Vitamin in 12-deficiency anemia

Since childhood, those forms of vitamin B12-deficiency anemia that are caused by a hereditary disruption of the formation of the internal factor of Kastla( it is necessary for absorption of vitamin B12 or absorption of vitamin B12 and the absence of a plasma protein of blood that carries the transfer of vitamin B12-trans-balamine. The Castle factor is transmitted by an autosomal recessive type of inheritance and is described in 24 boys and 23 girls. In the first year in children, blood counts remain at the limitIn the second year of life there is a sharp weakness, diarrhea, irritability. The child grows thin, the appetite disappears, waxy pallor, often yellowness of the sclera and skin, sometimes comes atrophy of the mucous membrane of the tongue with reddening of the papillae Often the liver and spleen increase.to be normal. In the study of pieces of mucosal tissue of the stomach, taken during the exercise of FGD, signs of atrophy are not detected. Sometimes unconditioned reflexes sharply decrease. In the blood serum, a decrease in the vitamin B12 content is noted. Absorption of the vitamin B12 labeled with special methods is also reduced. In the event that a child, when performing a study with labeled vitamin B12, is given a normal gastric juice or concentrate of the internal factor of Castle, then the absorption of the vitamin comes back to normal.

In the literature, there is a description of the case of vitamin B12 deficiency in a 13-year-old boy, whose content of the internal factor of Castle was normal. However, the internal factor did not ensure the absorption of vitamin B12.The addition of normal gastric juice and an internal factor concentrate normalized the absorption of the vitamin. The cause of B12-deficiency anemia in this case was that a functionally inactive internal factor was formed in the boy's body.

Regardless of the causes of vitamin B12 deficiency, the hemopoietic tissue, digestive and nervous systems are affected. Gradually, the child has fatigue, weakness, rapid heartbeat, shortness of breath with physical exertion. Many children may complain of abdominal pain for a number of years.

Children with B12-deficiency anemia are often full, with a puffy, and with severe anemia pale yellow face. Sometimes a deficiency of vitamin B12 determines a slight rise in body temperature. Some people may have pain in the tongue, which is associated with the appearance of inflammation sites on it. However, signs of inflammation of the language, both objective and subjective, arise only in 1/4 of persons with vitamin B12 deficiency. In general, inflammation of the tongue is not a characteristic sign of vitamin B12 deficiency, since glossitis( inflammation of the tongue) also occurs with iron deficiency anemia. In some cases, there is an increase in the spleen, and sometimes the liver. The formation of gastric juice in most people with vitamin B12 deficiency is sharply reduced. When fluoroscopy of the stomach is often found violations of food evacuation, as well as pathological changes in the folds of the mucous membrane of the stomach. One of the characteristic signs of vitamin B12 deficiency is the damage to the nervous system, which is commonly called funicular myelosis. The earliest manifestations of this lesion of the nervous system are the appearance of a sensation of "crawling"( paresthesia) and impaired sensation with persistent light pain sensations that resemble tingling with pins, a feeling of cold, "cotton feet," numbness in the extremities. Less often there are girdling pains.

Often, there is severe muscle weakness, muscle atrophy is possible. To the phenomena of polyneuritis( lesions of several nerves at once) the involvement of the spinal cord joins. Lower extremities are affected primarily, in most cases symmetrically. With the progression of the process, surface sensitivity, the ability to distinguish between cold and hot, and pain sensitivity decreases. The lesion can spread to the stomach and even higher. Hands are less likely to be affected and less than the legs. In severe cases, vibration and deep sensitivity are disturbed. Some children lose their sense of smell, hearing, and taste. In rare cases, there may be mental disorders, delusions, auditory and visual hallucinations, and sometimes even epileptic seizures. In the most severe cases, depletion, lack of reflexes, persistent paralysis of the lower extremities are observed.

The main method of treating this type of anemia is intramuscular injection of vitamin B12 or its administration inside very high doses, sometimes together with the internal factor of Castle. However, antibodies to the foreign protein are produced very quickly, and absorption is impaired. For intramuscular administration, drugs such as cyanocobalamin and hydroxy cobalamin are used. The aqueous solution of cyanocobalamin very rapidly penetrates into the blood, the maximum concentration in the blood serum is observed 1.5-2 hours after administration. Almost all of the administered amount is excreted in the urine, of 1 mg of cyanobalamin in the body remains only 50-80 μg. Hydroxycobalamin from the injection site is absorbed as quickly as cyanocobalamin, its concentration in the serum becomes maximal 2 hours after administration. However, unlike cyanocobalamin, hydroxycobalamine significantly binds to blood proteins much better. After the administration of 1 mg of the drug in the body remains 25-33%.

There are long-acting products - vitamin complexes in the form of an oil suspension. A drug;enters the blood slowly, of 1 mg in the body remains 90-98%, but after the introduction of such drugs remain poorly absorbable infiltrates at the injection site. With funicular myelosis, large doses of vitamin B12( 1000 μg daily) are used.

In all cases of vitamin B12 deficiency, the use of a vitamin should lead to a quick and persistent positive result. Inefficiency of vitamin B12, most likely, indicates that you were diagnosed incorrectly.