Pernicious anemia prognosis. Pernicious anemia: symptoms and treatment Pernicious anemia and stomach cancer

About what it is - pernicious anemia, most patients find out in the doctor's office after taking blood tests. In ordinary life, people, as a rule, do not encounter this term. Pernicious anemia is a disease that is characterized by a violation of hematopoiesis against the background of a decrease in vitamin B12 in the body. Pernicious anemia is also called B12 deficiency anemia or Addison-Birmer disease.

According to ICD10, pernicious anemia was assigned code D51.0, and according to ICD 9, code 281.0.

As vitamin B12 levels decrease in the body, the bone marrow replaces normal red blood cell precursors with very large cells (megaloblasts). They do not have the possibility of further degeneration into erythrocytes, which leads to a decrease in their number. If treatment is not started in time, then anemia will develop in a person and the process of degeneration of the nervous tissue will begin.

Pernicious anemia - what is it?

For the first time the world learned about pernicious anemia in 1855 thanks to the work of the scientist Addison. He called this disease idiopathic anemia, that is, anemia of unknown origin.

This violation was described in more detail by a scientist named Brimer, which happened in 1868. It was he who gave the name to the disease, which has come down unchanged to our times. Pernicious anemia means pernicious anemia.

For a long time, this disease was considered incurable. However, in 1926, scientists Minot and Murphy found that pernicious anemia can be cured by eating raw liver. At that time, this innovative method of treatment was called liver therapy.

The next scientist who continued to study the problem of pernicious anemia is W. B. Castle. Based on the scientific works of his predecessors, he found that in addition to hydrochloric acid and pepsin, the human body produces another internal factor containing mucoids and peptides. This substance is produced in the mucous membrane of the stomach. It is this internal factor that combines with vitamin B12, which comes from outside into an unstable, but mobile complex. It penetrates into the plasma part of the blood, through it enters the liver and settles in it in the form of a protein-B12-vitamin complex. It is this compound that takes an active part in the process of hematopoiesis. Castle was able to determine that in people who suffer from B12-deficiency anemia, it is precisely the third intrinsic factor (Castle factor), which is produced in the gastric mucosa, that is missing. However, at that time, the scientist could not establish that vitamin B12 was an external factor.

This became known only in 1948 thanks to the scientists Ricks and Smith.

It is impossible to call B12-deficiency anemia a rare disease. It is diagnosed in every 110-180 people out of 100,000 people. Most people with B12 deficiency anemia live in Scandinavia and the UK. Moreover, these are mostly patients of a fairly mature age. However, if a burdened history is traced in the family, then pernicious anemia can develop at a young age. Women are more likely to suffer from B12 deficiency anemia than men. For every 10 female patients, there are 7 males.

Pernicious anemia can have three degrees of severity:

With a decrease in the level of hemoglobin in the blood to 90-110 g / l, anemia is considered mild.

With a drop in the level of hemoglobin in the blood to 70-90 g / l, they speak of anemia of moderate severity.

If the hemoglobin level falls below 70 g/l, then anemia is severe.

Depending on what caused the development of pernicious anemia, the following forms are distinguished:

Alimentary (nutritin) anemia, which is most often diagnosed in children at an early age. However, this disorder can also be observed in adults who deliberately limit their diet in animal products. Also at risk are premature babies, formula-fed babies, and babies fed goat's milk.

Classical pernicious anemia, which develops against the background of atrophic processes in the gastric mucosa. This leads to the fact that the cells of the body are not able to produce intrinsic factor.

Juvenile pernicious anemia, which manifests itself with functional insufficiency of the fundic glands. They become unable to produce glandular mucoprotein. In this case, the gastric mucosa works as expected. If you start treatment of juvenile anemia, you can achieve a complete recovery.

Familial pernicious anemia (Olga Imerslund's disease) is also distinguished. It develops when there is a violation of the transport and absorption of vitamin B12 in the intestine. A clear diagnostic sign of such a violation will be.

The reasons that can lead to the development of pernicious anemia can be as follows:

Pernicious anemia (syn. Addison-Birmer disease, b12 deficiency anemia, pernicious anemia, megaloblastic anemia) is a pathology of the hematopoietic system that occurs against the background of a significant lack of vitamin B12 in the body or due to problems with the absorption of this component. It is noteworthy that the disease can occur after about 5 years after the cessation of the intake of such a component into the body.

The formation of such a disease can be influenced by a large number of predisposing factors, ranging from poor nutrition to a wide range of diseases associated with many internal organs and systems.

The clinical picture is nonspecific and includes:

pallor of the skin;
fluctuations in heart rate;
shortness of breath
weakness and malaise;
sensitivity disorder.

Diagnosis of b12-deficiency anemia is possible with the help of information obtained during laboratory blood tests. However, to search for a causative factor, instrumental procedures and activities carried out personally by the clinician may be required.

Treatment of the disease consists in the use of conservative methods, including:

taking medications;
adherence to a specially formulated sparing diet.

The International Classification of Diseases of the Tenth Revision allocates a separate code for such a disorder. It follows that megaloblastic anemia has the ICD-10 code D51.

Etiology

Addison-Birmer disease is considered a fairly rare disease that in the vast majority of situations occurs in people over the age of 40 years. However, this does not mean at all that pathology cannot develop in people of a different age, including children. In addition, it is noted that representatives of the weaker sex are most often affected by this disease.

Normally, the human body needs vitamin B12 daily in volumes from 1 to 5 micrograms. This dosage is often satisfied by the intake of this substance with food. From this it follows that most often pernicious anemia is the result of malnutrition.

In addition, the cause of pernicious anemia may be the following:

insufficient amount of internal factor Castle, which is also called a glycoprotein;
structural changes in the stomach or small intestine;
infiltration or pathogenic bacteria that absorb vitamin B12;
the formation of malignant tumors;
chronic form of alcoholism;
irrational use of drugs;
complete or partial removal of the stomach;
diverticula of the small intestine;
tuberculosis of the ileum;
dysfunction of the thyroid gland;
diseases of the liver and kidneys;
vegetarianism.

The main risk factors that increase the likelihood of developing such a disease are advanced age and the presence of gastric pathologies in the clinical history.

Megaloblastic anemia in newborns is most commonly associated with increased intake of vitamin B12, which is found in breast milk. Infants whose mothers do not eat meat often suffer.

Classification

Pernicious anemia has several degrees of severity, which differ depending on the concentration of hemoglobin in the blood:

mild degree - the level of iron-containing protein is 90-110 g / l;
moderate degree - indicators vary from 70 to 90 g / l;
severe - contains less than 70 g / l of hemoglobin.

Specialists from the field of genetics distinguish a group of people who develop a similar disease against the background of aggravated heredity. Thus, there are the following forms of malignant anemia caused by genetic disorders:

classical, in which there is a violation of the absorption of vitamins B12;
juvenile, when there are signs of an autoimmune condition;
teenage, supplemented by the Imerslund-Gresbek symptom complex;
congenital pernicious anemia, which presumably develops against the background of a gene mutation.

Symptoms

Megaloblastic anemia has non-specific symptoms, that is, those that cannot accurately indicate the course of this particular disease. The main external clinical signs of such a disease are:

increased heart rate;
pallor of the skin;
dizziness;
weakness and fatigue;
murmurs in the heart;
a slight increase in temperature indicators;
shortness of breath during physical activity;
loss of appetite;
stool disorder;
dryness, burning and pain in the tongue;
the acquisition of a crimson hue from the tongue;
numbness and limited mobility of the limbs;
muscle weakness;
change in gait;
paraparesis of the legs;
urinary and fecal incontinence;
violation of pain, tactile and vibration sensitivity;
sleep problems, up to its complete absence;
hallucinations;
cognitive decline;
in female representatives;
decrease in sexual attraction to the opposite sex;
loss of body weight;
tinnitus;
the appearance of "flies" before the eyes;
fainting states.

Symptoms of pernicious anemia in children, in addition to the above, include:

growth retardation;
violation of harmonious development;
a decrease in the resistance of the immune system, which is why inflammatory and infectious diseases very often occur, and chronic diseases are much more severe.

Diagnostics

A hematologist can make a diagnosis of Addison-Birmer disease, but specialists such as a gastroenterologist, pediatrician, and neurologist may also be involved in such a process.

The basis of diagnostic measures is the data obtained in the course of laboratory studies, but they must necessarily be preceded by such manipulations as:

the study of the medical history, which is carried out to search for the main pathological etiological factor;
collection of family and life history of the patient;
measurement of heart rate and temperature indicators;
a thorough physical and neurological examination;
listening to the sounds of human organs with a phonendoscope;
a detailed survey of the patient to obtain detailed information regarding the present symptom complex.

Among the laboratory studies it is worth highlighting:

general clinical and biochemical blood tests;
general urine analysis;
microscopic examination of punctate and biopsy;
coprogram.

Instrumental diagnostics involves the implementation of:

FGDS and ECG;
ultrasonography of the abdominal cavity;
radiography and irrigography;
electroencephalography;
CT and MRI;
myelograms;
gastroscopy;
endoscopic biopsy;
bone marrow puncture.

Pernicious anemia must be differentiated from other types of anemia such as:

folic acid deficiency.

Treatment

Treatment of megaloblastic anemia is based on the use of conservative therapeutic measures. First of all, correction of the conditions that led to the formation of such a disease is required. In this case, the scheme is selected individually for each patient.

intramuscular injections, when preparations containing vitamin B12 are administered;
diet therapy, which shows the consumption of food enriched with animal protein;
blood transfusion;
use of traditional medicine recipes.

Since the treatment of b12-deficiency anemia will not be complete without a sparing diet, it is recommended that patients, along with taking medications, be introduced into the diet:

dietary varieties of meat and fish;
dairy and sour-milk products;
seafood;
hard cheese;
chicken eggs;
mushrooms and legumes;
corn and potatoes;
boiled sausage and sausages.

Treatment of pernicious anemia includes the use of alternative medicine prescriptions. The most effective components of healing decoctions and infusions are:

nettle;
dandelion root;
yarrow;
fireweed;
buckwheat flowers;
birch leaves;
clover;
sagebrush.

In general, the therapy of such a disease lasts from 1.5 to 6 months.

Possible Complications

Pernicious anemia in the complete absence of treatment and ignoring clinical signs can lead to the development of the following complications:

funicular myelosis;
coma;
violation of the functioning of vital organs, such as the kidneys or liver;
peripheral;
formation;

Prevention and prognosis

To prevent the development of such a disease, people should only follow a few simple rules. Thus, the prevention of b12-deficiency anemia includes the following recommendations:

maintaining a healthy and active lifestyle;
complete and balanced nutrition;
taking medications only as prescribed by the attending physician;
taking courses of vitamin therapy after surgery;
early diagnosis and elimination of any diseases that lead to a decrease in the production or absorption of vitamin B12;
regular visits to a medical institution for a comprehensive examination.

The prognosis for megaloblastic anemia in the vast majority of situations is favorable, and complex long-term treatment allows not only to completely recover from such a disease, but also get rid of the provoking factor, which will reduce the chances of relapses and complications.

Is everything correct in the article from a medical point of view?

Answer only if you have proven medical knowledge

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.

A useful confirmation of the correctness of the diagnosis is the hematological effect of vitamin 12 treatment. This effect may be masked by the inappropriate use of folic acid in patients with presumably uncomplicated vitamin B12 deficiency.

Folate Deficiency Diagnosis

The most informative way to detect folic acid deficiency is to determine its concentration in red blood cells. Folic acid enters erythrocytes during bone marrow erythropoiesis and is subsequently not included in mature erythrocytes. In this sense, erythrocytes are tissue, and the concentration of folic acid in them (145-450 ng / ml of total erythrocyte volume) is about 20 times or more higher than in serum. The content of folic acid in erythrocytes changes only when young cells with a different level of folates enter the circulation and therefore occur slowly. Decreased erythrocyte folate levels are characteristic of long-term folic acid deficiency.

sa, it does not necessarily indicate a deficiency of folic acid. Even the slightest hemolysis in a blood sample taken causes an increase in serum folate and distorts the result of the study.

The megaloblastic anemia in this patient can be considered to be due to folic acid deficiency if the serum vitamin B12 level is normal or if its absorption is not impaired, regardless of its serum content. Persistent megaloblastosis refractory to vitamin B12 therapy also indicates folic acid deficiency.

PERNICIOUS ANEMIA

Definition

Pernicious anemia is a disease characterized by megaloblastic hematopoiesis and (or) changes in the nervous system due to vitamin B12 deficiency, which occurs with severe atrophic gastritis.

Frequency

Among the inhabitants of Northern Europe and in populations of immigrants from Northern Europe, the frequency of pernicious anemia (PA) is


stakes 110-180					population.
		reaches 1%.
			was 2.5%,			and among the inhabitants
	in North West England was 3.7%
		family		predispositions

the patient population was younger. The ratio of sick women and men is constantly 10:7.

Etiology

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

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

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

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

The third etiological factor is represented by the immune component. Two types of autoantibodies have been found in PA patients:

parietal cells and intrinsic factor.

The method of immunofluorescence in the serum of 80-90% of patients with PA reveals antibodies that react with the parietal cells of the stomach. The same antibodies are present in the serum of 5-10% of healthy individuals. In elderly women, the frequency of detection of antibodies to the parietal cells of the stomach reaches 16%. Microscopic examination of biopsies of the gastric mucosa in almost all individuals with serum antibodies to the parietal cells of the stomach reveals gastritis. The introduction of antibodies to the parietal cells of the stomach in rats leads to the development of moderate atrophic changes, a significant decrease in the secretion of acid and intrinsic factor. These antibodies obviously play an important role in the development of atrophy of the gastric mucosa.

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

IgG. In some patients, antibodies are present only in gastric juice. Based on the detection of antibodies in both serum and gastric juice, it can be concluded that such antibodies to intrinsic factor are detected in approximately 76% of patients.

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

cellular immunity to intrinsic factor, it turns out that the immune component is present in 24 out of 25 patients with PA.

According to modern concepts, lymphocytes contain all the necessary information for the production of any anti-

produce "autoantibodies" against parietal cells, intrinsic factor, and quite often against cells of the thyroid gland, parathyroid glands, adrenal glands and the islets of Langerhans. The tendency to develop autoantibodies is familial, in any case, these antibodies are found with high frequency in healthy relatives, and some relatives develop corresponding diseases. It is unclear what is primary in the development of atrophic gastritis. Antibodies to parietal cells interfere with normal mucosal regeneration. It is possible that it is the antibodies that trigger the atrophic process. Steroids, destroying lymphocytes, contribute to the reverse development of the process

sa and regeneration of the atrophied mucous membrane. Atrophy significantly reduces the volume

I eat gastric secretion and the production of intrinsic factor.

Antibodies to intrinsic factor neutralize its residual amounts, resulting in the absorption of vitamin B)