• the growth of white blood is inhibited, which contributes to the formation of leukopenia and relative lymphocytosis;
• The number of platelets decreases, but growth in size is activated;
• In the bone marrow, blast cells of the erythrocyte series of different maturity predominate.

During the period of remission, bone marrow hematopoiesis returns to normal.

Treatment for pernicious anemia

The main direction in medical therapy of this disease is to eliminate vitamin B12 deficiency. For this purpose it is assigned medicinal product Oxycobalamin, which is considered the most effective in the first stage of treatment.

If after six months there is a lack of iron, then iron supplements in tablets.

As a result of treatment, the number of reticulocytes increases, health improves, dizziness disappears, and strength appears in the limbs. It will take at least a month and a half to stabilize.

Features of the flow B 12 deficiency anemia

Difficulties in diagnosis arise when there are clinical symptoms no changes in hematopoiesis. In this case, a diagnosis is made atrophic gastritis, not Addison-Biermer disease.

Fluctuations in the correctness of the diagnosis appear when negative reaction to the administration of vitamin B12 and the absence of neurological signs. It is also worth considering that the effectiveness of treatment can be eliminated by the patient’s existing diseases:

• pyelonephritis in chronic form;
• kidney dysfunction;
• the presence of infection in the body for a long time;
• diseases thyroid gland;
• malignant formations.

Forecast

Nowadays it is rare to see running form pernicious anemia, this is only possible in the absence of therapeutic therapy. At the moment, the disease is curable, but requires medical supervision and prevention of remission.

With a long course of the disease, patients exhibit concomitant pathology:

1. toxic diffuse disease the thyroid gland is found in 1.8% of patients;
2. the endocrine disease myxedema is detected in 2.4% of cases.

The primary symptoms of cancer are:

• nonspecific weight loss;
• resistance to the drug Cyanocobalamin;
• restoration of hematopoiesis with existing symptoms.

Incomplete study of the causes and consequences of Addison-Birmer anemia is a reason for the patient to take an active position in preventive actions against relapses. To do this, you should eat well and properly, give up bad habits and monitor your health.

Malignant anemia was described in 1885 by Addison in his book on bronze disease of the adrenal glands under the name idiopathic anemia and by Birmer in 1872 under the name progressive pernicious anemia.
For a long time, this disease was classified as a “primary” anemia. believing that its cause lies deep in the body. Already in 1870, based on pronounced cases of complete atrophy of the digestive tract, the cause of anemia was considered to be insufficiency digestive function. However, for many years the prevailing opinion was that “anemia occurs due to damage bone marrow intestinal toxins or as a result of oral (“oral”) focal infection. Botkin established the significance for individual cases of malignant anemia of invasion by the broad tapeworm, and explained the mechanism of anemization itself as a reflex disturbance in the activity of the hematopoietic center in the brain. Gastric achylia, which constantly accompanies malignant anemia, has attracted the attention of scientists. Achilia apparently develops not so much as a result of inflammatory gastritis, but rather from a neurodystrophic effect, especially with a lack of vitamins and protein in the diet. The development of anemia is often preceded by liver diseases (cholecystitis, cholecystohepatitis), which can disrupt metabolism and worsen gastric trophism. Apparently, as a result of persistent metabolic disorders and disturbances nervous regulation gastric secretion under the influence adverse influences Multiple cases of malignant anemia may also occur in one family. As a result of the same reasons, due to damage to the stomach in the family of a patient with malignant anemia, there may be cases of chlorosis, or in the patient himself, signs of this disease appear as if replacing chlorosis. In the patient himself, achylia can be diagnosed ten years before the development of typical anemia. Using the gastroscopy method, it was possible to detect areas of regeneration of the gastric parenchyma in patients during remissions, especially under the influence replacement therapy and intensive vitaminization, which to a certain extent explains the undulating course of the disease and shows the dependence of the course of malignant anemia on environmental factors. The glandular tissue of the stomach can undergo further pathological restructuring and give rise to polypous growths and cancerous degeneration. Work in recent years has clarified the mechanism of development of anemia and damage to the central nervous system, depending on the disorder gastrointestinal digestion and nutrition, based on the revealed great medicinal value of the liver diet for malignant anemia.
It should be considered proven that healthy person During the process of gastric digestion, in addition to the breakdown of proteins by pepsin, a special anti-anemic substance is formed, which is absorbed in the intestine, deposited, like glycogen, protein, in the liver and, as needed, consumed in the bone marrow, ensuring normal maturation of red blood cells. In patients with malignant anemia, this substance is not formed in the stomach, and they do not have it in the liver; therefore, hematopoiesis in the bone marrow does not go beyond megaloblasts and anucleate large erythrocytes (megalocytes), as in the fetus; With calf liver or its extracts, patients receive this missing substance, which ensures the formation of normal normoblasts in the bone marrow, as well as anucleate red blood cells.
Castle in 1928 carried out the following experiment, which proved the role of the stomach in hematopoiesis. When feeding a patient with malignant anemia meat digested in a thermostat with normal gastric juice, the composition of the blood quickly improves, while the gastric juice of a patient with malignant anemia, even with the addition of nepsin and hydrochloric acid, does not have such an effect. The active principle of meat, as well as eggs, cereals, and yeast, which act similarly, is probably close to vitamins of the B complex. The formation of an antianemic substance can be represented in the form of the following scheme: external factor (thermostable - resistant to heat) + internal factor (thermolabile - destroyed when heated - specific gastric enzyme) = a heat-labile antianemic substance deposited in the liver.
A specific enzyme is produced in humans mainly by the fundic glands, and perhaps only in minute quantities by other parts gastrointestinal tract. The chemical nature of the antianemic substance has not been clarified, although last years A vitamin containing cobale, vitamin B 12, which acts especially energetically in this direction, has been isolated.
For the late stages of pernicious anemia, damage to the central nervous system is extremely characteristic in the form of degeneration of the posterior and lateral columns of the spinal cord, mainly in the cervical part; the development of this “funicular myelosis” is also associated with a digestive defect - underproduction in the stomach and intestines of a special substance, in the absence of which As with pellagra, demyelination and degeneration of the axial cylinders of the central neurons occur.
Severe anemia occurs with progressive atrophy of the stomach and intestines (malignant anemia in its own form and with sprue), after extensive resection of the stomach (“agastric” malignant anemia), with impaired absorption of the antianemic substance by the intestinal wall (gastrocolic fistula, sprue) and increased its destruction inside the intestine (with stenosis of the small intestine, with infection with a wide tapeworm). Malignant anemia can occur in pregnant women due to increased consumption of hematopoietic substance for fetal hematopoiesis, and finally, due to a lack of external factor(relevant vitamins) with prolonged malnutrition.
The immediate mechanism for the development of anemia appears to be the following form. Defective red blood cells released by the bone marrow, as well as pathological red blood cells when hemolytic jaundice, are easily destroyed in the spleen and other places where reticuloendothelial tissue accumulates. The number of red blood cells progressively falls despite hyperplasia of active bone marrow.
The consequence of increased breakdown of red blood cells is jaundice in patients, increased content in the blood of indirect bilirubin, in feces and urine - urobilin, although in significantly smaller quantities than with hemolytic jaundice, due to more deep violation pigment metabolism with the formation of porphyrin and hematin. In the blood serum, the iron content is increased, which is deposited in Kupffer cells and in the parenchyma on the periphery of the liver lobules, in the lungs, spleen, kidneys - homosiderosis of the organs, giving them a rusty tint. Anatomically, a crimson-red brain is also characteristic in the diaphysis of long bones, for example, the femur, rich in megaloblasts, with scanty foci of the formation of granular leukocytes and megakaryocytes. The same metaplasia can occur in a mildly enlarged spleen. At autopsy, fatty degeneration of the liver, degeneration of the kidneys, hemorrhages in the serous membranes, retina, and brain are found.
During remission, megaloblasts are replaced by erythroblasts, normoblasts and ordinary erythrocytes, pathological hemolysis stops, the need for colossal hematopoiesis decreases, the bone marrow of the thigh acquires a normal fatty appearance, and the punctate sternum does not contain megaloblasts after several days of liver treatment.

Clinical picture. Patients complain of gradually increasing general weakness, shortness of breath, palpitations, dizziness, heart pain, often swelling of the legs or general swelling, and fever. At first glance, the doctor’s attention is attracted by the general appearance of the patient: in front of him is an elderly man who looks older than his years, or a woman 30-40-50 years old, often graying early with bloodless mucous membranes and skin of a pale lemon-yellow hue; the patients are not very emaciated, often even overweight. On the face, torso, arms there are pigment spots (chloasma) and areas of depigmentation (vitiligo), wen. Patients often come with a diagnosis of heart disease, cardiosclerosis, angina pectoris or stomach cancer. Upon detailed questioning, it is possible to find out that the patient has been experiencing burning pain in the tongue for the last few months from spicy food, periodic diarrhea, and when examining gastric juice, achylia has long been established; that before, for example, towards the end of last winter, the patient’s pallor attracted the attention of others, and a blood test revealed anemia; V Lately The patient's fingertips go numb and a crawling and tingling sensation is felt in the hands and feet (paresthesia). There is often a history, especially in women, of attacks of hepatic colic and cholecystohepatitis.
Swelling can reach the level of anasarca with ascites, hydrothorax, edematous pads on the back of the hands, on the lower back and sacrum, sometimes swelling is limited to the legs, puffiness of the face. With very severe anemia, a few petechiae are found on the skin and minor hemorrhages in the mucous membranes. With pressure, pain in the sternum (sternalgia), ribs.
The cardiovascular system presents the usual changes for severe anemia: increased cardiac activity with increased pulsation of the carotid and other arteries with increased pulse pressure; sharp systolic murmur at all orifices of the heart from vortex movements of blood with reduced, often twice the norm, viscosity, with a sharp acceleration of blood flow. Those conditions cause a murmur heard on the jugular bulb, preferably on the right. This continuous spinning noise intensifies during inhalation, when venous blood rushes into the chest with even greater force. Blood mass is only slightly reduced: the loss of erythrocyte mass is compensated, as in general with anemia, by an increase in the liquid part of the blood. Acceleration of blood flow and other adaptive mechanisms of blood circulation ensure more or less normal respiratory function blood; this must be seen as an explanation amazing fact that patients with severe malignant anemia are often still capable of heavy physical work. Edema is, as a rule, “protein-free” in nature, i.e. associated with low content protein in blood serum. With prolonged anemia due to anoxemia, fatty degeneration of organs develops, including “tiger heart”. In this case, there may be signs of true circulatory failure with expansion of the cavities of the heart, increased venous pressure, slowing of blood flow, etc. With severe anemia, attacks of angina pectoris of a functional apoxemic nature may begin, stopping later with an improvement in blood composition. Of course, in elderly patients one has to take into account the possibility of angina pectoris due to coronary sclerosis.
The digestive organs are characterized by a tongue that is clean, bright red, smooth, devoid of papillae, atrophic, sometimes covered with aphthous vesicles or superficial ulcers (glossitis). Burning pain in the tongue is sometimes the main complaint of patients. The same burning pain can occur in the esophagus due to similar esophagitis. Dyspeptic complaints from the stomach are uncharacteristic, although due to the atrophic process, the secretion of hydrochloric acid cannot be caused and subcutaneous injection 0.5 mg of histamine, i.e. there is histamine-resistant achylia (The absence of a hematopoietic enzyme in the patient’s gastric juice can be proven by biological tests: 1) repeated feeding of another patient with undoubted pernicious anemia in the acute stage with meat, which was each time subjected to digestion in a thermostat by the gastric juice of the patient patient, does not cause remission; 2) subcutaneous injection of neutralized gastric juice of a patient into rats does not, unlike normal juice, cause an increase in the number of reticulocytes (the so-called rat-reticulocyte test). With extreme degrees of anemia, persistent vomiting may occur, making it impossible to ingest the liver. Periodically occurring diarrhea is of the nature of enteritis, accompanied by bloating, rumbling, and pain near the navel.
The liver is usually enlarged during exacerbations; Sensitivity in the area of ​​the gallbladder and other signs of cholecysto-hepatitis are common.
A slight enlargement of the spleen is observed in most untreated cases.
On the part of the central nervous system, signs of damage mainly to the posterior columns of the spinal cord are found - decreased and absent reflexes, ataxia, significant impairment of deep sensitivity while maintaining superficial sensitivity (“pseudotabes”); The lateral columns are also affected to a lesser extent, with spastic phenomena predominating and disorders of surface sensitivity often being detected early. More often, the spinal cord lesion is mixed, with a predominance of the posterior column type. Flaccid or spastic paralysis of the lower extremities develops, and later the sphincters of the bladder and rectum are disrupted. Less common are degenerative processes in the brain with a varied picture of general asthenia, psychosis, as well as peripheral neuritis. Patients often complain of memory loss and irritability.
When the number of red blood cells drops to 2,000,000 or below, there is almost always a significant fever of one or another, usually of the wrong type, simulating malaria, typhoid fever, sepsis and others infectious diseases. The increase in temperature can reach 39-40° and is apparently associated with a sharp breakdown of the blood or rejuvenation of the bone marrow; this aseptic “anemic” fever quickly ceases when the blood composition improves.
Most characteristic changes blood following. There is a high color index, above one, depending on the presence of large erythrocytes-macrocytes, excessively stained with hemoglobin (hyperchromia), which creates a deceptive impression of a good blood composition during a cursory examination of the smear (as opposed to iron-deficiency anemia, in which the erythrocytes remain completely unstained in the center ). Thus, with 40% hemoglobin, 1,500,000 red blood cells are often determined (30% of the norm), i.e., the color index is equal to 1.3. The color index remains high for a long time and with a significant improvement in red blood, without falling, as a rule, even during remissions below 0.7-0.8, which is in sharp contrast with the low color index of patients with chlorosis. White blood is characterized by leukopenia with polysegmented neutrophils - five-, seven-lobed, etc. - the so-called shift to the right in the neutrophil series.

Upon careful examination of a stained smear, a variety of other cellular forms are found: pathognomonic megaloblasts with a characteristic lattice-like structure of the nucleus (“like raindrops in the sand”) and often basophilic protoplasm; megalocytes-anucleate giant erythrocytes over 12 r. diameter; poikilocytes (erythrocytes of the most bizarre shape - in the form of a tennis racket, ribbon); fragments of erythrocytes, polychromatophils, erythrocytes with basophilic punctation, with Cabot rings, Jolly bodies, neutrophilic myelocytes, etc.

An increase in the number of reticulocytes, eosinophils, and platelets indicates the restoration of normal bone marrow hematopoiesis and is a good indicator of the onset of remission. Hepatic therapy naturally causes a steep rise in the number of reticulocytes on the 7-10th day with a slower subsequent decline. Following the peak of reticulocytes, from the 10th to 14th day of treatment, there occurs a constant long-term increase in the number of red blood cells and hemoglobin, which continues after the fall in reticulocytosis. Eosinophil count during raw liver treatment for a long time remains extremely high, reaching 50-60% of all leukocytes; liver extracts give only moderate eosinophilia.

Turning, complications and outcomes. The onset of the disease is gradual. Obviously, at least six months or a year passes before blood will fall to those low numbers at which the patient usually consults a doctor. A significant deterioration in the condition is often preceded by attacks of glossitis with diarrhea, as with other deficiency diseases, or by an accidental acute infection.
Before the introduction of liver therapy, the disease fully justified its name as pernicious (“disastrous”) and progressive. True, even without treatment, the disease gave one or two, rarely three characteristic remissions lasting from 2-3 months to 1 year, still leading to death usually after 1-3 years, as an exception, after 7-10 years. Treatment with the liver significantly changed the course of the disease, making it possible to immediately induce remission at the first attack and maintain this state of practical health and full performance, apparently for an indefinitely long time, at least up to 10-15 years. However, the disease remains serious due to the often late recognition of many complications (pyelitis, cholecystitis, protein-free edema) and especially due to the difficulty of carrying out long-term replacement treatment liver; in the end, the disease still leads to severe damage to the spinal cord with paralysis, urinary infection (urosepsis), pneumonia and death.

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A severe attack, not recognized and not treated in a timely manner, can lead to a peculiar comatose state - coma perniciosum, when patients with a hemoglobin amount of about 10% (difficult to determine accurately), general edema, jaundice, hypothermia, circulatory disorders experience severe lethargy, drowsiness, even complete loss of consciousness, and bring the patient out of this dangerous condition only succeeds urgent measures: drip blood transfusion, parenteral administration of active liver drugs into high dose, cardiovascular drugs, oxygen therapy.
A completely different picture is presented by patients in a state of remission, when complete absence complaints, neither the appearance of the patient nor the examination of individual organs (normal color of the skin and mucous membranes, an enlarged spleen and liver), nor the examination of the blood (normal number of red blood cells and hemoglobin; the most persistent morphological changes are macrocytosis with hyperchromia and leuko-neutropenia, but they, apparently, can disappear; even puncture of the sternum reveals normoblastic bone marrow). But this well-being is under constant threat from the remaining impaired activity of the nervous system and digestive tract: attacks of diarrhea, exacerbation of glossitis, development of polyposis and stomach cancer, and most importantly, nervous symptoms may progress. Even with normal composition blood, the patient can become severely disabled, bedridden due to paraplegia, etc. Ignoring liver therapy can also lead to relapse of anemia.

Pernicious-like macrocytic a blood picture without other classic signs of malignant anemia can be caused by diseases such as liver cirrhosis, malaria, acute leukemia, etc. Chronic leukemia, especially lymphatic, is sometimes combined with pernicious anemia - actually “leukanemia”. In familial hemolytic jaundice, the anemia is hyperchromic, but at the same time microcytic in nature; This disease is distinguished by a unique, well-defined clinical picture.

And plastic anemia (aleukia), and acute leukemia are often misdiagnosed as “acute pernicious anemia.” Both diseases have a very similar clinical picture, which differs, however, significantly from pernicious anemia; There are also significant hematological differences.

Cancer anemia, for example, in gastric cancer, it is usually easy to differentiate from malignant anemia by a low color index, neutrophilia with normal or increased number leukocytes, the presence of persistent gastric complaints, and most importantly, a defect in the filling of the stomach on an x-ray. X-ray examination makes it possible to recognize gastric polyposis, which often also causes severe anemia.
It should, however, be noted that with malignant anemia, swelling of the gastric mucosa can give an x-ray picture similar to a filling defect, and most importantly, that with a long course of malignant anemia can lead to true gastric neoplasm. This combination can be recognized, in addition to a persistent x-ray picture, by continuous deterioration of the patient’s condition with severe cachexia, unusual for malignant anemia, a positive blood symptom - blood in the stool, in vomit, leukocytosis (and thrombocytosis). In isolated early recognized cases, such patients underwent radical surgery to remove the tumor, and they recovered with liver replacement therapy.
In addition to cancer, other severe anemia is often incorrectly mistaken for malignant anemia. hypochromic anemia, such as: anemia with prolonged hemorrhoidal bleeding, with chronic azotemic nephritis (bright anemia). At first impression (pale face, swelling of the eyelids and other signs of sclerotic cachexia), an elderly patient with atherosclerosis, as well as patients with edematous disease or lipoid nephrotic syndrome, can be mistaken for a patient with pernicious anemia, but in these diseases the red blood is almost not affected .
Due to the presence of fever, along with swelling of the spleen, leukopenia, anemia, pernicious anemia is sometimes mistakenly diagnosed as malaria (bright large basophilic punctuation and Cabot rings in erythrocytes are also often mistaken for the stage of development of malarial plasmodium), typhoid fever (diarrhea, leukopenia, etc.), sepsis-endocarditis lenta (heart murmur, pulsation of arteries, enlarged spleen, etc.).
Finally, often significant damage to the spinal cord in malignant anemia leads to an erroneous diagnosis of nervous suffering itself, especially tabes dorsalis, multiple sclerosis, spinal cord tumors, polyneuritis; this mistake is even easier to make if, after treatment with the liver, only an erased anemic syndrome remains. There are known forms of funicular myelosis due to insufficiency of gastrointestinal digestion without anemia at all. In contrast to tabes dorsalis, in malignant anemia, the cerebrospinal fluid remains normal, pupillary reactions, as a rule, are preserved, motor muscle strength is sharply impaired, and shooting pains are unusual. The difference from multiple sclerosis is that it is more old age sick, absence eye symptoms and defeats optic nerve, lack of deep reflexes, sphincter dysfunction only in late stages diseases.

Prevention. It should be remembered that every patient with persistent achylia, as well as after extensive gastrectomy, may develop severe anemia, so such individuals must be systematically monitored general condition and blood composition (hyperchromia, macrocytosis, etc.), provide them with a nutritious diet, and, if necessary, apply early treatment of anemic syndrome and other measures. Thus, it will be possible to reduce the number of patients with malignant anemia who visit a doctor for the first time with severe anemia (often with a red blood cell count of about 2,000,000), requiring hospitalization and leading to long-term disability. A general correct hygienic regime and protecting the nervous system from difficult experiences are also of undoubted importance in preventing the disease.

Treatment. Treatment of malignant anemia is aimed primarily at resolving general regime, improving the neurotrophic regulation of the digestive organs and other systems, eliminating various foci of irritation (infectious diseases, inflammation of the gallbladder, etc.), providing adequate nutrition, especially substances that are most closely related to trophism - the gastrointestinal tract, hematopoietic organs and nervous system (separate fractions of vitamin B, autoclaved yeast, etc.). During exacerbation of the disease, bed rest is necessary. The food is varied, sufficient, always with normal amount complete proteins - meat, eggs, milk; the same principle of nutrition is observed in case of extreme degrees of anemia and the presence of diarrhea - meat soufflé, whipped egg whites, fresh mashed cottage cheese, yogurt, etc.
Liver is both food and the best remedy; usual dose its-200 g per day. Fresh liver (veal, bovine) is washed in warm water, cleaned of connective tissue fibers, passed through a meat grinder and given raw or lightly scalded on the outside with boiling water on a sieve, with any seasonings, depending on the patient’s taste - salt, onion, pepper, garlic, as well as in the form of sandwiches, sweet dishes, etc. At the first time, when the treatment of malignant anemia with the liver was proposed (1926), it was considered necessary to prescribe a special diet, low in fats and rich in fruits. It soon became clear, however, that liver treatment is valid for any diet, although it is advisable to provide the patient with complete protein nutrition. The addition of hydrochloric acid is desirable, as with any achilia. Raw liver poses no risk to helminthic infestation; the often developing very high eosinophilia is a consequence of ingesting raw liver as such. Diarrhea does not contraindicate treatment with raw liver; on the contrary, with such treatment it usually stops soon.
Various liver concentrates for oral administration - liquid, dried powder - have practically less value; they do not always satisfy the taste of patients, and most importantly, they are not always active enough; One of the best is liver extract, prescribed in a dose of about 2 tablespoons per day. “Gastrocrine”, a dried pork stomach, also has a therapeutic effect, containing, in addition to the internal factor, formed in pigs mainly by the pyloric glands, also external muscle layers stomach.
Fresh veal liver is a reliable carrier of an antianemic substance; in addition, it is rich in vitamins, iron, copper. If the patient refuses to take the liver orally, as well as in severe, life-threatening conditions and, of course, when sharp violation absorption by the intestine, preference should be given to parenteral administration of liver preparations.
Active injectable drugs, for example, Soviet Campolon, Hepalon, Hepatium, are administered intramuscularly, usually 1-2 ml, and in the most severe cases up to 5-8 ml per day (the so-called “Campolon shock” treatment) until obvious remission begins. In the future, they ensure a rapid increase in red blood to normal numbers, which requires at least 2-4 intramuscular injections of 1-2 ml of the active drug per week or daily intake of raw liver. In cases of moderate severity (with the number of red blood cells about 1,500,000 and hemoglobin about 40%), the patient’s well-being improves significantly by the end of the first week of treatment. On the 7-10th day, a peak of reticulocytosis is observed, followed by an increase in the number of red blood cells and hemoglobin, which occurs the more vigorously, the lower the initial numbers. Having achieved a stable remission during treatment with raw liver, they often take a break for several weeks, and when treating with injections they are content with 1-2 injections per week or even more rare.
In cases of apparent ineffectiveness of liver therapy, there is often an incorrect diagnosis of malignant anemia or insufficient dosage of the liver. Thus, in case of infectious complications - pyelitis, pneumonia, as well as in some less treatable patients, a double dose of 400 g of raw liver per day may be required. In these cases, as well as in cases of extreme anemia, an additional drip blood transfusion of 100-150 ml or more or, better, erythrocyte mass (suspension) of 100-200 ml is indicated.
Recently, it has been recommended to use treatment with vitamin B2, which is active in very small doses and, moreover, has a good effect on blood restoration and, when prescribed in a timely manner, apparently prevents damage to the nervous system. (Another antianemic vitamin, folic acid, does not prevent the neurological manifestations of the disease and therefore is currently considered less indicated for malignant anemia.)
To prevent and improve nerve damage, a valuable addition to liver treatment, especially when treating with injections of liver drugs, is the systematic administration of vitamin B 1 (thiamine under the skin or orally, yeast autoclaved in an incubator along with gastric juice); for spastic paralysis, motor-mechanotherapy is carried out, training in movements, walking, as with tabes, etc.
Arsenic currently does not find supporters in the treatment of malignant anemia; iron is indicated especially in the simultaneous presence of iron deficiency anemia.
In cases of symptomatic and malignant anemia - with widespread tapeworm, pregnancy, agastric anomia, etc. - also, first of all, vigorous treatment is carried out with raw liver or injections of appropriate drugs (injections are required for sprue, gastrocolic fistula, when absorption from the intestine is obviously extremely reduced), blood transfusion. In this way, it is possible to bring pregnant women to a normal delivery, in case of infestation with the broad tapeworm, significantly improve the blood composition and the entire clinical picture, after which they carry out treatment with fern, which is contraindicated in the serious condition of patients due to its general toxic effect and the liver damage it causes; for gastrocolic fistula and small intestinal stenosis, early surgical intervention is indicated before severe cachexia occurs.

Description of pernicious anemia

Pernicious anemia is an endogenous B12 vitamin deficiency caused by atrophy of the glands of the fundus of the stomach that produce gastromucoprotein. This leads to impaired absorption of vitamin B12, necessary for normal hematopoiesis, and the development of pathological megaloblastic hematopoiesis, resulting in “pernicious” type anemia. People over the age of 50 get sick.

Characterized by disorders of the cardiovascular, nervous, digestive and hematopoietic systems. The complaints of patients are varied: general weakness, shortness of breath, palpitations, pain in the heart, swelling of the legs, a crawling sensation in the hands and feet, gait disorder, burning pain in the tongue, periodic diarrhea. The patient's appearance is characterized by pale skin with a lemon-yellow tint. The sclera is subicteric. The patients are not exhausted. When researching of cardio-vascular system Anemic sounds associated with decreased blood viscosity and increased blood flow are typical.

On the part of the digestive organs, the so-called Gunter'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 detected. 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, red blood cells with Jolly bodies, Cabot rings, leukopenia, thrombocytopenia (during exacerbation).

Treatment is carried out with vitamin B12-100-200 mcg intramuscularly daily or every other day until remission occurs. If an anemic coma occurs, urgent hospitalization, blood transfusion, preferably red blood cells (150-200 ml). Maintenance therapy with vitamin B12 is necessary to prevent relapses. Systematic monitoring of blood composition in people with persistent achylia, as well as those who have undergone gastrectomy, is indicated. Patients suffering from pernicious anemia should be under dispensary observation(stomach cancer may occur).

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

Treatment 100-200 mcg is administered intramuscularly daily or every other day before the onset. If an anemic coma occurs, urgent hospitalization is recommended, preferably red blood cell mass (150-200 ml). Maintenance therapy with vitamin B12 is necessary to prevent relapses. Systematic monitoring of blood composition in people with persistent achylia, as well as those who have suffered, is indicated. Patients suffering from pernicious anemia should be under medical supervision (stomach cancer may occur).

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

Clinical picture (symptoms and signs). Persons over the age of 40-45 years become ill. Characterized by disorders of the cardiovascular, nervous, digestive and hematopoietic systems. The complaints of patients are varied: general weakness, shortness of breath, palpitations, pain in the heart, swelling of the legs, dizziness, a crawling sensation in the hands and feet, gait disorder, burning pain in the tongue and esophagus, periodic diarrhea. The patient's appearance is characterized by pale skin with a lemon-yellow tint. The sclera is subicteric. The patients are not exhausted. The face is puffy, swelling in the ankles and feet. Edema can reach large degrees and be accompanied by ascites and hydrothorax. From the cardiovascular system - the appearance of systolic murmur at all orifices of the heart and the “spinning top” murmur at the bulb of the jugular vein, which is associated with a decrease in blood viscosity and acceleration of blood flow; Anoxemic angina is possible. 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 (Hunter's) glossitis, the tongue is clean, bright red, devoid of papillae. Analysis of gastric juice usually reveals histamine-resistant achylia. Periodic diarrhea is a consequence of enteritis. The liver is enlarged and soft; in some cases - a slight enlargement of the spleen. If the number of red blood cells drops significantly (below 2,000,000), 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). 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, clonus, crawling sensation, numbness of the limbs, girdle pain, impaired vibration and deep sensitivity, sensory ataxia and dysfunction pelvic organs; less commonly, 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). As the disease worsens, the number of reticulocytes in the blood sharply decreases. The appearance of a large number of reticulocytes portends imminent 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 (color table, Fig. 3)], individual megaloblasts (color 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 neutrophil series, giant, polysegmented neutrophils are found. Along with a shift of neutrophils to the right, a shift to the left is observed with the appearance of juvenile forms and even myelocytes. The number of platelets during an exacerbation is significantly reduced (to 30,000 or less), but 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 (color table, Fig. 6).

Symptoms of the disease develop gradually. Many years before the disease, gastric achylia is detected. At the onset of the disease, general weakness is noted; patients complain of dizziness, palpitations at the slightest physical stress. Then dyspeptic symptoms and paresthesia are added; patients consult a doctor, already in a state of significant anemia. The course of the disease is characterized by cyclicity - alternating periods of improvement and deterioration. In the absence of proper treatment, relapses become increasingly prolonged and severe. Before the introduction of liver therapy into practice, the disease fully justified its name “disastrous” (pernicious). During the period of severe relapse - severe anemia and rapid progression of all 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 severe anemia of all organs, with the exception of the red bone marrow; the latter, being in a state of hyperplasia, fills the diaphyses of the bones (color table, Fig. 7). Fatty infiltration of the myocardium (“tiger heart”), kidneys, and liver is noted; in the liver, spleen, bone marrow, lymph nodes- hemosiderosis (color 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 is adenia. 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 (conversion of erythroblast into erythrocyte); 5 - 9 - nuclear disintegration with the formation of Jolly bodies in basophilically punctured (5, 6) and polychromatophilic (7 - 9) erythrocytes; 10 and 11- Jolly bodies in orthochromic erythrocytes; 12 - chromatin particles in erythrocytes; 13 - 16 - Cabot rings in basophilically 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 punctuation (5), megaloblasts (6), polysegmented neutrophil (7) , anisocytosis and poikilocytosis (8).

Rice. 6. Bone marrow in pernicious anemia (initial remission 24 hours after administration of 30 mcg of vitamin B12): 1 - normoblasts; 2 - metamyelocytes; 3 - band 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 20s, raw liver, especially lean veal liver, minced 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 production of liver extracts, especially for parenteral administration (campolon, antianemin). The specificity of the action of liver drugs in pernicious anemia is due to the content of vitamin B12 in them, which stimulates the normal maturation of erythroblasts in the bone marrow.

The greatest effect is achieved with parenteral administration 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 administration of vitamin B12 is effective only in combination with simultaneous administration internal antianemic factor (gastromucoprotein). Currently, favorable results have been obtained from the treatment of patients with pernicious anemia through the internal use of the drug mucovita (available in the form of pills) containing vitamin B12 (200-500 mcg each) in combination with gastromucoprotein (0.2). Mukovit is prescribed 3-6 tablets per day daily until the onset of reticulocyte crisis and then 1-2 times a day until the onset of hematological remission.

The immediate effect of anti-anemic therapy in the sense of replenishing the blood with newly formed red blood cells begins to affect from the 5-6th day of treatment with an increase in reticulocytes to 20-30% and higher (“reticulocyte crisis”). Following the reticulocyte crisis, the amount of hemoglobin and red blood cells begins to increase, which reaches normal levels after 3-4 weeks.

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. For funicular myelosis, vitamin B12 is used intramuscularly in large doses of 200-400 mcg, in severe cases, 500-000 (!) mcg per day] until complete clinical remission is achieved. The total dose of vitamin B12 during a 3-4 week course of treatment for anemia is 500-1000 mcg, for funicular myelosis - up to 5000-10,000 mcg and higher.

The effectiveness of vitamin B12 therapy has a known limit, after which the increase in blood counts stops and anemia becomes hypochromic; During this period of illness, it is advisable to use treatment with iron preparations (2-3 g per day, washed down with diluted hydrochloric acid).

The issue of using blood transfusions for pernicious anemia is decided in each case according to indications. An absolute indication is pernicious coma, which poses a threat to life due to increasing hypoxemia. Repeated blood transfusions or (better) red blood cells (250-300 ml each) often save the lives of patients until 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 relapse 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 blood composition of persons who have undergone extensive gastrectomy, as well as those who have persistent gastric achylia, provide them with a nutritious 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 gastric achylia and especially pernicious anemia are more likely than others to develop stomach cancer. Therefore, all patients with pernicious anemia should be under clinical observation and undergo an annual control X-ray examination of the stomach.

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

It was once believed that the root cause of this disease was intoxication. However, the source of intoxication remained unknown; For differential diagnosis, we relied on the most characteristic points and pathological anatomy of the disease.

Some gave great importance state of the bone marrow in malignant anemia, for example Ehrlich, who called this condition “a return to the embryonic state.” Others attached particular importance increased activity blood-destructive system (based on determining the daily amount of urobilin in feces and bilirubin in bile).

It seemed to many that it was significantly interested in the pathogenesis of the disease, although it did not always turn out to be increased. Proof of the participation of the spleen in the pathogenesis of the disease was the long remissions that occurred after. 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 was lost, while others believed that splenectomy removed an organ that inhibited the erythropoietic activity of the bone marrow.

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

Currently, the cause of Addison-Biermer disease is considered to be a lack of hematopoietic vitamin B12 and folic acid. Deficiency of this vitamin develops due to functional or anatomical disorders of the fundic glands of the stomach of a neurotrophic nature; the same vitamin deficiency occurs with Achilles gastritis (syphilis, polyposis or) or agastria (gastrectomy or exclusion of the stomach by others), with helminthic infestation (wide tapeworm), pregnancy, sprue (protracted enteritis), with resection or exclusion of the small intestine. These are all secondary forms; in some of them the disease proceeds without nervous phenomena, achylia and is cured with the elimination of etiological factor. And finally, vitamin B12 deficiency can be of exogenous origin - lack of vitamin B12 food products. Pathogenetically, we are talking about a violation of bone marrow hematopoiesis (impaired maturation of the formed elements of the erythroid germ according to the type of return to embryonic hematopoiesis).

The hemolysis that accompanies this form of anemia does not place it among the 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 after 40 years of age (before 25 years of age it was extremely rare), equally often in men and women. It all starts with achylia and changes in the nervous system. Weakness, dizziness appear, and then signs of anemia - shortness of breath, palpitations with minor physical exertion. Along with anemia, glossitis occurs (pain and burning in the tongue) - a pathognomonic symptom of pernicious anemia. Subsequently, the 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 towards obesity. The liver is enlarged, the spleen is not. If occasionally the spleen turns out to be enlarged, then this should not be considered an indication for splenectomy, as was the case before the 20s of our century due to misconceptions about the essence of the disease.

The course of pernicious anemia is cyclical - 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 clearing; there are few polychromatophils and reticulocytes (their appearance portends remission).

Until now, hyperchromic anemia with phenomena of the embryonic type of hematopoiesis (megalocytes from megaloblasts) is the main characteristic feature that distinguishes true pernicious anemia from other anemias. The rest of 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 characteristic features blood smear and occur in significant numbers only on the eve of remissions. As a rule, there is also leukopenia with relative lymphocytosis; hypersegmented forms are found among neutrophils; sometimes myelocytes are detected (a sign of special irritation of the bone marrow). There are always few platelets. Blood serum is dark yellow, especially in moments of deterioration (hemolysis); In parallel with bilirubinemia, urobilinuria is observed. These phenomena directly depend on the severity of pernicious anemia, and therefore may be completely absent during the period of remission. Significant deterioration may be combined with symptoms hemorrhagic diathesis. Malnutrition of the heart muscle (due to hypoxia associated with anemia) affects the negative T wave on the electrocardiogram.

In the pathological 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, which maintains the balance of iron metabolism in the body, while extracellular hemolysis disrupts it. That is why in pernicious anemia there is hyperchromemia, and in aplastic anemia there is hypochromemia.

Pathoanatomical changes in the spleen with pernicious anemia appear macroscopically in the form of a particularly strong overflow of blood; the histological picture shows a significant overflow of the spleen pulp with red blood cells located more around the trabeculae and follicles; the latter are almost always preserved, and in some cases their number is even increased. Sometimes extramarrow hematopoiesis is observed in the form of the appearance of scattered myeloid foci located near the vascular adventitia. According to some, there are also vascular changes, especially in the form of thickening of the walls of the central arteries and deposition of hyaline in the intimal area. Hyaline degeneration of the small vessels of the spleen is a very common occurrence in people between 10 and 40 years of age, and even more common in older people. At the same time, in small vessels the entire intima is degenerated.

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; Extramarrow hematopoiesis is also sometimes observed in the lymph nodes and liver.

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

Agastric anemia - anemia due to loss of the anti-anemic function of the stomach (after removal of the stomach or in some of its diseases). Anemia develops as pernicious anemia, but more often as achilic chloranemia. The fears that such anemia always entails are exaggerated. Severe anemia of the malignant type sometimes occurs only after total gastrectomies (about 8%); treatment in these cases is not unsuccessful, and postponing surgery to prevent anemia is dangerous from an oncological point of view. Conventional gastrectomy, especially when peptic ulcer, is sometimes accompanied (15-20% of cases) by slight anemia of the chlorine-anemic order, which responds well to treatment with iron.

Treatment of pernicious anemia

Currently, pernicious anemia is cured with organotherapy and vitamin therapy. It is recommended to take 100 g of raw veal liver (passed through a meat grinder) twice a day (washed down with diluted hydrochloric acid - 25 drops in half a glass of water) 2 hours before regular meals for 5-6 weeks. Liver extracts for internal use and parenterally. The effectiveness of all of these treatment methods depends on the content of hematopoietic vitamin B12 in them. Liver extract has been successfully used recently.

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

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

Anemia in pregnant women is curable with vigorous parenteral liver therapy, Campolon (termination of pregnancy is allowed only in case of ineffective treatment).

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

Prognosis for pernicious anemia

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