Intrinsic factor is necessary for the absorption of the vitamin. Castle factor, what do you eat it with? Preparing for analysis
An internal factor such as a lack of complex proteins in the stomach often leads to a deficiency of iron and vitamin B12 in the body and causes anemia. Anemia affects children and the elderly. The pathology is treated in a hospital setting. Preventing relapses requires normalizing nutrition, adding animal products to the diet, as well as prescribing parenteral administration of cyanocobalamin.
What causes anemia?
What is Castle factor deficiency?
With a lack of vitamin B12 and iron, anemia occurs, which is often diagnosed in children in the early period of development, pregnant women, and also in older people. Pathology occurs if the necessary substances are not absorbed and processed. Castle factor is a complex protein that converts vitamins. If there are not enough enzymes in the body, then deficiency anemia with severe neurological complications.
Causes
Doctors distinguish 2 types of Castle factors: external, which enters the body with animal food, and internal, formed in the gastric mucosa by cells responsible for the synthesis of hydrochloric acid. They produce vitamin B12, which is then transported to small intestine, and from it with blood flows to the liver, where it is stored and distributed throughout the tissues. Vitamin deficiency caused by external reasons, takes a long time to form, sometimes years, and is associated primarily with poor nutrition. There are also internal reasons associated with various pathologies. Castle factor deficiency is caused by:
Castle factors or antianemic substances are named after the American hematologist Castle.
How to recognize?
Symptoms manifest themselves equally in all patients and are divided into 3 large groups: neurological, anemic and dyspeptic. The patient loses weight, changes in stool character are noted. The patient is prone to hungry fainting and cramps, gets tired quickly, and has inadequate taste preferences, cardiac arrhythmia, spots in the eyes, unmotivated nausea and vomiting, nervousness, and apathy are noted. A characteristic feature is the persistent crimson color of the tongue.
Diagnostic procedures
To make a diagnosis, you need to do a full examination. This pathology is dealt with by a hematologist. It is impossible to recognize disorders by interviewing the patient and studying the anamnesis. Appointed laboratory research, including a biochemical or complete blood test and bone marrow puncture. If there are complications, additional consultations are held with doctors of the relevant profile, who, in turn, can take additional measures to obtain a complete diagnostic picture of the disease.
Therapy and prevention
Treatment iron deficiency anemia is carried out in a hospital setting, which allows monitoring the patient’s condition by monitoring the level of Castle factor and its formation. The main drug for therapy is a solution of vitamin B12, which is administered intramuscularly first large doses, then they are gradually reduced. In addition to medicinal effects, a nutritious diet, walks in the air, and exercise therapy are important. Prevention of pathology comes down to ensuring that the body receives a sufficient amount of cyanocobalamin from products of animal origin, among which the most useful are eggs, nuts, seafood, and liver. A balanced diet will normalize the patient’s condition and prevent relapse.
Vitamin B12
Vitamins B 12 call the group cobalt-containing biologically active substances called cobalamins, related to the so-called., ancient natural biocatalysts. These include cyanocobalamin itself, hydroxycobalamin and twocoenzymeforms of vitamin B12: methylcobalamin And adenosylcobalamin . In a narrower sense vitamin B12 called cyanocobalamin, 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. Moreover, only in the molecule of this vitamin there is a special chemical bond between cobalt and carbon atoms that 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, they are distinguished different types vitamin B12 - cyanocobalamin, already known to us, as well as hydroxycobalamin, methylcobalamin and adenosinecobalamin. In the future, we will call all of them by the collective names “vitamin B12”.
True Vitamin B12 (Cobalamin)
A striking feature of the metabolism of classical propionic acid bacteria is a high level of formation of corrinoids, compounds of the vitamin B12 group (the structure of corrin is shown below on the left - is the parent structure of corrinoids and a number of coenzymes.)
Corrinoids are a group of methylated and reduced tetrapyrrole compounds containing a cobalt atom at the center of the corrin ring, which forms a unique covalent bond with the β-ligand carbon, essential for chemical and biochemical reactions (see figure of the spatial structure of adenosylcobalamin, a coenzyme of vitamin B12).
In nature, all corrinoids are synthesized only by prokaryotic microorganisms - representatives of both phylogenetic domains (empires): Bacteria And Archaea. Consequently, all organisms that require corrinoids, including humans, depend on the microorganisms that synthesize them. The entire group of corrinoid compounds is often referred to as “vitamin B12.” However, there is the concept of “true vitamin B12”, which refers to cobalamin.
The latter is characterized by the presence of a “lower” α-ligand of the cobalt atom with a nucleotide, the specific base of which is 5,6-dimethylbenzimidazole (5,6-DMB). It is this corrinoid (cobalamin) that functions in the human body in two coenzyme forms (as adenosyl- or methylcobalamin, β-ligands), which determines the medical aspect of the study of the biochemistry of cobalamin. Cyanocobalamin, containing a CN group as the “top” β-ligand of the cobalt atom, is a commercial form of vitamin B12. Classic PCBs synthesize true vitamin B12 (cobalamin) in large quantities (500-1500 mcg/g).
There are only two enzymes in the human body with coenzymes B12:
- Methylmalonyl-CoA mutase, an enzyme that uses as a cofactor adenosylcobalamin, catalyzes the rearrangement of atoms in the carbon skeleton. As a result of the reaction, succinyl-CoA is obtained from L-methylmalonyl-CoA. This reaction is an important link in the chain of reactions of catabolism of proteins and fats.
- 5-Methyltetrahydrofolate homocysteine methyltransferase, an enzyme from the groupmethyltransferases, using as a cofactor methylcobalamin, catalyzes the conversion of the amino acid homocysteine to the amino acid methionine.
Chemical formula cyanocobalamin: C 63 H 88 Co N 14 O 14 P
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.
As you know, vitamin B12 deficiency leads to the development of pernicious anemia, which in the middle of the 19th century sounded like a death sentence and could not be treated. Ways to get rid of of this disease were discovered by chance during an experiment on dogs. An American doctor, George Whipple, provoked the development of pernicious anemia (pernicious anemia) in experimental animals by causing bleeding, and then fed the dogs a variety of foods to determine which foods speeded up recovery. During an experiment, the scientist discovered that eating liver in large quantities quickly cured a disease caused by blood loss. Based on these data, George Whipple suggested that daily intake This product leads to the elimination of pernicious anemia.
Further clinical researches, conducted by doctors William Parry Murphy and George Richards Minot, were aimed at isolating the “healing” substance from the liver. During tests, pathophysiologists discovered that completely different liver substances can treat anemia in dogs and people. As a result, Murphy and Minot discovered a specific factor found in liver juice in 1926. This was the first impetus for the study of the “fatal” disease.
Over the next 2 years, patients with anemia were supposed to drink juice daily and eat liver “flesh” in large quantities (up to 3 kg). However, long-term consumption of raw liver disgusted patients and the search for an alternative medicine became urgent. In 1928, for the first time, chemist Edwin Cohn developed a liver extract that was 100 times more concentrated than animal by-product. The resulting extract became the first active agent in the fight against a merciless disease.
In 1934, “for their discoveries concerning the use of the liver in the treatment of pernicious anemia,” three American doctors, William Parry Murphy, George Maikot, and George Whipple, received the Nobel Prize. This event ultimately led to the birth of soluble vitamin B12. 14 years later, in 1948, Lester Smith (England), as well as Edward Rickes and Karl Folkers (USA), were the first to obtain pure cyanocobalamin in crystalline form. However, it took several more years to determine its structure using X-ray diffraction analysis, which turned out to be extremely complex.In the late 1950s, scientists also developed a method for obtaining large quantities of the vitamin from bacterial cultures. Thanks to this, a fatal disease of that time called " pernicious anemia", began to respond to treatment. In 1955, the English chemist and biochemist Dorothy Mary Crowfoot Hodgkin determined the spatial configuration, the chemical structure of the molecule, for which she was awarded the Nobel Prize in 1964.
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: .
Propionic acid bacteria synthesize a large number of
, which regulates basic metabolic processes in the body, contributes to increased immune status the body, improve overall well-being by activating protein, carbohydrate and fat metabolism, increase resistance to infectious diseases, improve blood quality, and participate in the synthesis of various amino acids and nucleic acids. However, the synthesis of vitamin B12 by its own intestinal flora person is insignificant. With a lack of vitamin B12, gastrointestinal diseases, dysbacteriosis, anemia. Therefore, probiotic products containing propionic acid bacteria- producers of vitamin B12.
NOTE: It should be especially noted that the content vitamin B12
in products , fermented by the developed starter cultures of propionic acid bacteria is thousands (!) times higher than its amount in products made from traditional starter cultures containing similar cultures, but with the addition of lactic acid bacteria.Among modern methods enrichment fermented milk products vitamins, it is precisely this microbial supersynthesis of vitamin B12 that is 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. It should be noted that vitamin B12 is localized inside PCB cells, for which it is endometabolite. The vitamin enters the gastrointestinal tract only as a result of autolysis of PCB cells. This process is quite pronounced, because (about 30%) dies in aggressive environment Gastrointestinal tract (B12 is absorbed mainly in the ileum). This ensures that the human body is supplied with additional vitamin B12. In this regard, fermented PCB products are of particular importance, where it is possible to increase the accumulation of microbial biomass and, accordingly, the amount of absorbable vitamin B12.
About fermentation, see here: Features of fermentation
About synthesis, see here:
See also:
CASTLE FACTORS
Like most vitamins, B12 can exist in various forms and take 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 intrinsic factor, which is a unique protein(more precisely, a compound consisting of a protein part and mucoids-
secretion secreted by cells of the gastric mucosa)produced in the stomach, vitamin B12 cannot access the 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 belongs to external factors Castle. Interior Castle's 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, with atrophic gastritis , cancer), when part of the stomach or small intestine is removed, etc. Its release 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 translation folic acid into the active form, in the synthesis of methionine, coenzyme A, antioxidant glutathione, succinic acid, myelin. It controls DNA synthesis (therefore, cell division), maturation of red blood cells, increases the level of T-suppressors, which helps limit autoimmune processes. For information on the functions of vitamin B12, see also here at the link arrow
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. Cells become poorly sized and begin to function ineffectively, a condition called pernicious anemia(or "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.
See also: Vitamin B12 in the treatment of diseases of the nervous system
Vitamin B12and musculoskeletal system
At the very Lately 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 women in menopause 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, helping to normalize 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 requirements for vitamin B12 according toMethodological recommendations MP 2.3.1.2432-08about the norms of physiological needs for energy and nutrients for various population groups of the Russian Federation:
- The upper acceptable level has not been established.
- Physiological requirement for adults - 3 mcg/day
Water-soluble vitamin B12 is non-toxic. Vitamin B12 injections are also found to be safe.Because the vitamin is non-toxic, it is widely used in high doses for many types of incurable chronic ailments such as arthritis and psoriasis. It is also used as a remedy to relieve fatigue, ailments and pain.Upper limit of B12 absorption under normal conditions on average is 1.5 mcg when taken with food up to 50 mcg of the vitamin.When vitamin B12 is taken above its binding capacity, the excess is excreted in urine (and feces). Note ed.: in some pathologies, vitamin B12 supplied with food may not be absorbed at all and may be completely excreted from the body - the causes of B12 deficiency will be discussed separately.
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Age |
Daily requirement in vitamin B12, (mcg) |
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Infants |
0 - 3 months |
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4 - 6 months |
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7 - 12 months |
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Children from 1 year to 11 years |
1 — 3 |
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3 — 7 |
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7 — 11 |
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Men (boys, young men) |
11 — 14 |
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14 — 18 |
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> 18 |
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Women (girls, girls) |
11 — 14 |
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14 — 18 |
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> 18 |
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Pregnant and nursing |
Vitamin B12 deficiency
The rate at which B12 levels change depends on how much B12 comes from the diet, how much is excreted, and how much is absorbed. In young children, B12 deficiency can appear much more quickly. In the elderly due to decreased acidity gastric juice, decreased function of parietal (parietal) cells, there is a high risk of developing B12 deficiency. However, up to 100% of B12 taken from food can be excreted in the feces.
Symptoms potentially associated with vitamin B12 deficiency: dandruff, decreased blood clotting, numbness in the legs, decreased reflexes, red tongue, difficulty swallowing, tongue ulcers, fatigue, tingling in the legs, disorder menstrual cycle.
The signs of vitamin B12 deficiency vary widely. Its insufficient amount manifests itself as a complex syndrome that includes physical, neurological and mental disorders. Physical disorders manifest themselves as weakness, fatigue, memory impairment, headaches, tachycardia, pallor skin, dizziness, dandruff, decreased blood clotting, numbness in the legs, decreased reflexes, red tongue, difficulty swallowing, tongue ulcers, fatigue, tingling in the legs, menstrual irregularities. They also include digestive problems: lack of sense of taste, loss of appetite and eventually weight loss. Neurological disorders often appear first. These include:
- paresthesia of fingers;
- constant weakness;
- sensitivity disorders;
- muscle weakness and decreased muscle tone;
- atrophy optic nerve(weakened vision, which can result in blindness);
- pyramidal syndrome.
Mental disorders include cognitive impairment, dementia, behavioral disturbances, apathy, irritability, confusion, or depression. Vitamin B12 deficiency is detected more often in people susceptible to depression than in “normal” (i.e., not prone to depression).Although B12 deficiency is not the only cause of the symptoms listed, B12 deficiency should be considered as a possible underlying factor whenever any of the symptoms mentioned are present.
CAUSES OF VITAMIN B12 DEFICIENCY
See also: Causes of vitamin B12 deficiency in humans (Stroinski, 1987)
Cause of vitamin deficiency AT 12 in 50-70% of patients (more often in young and middle-aged people, somewhat more often in women) there is insufficient secretion of the gastric mucosa of intrinsic factor Castle (IFC), caused by the formation of antibodies to the parietal cells of the stomach that produce IFC, or to the binding site of IFC with vitamin B12. In approximately 20% of cases, there is a hereditary history of VPA deficiency. In these cases, the consequence of vitamin B12 deficiency is the development of so-called pernicious anemia. In addition, vitamin B12 deficiency can be caused by a stomach tumor, gastrectomy, malabsorption syndrome, helminthiasis and dysbacteriosis, and an unbalanced diet. Other reasons include hereditary diseases characterized by a defect in the production of proteins that bind to vitamin B12, or a defect in the formation of active forms of the vitamin; metabolic disorders and/or increased need for vitamins (thyrotoxicosis, pregnancy, malignant neoplasms), as well as long-term use H2 receptor blockers and inhibitors proton pump. It should be noted that the reserve of vitamin B12 in the body, even with limited supply, is enough for 3-4 years.
Stomach problems.
As already indicated (see above), disturbances in the functioning of the stomach can contribute to a lack of vitamin B12. This can happen for two reasons:
Firstly, stomach diseases can cause disruption of the functioning of stomach cells. Cells may stop producing a substance needed to absorb B12 called intrinsic factor. Without intrinsic factor, vitamin B12 cannot be absorbed from the gastrointestinal tract into the body's cells.
Secondly, insufficient secretion of gastric juice. Lack of stomach acid (a condition called hypochlorhydria) reduces the absorption of vitamin B12, since most B12 in foods is attached to food proteins, and stomach acids necessary to separate B12 from these proteins.
Third, small intestinal bacterial overgrowth syndrome ( SIBO), which is caused by a decrease in the secretion of hydrochloric acid in the stomach and impaired motility of the small intestine. During the development of SIBO, various anaerobic and facultative gram-negative aerobes competitively utilize dietary cobalamin. Intrinsic factor inhibits the utilization of cobalamin by gram-negative aerobic flora, but is not able to counteract the gram-negative anaerobic flora that absorb this vitamin.
Intestinal dysbiosis. Today everyone knows about the exceptional importance of intestinal microflora in the regulation of metabolic processes in the body. As practice shows, the main cause of B12 deficiency is not a lack of balanced nutrition, but disturbances in the processes of micronutrient absorption in the small intestine, which are regulated by the host’s own gastrointestinal microflora. Therefore, intestinal dysbiosis is also one of the main causes of B12 deficiency. The causes of microflora imbalance are different (usually secondary), ranging from the diseases described above, to such as: the consequences of intestinal infections, bad habits, other diseases, incl. stress, antibiotic therapy, etc. It is known that in addition to pathogenic bacteria, causing diseases, there are bacteria that use cobalamin for their own purposes, thereby interfering with its absorption by the human body. Based on the above, it would be reasonable to assume that in modern conditions probiotic therapy, incl. using propionic acid bacteria - B12 producers, is effective tool in the prevention of hypovitaminosis B12.
Vegetarianism.
The ability of a strict vegetarian diet to supply sufficient amounts of vitamin B12 remains controversial, despite growing evidence supporting vegetarianism and its nutritional adequacy.
Firstly, most animals, including humans, are able to accumulate and store vitamin B12.The main place accumulation of vitamin B12 The human body contains the liver, which contains up to several milligrams of this vitamin. It enters the liver with animal foods, in particular meat products, or synthesized intestinal microflora, provided that cobalt (Co) is supplied with food. The daily requirement for cyanocobalamin for an adult (from 14 years of age) is approximately 0.003 mg.
Secondly, the unreliability of the plant as a source of vitamin B12. Since no plant contains B12, the amount of vitamin B12 in plant foods depends on microorganisms (bacteria, yeast, mold and fungi) that produce the vitamin. Fermented bean products (tofu, tempeh, miso, tamari, shoyu) may contain significant amounts of vitamin B12 or none at all, depending on the bacteria, molds, fungi and fungi used to produce them. The B12 content of algae also varies depending on the distribution of microorganisms in the surrounding marine environment. Depending on the environment in which they are grown, brewer's yeast and nutritional yeast can be important sources of vitamin B12 in a strict vegetarian diet. Therefore, today in a plant-based diet it is recommended to consume fortified (fermented with B12 producers) foods. See below for fermentation.
What medications affect vitamin B12?
The categories of drugs that can reduce the supply of vitamin B12 in the body include: antibiotics (kanamycin, neomycin), antineoplastic drugs (methotrexate), anticonvulsants (phenytoin, primidone), anti-gout drugs (colchicine), antihypertensive drugs (methyldopa), drugs for the treatment of Parkinson's disease (levodopa), antipsychotics (aminazine), anti-tuberculosis drugs (isoniazid), cholesterol-lowering drugs (clofibrate), potassium chloride, blood sugar-lowering agent.
Smoking and vitamin B12
We will not discuss the relationship between smoking and B12 deficiency here, but will merely comment on one study that some readers have suggested that long-term consumption of large amounts of B12 may increase the risk of cancer. We simply have to make a clarification, since such speculation is presented as evidence, though of who knows what. This is the study we are talking about: Theodore M. Brasky,et. al. Long-Term, Supplemental, One-Carbon Metabolism-Related Vitamin B Use in Relation to Lung Cancer Risk in the Vitamins and Lifestyle (VITAL) Cohort. Journal of Clinical Oncology, 2017. In this work, it was suggested that in men, long-term consumption of large amounts of vitamins B6 and B12 may increase the risk of developing lung cancer (for women, this conclusion was not confirmed in this statistical study).
However, it is worth describing in detail the conditions of the study: men who took part in the statistical (!) study daily (!)within (!) 10 yearsconsumed high doses of vitamin preparations, were aged from 50 to (!) 76 years and had a long (!)
smoking history, which in itself raises many questions regarding the level of reliability of the conclusions drawn about the cause-and-effect relationship of the increased risk of lung cancer. The author of the work, Theodore M. Braschi, put an end to the results obtained. He noted that he plans to hold a second more ambitious study to confirm the results of the first. That is why it is simply unacceptable to present these statistical conclusions as proof of anything. In conclusion, we note that the task itself daily multi-year absorption high doses
vitamin B12 is not placed at all, because without scientific interest, no one needs this and when consuming food products (even fermented PCB) or microbiological dietary supplements (not injections or special vitamin preparations) penetration of excess B12 into organs and tissues physically impossible. Moreover, vitamin B12 is non-toxic andsurplusare excreted from the body(cm. ).
Sources of vitamin B12
So what do we have? Humans and animals usually provide themselves with vitamin B12 as a result of the consumption of foods of animal origin and its production by the microflora of the digestive tract (see: Vitamin B12). However, given that the synthesis of vitamin B12 by intestinal flora is insignificant, the vitamin must enter the body from the outside.
Since vitamin B12 cannot be produced by plants, its content depends on their association with microorganisms (for example, bacteria in the soil). Because of their ability to store vitamin B12, animals contain more of the vitamin than plants.
Therefore, are excellent sources of vitamin B12 limited to animal foods? No. And here, unfortunately, it is not always possible to get a sufficient amount of vitamin B12. This is primarily due to the quality of the products and their industrial processing. If we talk about reliable food sources B12, then today these are the productsfermented by microorganisms that produce cobalamin (B12).The developed technologies now make it possible to obtain B12-containing products from almost any type of food raw material, both plant and animal origin. In this case, propionic acid bacteria are used as powerful B12 producers.
[13-083 ] Antibodies to intrinsic Castle factor, IgG
1620 rub.
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Detection of antibodies to intrinsic Castle factor in the patient’s blood is a test that allows diagnosing the autoimmune cause of vitamin B12 deficiency.
Synonyms Russian
Antibodies to intrinsic Castle factor.
English synonyms
IF Antibody; IF Antibody Type I or Type II; Intrinsic Factor Binding Antibody; Intrinsic Factor Blocking Antibody; Anti-intrinsic Factor.
Research method
Enzyme-linked immunosorbent assay (ELISA).
Units
What biomaterial can be used for research?
Venous blood.
How to properly prepare for research?
- Do not smoke for 30 minutes before the test.
General information about the study
IN medical practice determination of antibodies to intrinsic Castle factor in the blood in combination with clinical manifestations is used to diagnose pernicious anemia.
Pernicious anemia is a type of anemia caused by a deficiency of vitamin B12 in the body. The main causes of this disease include atrophic gastritis, an autoimmune pathology in which the body produces antibodies to the internal Castle factor, which promotes the absorption of vitamin B12 in the intestine. Very rarely, pernicious anemia is inherited (congenital pernicious anemia). In adults, symptoms of such anemia usually appear after the age of 30 years, more often after 60 years.
Some people have no symptoms, but most often the disease may be accompanied by the following clinical manifestations: diarrhea or constipation; increased fatigue, decreased performance, dizziness, loss of appetite, pale skin, decreased concentration, shortness of breath during exercise, swollen red tongue, bleeding gums. With a long-term lack of vitamin B12 in the body, the nervous system can be affected: numbness and tingling in the hands and feet, depression, loss of balance, confusion.
The main focus of therapy is to increase the level of vitamin B12 in the body.
What is the research used for?
- Examination of patients with suspected pernicious anemia;
- differential diagnosis with other anemias;
- For preventive examination healthy people when performance decreases.
When is the study scheduled?
- If diarrhea or constipation is detected; increased fatigue, decreased performance, dizziness, loss of appetite, pale skin, decreased concentration, shortness of breath during exercise, swollen red tongue, bleeding gums, etc.;
- in the presence of Addison's disease, chronic thyroiditis, hyperthyroidism, secondary amenorrhea, type 1 diabetes mellitus, gonadal dysfunction, vitiligo.
What do the results mean?
Reference values: 0 - 6 AU/ml.
If the level of the studied antibodies is within the reference values, it means that the level of intrinsic Castle factor in the body is not reduced due to autoimmune effects, but pernicious anemia may occur.
If the test antibodies are detected in the blood, it means that anemia may be associated with a lack of vitamin B12 in the body.
What can influence the result?
A pronounced comorbid background may reduce the specificity of the method and require targeted differential diagnosis.
Important Notes
- Causes that increase the likelihood of developing the disease include Addison's disease, chronic thyroiditis, hyperthyroidism, secondary amenorrhea, type 1 diabetes mellitus, gonadal dysfunction, vitiligo.
- Vitamin B12 (cyanocobalamin)
- General blood analysis
- Vitamin B9 (folic acid)
- Vitamin B1 (thiamine)
- Vitamin B5 (pantothenic acid)
- Vitamin B6 (pyridoxine)
Who orders the study?
Hematologist, gastroenterologist, therapist, general practitioner.
Literature
- Bunting RW, Bitzer AM, Kenney RM, et al: Prevalence of intrinsic factor antibodies and vitamin B12 malabsorption in older patients admitted to a rehabilitation hospital. JAGS 1990; 38(7):743-747.
- Waters HM, Dawson DW, Howarth JE, et al: High incidence of type II autoantibodies in pernicious anemia. J Clin Pathol 1993; 46(1):45-47.
- Tietz NW (Ed): Clinical Guide to Laboratory Tests, 3rd ed. W. B. Saunders, Philadelphia, PA, 1995.
- Henry JB: Clinical Diagnosis and Management by Laboratory Methods, 20th ed. Saunders, 2001.
- Lahner E, Annibale B; Pernicious anemia: new insights from a gastroenterological point of view. World J Gastroenterol. 2009 Nov 7;15(41):5121-8.
- Malizia RW, Baumann BM, Chansky ME, et al; Ambulatory dysfunction due to unrecognized pernicious anemia. J Emerg Med. 2010 Apr;38(3):302-7. Epub 2007 Dec 3.
- Turner MR, Talbot K; Functional vitamin B12 deficiency. Pract Neurol. 2009 Feb;9(1):37-41.
- Vlasveld LT; Low cobalamin (vitamin B12) levels in multiple myeloma: a retrospective study. Neth J Med. 2003 Aug;61(8):249-52.
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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 up to late stages has mild symptoms, but lesions of the gastric mucosa occur many years before the development of anemia. TO clinical manifestations diseases include weight loss, general weakness, damage to the peripheral nervous system (the most common is paresthesia), 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 research To diagnose pernicious anemia, such as the Schilling test (a method for detecting malabsorption of cyanocobalamin, which involves 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. With absence 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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Castle's internal factor
Castle's internal factor– a protein that is produced in the gastric mucosa that binds, transports and ensures the absorption of vitamin B12. Antibodies to intrinsic Castle factor are complexes that reduce the amount of this glycoprotein. A blood test to determine the content of antibodies of this type is used in gastroenterology, neurology, and hematology. It is prescribed in combination with a clinical blood test, a test for vitamin B12 and antibodies to myelin basic protein. The results are used for early diagnosis of hypoacid gastritis, pernicious anemia, demyelinating diseases of the nervous system, as well as autoimmune pathologies. Blood is taken for testing from a vein. Enzyme immunoassay methods are used to detect antibodies. Normally the result is negative. The study is carried out within 11 working days.
Antibodies to intrinsic Castle factor are specific immunoglobulins that interact with intrinsic Castle factor, disrupting its binding to vitamin B12 and absorption by the small intestinal mucosa. Intrinsic Castle factor is classified as a glycoprotein in its chemical structure. It is produced in the cells of the stomach lining and enters the small intestine. The main function of this protein is to ensure the absorption of vitamin B12. The internal factor is able to bind, transport and stimulate the absorption of cobalamin even with changes in the aggressiveness of gastric juice, increased exposure to pepsin and perchloric acid, so gastritis does not affect the functions of the glycoprotein.
In clinical and laboratory practice, antibodies to intrinsic Castle factor are considered as a highly specific marker of B12-deficiency anemia. There are two types of these immunoglobulins. Blocking antibodies prevent cobalamin from binding to intrinsic factor. They are more active at higher alkalinity internal environment stomach. The other type is binding antibodies. They disrupt the attachment of internal factor with vitamin B12 to the receptors of the intestinal mucosa, that is, they interfere with absorption. The result of the action of both types of antibodies is a deficiency of vitamin B12 in the body.
When testing blood for antibodies to intrinsic Castle factor, the total amount of antibodies of two types is revealed, since their separation is not of particular clinical significance. To perform the analysis, blood is taken from a vein. The presence and concentration of antibodies are determined by the enzyme immunoassay method. The main areas of application of the analysis are hematology and gastroenterology, as auxiliary test it is used in neurology and rheumatology.
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 to early detection 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 V nervous system, therefore, the study of antibodies to the internal factor may 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. That's why this test It is recommended to combine it 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 general analysis blood, 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 performance 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.