Vitamin B12 deficiency is a disease caused by an insufficient content of vitamin B12 in the body. It is manifested by anemia, inflammation and burning of the tongue, the formation of redness on the skin, increased fatigue, insomnia, decreased appetite, abdominal pain, stomach upset, weight loss, numbness of fingers and muscle pain. With a prolonged course of the disease, encephalopathy, paralysis and osteoporosis may develop. The diagnosis is based on the data of a clinical survey and the results of a study of vitamin B in venous blood. Replacement therapy with vitamin preparations, correction of the diet is used for treatment.
ICD 10
E53.8 Insufficiency of other refined B vitamins
Meaning
Vitamins B12 – cobalt-containing biologically active substances, cobalamines. This group of compounds is represented by cyanocobalamin, hydroxocobalamin, methylcobalamin and cobamamide. A significant part of the vitamin enters the body in the form of cyanocobalamin, so you can find the use of the name of this substance as a synonym for vitamin B12. Synonymous names of vitamin B12 deficiency are vitamin deficiency B12, deficiency of the external factor Castle. The disease is most common among elderly and senile patients. According to epidemiological data, at least 15% of people over 60 years of age suffer from vitamin B12 deficiency.
Vitamin B12 deficiency causes
Normally, vitamin B12 is sent to the stomach, and then to the intestines with food. It forms a complex with a special enzyme – the internal Castle factor, thanks to which it becomes digestible and absorbed by the epithelial cells in the ileum. In the intestinal mucosa, the compound binds to the transport protein transcobalamin. The main place of vitamin storage is the liver. A large amount is consumed by the muscles, spleen and kidneys. Vitamin is excreted by the gallbladder, reabsorbed in the intestine. vitamin B12 Deficiency develops when one or more links of the compound’s metabolism are disrupted. The causes of the disease are:
- Deficiency in the diet. The main suppliers of vitamin are animal products, so hypovitaminosis is more often diagnosed in vegetarians and people who follow strict diets for a long time. Cyanocobalamin is deposited by the liver and spleen, its reserves are large enough, it takes from 3 to 5 years for the deficiency to develop.
- Impossibility of absorption. Hypovitaminosis is promoted by diseases of the small intestine that disrupt the absorption of vitamin – celiac disease, Crohn’s disease, achlorhydria, as well as a reduction in the reabsorbing surface of the intestine after resection. A common cause of hypovitaminosis is congenital insufficiency of the internal factor or transcobalamin.
- Rapid elimination or decay. Pathologies of the kidneys and liver, alcoholism prevent the accumulation of vitamin, enhance its excretion. Vitamin loss occurs with helminthic invasions, for example, with infection with broad tapeworm.
- Increased consumption by the body. The risk of hypovitaminosis increases in the third trimester of pregnancy and during recovery after acute diseases. Vitamin metabolism increases with hyperthyroidism, thyrotoxicosis, alpha-thalassemia and hemolytic anemia.
Pathogenesis
Cobalamines act as coenzymes of the transmethylation –transfer reaction of the methyl group CH3. As a result of the multi-stage process, tetrahydrofolic acid is formed, which is necessary for the metabolism of proteins and nucleic acids. With its deficiency, the synthesis of purines, thymidine, DNA, RNA and proteins in cells is weakened. Thus, vitamin B12 deficiency contributes to a reduction in the production of the most frequently renewed cells – blood and epithelial cells.
The process of hematopoiesis changes pathologically: large, but immature red blood cells are formed in the bone marrow, unable to transfer oxygen to the tissues. Megaloblastic anemia develops. A decrease in the rate of renewal of epithelial cells is manifested by lesions of the digestive tract: the gastric mucosa atrophies, the release of pepsin and hydrochloric acid decreases, the tongue becomes bright red, hypersensitive to chemical stimuli. Vitamin B12 is involved in the formation of myelin, hypovitaminosis is accompanied by neurological disorders. Patients develop distal paresthesia, pain, gait and sensitivity disorders, tendon reflexes increase.
Vitamin B12 deficiency symptoms
Vitamin B12 deficiency has polymorphic symptoms, manifested by disorders in several body systems at once. The key sign of the disease is B12-deficiency anemia, in which patients experience general weakness, headaches, shortness of breath, nausea, vomiting and diarrhea. There are often swelling, redness and pain on the tongue (glossitis), focal skin lesions, especially in the distal extremities. Poor blood supply to the brain and spinal cord in children provokes a delay in physical and mental development: there is a lag in growth, slow formation of motor skills, muscle weakness and learning difficulties.
Disorders of the nervous system are represented by chronic fatigue, frequent headaches, dizziness, a decrease in intellectual and mnestic functions and attention, depression and irritability. Neurological syndromes include pain, tingling and numbness of the extremities, disorders of various types of sensitivity. From the gastrointestinal tract, constipation, an increase in the size of the liver, inflammation of the mucous membrane of the duodenum and stomach, the formation of ulcers in these departments are observed. Cardiovascular symptoms are less common: blood pressure decreases, the risk of atherosclerosis increases.
Complications
In the absence of treatment, prolonged vitamin B12 deficiency leads to severe diseases of the central nervous system. The intensification of degenerative processes provokes the development of paralysis of the lower extremities, weakens normal reflex reactions and causes pathological reflexes. Encephalopathy is gradually formed with a weakening of cognitive functions up to dementia and amnesia. Elderly patients have hallucinatory delusional disorders. Vitamin deficiency negatively affects the condition of the musculoskeletal system: bone tissue is thinning, osteoporosis is observed.
Diagnostics
The examination is prescribed for suspected megaloblastic anemia, malnutrition, patients with malabsorption syndrome, celiac disease, Crohn’s disease and alcoholism, elderly people with symptoms of depression, paranoia and confusion. Depending on the existing symptoms, the diagnosis is carried out by a hematologist, neurologist or gastroenterologist. It includes differentiation of B12-deficient anemia with other types of anemia, allows you to determine the cause of neurological disorders and mental disorders in old age. The following procedures are used to confirm the diagnosis of hypovitaminosis:
- Clinical survey. In conversation, patients present complaints characteristic of anemic and neurological syndrome: weakness, dizziness, shortness of breath combined with a feeling of numbness and tingling in the legs, decreased sensitivity in the extremities. A history of adherence to vegetarianism and strict diets, malnutrition, chronic intestinal diseases and malabsorption syndrome may be noted.
- Blood test. The results of the analysis determine a reduced level of erythrocytes and hemoglobin, hyperchromia, macrocytosis, poikilocytosis, leukopenia, thrombocytopenia, lymphocytosis, reduced or normal number of reticulocytes. Microscopy of erythrocytes reveals the presence of Jolly bodies and Cabot rings.
- Analysis for vitamin B12. The concentration of vitamin in the blood serum from the vein is being investigated. With hypovitaminosis, the final indicator is less than 191 pg /ml. A decrease in the concentration of vitamin B12 confirms its insufficiency, but does not correlate with the severity of anemia or neuropathy.
- Examination of bone marrow punctate. In some cases, a puncture of the red bone marrow is required. Macrocytic anemia is indicated by the presence of megaloblasts in a sample of biomaterial.
Vitamin B12 deficiency treatment
With severe hypovitaminosis, therapy is carried out in a hospital of a hematology or therapeutic department. Drug treatment is based on intramuscular or intravenous administration of cyanocobalamin preparations. In severe cases, intralumbal injections are necessary. In mild forms caused solely by dietary vitamin deficiency, oral medication without hospitalization is indicated. Together with cyanocobalamin, folic acid preparations are prescribed. The course of treatment lasts 1-2.5 months. Additionally, diet therapy is used, products rich in vitamin B12 are introduced into the daily diet of patients – liver, meat, fish, eggs, cheese.
Prognosis and prevention
Cyanocobalamin replacement therapy allows you to eliminate the neurological symptoms of hypovitaminosis in 2 weeks, reduce vitamin deficiency in 8 weeks and fill the body depot. With timely initiation of treatment before complications develop, the prognosis is favorable. In order to prevent relapses of the disease, patients are prescribed cyanocobalamin intramuscularly 1 time a week. To prevent the primary development of hypovitaminosis, it is necessary to adhere to a full diet, including daily intake of meat, offal, fish, eggs and cheese. Patients with impaired absorption of nutrients in the gastrointestinal tract