Antibodies to the internal factor of Castle, IgG (Intrinsic Factor Antibodies, IgG). Antibodies to intrinsic Castle factor, IgG Preparation for analysis

First described by W. Castle in 1929.

W. Castle's research served as the starting point in the creation of a well-known concept, according to the cut, as a result of the interaction of two factors - external, contained in raw meat, raw liver, yeast, and internal, produced by the gastric mucosa - the so-called. antianemic “principle” - a compound that ensures fiziol, the maturation of bone marrow cells, primarily erythronormoblasts. W. Castle's concept had the character of a working hypothesis.

External Castle factor, the nature of which was originally associated with a protein substance, is identified with cobalamin or vitamin B 12 (see Cyanocobalamin).

Castle's intrinsic factor is a substance that has the properties of a protein; it does not pass through the membrane during dialysis, is inactivated in normal gastric juice heated to 60°, and can be concentrated by methods of fractional separation of proteins. Glass (G. Glass) et al. (1952) isolated internal factor in crystalline form from gastric juice and showed that it is a gastromucoprotein, which he called “glandular (glandular) mucoprotein.” According to modern data, the internal factor is a complex compound consisting of peptides released: in the process of converting pepsinogen into pepsin, and mucoids secreted by: accessory cells of the gastric mucosa. The protein part of the complex determines its activity, and the mucoid part provides protection of vitamin B 12 from digestive enzymes and microbes. Accurate chem. structure of active groups: internal factor unknown. The main role of the internal factor is the formation of a labile complex with vitamin B 12, ensuring the transport of vitamin B 12 through the intestinal lumen and its resorption by the mucous membrane of the small (mainly ileal) intestine. Resorption of the vitamin B 12 + intrinsic factor complex at the level of intestinal epithelial cells is improved in the presence of calcium ions, bicarbonates and pancreatic enzymes. Further entry of vitamin B 12 into the portal bloodstream is carried out with the help of protein carriers - transcobalamins I (alpha globulin) and II (beta globulin). The resulting protein-B 12 vitamin complex is deposited in the liver. It is used, in addition to bone marrow, by nervous tissue and gland. tract.

According to modern researchers, not only gastric intrinsic factor, but also a number of other proteins can bind B 12. The existence of a protein in the intestine that promotes the absorption of vitamin B 12 in the ileum has been proven.

The presence of B 12-binding proteins (including intrinsic factor) in gastric juice is proven by the Singer test - “rat-reticulocyte reaction” (RRR, or RRR - Ratten Reticulocyte Reaction), the essence of the cut is that normal human gastric juice administered parenterally, causes an increase in the number of reticulocytes in rats. The gastric juice of a patient with pernicious anemia, who lacks an internal factor, does not cause such a reaction. More precisely, the presence of intrinsic factor in the test material is proven using various methods based on the specific inhibitory effect of antibodies blocking intrinsic factor (obtained from the serum of a patient with pernicious anemia), precipitation of intrinsic factor with a specially prepared (against this patient) rabbit antiserum, as well as immunodiffusion data and chromatography (allowing you to determine the composition of the amino acids and sugars included in the internal factor).

The degree of absorption of vitamin B 12 associated with the internal factor is judged by the Schilling test, which consists of the oral administration of cobalt-labeled vitamin B 12 (60Co B 12): normally, st. 10% of orally administered radioactive vitamin B 12 is determined in the urine, and with pernicious megaloblastic anemia, even in the stage of clinical and hematological remission achieved by parenteral administration of vitamin B 12, less than 2% of orally administered vitamin B 12 enters the urine; the increased radioactivity in the feces determined in this case indicates impaired absorption of vitamin B 12 due to the lack of internal factor.

According to research by I. M. Roitt et al. (1964), Glass (1972), etc., a decrease in the functional activity of gastric cells, accompanied by a decrease or complete cessation of the secretion of internal factor with the subsequent development of B 12-deficient megaloblastic (pernicious) anemia, occurs as a result of organ-specific autoimmunization. In this case, the antigen-antibody reaction occurs at the level of the gastric mucosa, both between parietal cells (their antigens) and antiparietal cell antibodies, and between the internal factor and antibodies against it. The presence of antiparietal cell antibodies is proven using immunofluorescence (see) - antibodies fixed in the cytoplasm of parietal cells are detected (Coons test).

Antibodies against intrinsic factor are also found in childhood forms of B 12 -deficiency anemia, occurring with impaired production of intrinsic factor, as well as in the blood of newborns (up to 3 weeks of age) born from mothers with megaloblastic anemia, whose blood contains antibodies against intrinsic factor .

The role of heredity in the development of intrinsic factor deficiency is proven by cases of detection of antiparietal cell antibodies, as well as antibodies that block both the intrinsic factor and the intrinsic factor + vitamin B 12 complex, in parents of patients with pernicious anemia. Katz and Allen (M. Katz, R. H. Allen, 1973) described cases of hetero- and homozygous inheritance of this trait.

Bibliography: Diseases of the digestive organs, ed. S. M. Ryssa, p. 182, L., 1966, bibliogr.; Kassirsky I. A. and Alekseev G. A. Clinical hematology, M., 1970; Lazovskiy Yu. M. About the localization of the antianemic factor in the stomach, Arkh. pathol., vol. 9, no. 1, p. 42, 1947, bibliogr.; Normal hematopoiesis and its regulation, ed. N. A. Fedorova, p. 341, M., 1976, bibliogr.; B e g e m a n n H. u. H a g w. e r t b H. G. Praktische Hamatologie, Stuttgart, 1974; Castle W. B. Observations on the etiologic relationship of achylia gastrica to pernicious anemia, Amer. J. med. Sci., v. 178, p. 748, 1929; D e s a i H. G. a. An t i a F. P. Vitamin B 12 malabsorption due to intrinsic factor deficiency in Indian subjects, Blood, v. 40, p. 747, 1972; K ass L. Pernicious anemia, Philadelphia, 1976, bibliogr.; Katz M., Mehlman C. S. a. Al 1 e n R. H. Isolation and characterization of an abnormal human intrinsic factor, J. clin. Invest., v. 53, p. 1274, 1974.

Castle factor: features of vitamin B12 deficiency

Castle factor is a special substance (complex proteins, proteins) that, through their combined interaction, stimulate hematopoietic processes in the body. They are named after the American hematologist W.B. Castle. Vitamin B12 is produced in the body through complex biochemical processes at the cellular level. The condition is often diagnosed in young children, adults and elderly patients. With a lack of B12, anemia develops, just like with a lack of iron. The occurrence of pathology is due to the inability to process or absorb folates, vitamin C and vitamin B12, which are responsible for the formation of anemic syndrome. Treatment of the pathology consists of correcting nutrition and intramuscular administration of the vitamin in proportion to the stage of development of B12-deficiency anemia (otherwise known as pernicious anemia).

Characteristics

Castle factor is a complex protein that is transformed into vitamin B12. B vitamins are essential in the production of red blood cells in the blood and the development of the nervous system. Vitamin deficiency causes serious neurological diseases, which without correction can have irreversible consequences for the patient. There are two types of Castle factors:

External B12 accumulates in the liver, milk and meat of animals, which is why a deficiency of this vitamin is so often observed in absolute vegetarians. Plant foods simply do not have B12 because plants are not able to synthesize the vitamin on their own. Intrinsic Castle factor is formed in the mucous tissues of the stomach by special cells that synthesize hydrochloric acid. Some of the proteins in the gastric mucosa are a kind of transport for B12, and its mucoid part protects against the aggressive effects of acids necessary for digestive processes. Complex interactions in the cavity and structures of the stomach produce vitamin B12 and deliver it to the small intestine. When interacting with other substances and cells, B12 is sent into the bloodstream and enters the liver, where it is distributed throughout the body and stored.

Important! Vitamin B12 deficiency is a long-term process that can last several years. The first signs often appear as vitamin deficiency increases.

Causes

There are cases when the Castle factor is in the stomach, but the protein has nothing to contact for further transportation. Such conditions may be associated with a lack of animal products in the diet or with various diseases. The risk group of patients consists of the following persons:

adherents of plant-based nutrition;
lovers of hungry diets;
those who have undergone surgery on the stomach and other organs of the gastrointestinal tract;
having autoimmune disorders;
forced to take medications for a long time.

Poor nutrition and social disadvantage, unsatisfactory living environment, abuse of strong alcohol and tobacco, cancer and other negative factors contribute to the development of B12-deficiency anemia.

Clinical manifestations

The symptomatic complex with Castle factor deficiency manifests itself in all patients in the same way. At first, the signs appear weakly, but over time the disturbances become persistent. Symptoms are combined into three main groups: anemic signs, dyspeptic, neurological. The predominant manifestations of certain signs are determined by the duration of anemia, which makes up the following general picture:

general weakness and malaise;
dizziness, frequent headaches;
the appearance of spots before the eyes, ringing in the ears;
fainting, increased heart rate and breathing;
weight loss, perversion of taste preferences;
crimson tongue syndrome (due to destruction of the papillae);
nausea and vomiting;
stiffness of movement, rapid muscle fatigue;
convulsive syndrome, nervousness;
apathy and emotional instability.

The pathology is quite dangerous due to the likelihood of chronic complications. It is not possible to check the presence of Castle factor on your own. The disease can only be determined by a detailed blood test (including antibody levels). If symptoms bother you for a long time against the background of absolute health, you should consult a doctor and undergo a full examination.

Treatment and diagnosis

Differential diagnosis is aimed at excluding iron deficiency anemia, as well as the absence of autoimmune factors. After a thorough examination, doctors plan further therapy.

Diagnostics

Before carrying out therapeutic measures, diagnostics is required, which consists of the following studies:

study of clinical history;
studying patient complaints;
detailed blood test;
sternum puncture (collection of bone marrow cells).

Consultation with a hematologist is required, and in case of a burdened clinical history of various organs or systems, with other specialists in the treatment profile.

Treatment process

For successful treatment, the patient must remain in the hospital for some time. This will allow for regular monitoring of his condition, monitoring the level of Castle factor and its production. The main drug for the treatment of B12-deficiency anemia is vitamin B12 solution for intramuscular administration. The initial dosage is usually high, after which it is significantly reduced. It all depends on the age of the patient and the severity of vitamin deficiency.

Important! In addition to drug correction, special attention is paid to the patient’s lifestyle: a nutritious diet, exclusion of harmful and toxic substances, physical exercise and daily walks in the fresh air, adherence to the regime (sleep, wakefulness, nutrition).

Prevention

Preventive measures are aimed at creating a complete diet. Products must ensure a complete supply of the vitamin to the body, as well as its maximum absorption. Foods fortified with vitamin B12 include:

any eggs;
leafy vegetables with a dark green color;
grain products;
any nuts;
seafood;
sea fish;
white meat;
berries and fruits;
offal (especially liver).

For mild pernicious anemia, nutritional correction, dietary supplements or a special nasal spray are sufficient. In case of severe disorders, intravenous administration of B12 is required. Particularly severe cases require lifelong treatment, which involves weekly administration of a certain dose of the drug subcutaneously or intramuscularly. Timely drug correction will help avoid serious complications in the future.

But perhaps it would be more correct to treat not the effect, but the cause?

Castle factor, what do you eat it with?

First, let's try to figure out what it is. There are two types: internal and external Castle factors. External is vitamin B12, well known to both doctors and patients. It is produced by bacteria and blue-green algae. Animals accumulate it in the liver, meat, and excrete it in milk. For the growth and development of embryos, a lot of this vitamin is found in the yolks of eggs. But plants cannot synthesize it, so vegetarians usually do not get it.

But our body produces intrinsic factor Castle on its own. It is formed in special cells of the gastric mucosa, the same ones that provide us with hydrochloric acid. Its protein part plays the role of a conductor, and the mucoid part acts as a protector from the digestive action of the aggressive environment of the digestive tract and ubiquitous bacteria. This complex compound helps secrete vitamin B12, combines with it and delivers it to the small intestine. There it finds specially designed cells and is absorbed into the blood along with it. Further, the path of the resulting complex of Castle’s internal and external factors lies in the liver. There it is stored and used as needed.

The nervous system cannot do without vitamin B12, but it is especially needed for the reproduction of new blood cells. The danger of a deficiency of this substance is a slow, imperceptible increase in symptoms.

Possible causes of Castle intrinsic factor deficiency:

A congenital genetic defect, when for some reason this substance is not produced enough or is completely absent
Diseases of the stomach in which the work of parietal cells is blocked or their number is sharply reduced (chronic gastritis with atrophy of the mucous membrane or stomach cancer)
Surgical removal of the stomach for various reasons
Often additional pathology from the endocrine system, autoimmune diseases are complicated by B12 deficiency anemia

Sometimes enough of it is produced, but the disease still develops. Why could this be?

Castle has an internal factor, but he has nothing to connect with - a strict vegetarian simply deprives himself of vitamin B12 completely
The work of the cells of the small intestine, which is responsible for the absorption of the resulting complex, is disrupted
Complete dysfunction of intestinal absorption, congenital or acquired. This is caused by celiac disease, multiple diverticula of the small intestine, some worms (diphyllobothriasis)
Condition after intestinal resection

Vitamin B12 and Castle factor deficiency clinic

The most well-known form of the disease associated with a deficiency of these factors is pernicious (megaloblastic) anemia. In addition to the expected pallor, brittle hair and nails, jaundice is associated with increased destruction of red blood cells. The tongue becomes very characteristic and remarkable - completely smooth due to atrophy of the papillae, shiny and bright - varnished. Often quite painful and unpleasant ulcers appear on it - aphthae. Appetite is significantly reduced, and an aversion to meat appears. The liver and spleen may enlarge, and the activity of the heart may be impaired. Of course, in addition to all this, a person feels weakness, loss of strength, and dizziness and darkening of the eyes are often noted.

On the part of the nervous system, the signs are even more sad, and everything begins very innocently, and does not make either the patient or his family wary. Initially, weakness appears in the legs, periodically there is a feeling of pins and needles, and reflexes decrease, which are usually determined at an appointment by neurologists. Over time, muscle weakness increases, the functioning of the pelvic organs is disrupted (the activity of the sphincters of the bladder and rectum, impotence develops in men). In some cases, mental abnormalities may appear, from neurosis to severe psychosis with hallucinations, and a progressive decline in intelligence.

Diagnosis and treatment

For correct diagnosis, in addition to the usual peripheral blood test, it is advisable to perform a puncture of the sternum to check bone marrow cells. In addition, you should definitely consult a hematologist. For the safety of the patient and to make the doctor more informative, it is recommended that a complete examination and initiation of treatment be carried out in a hospital.

Once the diagnosis and its possible cause become clear, therapy begins. The main drug for this pathology is vitamin B12 intramuscularly. The dose depends on the severity and severity of symptoms, the degree of deficiency of this important factor. Initially, injections are prescribed daily, then every other day, gradually switching to maintenance administration of the drug once a week.

Naturally, if it is possible to eliminate the internal deficiency of the vitamin in the blood, for example, by diversifying the menu and switching to less strict vegetarianism, removing helminths, this must be done.

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What are the effects of vitamin B12 deficiency on red blood cell production?

12-deficiency anemia ranks second in importance and frequency in the group of deficiency anemias. Vitamin B12 in the human body is indispensable for the proper synthesis of proteins that make up red blood cells. In the presence of the required amount of vitamin B12, normal-sized red blood cells are formed in the body (normoblastic type of hematopoiesis). In case of a lack of vitamin B12, the size of red blood cells changes; they are much larger than usual and are called megaloblasts, i.e., a type of hematopoiesis appears that is characteristic of the period of intrauterine development of the fetus. Therefore, B 12 deficiency anemia is also called megaloblastic.

Typically, B12 deficiency anemia can be easily treated with tablets or injections containing vitamin B12.

Vitamin B12 (cyanocobalamin)

Vitamin B12

DEFINITION OF VITAMIN B12

Vitamins B 12 are a group of cobalt-containing biologically active substances called cobalamins, which belong to the so-called. corrinoids, ancient natural biocatalysts. These include cyanocobalamin itself, hydroxycobalamin and two coenzyme forms of vitamin B12: methylcobalamin and 5-deoxyadenosylcobalamin. In a narrower sense, vitamin B12 is called cyanocobalamin, since it is in this form that the bulk of vitamin B12 enters the human body, without losing sight of the fact that it is not synonymous with B12, and several other compounds also have B12-vitamin activity. Cyanocobalamin is just one of them. Therefore, cyanocobalamin is always vitamin B12, but vitamin B12 is not always cyanocobalamin.

B12 is a complex of several substances that have similar biological effects. The main one among them is cyanocobalamin - solid dark red crystals. This color is due to the content of a cobalt atom in each large cyanocobalamin molecule. It is this atom that creates all the uniqueness of vitamin B12. No other vitamin in living nature contains metal atoms. In addition, only in the molecule of this vitamin there is a special chemical bond between the cobalt and carbon atoms, which is not found anywhere else in living nature. The cyanocobalamin molecule is the largest and bulkiest among the molecules of all vitamins. Each molecule of vitamin B12 has a region in which different atoms can be located. Depending on the type of these atoms, different types of vitamin B12 are distinguished - cyanocobalamin, already known to us, as well as hydroxocobalamin, methylcobalamin and deoxyadenosinecobalamin. At the same time, all these substances in the human body are converted into the active form of the vitamin - adenosylcobalamin, or cobamine. In the future, we will call all of them by the collective names “vitamin B12” or cyanocobalamin.

HISTORY OF THE DISCOVERY OF VITAMIN B12

Vitamin B12 (cyanocobalamin) is one of the more controversial members of the B-complex vitamin family. Although the full chemical structure of vitamin B12 was revealed only in the 1960s, research involving this vitamin has already been recognized with two Nobel Prizes. The first Nobel Prize in 1934 was awarded for the discovery that foods (particularly liver, a very rich source of vitamin B12) could be used to treat pernicious anemia (the inability of the blood to carry oxygen). The second prize, thirty years later, was awarded to chemists for discovering the exact chemical structure of this important vitamin.

SYNTHESIS OF VITAMIN B12

Vitamin B12 is unusual regarding its origin. Almost all vitamins can be extracted from a variety of plants or specific animals, but no single plant or animal is capable of producing vitamin B12. The exclusive source of this vitamin, according to modern data, are tiny microorganisms: bacteria, yeast, mold and algae. However, despite the fact that only a few microorganisms produce B12, the vitamin itself is required by the entire microbial community due to its unique properties. For more information about this, see the article: Vitamin B12 is a key link in the regulation of the metabolism of folic acid, ubiquinone and methionine.

Propionic acid bacteria synthesize large amounts of vitamin B12, which regulates basic metabolic processes in the body, helps improve the body’s immune status, improves overall well-being by activating protein, carbohydrate and fat metabolism, increases resistance to infectious diseases, improves blood quality, and participates in the synthesis of various amino acids , nucleic acids. However, the synthesis of vitamin B12 by the human intestinal flora is insignificant. With a lack of vitamin B12, gastrointestinal diseases, dysbacteriosis, and anemia occur. Therefore, probiotic products containing propionic acid bacteria, producers of vitamin B12, can play an important role in the prevention and treatment of these diseases.

NOTE: It should be especially noted that the content of vitamin B12 in products fermented with developed starter cultures of propionic acid bacteria is thousands (!) times higher than its amount in products made with traditional starter cultures containing similar cultures, but with the addition of lactic acid bacteria. Among modern methods of enriching fermented milk products with vitamins, it is precisely this microbial supersynthesis of vitamin B12 that is the most justified, since recent studies by doctors and microbiologists have confirmed that the most effective use of vitamins is in a coenzyme (associated with microbial cell protein) easily digestible form.

CASTLE FACTORS

Like most vitamins, B12 comes in different forms and goes by different names. The names for vitamin B12 contain the word form "cobalt" because cobalt is the mineral found in the center of the vitamin: cobrinamide, cobinamide, cobamide, cobalamin, hydroxcobalamin, methylcobalamide, aquacobalamin, nitrocobalamin, and cyanocobalamin.

Castle factors and vitamin B12

Vitamin B12 is unusual in that it depends on a second substance called intrinsic factor, which allows the vitamin to pass from the gastrointestinal tract to the rest of the body. Without the intrinsic factor, which is a unique protein (more precisely, a compound consisting of a protein part and mucoids - a secretion secreted by the cells of the gastric mucosa) produced in the stomach, vitamin B12 cannot access those parts of the body where it is needed.

Castle factors (Note: Named after the American physiologist and hematologist W.B. Castle)– these are substances necessary to maintain normal hematopoiesis. Vitamin B12 (cyanocobalamin) is one of Castle's external factors. Intrinsic Castle factor binds vitamin B12 and promotes its adsorption by the intestinal wall (absorption by epithelial cells of the ileum). The secretion of intrinsic factor Castle may decrease (or even stop completely) when the gastrointestinal tract is damaged (for example, during an inflammatory process, atrophic gastritis, cancer), when part of the stomach or small intestine is removed, etc. Its secretion increases under the influence of insulin and decreases under the influence of alcohol. If the release of intrinsic factor is impaired, the binding and absorption of vitamin B12 is impaired, which leads to the development of B12-deficient megaloblastic, or pernicious, anemia.

Functions of vitamin B12

Vitamin B12 is involved in the conversion of folic acid into its active form, in the synthesis of methionine, coenzyme A, the antioxidant glutathione, succinic acid, and myelin. It controls DNA synthesis (therefore, cell division), maturation of red blood cells, increases the level of T-suppressors, which helps limit autoimmune processes.

Perhaps the most well-known function of B12 is its role in the development of red blood cells. As noted above, vitamin B12 is one of Castle’s external factors, which are responsible in the body for maintaining normal hematopoiesis. When red blood cells mature, they require information contained in DNA molecules (DNA or deoxyribose nucleic acids, the substance in the nucleus of our cells that contains genetic information). Without vitamin B12, DNA synthesis fails and the information needed to make red blood cells cannot be obtained. The cells become poorly oversized and begin to function ineffectively, a condition called pernicious anemia. Most often, pernicious anemia is not caused by a lack of B12, but by a decrease in its absorption due to the lack of intrinsic factor.

Vitamin B12 and the nervous system

The second major task of vitamin B12 is its participation in the development of nerve fibers. Vitamin B12 is involved in the construction of protein and fat structures of the protective myelin layer. The myelin sheath, which covers neurons, forms less successfully with vitamin B12 deficiency. Although the vitamin plays an indirect role in this process, vitamin B12 supplementation has been reported to be effective in relieving pain and other symptoms of nervous system disorders.

One of the main tasks of vitamin B12 is to participate in the production of methionine, an amino acid that affects mental activity and the formation of a person’s emotional background. Vitamin B12, folic acid and methionine (as well as vitamin C) form a kind of working group that specializes mainly in the functioning of the brain and the entire nervous system. These substances are involved in the production of so-called monoamines - stimulants of the nervous system, which determine the state of our psyche.

Also, vitamin B12 and folic acid promote the production of choline (vitamin B4), which significantly affects mental activity and psyche. In the process of metabolism from it to the so-called. Cholinergic fibers produce the neurotransmitter acetylcholine, a substance that transmits nerve impulses. When a person needs to concentrate, the accumulated choline is converted into acetylcholine, which activates the brain.

A lack of choline threatens a real breakdown of the psyche. With choline deficiency, cholesterol is oxidized, combines with protein waste and clogs the “passages” in cell membranes, so necessary substances cannot enter the cell. The brain tries to transmit signals, but the passage channels become blocked, and the person loses the ability to think clearly and “falls into depression.” At the same time, sleep is disturbed, and brain cells and nerve endings begin to quickly die: the more cholesterol accumulates in the blood, the faster this process occurs. Since, with a lack of choline, entire colonies of cholinergic neurons die off, eventually there is a danger of incurable Alzheimer's disease, which is accompanied by absolute loss of memory and personality disintegration. Modern neurophysiologists are of the opinion that a significant proportion of people over 40 years of age in Western countries have already come close to this disease.

Recently, evidence has been obtained that vitamin B12 is also of great importance for bone formation. Bone growth can only occur when there is an adequate supply of vitamin B12 in osteoblasts (the cells that make bones). This is especially important for children during the period of active growth, as well as for menopausal women who experience hormonally caused bone loss - osteoporosis.

Vitamin B12 affects muscle growth because it is involved in the processes of protein metabolism and amino acid synthesis. It activates energy exchange in the body. It is also important that it supports the vital activity of the nerve cells of the spinal cord, through which centralized control of the muscles of the body occurs.

Vitamin B12 and metabolism

Vitamin B12 is required to circulate proteins throughout the body that are essential for cell growth and repair. Many of the key components of protein, called amino acids, become unusable in the absence of B12. Vitamin B12 influences the movement of carbohydrates and fats in the body.

In combination with folic acid (vitamin B9) and pyridoxine (vitamin B6), vitamin B12 normalizes the metabolism of methionine and choline, thereby having a beneficial effect on the liver, preventing its fatty degeneration. This is due to the fact that choline and the essential amino acid methionine are very strong lipotropic substances. Lipotropic substances are very important factors that contribute to the normalization of lipid and cholesterol metabolism in the body, stimulating the mobilization of fat from the liver and its oxidation, which leads to a decrease in the severity of fatty infiltration of the liver.

Also, according to the latest data, vitamin B12 deficiency leads to a lack of carnitine, the so-called quasi-vitamin (vitamin B or B11) - a substance that is a cofactor in metabolic processes that maintain CoA activity. Carnitine promotes penetration through mitochondrial membranes and the breakdown of long-chain fatty acids (palmitic, etc.) with the formation of acetyl-CoA, mobilizes fat from fat depots. In other words, carnitine is involved in the transport of fat molecules from the blood to mitochondria - the “energy stations” of cells, where fat is oxidized and provides energy to the entire body. Without carnitine, the content of breakdown products in the blood increases, since fat remains unprocessed. Also, this substance has a neurotrophic effect, inhibits apoptosis (the process of programmed cell death), limits the affected area and restores the structure of nervous tissue, normalizes protein and fat metabolism, incl. increased basal metabolism in thyrotoxicosis, restores the alkaline reserve of the blood, promotes economical consumption of glycogen and increases its reserves in the liver and muscles.

Daily intake of vitamin B12

Physiological needs for vitamin B12 according to Methodological Recommendations MP 2.3.1. on the norms of physiological needs for energy and nutrients for various groups of the population of the Russian Federation:

The upper acceptable level has not been established.
Physiological requirement for adults – 3 mcg/day

External factor

Castle's extrinsic factor is vitamin B12 (cobalamin, or cyanocobalamin), which is found in raw meat, raw liver, yeast, fish, eggs, and milk.

Internal factor

Castle's internal factor (gastromucoprotein) is a complex compound consisting of peptides that are cleaved from pepsinogen when it is converted into pepsin, and mucoids, a secretion secreted by the cells of the gastric mucosa (mucocytes). The mucoid part of the complex protects it from hydrolysis by digestive enzymes and utilization by intestinal bacteria; the protein part determines its physiological activity. The main role of Castle's intrinsic factor is the formation of a labile complex with vitamin B12, which is absorbed by the epithelial cells of the ileum. Absorption is enhanced in the presence of calcium ions, bicarbonates and pancreatic enzymes. In blood plasma, vitamin B12 binds to plasma proteins, forming a protein-B12-vitamin complex, which is deposited in the liver. It enhances the hematopoietic function of the bone marrow, as well as the functions of nervous tissue and glands. -kish. tract.

Violations

The secretion of intrinsic factor Castle may decrease or completely stop when the gastrointestinal tract is damaged. -kish. tract (for example, during an inflammatory process, cancer), when part of the stomach or small intestine is removed, etc. In these cases, the binding and absorption of vitamin B12 is impaired, which leads to the development of B12-deficient megaloblastic, or pernicious, anemia.

Indications

A test for antibodies to intrinsic factor in the blood is indicated for patients with vitamin B12 deficiency and pernicious anemia. Both conditions are accompanied by a decrease in body weight, increasing weakness, disorders of the peripheral nervous system (a frequent manifestation is a change in sensitivity), and inflammation of the tongue. Pernicious or B-12 deficiency anemia most often develops after age 40. Its combination with autoimmune diseases affecting the endocrine glands is typical. Therefore, as part of a comprehensive diagnosis, an analysis for antibodies to internal factor is prescribed for autoimmune thyroiditis, insulin-dependent diabetes mellitus, Addison's disease, as well as for autoimmune pathologies not related to endocrinopathies.

A test for antibodies to intrinsic Castle factor in the blood is used for the early detection of autoimmune gastritis (type A) and its differentiation from other diseases. The pathology is practically asymptomatic and rarely becomes the reason for seeking medical help. Often, autoimmune gastritis is discovered several years after its onset, when, due to a lack of vitamin B12, the production of red blood cells is disrupted and macrocytic anemia develops.

The basis for studying antibodies to the internal factor may be symptoms of anemia, as well as changes in a general clinical blood test - an increase in the size of red blood cells, an increase in erythrocyte hemoglobin, a decrease in the level of reticulocytes, the development of thrombocytopenia, leukopenia. Long-term pernicious anemia leads to irreversible changes in the nervous system, so the study of antibodies to the internal factor can be indicated for polyneuritis, ataxia, and demyelinating pathologies.

The advantage of testing for antibodies to intrinsic Castle factor is its high specificity for vitamin B12 deficiency and pernicious anemia. A limitation of the study is that these antibodies are produced in only 60% of patients with autoimmune gastritis. Therefore, this test is recommended to be combined with a blood test for ARVC.

Preparation for analysis and collection of material

The level of antibodies to intrinsic Castle factor is determined in venous blood. The collection procedure is performed in the morning, before meals. Preparation includes giving up alcohol, limiting physical and psycho-emotional stress during the previous 24 hours, and quitting smoking 30 minutes in advance. Blood is taken from the cubital vein using a puncture, stored and transported in sealed tubes. Before the test, the tubes are placed in a centrifuge unit, and then clotting factors are removed from the plasma.

Antibodies to intrinsic Castle factor are determined in venous blood serum by enzyme immunoassay. The procedure consists of two stages. At the first stage, antigens specific to intrinsic factor antibodies are introduced into the serum. At the second stage, the resulting complexes are colored during an enzymatic reaction. Based on the change in the density of the mixture, the concentration of the antibodies under study is calculated. Preparation of results takes 7-11 days.

Normal values

Normally, the result of a blood test for antibodies to intrinsic Castle factor is negative. Reference values range from 0 to 6 rel. units/ml Physiological factors do not affect the results of the study. It is also worth remembering that the absence of antibodies to the internal factor does not exclude the presence of diseases; the final indicators in any case require interpretation by a specialist.

Level change

The main reasons for increased levels of antibodies to intrinsic factor in the blood are vitamin B12 deficiency and pernicious anemia. If this result is combined with low blood test results for vitamin B12 and characteristic changes in the general blood test, then the diagnosis of B12 deficiency anemia is confirmed. In addition, the cause of an increase in the level of antibodies to the internal Castle factor in the blood can be atrophic gastritis, autoimmune and neurological diseases.

The reason for the decrease in the level of antibodies to the intrinsic factor in the blood during repeated studies is considered to be a positive response to therapy. Low levels during the initial examination are normal, but a negative result does not exclude the diagnosis of pernicious anemia.

Treatment of abnormalities

A blood test for antibodies to intrinsic Castle factor is a highly specific test for diagnosing B12 deficiency and pernicious anemia. In combination with an analysis for ARGC, it is used to identify autoimmune gastritis. The interpretation of the results and the prescription of treatment is carried out by the attending physician - hematologist, gastroenterologist, neurologist, rheumatologist.

Intrinsic factor, Castle Factor, Intrinsic Factor Antibody, Anti-intrinsic Factor, B221, B12/folate deficiency anemia, Blood and hematopoietic system, Stomach, duodenum 12

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Price: 1 430 715 ₽ RU-MOW

800 rub. RU-SPE 690 rub. RU-NIZ 690 rub. RU-ASTR 715 rub. RU-BEL 690 rub. RU-VLA 705 rub. RU-VOL 690 rub. RU-VOR 690 rub. RU-IVA 715 rub. RU-ME 650 rub. RU-KAZ 690 rub. RU-KLU 690 rub. RU-KOS 670 rub. RU-KDA 690 rub. RU-KUR 690 rub. RU-ORL 715 rub. RU-PEN 650 rub. RU-PRI 705 rub. RU-ROS 690 rub. RU-RYA 700 rub. RU-SAM 650 rub. RU-TVE 690 rub. RU-TUL 690 rub. RU-UFA 690 rub. RU-YAR

Description
Decoding
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Period of execution

The analysis will be ready within 1 day (except for the day of taking the biomaterial). You will receive the results by email. mail immediately when ready.

Completion period: 1 day (except for the day of taking biomaterial)

Preparing for analysis

Limit fatty and fried foods for 24 hours, eliminate alcohol and heavy physical activity, as well as x-rays, fluorography, ultrasound and physiotherapy.

4 hours before donating blood, do not eat food, drink only clean water.

Discuss with your doctor the medications you are taking and the need to stop them.

Antibodies to intrinsic factor

Intrinsic factor (Castle intrinsic factor) is an enzyme that converts the inactive form of vitamin B12 into the active one. It is synthesized by the parietal cells of the stomach and is a glycoprotein with a molecular weight of about 44 kDa. With the help of internal factroa, vitamin B12 is transported and absorbed in the small intestine. Insufficient absorption of vitamin B12 due to impaired secretion of intrinsic factor leads to pernicious anemia. This process is more common in people over 50 years of age. The prevalence of pernicious anemia or Burman's disease is estimated to be 0.1% of the general population and increases with age to 1%. As recent studies show, 1.9% of people over 60 years of age suffer from this pathology.

Without vitamin B12 (cyanocobalamin), normal reproduction of red blood cells and the functioning of the nervous system are impossible. When cyanocobalamin is taken from food under the influence of gastric juice, it is released, and then one of the two vitamin B12-binding proteins of gastric juice is added to it. In the duodenum, binding proteins are broken down by pancreatic proteases, vitamin B12 becomes free and binds to intrinsic factor. The labile complex formed by vitamin B12 and intrinsic factor binds to the epithelial cells of the ileum and vitamin B12 enters the bloodstream.

Pernicious anemia in adults usually occurs between the ages of 40 and 70 years. Pernicious anemia is often combined with autoimmune diseases, with autoimmune endocrinopathies, with the presence of antibodies to various receptors (chronic autoimmune thyroiditis, insulin-dependent diabetes mellitus, Addison's disease, vitiligo). The disease has mild symptoms until the late stages, but lesions of the gastric mucosa occur many years before the development of anemia. Clinical manifestations of the disease include weight loss, general weakness, damage to the peripheral nervous system (the most common are paresthesias), glossitis. Pernicious anemia is characterized by megaloblastic anemia, gastritis with the presence of antibodies to intrinsic factor, vitamin B12 deficiency, and neuropathy. In some cases, pernicious anemia occurs with a slight or moderate deficiency of vitamin B 12 and without pronounced macrocytosis.

Pernicious anemia is the result of long-term autoimmune processes aimed at destroying the gastric mucosa. There are two autoimmune processes that affect the absorption of vitamin B12 and, accordingly, the development of pernicious anemia:

Decreased production of intrinsic factor by gastric parietal cells. Pernicious anemia is characterized by a decrease in the synthesis of intrinsic factor.
Blocking by autoantibodies of the binding sites of the internal factor of Castle, necessary for the absorption of vitamin B12. The production of antibodies to intrinsic factor and antibodies to gastric parietal cells is observed. The pathological result of the action of antibodies to the internal factor is the same - lack of absorption of vitamin B12 in the intestine.

In a population of healthy people, antibodies to the intrinsic factor are quite rare, so their detection allows one to accurately determine the presence of pernicious anemia. Researchers have described two types of antibody data:

Type I autoantibodies, which block intrinsic factor, block the vitamin B12 binding site of intrinsic factor and prevent the uptake of vitamin B12.
Type II autoantibodies that bind intrinsic factor react with another intrinsic factor site and may prevent the intrinsic factor vitamin B12 complex from binding to binding sites in the small intestine.

A study by Conn D. A. showed that in a group of 66 samples with antibodies to intrinsic factor, all samples contained both type I and type II antibodies. The presence of pernicious anemia and antibodies to intrinsic factor is often associated with diseases such as Hashimoto's thyroiditis, Graves' disease, Lambert-Eaton syndrome, insulin-dependent diabetes mellitus, myasthenia gravis, rheumatoid arthritis, and hypoparathyroidism. It should also be noted that antibodies to intrinsic factor may be present in 3–6% of people with hyperthyroidism or insulin-dependent diabetes mellitus.

For the diagnosis of pernicious anemia, the combination of megaloblastic anemia, low serum vitamin B12 levels, and the presence of autoantibodies to intrinsic factor in the serum is essential. When determining antibodies to intrinsic factor, further studies to diagnose pernicious anemia, such as the Schilling test (a method for detecting malabsorption of cyanocobalamin, which consists of ingesting a certain amount of vitamin B12 labeled with radioactive cobalt, followed by examining its content in urine collected per day), may not be needed. The specificity of this test is high because antibodies to intrinsic factor are extremely rare in cases where vitamin B12 deficiency is not associated with pernicious anemia. In the absence of timely diagnosis and treatment of pernicious anemia, irreversible changes in the nervous system may occur. Prescribing B12 is unacceptable, since it not only does not improve the condition of patients with neurological disorders, but can also worsen it. This is why identifying undiagnosed cases is critical, especially for older people.

Interpretation of the results of the study "Antibodies to intrinsic factor"

Attention! Interpretation of test results is for informational purposes only, is not a diagnosis and does not replace medical advice. Reference values may differ from those indicated depending on the equipment used, the actual values will be indicated on the results form.

The titer of antibodies to intrinsic factor increases in pernicious (B12-deficiency) anemia and other autoimmune diseases. A decrease in antibody titer has no diagnostic value.

Unit of measurement: U/ml

Reference values: 0.93 - 1.19 U/ml

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Receive test results within the time frame specified on the website by email and, if necessary, at the medical center.

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The nervous system cannot do without vitamin B12, but it is especially needed for the reproduction of new blood cells. The danger of a deficiency of this substance is a slow, imperceptible increase in symptoms.

Possible causes of Castle intrinsic factor deficiency:

A congenital genetic defect, when for some reason this substance is not produced enough or is completely absent
Diseases of the stomach in which the work of parietal cells is blocked or their number is sharply reduced (chronic gastritis with atrophy of the mucous membrane or stomach cancer)
Surgical removal of the stomach for various reasons
Often additional pathology from the endocrine system, autoimmune diseases are complicated by B12 deficiency anemia

Sometimes enough of it is produced, but the disease still develops. Why could this be?

Castle has an internal factor, but he has nothing to connect with - a strict vegetarian simply deprives himself of vitamin B12 completely
The work of the cells of the small intestine, which is responsible for the absorption of the resulting complex, is disrupted
Complete dysfunction of intestinal absorption, congenital or acquired. This leads to multiple diverticula of the small intestine, some (diphyllobothriasis)
Condition after intestinal resection

Vitamin B12 and Castle factor deficiency clinic

From the nervous system The signs are even sadder, and everything begins very innocently, and does not make either the patient or his family wary. Initially, weakness appears in the legs, periodically there is a feeling of pins and needles, and reflexes decrease, which are usually determined at an appointment by neurologists. Over time, muscle weakness increases, the functioning of the pelvic organs is disrupted (the activity of the sphincters of the bladder and rectum, impotence develops in men). In some cases, mental abnormalities may appear, from neurosis to severe psychosis with hallucinations, and a progressive decline in intelligence.

Diagnosis and treatment

Useful video on the topic - “Vitamin B12 - what you eat it with”

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Antibodies to the internal factor of Castle, IgG (Intrinsic Factor Antibodies, IgG). Antibodies to intrinsic Castle factor, IgG Preparation for analysis

Castle factor: features of vitamin B12 deficiency

Characteristics

Causes

Clinical manifestations

Treatment and diagnosis

Diagnostics

Treatment process

Prevention

But perhaps it would be more correct to treat not the effect, but the cause?

Castle factor, what do you eat it with?

Possible causes of Castle intrinsic factor deficiency:

Sometimes enough of it is produced, but the disease still develops. Why could this be?

Vitamin B12 and Castle factor deficiency clinic

Diagnosis and treatment

What are the effects of vitamin B12 deficiency on red blood cell production?

Vitamin B12 (cyanocobalamin)

Vitamin B12

DEFINITION OF VITAMIN B12

HISTORY OF THE DISCOVERY OF VITAMIN B12

SYNTHESIS OF VITAMIN B12

CASTLE FACTORS

Castle factors and vitamin B12

Functions of vitamin B12

Daily intake of vitamin B12

External factor

Internal factor

Violations

see also

See what the "Castle Factor" is in other dictionaries:

Indications

Preparation for analysis and collection of material

Normal values

Level change

Treatment of abnormalities

Period of execution

Preparing for analysis

Antibodies to intrinsic factor

Interpretation of the results of the study "Antibodies to intrinsic factor"

So, why without a doubt Lab4U?

Possible causes of Castle intrinsic factor deficiency:

Sometimes enough of it is produced, but the disease still develops. Why could this be?

Vitamin B12 and Castle factor deficiency clinic

Diagnosis and treatment

Read along with this article: