B12 deficiency anemia is a collection of clinical signs gematologichesky arising from the change of morphology of red blood cells and disrupting the synthesis of RNA and DNA in bone marrow cells of hematopoiesis. The body of each adult human needs in a systematic replenishment of vitamin B12, the main sources are foods of animal origin. For the implementation of normal hematopoiesis, the body must be no more than 7 micrograms of cyanocobalamin per day. The peculiarity of the absorption of vitamin B12 requires the presence of gastric biermerin linking cyanocobalamin complex.
After receipt of the complex with cyanocobalamin in the small intestine are activated by the processes of absorption and availability of vitamin B12 in the peripheral blood stream and Deposit it in the liver and bone marrow tissue. For the process of megaloblastic hematopoiesis, in addition to maintaining normal levels of vitamin B12, it is obligatory 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 flow of its food in the amount of not less than 100 µg.
Vitamin B12 acts as activator of folic acid, which is directly involved in nucleic acids metabolism, which is crucial in the process of erythropoiesis.
A risk group for vitamin B12 deficiency anemia are men of advanced age with chronic diseases of the digestive system.
B12 folic acid deficiency anemia belongs to the category politologichni diseases, the occurrence of which is affected by a number of reasons, each of which can be attributed to one of two main mechanisms – disruption of the process of absorption of cyanocobalamin or excessive spending.
Violation of the process of absorption of vitamin B12 and folic acid can be triggered by a close etiological factors, of which the most common:
— atrophy of glands in the projection of the rats ‘ stomach fundus responsible for the production of biermerin;
— partial resection of the stomach;
— the presence of large space-occupying lesions of the stomach (polyps, malignant neoplasms, teratoma, bezoar);
— burn the mucosal of the stomach;
— violation of the synthesis biermerin parietal granulocytes in the mucosa of the stomach as a result of autoimmune disorders in the body;
— toxic damage of the mucous membrane of the stomach and small intestine alcohol and chemical compounds;
— chronic enteritis with atrophic disorders of the mucous membrane of the duodenum, accompanied by malabsorption.
Increased consumption of vitamin B12 is observed in helminth infection (difillobotrioz), prevalence of diverticulosis with localization in the small intestine and chronic pathologies of the liver. Megaloblastic anemia arises not only from insufficient levels of vitamin B12, but with a decrease in the body of folic acid, which develops in celiac disease, blind loop syndrome, chronic administration of an antagonist of folic acid, alcoholism. Physiological decline in the level of folic acid occurs only in pregnancy and its insufficient receipt with food.
Pathogenetic mechanisms of occurrence of megaloblastic type of hematopoiesis based on the violation of DNA synthesis of erythroblasts and an increase in terms of maturation of erythroid elements. At megaloblastic type of hematopoiesis is observed in the allocation of the flow of the peripheral blood erythrocytes of the modified form in which a percentage of the hemoglobin with the presence of inclusions in the form of Taurus Jolly and rings Kebot.
The mechanism of raising the level of indirect bilirubin in the blood due to increased destruction of erythrocytes changed in the spleen. As with all other types of anemia, megaloblastic anemia accompanied by significant shortening of life of red blood cells. The pathogenesis of the development of funicular myelosis, which is one of the manifestations of vitamin B12 deficiency anemia, based on violation of the synthesis of succinic acid and the accumulation of toxic metilenovoj acid.
The typical clinical picture of the B12-palaeolatitudes anemia develops gradually and is characterized by symptoms of Central nervous system, organs of the digestive tract and the appearance of characteristic signs of anemic syndrome.
Long before the appearance of signs of reducing the level of red blood cells in the peripheral blood, patients with megaloblastic anemia complain of increasing weakness and reduced work capacity, the emergence of a burning sensation in the mouth, lack of appetite. With the development of severe clinical symptoms of B12-deficiency anemia the patient has development of the pain syndrome in the epigastric region aching, regurgitation of acidic contents of the stomach, and dyspepsia (nausea and vomiting, associated with food intake, taste perversion, frustration of a chair).
Specific signs of vitamin B12 deficiency anemia is considered a constant compressive headache pain without radiation, weakness in lower limbs during prolonged walking, numbness of the peripheral parts of the upper and lower extremities, the appearance of paresthesia and disorders of skin sensitivity.
The initial examination of a patient with B12 deficiency anemia of severe degree of development is observed pale skin with lemon-yellow tint, ikterichnost mucous membranes of the oral cavity and conjunctiva, pastoznost lower extremities and face. A typical objective manifestations of megaloblastic anemia is the change in the mucous membrane of the tongue showed atrophy of the papillae and signs of inflammatory changes in the form of redness and the presence of aft.
Symptoms of Central nervous system when B12 deficiency anemia is a violation of both surface and deep sensitivity, the reduction reaction in the study of tendon reflexes and muscle atrophy of different localization. The appearance of the patient’s visual and auditory hallucinations, as well as the occurrence of delusions is evidence of the progression of vitamin B12 deficiency anemia.
Symptoms of the cardiovascular system are extremely rare and are a sign of severe vitamin B12 deficiency anemia. The most characteristic changes in this situation are: rapid heart rate, the appearance of systolic murmur in all points of auscultation, and the increase of borders of relative and absolute cardiac dullness.
Isolated deficiency in folic acid if the safety level of vitamin B12 in the body is accompanied by the appearance of the signs of glossitis and a complete lack of neurological symptoms.
Informative and available in the application method of diagnosis B12-palaeolatitudes anemia is a complete blood count. When B12-deficiency anemia in the peripheral blood formed characteristic changes as violations of the shape and size of red blood cells (macrocytosis, poikilocytosis) and the appearance of erythrocytes remnants of the nuclear substance (Taurus Jolly, Cabot rings) and a high color index.
Typical manifestations of megaloblastic type of anemia, distinguishing it from other forms of anemia, is the combination of anemic syndrome with a mild leukopenia and the appearance of giant neutrophils with hypersegmentation core. B12-palaeolatitudes anemia is not typical reticulocytosis, even given the decline in absolute numbers of reticulocytes.
In situation of difficult diagnosis of megaloblastic type of hematopoiesis the patient was recommended to performing sternal puncture and examination of punctate on the subject of hyperplasia of red sprout, and the presence of megaloblasts.
In order to distinguish deficiency of cyanocobalamin and folic acid recommended the study of blood serum of microbiological and radioimmunoassay method for the determination of the qualitative and quantitative content of vitamin B12. Criterion reduction of cyanocobalamin in the body is the detection of methylmalonic acid in the urine.
Biochemical blood only accompanied by elevated levels of bilirubin by its indirect fraction.
Treating patients should engage a hematologist with the involvement of specialists, if necessary (gastroenterologist, neurologist, oncologist and physiotherapist). The amount of therapeutic measures largely depends on the severity of B12-deficiency anemia, and the presence of signs of disorders of the cardiovascular, digestive and Central nervous systems.
Unlike other forms of anemia, B12 anemia palaeodiversity hard cured non-pharmacological methods that should be applied only as additional measures. Among non-drug methods of correction of deficiency of vitamin B12 and folic acid the most important is correction of eating behavior and the elimination of factors that exacerbate the disease (consumption of alcohol and drugs of certain groups, for example, most anticonvulsants).
Selection of adequate etiopathogenetic therapy is a mandatory criterion for achieving a positive result in the treatment of B12-deficiency anemia. With this purpose it is recommended to pay most attention to the diagnosis of the underlying disease, which is the instigator of the emergence of anemia, and selection of individual treatment regimens. So, if the helminthiasis of the small intestine, appropriate use of deworming with the strict observance of the dosage of the drug (Fenasala daily dose of 3 g orally) and ongoing monitoring of the stool.
In a situation when B12-deficiency anemia is severe and it occurs due to the presence of space-occupying lesions in the intestines and stomach, the patient shows a surgical intervention. To improve digestive and absorptive function of the intestine, particular attention should be paid to the normalization of intestinal flora, therefore, patients are recommended long-term use of Lacidofil 2 capsules 2 R./day, as well as enzymatic medicines (zantac 1 tablet during each meal).
As the pathogenetic treatment of B12-deficiency anemia use parenteral types of administration of Cyanocobalamin. The dosage administered depends on the severity of B12 deficiency and its associated anemia. Most often used this pattern of use of Cyanocobalamin: the first 10 days 500 mg 2 p/day, next month the drug is administered 1 time per week at a dose of 500 mg, then six months, the drug is taken 1 time per month at a dose of 500 mg. is Preferable to intramuscular or subcutaneous type of infusion.
In a situation when diagnosed with B12 deficiency anemia due to autoimmune disorders, pathogenetically justified is the appointment of prolonged corticosteroid therapy (Prednisone at a daily dose of 20 mg orally).
Exchange transfusion of whole blood and Packed red blood cells with B12-deficiency anemia is the exception to the rule and its application is justified only in the case of extremely severe course of the disease. The volume of transfusion is not more than 250 ml of erythrocytic mass the course of 5-6 infusions.
Indications for folic acid in therapeutic doses of 4 mg is it confirmed by laboratory methods deficit.