The blood that circulates throughout the body has a number of critical functions. It delivers oxygen, removes carbon dioxide and carries vital nutrients.
By transporting substances such as hormones to distant parts of the body, blood helps different parts of the body communicate with each other. These important functions are performed by blood cells paired with the liquid part of the blood ( plasma).
Most of the cells in plasma are red blood cells ( erythrocytes). White blood cells ( leukocytes) are also present, but in smaller quantities. Their role is to protect the body from foreign substances, including infections, viruses and fungi.
What is pernicious anemia?
Anemia-it is a condition that occurs when hemoglobin level(the iron-protein compound in the oxygen-carrying red blood cells) decreases and the body becomes too few red blood cells. When there are too few red blood cells due to a lack of vitamin B12, this condition is called pernicious anemia .
Term pernicious (from Lat. perniciosus - fatal, dangerous) was adopted many years ago, when there were no effective methods of therapy, and this condition inevitably led to the death of patients. Excellent treatments are available today and most people can lead normal lives with very few side effects.
Pernicious anemia can affect all racial groups, but the incidence is higher among fair-haired people, especially those with ancestors from Scandinavia or Northern Europe. Usually, the disease does not appear until the age of 30, although children may develop a juvenile form of the disease.
Alternative names for pernicious anemia are B12 deficiency anemia, megaloblastic anemia, disease (or anemia) Addison-Birmer.
Causes of pernicious anemia
Perniciousanemia is caused by a deficiency of vitamin B12, which is essential for normal red blood cell production. It is often hereditary. Risk factors include history autoimmune endocrine disorders, a family history of pernicious anemia and of Scandinavian or Northern European origin.
The meat and dairy products we eat are our main sources of vitamin B12. However, with the exception of strict vegetarians, pernicious anemia is not simply caused by not consuming enough of these foods, but by a malfunction in the complex process of the digestive tract through which vitamin B12 is absorbed.
In order for vitamin B12 to be absorbed by the small intestine, the cells that line part of the stomach must produce a substance called internal factor(IF).
This substance binds to vitamin B12 and both are absorbed in combination in the lowermost part of the small intestine ( ileum), right where the small intestine enters the large intestine. If the ileum is damaged or removed during surgery, the intrinsic factor combination will not be absorbed.
People with medical conditions such as who often have surgery to remove part of their ileum (the part of the small intestine where vitamin B12 is absorbed) should be screened for vitamin B12 deficiency and, if necessary, receive treatment.
Lack of intrinsic factor can also be congenital(present at birth). This form of pernicious anemia (called juvenile or congenital) is usually seen before the child is three years old. It is believed that even the transmission of this gene from only one parent can cause this disorder in a child.
Less common causes of decreased absorption of B12 include certain medications and, very rarely, increased B12 metabolism as a result of prolonged hyperthyroidism ... A very common cause of B12 deficiency in older people is inadequate intake of foods containing vitamin B12.
Pernicious anemia is also often seen in combination with some autoimmune endocrine(glandular) diseases such as type 1 diabetes hypoparathyroidism , Addison's disease and testicular dysfunction.
Symptoms and complications
In most cases, there are no early signs of pernicious anemia. As the disorder progresses, and decreased endurance during exercise or any activity. A noticeable heart palpitations can also be an obvious symptom of B12-deficiency anemia.
People with this disorder often have very low hemoglobin but symptoms of low hemoglobin such as fatigue are minor. They may also develop low white blood cell count(which is important for fighting infections) and platelets(which are necessary for blood clotting and bleeding control). However, infections and bleeding are rare in people with pernicious anemia.
Other symptoms that can develop include:
- pallor of the skin;
- painful, red, shiny tongue (see photo above);
- and weight loss;
- tingling sensation and and feet;
- violation of gait and balance (especially in the dark);
- mental changes, including memory loss, irritability, mild, and dementia;
- yellow-blue color blindness.
Left untreated, vitamin B12 deficiencies can gradually affect sensory and motor nerves and cause neurological effects. Anemia can also affect the gastrointestinal system and cardiovascular system, lead to tongue problems, impair smell, bleeding gums, and loss of deep tendon reflexes. In very advanced cases, paranoia, delirium and confusion can also occur.
Pernicious anemia is a chronic disease that progresses slowly and steadily. In the past, before much was known about the disease and there was no cure, it ended up causing death after years of suffering. Today the forecast is excellent. Replacement therapy with an adequate amount of vitamin B12 will correct the deficiency and allow the person to lead a normal life.
If the condition progresses for a long time before it is detected, it can damage certain parts of the body, most notably the nervous and digestive systems. Gastric polyps may develop, increasing the likelihood of developing stomach cancer. Vitamin B12 deficiency affects the appearance of epithelial cells on the cervix, and an untreated woman can get a false positive result with a Pap test.
Establishing diagnosis
If you have underlying symptoms of anemia, your doctor will likely do a variety of tests. One of these tests looks at the amount of vitamin B12 in the blood. The blood will be examined under a microscope to assess the size and shape of the red blood cells. In cases of pernicious anemia, these cells will be larger and fewer in number.
If the amount of vitamin B12 in your blood is found to be low, your doctor may perform additional tests to confirm that your body has sufficient levels to carry out regular cellular processes. In rare cases, a bone marrow examination is required to confirm the diagnosis.
Historically, the so-called Schilling test was previously performed, but in practice it is no longer carried out.
People with pernicious anemia have an increased incidence of stomach cancer. The doctor will need to watch for any clinical signs (eg, symptoms, positive trace test) that indicate a problem with the digestive system, and do additional research, such as x-ray or endoscopy(examination of the inside of the body with a thin, flexible tube with a small camera at the end).
Treatment and prevention of pernicious anemia
The amount of vitamin B12 containedin the body is directly related to the amount that is taken. The main treatment for pernicious anemia is injections ( cobalamin). Determining the amount of vitamin B12 you need can be difficult because it must also replace the vitamin B12 found in the liver.
At first, there may be 5 to 7 injections in a short period of time. This therapy usually makes sense for 48-72 hours, so there is no need for a blood transfusion. After all, injections can be given once a month and will likely continue indefinitely. It has recently been found that vitamin B12 can be administered orally in very high doses (0.5 to 2 mg per day) for maintenance therapy, making injections unnecessary.
Pernicious without the help of a doctor... However, a well-balanced diet is essential to provide other components needed for healthy blood cell development, such as folate, iron, and vitamin C.
Vitamin B12 therapy should be maintained throughout life unless the underlying cause of the deficiency is addressed.
Because there is an increasing familial incidence of pernicious anemia, family members should be aware that they are at greater risk of developing the condition and should seek immediate medical attention if they develop anemia or mental and neurological symptoms.
Forecast
As mentioned above, the disease is called pernicious anemia because it was fatal before its underlying causes were identified. The megaloblastic appearance of the cells led many to assume that this is a tumor disease. Patient responses to liver therapy indicated that nutritional deficiencies were the cause of the disorder. This became apparent in clinical trials following the release of vitamin B12.
Currently, early detection and treatment of pernicious anemia ensures normal and generally long life expectancy. However, delayed treatment allows for the progression of anemia and neurological complications.
If patients are not treated early in the disease, neurological complications can become permanent. Severe anemia can cause congestive or cause coronary insufficiency.
Although vitamin B12 therapy corrects anemia, it does not cure atrophic gastritis, which can progress to stomach cancer. The incidence of gastric adenocarcinoma is 2-3 times higher in patients with pernicious anemia than in the general population of the same age.
Interesting
Pernicious anemia
Chronic illness / anemia due to insufficient absorption of vitamin B 12
It occurs in adults as a result of stomach atrophy (cannot absorb vitamin B12). Wall cells in the stomach that produce an intrinsic factor necessary for the absorption of vitamin B12 and, if destroyed, result in a lack of this very important vitamin.
The name pernicious anemia has survived from the time when this type of anemia was fatal and has retained the name for historical reasons.
Due to a lack of vitamin B12 can cause a variety of diseases and conditions, but anemia includes only those caused by atrophic gastritis and loss of parietal cell function.
Dr. Addison was the first to describe the disease and before 1920 people died of the disease within a year to 3 years after diagnosis. Doctors investigated this anemia so that patients consumed more raw liver and juice in larger 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 solved the lack of this vitamin with tablets or injections!
Vitamin B 12 cannot be created / synthesized by the human or animal body so that it must be supplied with food. It is extremely important for the proper functioning of the brain and nervous system; it is involved in the metabolism of every cell in the body.
Most 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 is synthesized in the parietal cells of the stomach, not assimilating vitamin B12, the result: megaloblastic anemia.
Any illness or condition can lead to malabsorption of vitamin B12 deficiency and anemia is (although not always) a neurological condition.
Periodicity:
Most widespread in the North European population. British, Scandinavians, Irish, Scots, aged 40-70.
Problem:
Weight loss, temperature
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
Dysfunction of the thyroid gland
Diarrhea
Paresthesias: tingling in the hands / feet
Most difficult: neurological disorders: problems with balance, gait, muscle weakness. An elderly person with signs of dementia is diagnosed with a lack of vitamin B12, and memory problems, hallucinations, irritability can 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.
The presence of antibodies and internal factors in the blood.
THERAPY:
As you probably guessed, the therapy is vitamin B12 replacement. Vitamin B12 does not exist in nature, but is synthesized and applied to patients in the form of tablets, transdermal, in the nose or in the form of injections (intramuscularly, subcutaneously).
Today there are tablets that contain high doses of vitamin B12: 500-1000 mcg, so that there is a sufficient amount of vitamin to the cells in the body.
Is there any doubt, if anything, 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 65 years of age
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.
Disturbances of the cardiovascular, nervous, digestive and hematopoietic systems are characteristic. Complaints of patients are varied: general weakness, shortness of breath, palpitations, pain in the heart, swelling of the legs, a feeling of creeping in the hands and feet, gait disorder, burning pain in the tongue, periodic diarrhea. The patient's appearance is characterized by pallor of the skin with a lemon-yellow tint. The sclera are subicteric. The patients are not exhausted. When examining the cardiovascular system, anemic murmurs associated with a decrease in blood viscosity and an acceleration of blood flow are typical. On the part of the digestive organs, the so-called Gunter glossitis (the tongue is bright red, the papillae are smoothed), histamine-resistant achilia (the absence 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. Nervous system changes 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, Kebot's 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 case of anemic coma - urgent hospitalization, blood transfusion, better than erythrocyte mass (150-200 ml). Supportive therapy with vitamin B12 is necessary to prevent relapses. A systematic observation of the blood composition in people with persistent achilia, as well as those who have undergone gastric resection, is shown. Patients suffering from pernicious anemia should be under dispensary supervision (possibly stomach cancer).
1. Malignant 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's disease - as endogenous B12-avitaminosis due to atrophy of the fundic glands that produce gastromucoprotein, as a result of which the assimilation of vitamin B1a, which is necessary for normal, normoblastic, and hematopoiesis, is impaired. pathological, megaloblastic, hematopoiesis develops, leading to anemia of the "pernicious" type.
Clinical presentation (symptoms and signs). Persons over the age of 40-45 get sick. Disturbances from the cardiovascular, nervous, digestive and hematopoietic systems are characteristic. Complaints of patients are varied: general weakness, shortness of breath, palpitations, pain in the heart, swelling of the legs, dizziness, a feeling of creeping in the hands and feet, gait disorder, burning pain in the tongue and esophagus, recurrent diarrhea. The patient's appearance is characterized by pallor of the skin with a lemon-yellow tint. The sclera are subicteric. The patients are not exhausted. The face is puffy, with swelling in the ankles and feet. Edema can reach large degrees and be accompanied by ascites, hydrothorax. From the side of the cardiovascular system - the appearance of a systolic murmur at all openings of the heart and a "spinning top" noise on the bulb of the jugular vein, which is associated with a decrease in blood viscosity and accelerated blood flow; possible angina pectoris of anoxemic nature. 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 system - the so-called Hunter's (Hunter's) glossitis, the tongue is clean, bright red, devoid of papillae. Analysis of gastric juice, as a rule, reveals histamine-resistant achilia. Recurrent diarrhea is a consequence of enteritis. The liver is enlarged, soft; in some cases, a slight enlargement of the spleen. With a significant drop in the number of red blood cells (below), 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 palsy and tabic symptoms (the so-called pseudotabes): spastic paraparesis with increased and pathological reflexes, clonuses, creeping sensation, numbness of the limbs, girdle pain, impaired vibration and deep sensitivity, sensory ataxia and disorder pelvic organs; less often bulbar phenomena.
Blood picture. The most common symptom is hyperchromic type anemia. The morphological substrate of hyperchromia is large, hemoglobin-rich erythrocytes - macrocytes and megalocytes (the latter reach 12-14 microns and more). With an exacerbation of the disease, the number of reticulocytes in the blood sharply decreases. The appearance of a large number of reticulocytes portends an imminent remission.
The exacerbation of the disease is characterized by the appearance of degenerative forms of erythrocytes [poikilocytes, schizocytes, basophilic-punctured erythrocytes, erythrocytes with Jolly bodies and Kebot's 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 neutrophilic series, giant, polysegmented 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 an 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 (color table, Fig. 6).
The symptoms of the disease develop gradually. For many years before the disease, gastric achilia is found. At the beginning of the disease, general weakness is noted; patients complain of dizziness, palpitations at the slightest physical exertion. Then 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 a cyclical nature - 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 "disastrous" (pernicious). During a period of severe relapse - the sharpest anemization and rapid progression of all symptoms of the disease - a life-threatening coma (coma perniciosum) may develop.
Pathological anatomy. An autopsy of a deceased 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 (tsvetn. table, Fig. 7). Fatty infiltration of the myocardium ("tiger heart"), kidneys, liver is noted; in the liver, spleen, bone marrow, lymph nodes - hemosiderosis (printing table, Fig. 8). Changes on the part of the digestive organs are characteristic: the papillae of the tongue are atrophic, atrophy of the mucous membrane of the stomach and its glands is 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 case of anemia: 1 - 4 - erythrocytes of the last stage of normal hematopoiesis (transformation of erythroblast into erythrocyte); 5 -9 - disintegration of the nucleus with the formation of Jolly bodies in basophilic punctate (5, 6) and polychromatophilic (7 - 9) erythrocytes; 10 and 11 - Jolly bodies in orthochromic erythrocytes; 12 - chromatin dust particles in erythrocytes; 13 - 16 - Kebot's rings in basophilic punctured (13, 14) and orthochromic (15, 16) erythrocytes (pernicious anemia); 17 - 23 - basophilic punctured erythrocytes with lead anemia; 24 and 25 - polychromatophilic erythrocytes (microcyte and macrocyte); megalocyte (26) and poikilocyte (27) with pernicious anemia; 28 - normocyte; 29 - microcytes.
Rice. 5. Blood in case of pernicious anemia (severe relapse): megalocytes orthochromic (1) and polychromatophilic (2), erythrocytes with Kebot's rings (3), Jolly bodies (4) with basophilic puncture (5), megaloblasts (6), polysegmented neutrophil ( 7), anisocytosis and poikilocytosis (8).
Rice. 6. Bone marrow in case of pernicious anemia (initial remission 24 hours after administration of 30mkg 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 with pernicious anemia (reaction to Prussian blue).
Treatment. Since the 1920s, raw liver has been used with great success for the treatment of malignant anemia, especially lean veal, minced (200 g per day). A great achievement in the treatment of pernicious anemia was the manufacture 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 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 administration of vitamin B12 is effective only in combination with the simultaneous intake of an 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 mukovita (produced in the form of pills) containing vitamin B12 (200-500 μg each) in combination with gastromucoprotein (0.2). Mukovit is prescribed 3-6 pills a day every day before the onset of a reticulocytic crisis and then 1-2 times a day until hematological remission occurs.
The immediate effect of antianemic therapy in terms of blood replenishment with newly formed erythrocytes begins to affect from the 5-6th day of treatment by the rise of reticulocytes to 20-30% and higher ("reticulocytic crisis"). Following the reticulocytic crisis, the amount of hemoglobin and erythrocytes 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. In case of funicular myelosis, vitamin B12 is applied 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, with funicular myelosis - up to 5000 mcg and more.
The effectiveness of therapy with vitamin B12 has a certain limit, upon reaching which the increase in blood quantitative parameters stops and anemia becomes hypochromic; during this period of the disease, it is advisable to apply treatment with iron preparations (2-3 g per day, washed down with diluted hydrochloric acid).
The question of the use of blood transfusions for pernicious anemia in each case is decided according to the indications. An unconditional indication is pernicious coma, which poses a threat to life due to increasing hypoxemia. Repeated transfusions of blood or (better) erythrocyte mass (250-300 ml each) often save the lives of patients until the therapeutic effect of vitamin B12 appears.
Prevention. The minimum daily human need for vitamin B12 is 3-5 mcg, therefore, in order to prevent recurrence of pernicious anemia, it is 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 extensive resection of the stomach, as well as those with persistent achilia of the stomach, provide them with a full-fledged 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 achilia of the stomach and especially pernicious anemia are more likely to develop stomach cancer than others. 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 the intoxication remained unknown; for differential diagnosis they relied on the most characteristic moments of the clinic and the pathological anatomy of the disease.
Some attached great importance to the state of the bone marrow in malignant anemia, for example Ehrlich, who called this state "a 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. Long-term remissions after splenectomy were evidence of the involvement of the spleen in the pathogenesis of the disease. 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, and still others believed that splenectomy removes the organ that inhibits the erythropoietic activity of the bone marrow.
The onset of remission after other methods of treatment, as well as the return of the disease and 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-Birmer disease is considered to be a lack of hematopoietic vitamin B12 and folic acid. Deficiency 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 vitamin deficiency occurs with achilic gastritis (syphilis, polyposis or stomach cancer) or agastria (gastrectomy or turning off the stomach by other operations), with helminthic invasion (wide tapeworm), pregnancy, sprue (prolonged enteritis), with resection or shutdown of the small intestine. These are all secondary forms; with some of them, the disease proceeds without nervous phenomena, achilia and is cured with the elimination of the etiological factor. And, finally, vitamin B12 deficiency can be of exogenous origin - a lack of vitamin B12 in food. Pathogenetically, we are talking about a violation of bone marrow hematopoiesis (a 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 rank it among hemolytic anemias, since we are talking about the destruction of erythrocytes in the bone marrow itself due to a violation of hematopoiesis.
Pernicious anemia symptoms
The disease affects people over the age of 40 (earlier than 25 years are extremely rare), equally often men and women. It all starts with achilia and changes in the nervous system. Weakness, dizziness appear, and then signs of anemia - shortness of breath, palpitations with minor physical exertion. Simultaneously with anemia, glossitis occurs (pain and burning sensation 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 it were, 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 turns out to be 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 nature of the disease.
The course of pernicious anemia is cyclical - deterioration is replaced by remission, 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 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 erythrocytes, 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 remission. As a rule, there is also leukopenia with relative lymphocytosis; hypersegmented forms are found among neutrophils; sometimes myelocytes are found (a sign of particular irritation of the bone marrow). There are always few platelets. Dark yellow blood serum, especially at moments of deterioration (hemolysis phenomena); parallel to bilirubinemia, urobilinuria is observed. These phenomena directly depend on the severity of pernicious anemia, therefore, they may be completely absent during the period of remission. Significant deterioration can be combined with symptoms of 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, lymph nodes. In the spleen, iron is found mainly intracellularly, and this differs 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 violates it. That is why, with pernicious anemia, there is hyperchromemia, and with aplastic anemia, hypochromemia.
Pathological changes in the spleen with pernicious anemia appear already and macroscopically in the form of a particularly strong overflow of its 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 extraboneous cerebral hematopoiesis is observed in the form of the appearance of diffuse 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 deposits of hyaline in the intima. Hyaline degeneration of the small vessels of the spleen is very common in people between the ages of 10 and 40, 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, extraboneous 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 gastric and intestinal mucosa. Changes in the adrenal glands are found in the form of a decrease in lipoids and chromaffin substance.
Agastric anemia - anemia due to loss of antianemic 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. 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 the operation to prevent anemia is dangerous from an oncological point of view. The usual resection of the stomach, especially in peptic ulcer disease, is sometimes accompanied (15-20% of cases) with a small anemia of the chlorine-anemic order, which responds well to iron treatment.
Pernicious anemia treatment
Currently, pernicious anemia is cured by organ and vitamin therapy. Recommended raw veal liver (minced) twice a day, 100 g (washed down with diluted hydrochloric acid - 25 drops in half a glass of water) 2 hours before a regular meal for 5-6 weeks. Hepatic extracts for internal use and parenteral. The effectiveness of all the listed methods of treatment 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 the liver itself, as indicated above) should 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 the muscles, 2-4 ml daily. You can also use the intramuscular injection of pure (crystalline) vitamin B12, 15-30 μg.
For functional myelosis, raw liver (rich in vitamins B1 and B12) is most effective.
Anemia of pregnancy is cured by vigorous parenteral hepatic therapy, campolon (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 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 a broad tapeworm, the expulsion of the latter or specific anti-syphilitic treatment leads to full recovery.
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A drop in hemoglobin levels is observed in more than 1/3 of cancer patients. Anemia in cancer is measured by the level of blood oxygen saturation, which in this case decreases to less than 12 g / dL. This state of the body is also often observed in patients who have undergone a course of 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:
- Slowing down the production of red blood cells.
- Accelerated destruction of blood corpuscles.
- 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 renal 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 cancer anemia
The first symptoms of the disease are considered to be a sharp pallor of the skin and impaired 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 overall health. Patients report constant malaise, muscle weakness, rapid fatigue and loss of working capacity.
Cancer anemia is diagnosed on the basis of a detailed blood test. A quantitative study of the circulatory system is recommended to be carried out 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 drugs is the rapid restoration of normal hemoglobin parameters. At the same time, this technique has a short-term therapeutic effect. Many experts do not recommend prescribing a transfusion to cancer patients from the first days of anemia. In the initial period, the patient's body independently copes with the insufficiency of erythrocytes. Compensation is achieved by altering blood viscosity and oxygen uptake.
Blood transfusion is mainly carried out in the presence of a vivid 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.
Stimulating the production of red blood cells:
Many clinical studies indicate the high efficacy of the hormonal drugs erythropoietin. In many cases, this therapy option can replace systematic blood transfusion. In this case, special attention should be paid to patients with chronic renal failure. For these patients, there is an increased risk of premature mortality.
The use of iron preparations:
Iron deficiency is observed in about 60% of cancer patients. Iron deficiency can be caused by:
- chronic internal bleeding;
- surgical interventions on the organs of the gastrointestinal tract;
- cancerous anorexia.
What are the dangerous consequences of anemia in cancer?
Many doctors believe that anemic condition accompanies to one degree or another the course of all oncological diseases. The danger of a deficiency of erythrocytes lies in the development of oxygen starvation of all tissues and body systems. Also, the disease is usually aggravated by chemotherapy and radiation therapy.
Forecast
The consequences of the disease depend on the stage of the primary diagnosis of the tumor process. Erythrocyte insufficiency, which is detected in the early stages of oncology, has a favorable prognosis. In this case, a positive outcome 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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Malignant anemia
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 that is produced in the stomach. Intrinsic factor is essential for the absorption of vitamin B12. Pernicious anemia is often associated with an autoimmune-mediated attack by gastric parietal cells and / or intrinsic factor. Anemia is an inadequate supply of oxygen to the body's cells by red blood cells. The earlier the treatment of pernicious anemia begins, the better the result.
Causes of pernicious anemia
There are many possible causes of pernicious anemia. Some of them are listed below.
- Atrophic gastritis (stomach inflammation);
- Removal of all or part of the stomach;
- The immune system's response (in the form of an attack) to:
- Intrinsic Factor - 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;
- Basedow's disease;
- Myasthenia gravis;
- Secondary amenorrhea;
- Hypoparathyroidism;
- Hypopituitarism;
- Testicular dysfunction;
- Chronic thyroiditis;
- Vitiligo;
- Idiopathic adrenal cortex insufficiency;
- Origin: Northern Europe and Scandinavia;
- Age: over 50.
Symptoms of pernicious anemia
The symptoms of pernicious anemia can vary. Symptoms can change or worsen over time. These symptoms can be caused by other diseases. It is necessary to inform the doctor if any of them appear.
Symptoms may include:
- Tingling sensation in your feet or hands;
- Intermittent constipation and diarrhea;
- A burning sensation on the tongue or a sensitive red tongue;
- Significant weight loss;
- Inability to distinguish between yellow and blue;
- Fatigue;
- Pallor;
- Altered taste sensations;
- Depression;
- Impaired balance, especially at night;
- Tinnitus;
- Chapped lips;
- Yellow skin;
- Fever;
- Inability to feel the vibrations in the legs;
- Dizziness when moving from a sitting to a standing position;
- Cardiopalmus.
Diagnosis of pernicious anemia
Tests for diagnosing pernicious anemia include:
- Complete blood count - counts the number of red and white blood cells in the blood;
- A vitamin B12 level test, which measures the amount of vitamin B12 in your blood;
- Measuring the amount of methylmalonic acid in the blood - this test shows if there is a vitamin B12 deficiency;
- Homocysteine level is a test that measures the amount of homocysteine in the blood (homocysteine is a component that participates in the formation of protein). Homocysteine levels will be elevated if there is a deficiency of vitamin B12, folate, 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;
- Measuring the amount of a protein called intrinsic factor (Castle factor) - usually done in the stomach
- Prussian blue staining of bone marrow is a test that shows if there is an iron deficiency.
Treatment of pernicious anemia
Treatment may include:
Vitamin B12 injections
Treatment consists of intramuscular injection of vitamin B12. These injections are necessary because the intestines cannot absorb the required amount of vitamin B12 without the presence of an intrinsic factor in the stomach.
Oral vitamin B12
The procedure consists of taking increased doses of vitamin B12 orally.
Intranasal vitamin B12 intake
The doctor gives the patient vitamin B12 preparations, which are administered through the nose.
Oral iron supplementation
Prevention of pernicious anemia
To reduce the likelihood of developing pernicious anemia, the following steps should be taken:
- Long-term excessive alcohol consumption should be avoided;
- Ask your doctor for iron deficiency tests;
- Get tested if your doctor suspects Helicobacter Pylori infection.
Pernicious anemia
Pernicious anemia is a violation of the red sprout 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 made according to the results of laboratory tests (clinical and biochemical blood tests, bone marrow puncture). Treatment for pernicious anemia includes a balanced diet, intramuscular administration of cyanocobalamin.
Pernicious anemia
Pernicious anemia is a type of megaloblastic deficiency anemia that develops with insufficient endogenous intake or assimilation of vitamin B12 in the body. "Pernicious" in translation from Latin means "dangerous, disastrous"; in the domestic tradition, such anemia was previously called "malignant anemia". In modern hematology, B12-deficiency anemia and Addison-Birmer disease are also synonyms for pernicious anemia. The disease occurs more often in elders, somewhat more often in women. The prevalence of pernicious anemia is 1%; however, about 10% of elderly 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 mcg. It is satisfied due to the intake of vitamin with food (meat, dairy products). In the stomach, under the action of enzymes, vitamin B12 is separated from the dietary protein, however, for absorption and absorption into the blood, it must combine with glycoprotein (Castle's factor) or other binding factors. The absorption of cyanocobalamin into the bloodstream occurs in the middle and lower part 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. Alimentary reasons are due to insufficient intake of vitamin B12 from food. This can occur with fasting, vegetarianism, and diets that exclude animal protein.
Endogenous causes imply a violation of the assimilation of cyanocobalamin due to a deficiency of Castle's intrinsic factor with its sufficient intake from outside. Such a mechanism for the development of pernicious anemia occurs in atrophic gastritis, a condition after gastrectomy, the formation of antibodies to Castle's intrinsic factor or parietal cells of the stomach, and a congenital absence of a factor.
Impaired absorption of cyanocobalamin in the intestine can be observed with 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.
The absorption of vitamin B12 is impaired in patients who underwent resection of the small intestine with the imposition of a gastrointestinal anastomosis. Pernicious anemia can 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 assimilation of vitamin B12.
In conditions of vitamin B12 deficiency, a deficiency of its coenzyme forms occurs - methylcobalamin (participates in the normal course of erythropoiesis) and 5-deoxyadenosylcobalamin (participates in metabolic processes in the central nervous system and peripheral nervous system). Lack of methylcobalamin disrupts the synthesis of essential amino acids and nucleic acids, which leads to a disorder in the formation and maturation of erythrocytes (megaloblastic type of hematopoiesis). They take the form of megaloblasts and megalocytes, which do not carry out 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, the synthesis of myelin is disrupted, which is accompanied by degeneration of the myelin layer of nerve fibers - this is due to the damage to the nervous system in pernicious anemia.
Pernicious anemia symptoms
The severity of the course of pernicious anemia is determined by the severity of circulatory-hypoxic (anemic), gastroenterological, neurological and hematological syndromes. Signs of anemic syndrome are nonspecific and reflect 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. Auscultation of the heart may result in a “spinning top” murmur or systolic (anemic) murmurs. Outwardly, there is a pallor of the skin with a subicteric shade, puffiness of the face. Long-term "experience" of pernicious anemia can lead to the development of myocardial dystrophy and heart failure.
Gastroenterological manifestations of B12-deficiency anemia are decreased appetite, instability of the stool, hepatomegaly (fatty degeneration of the liver). The classic symptom found in pernicious anemia is a “lacquered” crimson tongue. Characterized by the phenomenon of angular stomatitis and glossitis, burning and pain in the tongue. During gastroscopy, atrophic changes in the gastric mucosa are detected, which are confirmed by endoscopic biopsy. Gastric secretion is sharply reduced.
The neurological manifestations of pernicious anemia are caused by damage to neurons and pathways. Patients indicate numbness and stiffness of the limbs, muscle weakness, gait disturbance. 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, Romberg and Babinsky's symptoms, signs of peripheral polyneuropathy and funicular myelosis. With B12-deficiency anemia, mental disorders can develop - insomnia, depression, psychosis, hallucinations, dementia.
Diagnostics of the pernicious anemia
In addition to a hematologist, a gastroenterologist and a neurologist should be involved in the diagnosis of pernicious anemia. Deficiency of vitamin B12 (less than 100 pg / ml at the rate of pg / ml) is established during a biochemical blood test; it is possible to detect Ab to parietal cells of the stomach and to Castle's intrinsic factor. For a general blood test, pancytopenia is typical (leukopenia, anemia, thrombocytopenia). Microscopy of a peripheral blood smear reveals megalocytes, Jolly's and Cabot's bodies. The study of feces (coprogram, analysis for eggs of worms) can reveal steatorrhea, fragments or eggs of a wide tapeworm in diphyllobothriasis.
Schilling's test allows you to determine the violation of absorption of cyanocobalamin (by excretion with urine labeled with a radioactive isotope of vitamin B12, taken orally). Puncture of the bone marrow and the results of myelogram 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, EGD, X-ray 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 folate deficiency, hemolytic and iron deficiency anemia.
Pernicious anemia treatment
The 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 stomach cancer.
In order to replenish the cyanocobalamin deficiency, intramuscular injections of vitamin B12 are prescribed. Correction of conditions that led to B12-deficiency anemia is required (deworming, taking enzyme preparations, surgical treatment), and with an alimentary nature of the disease, a diet with a high content of animal protein. If the production of Castle's intrinsic factor is impaired, 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 return to normal after 1.5-2 months. The neurological manifestations persist for the longest time (up to 6 months), and when treatment is started late, they become irreversible.
Prevention of pernicious anemia
The first step towards preventing pernicious anemia should be good nutrition, ensuring sufficient intake of vitamin B12 (consumption of meat, eggs, liver, fish, dairy products, soy). Timely therapy of gastrointestinal tract pathologies that disrupt the absorption of the vitamin is necessary. After surgical interventions (resection of the stomach or intestines), it is necessary to carry out supportive courses of vitamin therapy.
Patients with B12-deficiency anemia are at risk of developing diffuse toxic goiter and myxedema, as well as stomach cancer, therefore, they need to be monitored by an endocrinologist and gastroenterologist.
Anemia is a disease characterized by a decrease in the concentration of hemoglobin in the blood. Today we will talk about pernicious anemia, we will also briefly consider other types of anemia (classification and severity).
Pernicious anemia is a serious pathology that develops as a result of a deficiency of vitamin B12 in the body. This disease has several names: malignant anemia, Addison-Birmer disease, megaloblastic anemia, B12-deficiency anemia.
A bit of history
In 1855, the English doctor Thomas Addison first described this disease. In 1872, German physician Anton Birmer studied the disease in more detail. It was he who called the disease pernicious, or pernicious anemia. However, it was not known at the time what treatment was needed for this type of anemia. And only in 1926, a group of doctors found that the symptoms of the disease completely disappear after the introduction of a raw liver into the patient's diet. The same experts proved that such a disease is based on a condition in which the stomach, due to congenital pathology, is not able to secrete a special substance (Castle factor), which helps to absorb vitamin B12 in the intestine. For this discovery, scientists were awarded the Nobel Prize.
Types of anemia: classifications
What are the types of anemia? This ailment develops for various reasons, and the medical history may be different. Anemia is classified into the following types:
Posthemorrhagic - the disease develops against the background of acute or chronic blood loss (injury, bleeding).
Hemolytic - the occurrence of pathology is associated with increased destruction of red blood cells.
Deficiency - the disease develops due to a lack of substances necessary for hematopoiesis (iron, vitamins and other trace elements).
Hypoplastic - the most severe type of anemia, this condition occurs as a result of a violation of hematopoiesis in the bone marrow.
Anemia: the severity of the disease
In addition to the above classification, clinicians distinguish between the disease and the severity. This indicator depends on the concentration of hemoglobin. The disease of anemia of severity has the following:
average - the amount of hemoglobin for men is 80-100 g / l, for women - 70-90 g / l;
severe - the hemoglobin level falls below the above limits.
Causes of pernicious anemia
Before answering the question: "How to treat pernicious anemia?", It is necessary to find out what contributed to its occurrence. This ailment can develop for various reasons. As mentioned above, the main one is the lack of vitamin B12 in the body. Also, pernicious anemia can develop as a result of:
Signs of the disease
How does pernicious anemia manifest? Symptoms can be overt or indirect. Signs of Addison-Birmer disease include:
bright red (scarlet) tongue, which becomes "varnished" due to deformation of receptors;
dysfunction of the nervous system;
gastric achilia - a condition in which there is no hydrochloric acid and enzymes in gastric juice;
the presence of pathological erythrocytes, anemia;
the formation of unnaturally large cells (megaloblasts) in the bone marrow instead of red blood cells.
Indirect symptoms of the disease are:
weakness, drowsiness, decreased vitality;
painful sensations in the mouth and tongue;
limb pain;
weight loss, loss of appetite.
These signs of pathology develop most often. In rare cases, pernicious anemia can manifest itself:
change in gait;
violation of urination;
deterioration of vision;
sexual dysfunction;
hallucinations;
mental disorders.
Development of pernicious anemia during pregnancy
The disease can develop in pregnant women. Pernicious anemia occurs as a result of insufficient intake of folic acid and cyanocobalamin in the body of the expectant mother. In this case, a decrease in the level of red blood cells occurs in the blood, but hemoglobin remains normal or increases. The disease develops rather slowly, and in order to diagnose "pernicious anemia" at an early stage, it is necessary to conduct a clinical blood test. Therefore, the timely conduct of all tests prescribed by the doctor is extremely important. The disease is manifested by pallor of the skin, weakness, increased fatigue, later digestive disorders join. Damage to the nervous system is extremely rare; a slight decrease in sensitivity in the limbs may be observed.
During pregnancy, pernicious anemia must necessarily be cured, since in most cases the pathology can provoke placental abruption, the risk of premature birth and the birth of a still child.
Treatment of the disease is carried out according to the general scheme.
Pernicious anemia in children
Most often, this ailment develops in children with hereditary pathologies of the digestive system, as a result of which the absorption of vitamin B12 is impaired. In rare cases, a baby may develop pernicious anemia when breastfeeding by a vegetarian mother. A blood test makes it possible to make a correct diagnosis already in the third month of life, the symptoms of pathology begin to appear only when the child reaches 3 years of age. On examination, the doctor can detect dryness and peeling of the skin, glossitis, and enlargement of the spleen. Indigestion is observed, appetite decreases. In severe cases, the child may lag behind in development.
Diagnosis of the disease
The most obvious manifestation of pathology is observed in the composition of the blood. As a rule, all patients have a low concentration of vitamin B12 in the serum. For the absorption of the vitamin, an additional introduction of an intrinsic factor is required. Also, a urine test is carried out, since a comparative analysis of the composition of urine and blood makes it possible to make a diagnosis more accurately.
It is very important to find the root cause of the disease. Experts conduct a study of the gastrointestinal tract for the possible detection of gastritis, ulcers and other pathologies, as a result of which the absorption of vitamin B12 could be impaired.
Pathology treatment
If pernicious anemia is diagnosed, treatment is carried out with the introduction of medications such as "Oxycobalamin" or "Cyanocobalamin". The drugs are administered by injection. First of all, it is necessary to bring the concentration of vitamin B12 to normal values, later the number of injections is reduced, and the injected drug has only a supporting effect. After the therapy, patients will have to constantly monitor the level of the vitamin and periodically undergo a preventive course of injections of the drug.
In some cases, during treatment, patients may experience a decrease in the concentration of iron in the body. This usually happens after 3-6 months of treatment. In such a situation, additional administration of medications that restore iron levels is required.
With successful therapy, all manifestations of the disease gradually disappear. The duration of the recovery period can be 6 months. The content of vitamin B12 is normalized 35-70 days after the start of treatment.
In the course of treatment, neuropathy is eliminated, and urinary incontinence and other symptoms disappear in all patients. Vision, which has been impaired as a result of optic nerve atrophy, is unfortunately not restored. But if visual impairment has arisen due to macular hemorrhages, then recovery occurs quickly enough.
It should be borne in mind that in some cases, after treatment, serious diseases such as toxic goiter, myxedema, and stomach cancer may develop. However, this happens quite rarely (no more than in 5% of cases).
Nutrition principles
We have found out how to treat pernicious anemia, but we should not forget about a balanced diet. The daily diet should contain sufficient amounts of vitamins and proteins. Be sure to regularly eat beef, rabbit meat, seafood, eggs, dairy products, legumes. It is recommended to limit the amount of fats in the diet, as they inhibit the processes of hematopoiesis in the bone marrow. You should also stop smoking and drinking alcoholic beverages. Positive emotions and support of family and friends are extremely important for successful treatment. Be attentive to your body, get tested regularly and immediately react to the slightest changes in your health.
With pernicious anemia, the process of the red sprout of hematopoiesis is disrupted. Irreversible phenomena associated with a lack of vitamin B12 occur in the body. In this case, there are deviations from various body systems.
Including systems that undergo a pathological process include digestive pathology. That is, damage to the digestive system. The functioning of the stomach and liver is impaired. 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 B 12 deficiency is replenished as a result of the consumption of foods containing these vitamins.
The lifestyle of a person is of great importance in the processes of assimilation of the vitamin. People who lead a lifestyle associated with fasting are most susceptible to pernicious. Therefore, appropriate treatment is required.
Much also depends on the concomitant pathology. In some cases, the disease occurs as a result of pathological processes. It is known that disturbances 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 correct functioning of the internal organs.
Causes
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 pathway for the intake of vitamins B 12 into the human body. Therefore, the causes of the disease are associated with the presence of adverse factors.
What kind of diseases lead to pernicious anemia? Most often, the etiology of pernicious anemia is associated with the following pathological factors:
- atrophic gastritis;
- the impact of medical interventions (gastrectomy);
- Castle's intrinsic factor.
Enteritis, chronic pancreatitis, Crohn's disease are of great importance in the etiology of the disease. Also, tumor formations in the intestine play a role. Often the causes of pernicious anemia are.
The causes of pernicious anemia are alcohol intoxication. Or the effects of drugs. What exactly drugs cause pernicious anemia:
- colchicine;
- neomycin;
- contraceptives.
Symptoms
Pernicious anemia is mainly 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. These are pallor of the skin, puffiness of the face. Complications of these conditions are also frequent. Myocarditis occurs.
In some cases, heart failure can develop. On the part of the digestive system, there is a decrease in appetite. In most cases, dyspepsia may occur. It is expressed in the phenomena of loose stools.
Pernicious anemia is characterized by an enlarged liver. This is the most powerful argument for the development of anemia associated with a lack of vitamin B 12. The tongue with this disease has a crimson color.
Often the mucous membrane of the mouth suffers. At the same time, stomatitis, glossitis and other pathologies are noted. The patient feels a burning sensation in the tongue. That is why appetite decreases sharply.
Low acidity gastritis 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, the phenomena of damage to neurons are possible. That is the network of nerve cells in the body. In this case, the following symptoms are noted:
- numbness and stiffness of the limbs;
- muscle weakness;
- violation of gait.
The patient may experience incontinence. Moreover, urinary and fecal incontinence. Sensitivity is impaired. The patient, especially in old age, notes:
- insomnia;
- depression;
- hallucinations.
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Diagnostics
Anamnesis is of great importance in the diagnosis of pernicious anemia. Anamnesis involves the collection of the necessary information. This information relates to the possible causes of the disease. The clinical picture is established.
Diagnostics consists in an objective examination of the patient. In this case, there are complaints from the patient. Also the presence of signs of anemia. Biochemical research is also used.
It involves the detection of Ab 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.
The analysis of feces is of great importance in the diagnosis of the disease. In this case, the coprogram plays a 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 bone marrow biopsy. This allows you to determine the increase in the number of megaloblasts. The FGDS method is widely used. In some cases, stomach x-rays are taken.
Diagnostics is also aimed at identifying cardiac pathologies. Therefore, electrocardiography, ultrasound examination of the abdominal organs are used. An MRI of the brain may be required.
Prevention
Preventive measures are aimed at replenishing 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;
- a fish;
- dairy products.
A prerequisite for 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 have been carried out, 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 assimilation of essential substances.
Consultation of specialists 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 attached 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.
The stomach should also be checked. This event is associated with the use of gastroscopy. This allows you to identify a tumor in the stomach. Which is a common complication of this disease. Or else the most significant reason for its development.
It is advisable to administer vitamin B 12 intramuscularly. The patient's condition is also directly corrected. In this case, the following activities are relevant:
- elimination of helminths;
- taking 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 adjustments include an animal protein diet.
If the patient's condition is preceded by anemic coma. Which is also a common complication, then you should resort to blood transfusion. That is, apply blood transfusion methods.
In adults
Pernicious anemia in adults may occur in some cases. This is primarily due to various pathologies. This is especially appropriate in old age. Anemia is most dangerous after seventy years.
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 up a time span of four years. The course of the disease in the elderly is rather severe. First of all, this is due to the following factors:
- the presence of neurological disorders for a long time;
- lifelong use of drugs;
- the occurrence of complications.
Adults are forced to live with drugs. Moreover, these drugs should directly restore the vitamin B12 deficiency. If the cause of the vitamin deficiency is a tumor, then an adult is most susceptible to complications.
Symptoms of pernicious anemia in adults differ as follows:
- decreased performance;
- lethargy;
- dizziness;
- insomnia.
Insomnia is a significant symptom of the disease in adults. 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. The causes of the disease in adults include:
- pathology of internal organs;
- malignant neoplasms;
- medicinal substances;
- intoxication of the body.
In children
Pernicious anemia in children is manifested by the presence of severe symptoms. Children with anemia lag behind in development. They are 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:
- brittle nails;
- pallor of the skin;
- weakness;
- dizziness.
In severe cases, children develop stomatitis. Children with pernicious anemia are at risk for respiratory pathology. More often they get sick with bronchitis and pneumonia. In young children, tearfulness, exhaustion is noted.
Children often have tachycardia. Blood pressure may decrease. Up to the development of a 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 also depends on the presence of the underlying disease. With malignant pathology, the prognosis is poor. In the presence of cardiac abnormalities, the prognosis is also the worst.
The disease is quite long. The prognosis will directly depend on the patient's condition. Also from the course of the underlying disease. And, of course, on the availability of adequate therapy.
Exodus
Death with pernicious anemia is possible if there is a malignant tumor. Even in the presence of long-term treatment therapy, the outcome will depend on further action. The outcome is favorable if the patient follows some of the recommendations.
First of all, the outcome will depend on the correction of lifestyle and nutrition. Especially in the presence of an intoxicating factor and alimentary etiology. In people after seventy years, the outcome is often unfavorable.
Recovery is possible. But medical therapy is quite long. It can vary from several years. Moreover, the outcome in this case may be associated with lifelong intake of this vitamin.
Life span
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 the longevity.
If the disease was eliminated in a timely manner, then the life expectancy increases. If the diagnosis is late, which may 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 anemic coma worsens the quality of life, shortens its duration. Urgent action must be taken.
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