^

Health

A
A
A

Lack of vitamin B12

 
, medical expert
Last reviewed: 19.11.2021
 
Fact-checked
х

All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.

We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.

If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.

Vitamin B 12 (cobalamin - Cbl) enters the body mainly with products of animal origin (such as meat, milk) and absorbed by absorption. Absorption of vitamin B 12 - a multi-stage process, including:

  • proteolytic release of cobalamin from proteins;
  • the addition of cobalamin to the protein of the gastric secretion (internal factor - IF, the factor of Castle);
  • recognition of the complex "IF-cobalamin" receptors of the mucous membrane of the ileum;
  • transport through the malignant enterocytes in the presence of calcium ions;
  • release into circulation of the portal vein system in a complex with transcobalamin II (TC II) - a protein of blood serum.

Usually, vitamin B 12 deficiency (deficiency) in young children is caused by its inadequate intake of food into the mother's body.

The most frequent violation of absorption of vitamin B 12 - pernicious anemia. This is a chronic disease that develops as a result of a disruption of cobalamin intake due to IF deficiency in the gastric secretion. Insufficient content of IF in the gastric secretion can be caused by a congenital deficit of this factor or acquired causes, including immune factors (the production of autoantibodies against IF and parietal cells of the gastric mucosa).

To release cobalamin from the protein complex, in the form of which the compound comes with food, an acid reaction of the medium and the pepsin activity of the gastric juice are necessary. That is why pernicious anemia develops with certain diseases of the stomach (atrophic gastritis, partial gastrectomy).

In the absence or damage of IF, the entry of cobalamin into enterocytes becomes impossible, which leads to the development of pernicious anemia. Insufficient IF can be both congenital and acquired.

Violation of the metabolism of vitamin B 12 in many cases develops with insufficient protein nutrition (kwashiorkor), liver diseases. Some medicines affect the absorption and metabolism of vitamin B 12.

trusted-source[1], [2], [3], [4], [5], [6], [7], [8], [9]

Metabolism of vitamin B 12

Vitamin B 12 (cobalamin) - is a part of products of animal origin only: meat, liver, milk, eggs, cheese and others (the vitamin in the tissues of animals is a derivative of bacteria). Under the influence of culinary processing and proteolytic enzymes of the stomach, it is released and quickly binds to "R-binders" (trans-cobalamin I and III) - proteins with rapid electro-phoretic mobility, compared to the internal factor; to a lesser extent, vitamin B 12 is combined with an internal factor (WF, factor of Castle) - glycoprotein, produced by parietal cells of the fundus and the body of the stomach.

Metabolism of vitamin B12

Pathogenesis

In plasma, vitamin B 12 is present in the form of coenzymes - methyl cobalamin and 5'-deoxyadenosyl cobalamin. Methylcobalamin is necessary to ensure normal hematopoiesis, namely for the synthesis of thymidine monophosphate, which is part of the DNA, and the formation of tetrahydrofolic acid. Violation of the formation of thymidine with a deficiency of vitamin B 12 leads to a violation of the synthesis of DNA, slowing down the normal processes of maturation of hemopoietic cells (lengthening phase S), which is expressed in megaloblastic hematopoiesis.

The pathogenesis of vitamin B12 deficiency

Symptoms of lack of vitamin B 12

Isolated hereditary and acquired forms of vitamin B 12- deficiency anemia.

Hereditary forms of vitamin B 12 deficiency anemia are rare. Clinically characterized by a typical picture of megaloblastic anemia with the presence of symptoms of lesions of the gastrointestinal tract and the nervous system.

Symptoms of the disease appear gradually. Initially, there is a worsening of appetite, aversion to meat, dyspeptic phenomena are possible. The most pronounced anemic syndrome - pallor, light icteric skin with a lemon-yellow hue, subclicity sclera, weakness, malaise, fatigue, dizziness, tachycardia, shortness of breath even with a little physical exertion.

Symptoms of lack of vitamin B12

What's bothering you?

How to examine?

Treatment of deficiency of vitamin B 12

Prevention is carried out in the case of gastrectomy and resection of the ileum.

The initial daily dose of vitamin B 12 is 0.25-1.0 mg (250-1000 μg) for 7-14 days. As an alternative scheme (with the ability of the body to store vitamin for a long time) use intramuscular injection of the drug in a dose of 2-10 mg (2000-10 000 μg) monthly. In most cases, therapy is carried out for life.

Treatment of vitamin B12 deficiency

Использованная литература

Translation Disclaimer: For the convenience of users of the iLive portal this article has been translated into the current language, but has not yet been verified by a native speaker who has the necessary qualifications for this. In this regard, we warn you that the translation of this article may be incorrect, may contain lexical, syntactic and grammatical errors.

You are reporting a typo in the following text:
Simply click the "Send typo report" button to complete the report. You can also include a comment.