B12-deficiency anemia is a combination of clinical and hemolytic signs that arise as a result of a change in the morphology of erythrocytes and a violation of the synthesis of RNA and DNA in the bone marrow cells of hematopoiesis. The body of every adult person needs a systematic replenishment of vitamin B12, the main sources of which are food products of animal origin. To perform normal hematopoiesis, the body needs no more than 7 μg of cyanocobalamin per day. The peculiarity of absorption of vitamin B12 is the mandatory presence of gastric gastromucoprotein, which binds cyanocobalamin into the complex.
After the complex with cyanocobalamin enters the small intestine, the absorption and intake of vitamin B12 into the peripheral blood stream and its deposition in the liver and bone marrow tissue are activated. For the implementation of the megaloblastic hematopoiesis process, in addition to maintaining the normal level of vitamin B12, it is imperative to maintain the level of folic acid. To maintain a sufficient level of folic acid in the body, a necessary condition is a constant daily intake of food with food products in a volume of not less than 100 μg.
Vitamin B12 acts as an activator of folic acid, which takes a direct part in the exchange of nucleic acids, which are crucial in the process of erythropoiesis.
Causes of B12-deficiency anemia
The risk group of B12-deficient anemia is the elderly men suffering from chronic diseases of the digestive system.
B12 folic-deficiency anemia belongs to the category of polyethiologic diseases, the occurrence of which is influenced by a number of causes, each of which can be attributed to one of the two main mechanisms - a violation of the absorption of cyanocobalamin or excessive consumption of it.
Violation of the absorption process of vitamin B12 and folic acid can be triggered by a number of etiological factors, of which the most common are:
- the presence of atrophy of glands in the projection of the fundus of the stomach, responsible for the production of gastromucoprotein;
- partial resection of the stomach;
- the presence of large volume formations in the stomach cavity (polyps, malignant neoplasms, teratoma , bezoar);
- burn lesion of the stomach mucosa;
- disruption of gastromucoprotein synthesis by parietal granulocytes of the gastric mucosa as a result of autoimmune disorders in the body;
- toxic damage to the gastric mucosa and small intestine by alcohol and chemical compounds;
- chronic enteritis with atrophic disorders of the mucous membrane of the duodenum, accompanied by a violation of absorption processes.
Increased consumption of vitamin B12 is observed in helminthic invasion (diphyllobothriasis), a widespread diverticulosis with localization in the small intestine and chronic liver pathologies. Megaloblastic anemia occurs not only with an insufficient level of vitamin B12, but also with a decrease in the body of folic acid, which develops with celiac disease, blind loop syndrome, long-term administration of a folic acid antagonist, alcoholism. Physiological decrease in the level of folic acid is observed only with pregnancy and inadequate intake of foodstuffs.
Pathogenetic mechanisms of the appearance of megaloblastic hematopoiesis are based on the violation of the synthesis of erythroblast DNA and the increase in the maturation of elements of the erythroid germ. In the megaloblastic type of hematopoies, a redistribution of red blood cells in the peripheral blood stream is observed, in which a large percentage of hemoglobin is observed, with inclusions in the form of Jolly bodies and Kebot rings.
The mechanism of increasing the level of indirect bilirubin in the blood is caused by increased destruction of the changed erythrocytes in the spleen. As with all other types of anemia, megaloblastic anemia is accompanied by a significant reduction in the life span of erythrocytes. The pathogenesis of the development of funicular myelosis, which is one of the manifestations of B12-deficient anemia, is based on a violation of the process of synthesizing succinic acid and accumulation of toxic methylamine acid.
Symptoms of B12-deficient anemia
A typical clinical picture with B12 folio-deficient anemia develops gradually and is characterized by symptoms of damage to the central nervous system, digestive system organs and the appearance of characteristic signs of anemic syndrome.
Long before the appearance of signs of a decrease in the level of erythrocytes in peripheral blood, patients with megaloblastic anemia complain of growing weakness and disability, a burning sensation in the oral cavity, and a lack of appetite. With the development of severe clinical symptoms of B12-deficiency anemia, the patient develops a pain syndrome in the epigastric region of the aching nature, belching acidic stomach contents, as well as dyspeptic disorders (nausea and vomiting, food-related problems, perversion of taste preferences, stool disorder).
Specific signs of B12-deficiency anemia are the appearance of a constant constrictive headache without irradiation, weakness in the lower extremities with prolonged walking, numbness of the peripheral parts of the upper and lower extremities, the appearance of paresthesias and the violation of skin sensitivity.
At the initial examination of the patient with B12-deficiency anemia of a pronounced degree of development, paleness of the skin with a lemon-yellow hue, ictericity of the mucous membranes of the oral cavity and conjunctiva, pastosity of the lower limbs and face are observed. Typical objective manifestations of megaloblastic anemia is a change in the mucous membrane of the tongue with the manifestation of atrophy of the papillae and signs of inflammatory changes in the form of reddening and the presence of aphthae.
Symptoms of central nervous system damage with B12-deficient anemia are a violation of both surface and deep sensitivity, a decrease in the response in the study of tendon reflexes and the development of muscular atrophy of different localization. The appearance of visual and auditory hallucinations in the patient, as well as the appearance of delusional ideas, indicates the progression of B12-deficient anemia.
Symptoms of cardiovascular damage are extremely rare and are a sign of a severe course of B12 deficiency anemia. The most characteristic changes in this situation are: increased heart rate, the appearance of systolic noise in all auscultative points, as well as an increase in the boundaries of relative and absolute cardiac dullness.
Isolated deficiency of folic acid, provided that the level of vitamin B12 in the body is preserved in the body is accompanied by the appearance of signs of glossitis and complete absence of neurologic symptoms.
Diagnosis of B12-deficiency anemia
Informative and accessible in the application of the method of diagnosis of B12-folia deficiency anemia is a detailed blood test. With B12-deficiency anemia, characteristic changes in the composition of peripheral blood are formed in the form of a violation of the shape and size of erythrocytes (macrocytosis, poikilocytosis), the appearance of nuclear substance residues (Jolly's body, Kebot's ring) in erythrocytes, as well as an increased color index.
Typical manifestations of megaloblastic anemia, distinguishing it from other forms of anemia, is the combination of an anemic symptom complex with mild leukopenia and the appearance of giant neutrophils with a hypersegmented nucleus. For B12 folio-deficient anemia, reticulocytosis is not characteristic, even considering the decrease in the absolute numbers of reticulocytes.
In the situation of difficult diagnosis of the megaloblastic type of hemopoiesis, the patient is recommended to perform a sternal puncture and examination of the puncture for hyperplasia of the red shoot and the presence of megaloblasts.
In order to distinguish between the deficiency of cyanocobalamin and folic acid, a blood serum test using a microbiological and radioimmunoassay method is recommended to determine the quantitative and qualitative content of vitamin B12. The criterion for lowering the level of cyanocobalamin in the body is the detection of methylmalonic acid in the analysis of urine.
Biochemical blood test is accompanied only by an elevated level of bilirubin due to its indirect fraction.
Treatment of B12-deficiency anemia
Patients should be treated by a hematologist with the involvement of specialists of a narrow profile, if necessary (gastroenterologist, neurologist, oncologist and physiotherapist). The volume of therapeutic measures depends to a greater extent not on the severity of B12-deficiency anemia, but on the presence of signs of disruption of the cardiovascular, digestive and central nervous system.
Unlike other forms of anemia, B12-folia deficiency anemia is difficult to cure by non-pharmacological methods, which should be used only as additional measures. Among the non-pharmacological methods of correction of vitamin B12 deficiency and folic acid, correction of eating behavior and elimination of factors aggravating the course of the disease (use of alcohol and drugs of certain groups, for example, the majority of anticonvulsants) is of the greatest importance.
Adequate selection of etiopathogenetic therapy is an obligatory criterion for achieving a positive result in the treatment of B12-deficiency anemia. For this purpose, it is recommended to pay the greatest attention to the diagnosis of the underlying disease, which is the provoker of the occurrence of anemia, and the selection of an individual treatment regimen. So, with the existing small intestine helminthiasis, it is advisable to use deworming with the obligatory observance of the dosage of the drug (Fenasal in a daily dose of 3 g orally) and constant monitoring of stool analysis.
In a situation where B12-deficiency anemia proceeds in severe form and its occurrence is caused by the presence of volumetric formations in the intestine and stomach, the patient is shown surgical intervention. In order to improve the digestive and absorption functions of the intestine, special attention should be paid to the normalization of the intestinal flora, in this connection, patients are recommended long-term use of Lacidophil 2 capsules 2 r. / Day, as well as enzymatic medicines (Mezim for 1 pills at each meal ).
As a pathogenetic treatment of B12-deficient anemia, parenteral types of administration of Cyanocobalamin are used. The dosage of the drug administered depends on the severity of vitamin B12 deficiency and the associated anemic syndrome. Most often, such a scheme is used Cyanocobalamin: the first 10 days of 500 mg 2 r / day, the next month the drug is administered 1 time a week in a single dose of 500 mg, then six months the drug is taken once a month at a dose of 500 mg. Intramuscular or subcutaneous infusion is preferred.
In a situation where B12-deficiency anemia due to autoimmune disorders is diagnosed, the use of prolonged corticosteroid therapy (Prednisolone at a daily dose of 20 mg orally) is pathogenetically justified.
Replaced transfusion of whole blood and erythrocyte mass with B12-deficiency anemia is the exception to the rule and its use is justified only in case of extremely severe course of the disease. The volume of transfusion is not more than 250 ml of erythrocyte mass with a course of 5-6 infusions.
Indication for the appointment of folic acid in a therapeutic daily dose of 4 mg is its laboratory-confirmed deficiency.