Pyridoxine solution for injection 50 mg/ml - - Catalog Production of medicines

pharmachologic effect

Vitamin B6. Entering the body, it is phosphorylated, converted into pyridoxal-5-phosphate and is part of enzymes that carry out decarboxylation, transamination and racemization of amino acids, as well as the enzymatic conversion of sulfur-containing and hydroxylated amino acids. Participates in tryptophan metabolism (participation in the reaction of serotonin biosynthesis). Isolated deficiency of pyridoxine is very rare, mainly in children on special artificial nutrition (manifested by diarrhea, cramps, anemia, and peripheral neuropathy may develop).

Magnesium and vascular endothelial inflammation

During pregnancy, the activity of the body's systemic inflammatory response significantly increases. First, it is inevitable that the mother's immune system will react to fetal tissue. Second, a certain degree of inflammatory component is required for successful blastocyst attachment and invasion [15] and subsequent placental growth. Thirdly, the mother's immune system is important for protecting the fetus from possible intrauterine infections. At least 25% of all preterm births are caused by intrauterine infections. Due to an increase in the levels of pro-inflammatory cytokines - IL-1 (see Fig. 1, color inset)

Figure 1. Spatial structure of interleukin-1 (PDB 4i1b). and TNF - premature uterine contractions occur and, as a result, premature birth [17]. Thus, during pregnancy, the use of drugs that reduce the body’s excessive systemic inflammatory response and at the same time do not interfere with the functionally necessary systemic inflammatory response is required.

Magnesium-based preparations are ideal for solving both problems. Magnesium modulates cellular events associated with inflammation. Experimental work examining magnesium deficiency in rats has shown activation of leukocytes and macrophages, secretion of inflammatory cytokines, acute phase proteins, and increased production of free radicals [14]. Low levels of magnesium in body tissues stimulate the synthesis/secretion of interleukins - IL-1α, IL-6 and monocyte-endothelial interaction mediator protein (VCAM gene). Under conditions of magnesium deficiency, the most noticeable increase in the level of IL-6 and acute phase protein - MCP-1 [4].

Conversely, increasing extracellular magnesium reduces the inflammatory response. High levels of Mg promote the proliferation and migration of endothelial cells, stimulating angiogenesis [4]. Transcriptional studies of the molecular effects of magnesium have shown that magnesium deficiency leads to changes in the transcription of more than 20 genes. For the most part, these are genes involved in the antioxidant response of the cell, regulation of the cell cycle, apoptosis and cell adhesion [16].

Magnesium and atherosclerosis

Pregnant women are relatively young (mostly under 35 years old) women, and, as a rule, they are characterized by a normal condition of the arteries. However, due to widespread malnutrition and the increasing trend towards obesity, atherosclerosis is beginning to play an increasingly important role in the health of pregnant women. The fetus's need for building materials (in particular, fats) also leads to an intensification of fat metabolism and an increase in lipid levels in the blood of a pregnant woman. All this contributes to the formation of atherosclerotic plaques, which are one of the risk factors for thrombophilia.

The formation of atherosclerotic plaques is provoked by an increased inflammatory response of the vascular endothelium and excessive concentrations of lipids in the blood plasma. Lipids obtained from food are converted in the small intestine into 200-500 nm particles - chylomicrons. 99% (by volume) of these fat particles consist of triglycerides (TG) stabilized by apolipoproteins. The ten major apolipoproteins (ApoA1, ApoA2, ApoA4, ApoB48, ApoB100, ApoC1, ApoC2, ApoC3, ApoD, and ApoE) are synthesized and secreted by the liver and small intestinal tissue. When foods consumed contain more fat than the body requires, excess TG and cholesterol are exported from the liver into the blood in the form of VLDL (very low-density lipoprotein) particles, stabilized mainly by apolipoproteins ApoB100, ApoE, as well as ApoC3 and ApoC2.

The cleavage of TG from VLDL by the enzyme LPL (lipoprotein lipase) leads to the formation of LDL (low-density lipoprotein) particles. At the same time, the liver synthesizes small (8-20 nm) HDL (high-density lipoprotein) particles that contain a range of apolipoproteins and serve as “scavengers” of cholesterol from the bloodstream, which they carry back to the liver. If the normal functioning of the fat processing mechanism described above is disrupted due to an unbalanced diet or due to certain genetic defects, then various conditions arise, leading in most cases to the deposition of cholesterol on the walls of blood vessels - the initial stage of atherosclerosis.

In addition to this general scheme of the atherosclerotic process leading to thrombosis, there are a number of other factors that determine the tendency to form atherosclerotic plaques and their parameters. These factors are associated primarily with the processes of inflammatory and immune responses. Causes of inflammation, direct or indirect, include the influence of bacteria, poor diet, destructive habits, and genetic predispositions.

With magnesium deficiency in the blood, the content of TG, chylomicrons, VLDL and LDL is increased. The level of vital HDL, on the contrary, is reduced. Magnesium deficiency affects the fatty acid composition of lipids. Against the backdrop of increased consumption of fats and simple carbohydrates, the need for magnesium increases sharply, the element is rapidly consumed and its excretion in the urine increases.

It should be noted that the molecular mechanisms through which magnesium affects atherosclerotic processes is an issue that requires separate research. From a molecular point of view, magnesium is required by the active sites of mitochondrial enzymes of fatty acid metabolism. These mitochondrial proteins are, first of all, coenzyme A (CoA) ligases of long-chain fatty acids (genes ACSL1, ACSL3, ACSL4, ACSL5, ACSL6) and also acyl-CoA synthases (genes ACSM1, ACSM2A, ACSM2B, ACSM3 and ACSM5 ). Long-chain fatty acid CoA ligases activate fatty acid chains for cellular lipid synthesis and degradation through the β-oxidation pathway. CoA ligases vary in substrate specificity: for example, ACSL1 preferentially uses palmitoleate, oleate, and linoleate; ACSL3 predominantly utilizes myristate, laurate, arachidonate and eicosapentaenoate, while ACSL5 has a very broad spectrum of substrates, including almost all biologically important saturated fatty acids. Acyl-CoA synthases (ACSM) attach chains of medium and short fatty acids to coenzyme A (see Fig. 2, color insert)

Figure 2. Model of the all-atom structure of acyl-CoA synthase. The substrate analogue is shown as a lattice model. All acyl-CoA synthases have very similar full-atomic structures; the magnesium ion (sphere) is an integral part of the active center. and are also characterized by differences in substrate specificity. Magnesium deficiency causes a significant decrease in the catalytic activity of these enzymes, which contributes to the adverse changes in the lipid profile mentioned above.

Magnesium and connective tissue structure

Connective tissue forms the outer lining of the blood vessel. Therefore, the state of connective tissue cannot directly influence the development of thrombophilia. However, with a deficiency of connective tissue, the rather rigid outer lining of the vessels will be damaged, which will inevitably lead to a higher frequency of microdamage to these vessels. Consequently, the tendency to form blood clots will increase.

During pregnancy, both magnesium deficiency and connective tissue deficiency are observed quite often. Connective tissue deficiency is one of the long-term consequences of magnesium deficiency. Previously, we analyzed the molecular mechanisms through which magnesium strengthens the structure of connective tissue [2]. At least 20 proteins are involved in magnesium-dependent regulation of connective tissue. Possible mechanisms of the influence of magnesium deficiency on the synthesis and degradation of connective tissue include activation of matrix metalloproteinases, lysyl oxidase, glutaminase, slowdown of the synthesis of collagen, elastin and hyaluronan (see Fig. 3, color insert).

Figure 3. Magnesium and connective tissue structure: molecular mechanisms. With Mg2+ deficiency, protein synthesis of connective tissue slows down, the activity of matrix metalloproteinases increases, and the extracellular matrix is progressively degraded as the structural support of the tissue (in particular, collagen fibers) is destroyed faster than it is synthesized.

Magnesium and vasoconstriction

Pregnancy often has a stressful effect on the body of the expectant mother. The consequence of constant stress is a chronic increase in the levels of catecholamines: adrenaline and norepinephrine in the blood plasma. The physiological effects of catecholamines are varied: increased heart rate, increased stroke volume, increased blood pressure, glycogenolysis and lipolysis. One of the main physiological effects of catecholamines is vasoconstriction, which reduces blood circulation in the mother-placenta-fetus system and increases the likelihood of thrombus formation.

Magnesium promotes vasodilation through several parallel molecular mechanisms. Catecholamines that enter the bloodstream are rapidly converted to deaminated and other low-active products by monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT). The last enzyme (see Fig. 4 on the color insert)

Figure 4. Spatial structure of catechol-O-methyltransferase. A magnesium ion (sphere) is shown along with a substrate analog bound in the active site of the enzyme (PDB code 1JR4). also catalyzes O-methylation of products produced by MAO, which leads to conjugation with glucuronide and increased urinary excretion. Magnesium ion is an integral part of the active site of COMT, such that sufficient levels of magnesium are necessary for efficient degradation of catecholamine vasoconstrictors.

There are a number of other mechanisms through which magnesium affects vascular smooth muscle. Increased plasma magnesium concentrations correlate with increased synthesis of nitric oxide (a potent vasodilator), in part through increased levels/activity of endothelial NO synthase [13]. Magnesium deficiency promotes an increase in aldosterone levels when stimulated by angiotensin-2, along with a significant increase (up to 75%) in the level of endothelin-1 circulating in the blood (J. Nadler et al., 1993; V. Serebruany et al., 1996).

Pyridoxine, hyperhomocysteinemia and thrombophilia

Elevated plasma homocysteine levels (hyperhomocysteinemia) are one of the additional factors leading to both excessive vasoconstriction (due to increased catecholamine levels [24]) and a proinflammatory effect. A meta-analysis of 11 studies concerning idiopathic pregnancy loss found that elevated homocysteine levels are associated with the disease [12]. Arterial and venous thrombosis occur 2-4 times more often in patients with hyperhomocysteinemia [9, 25].

The main way to compensate for hyperhomocysteinemia is to take B vitamins: folic acid (vitamin B9), pyridoxine (B6) and cyanocobalamin (B12). Pyridoxine, as well as its derivatives (such as pyridoxal, pyridoxal phosphate and pyridoxamine, Fig. 5)

Figure 5. Forms of vitamin B6 (from left to right): pyridoxine, pyridoxal and pyridoxamine. necessary for the metabolism of carbohydrates, proteins and fats, the formation of red blood cells, maintaining sodium-potassium balance and reducing the level of homocysteine in the blood. Vitamin B6 deficiency due to insufficient dietary intake has been associated with increased blood pressure (K. Lal et al., 1995).

From a molecular point of view, pyridoxine deficiency reduces the activity of cystathionine-β-synthetase (CBS, CBS gene, see Fig. 6, color insert),

Figure 6. Cystathionine β-synthetase dimer (PDB code 1jbq). The pyridoxal phosphate molecule is located in the active site. which leads to hyperhomocysteinemia and activation of serine hydroxymethyltransferase (SHMT, SHMT1 gene, see Fig. 7, color insert),

Figure 7. Spatial structure of serine hydroxymethyltransferase (PDB code 1bj4). The pyridoxal phosphate molecule is located in the active site. which leads to increased S-adenosylmethione (SAM) levels [10]. Both high homocysteine levels and high SAM levels correspond to increased blood catecholamine levels due to decreased COMT enzyme activity [24]. A decrease in COMT activity leads to an increase in the biological half-life of catecholamines in the blood and to chronic vasoconstriction.

In addition to its effects on vasoconstriction, pyridoxine also directly affects platelet aggregation. Vitamin B6 significantly prolongs bleeding time (from 4.1 to 6.8 minutes; p = 0.006), namely through inhibition of platelet aggregation when stimulated with ADP or adrenaline (V. van Wyk et al., 1992).

The use of magnesium preparations for thrombophilia in pregnant women in the light of evidence-based medicine

Above, an analysis was carried out of the effects of magnesium and pyridoxine on various pathophysiological processes leading to thromboembolism. These mechanisms (summarized in Fig. 8, see color plate)

Figure 8. Molecular mechanisms of the effects of magnesium and pyridoxine on thrombus formation. based on research in basic medicine and experimental pharmacology. Next, we review evidence-based medicine data on the use of magnesium and pyridoxine preparations for the treatment and prevention of thrombotic complications.

Patients with chronic magnesium deficiency may experience non-obstetric, general somatic diseases: deep vein thrombosis, relatively early (before 50 years) cardiovascular diseases, a negative reaction to estrogen-containing drugs, etc.

Studies of the effect of magnesium on thrombus formation have been carried out at least since the 20s of the last century, and the prescription of magnesium for the treatment/prevention of thrombotic complications has been known for a long time (M. Gorbenko, 1950). The medical community is no less well informed about the intravenous use of magnesium sulfate for the prevention of eclampsia in pregnant women [11]. Magnesium sulfate infusions also prolong clotting time during pregnancy and reduce blood pressure [18].

The use of magnesium has a positive effect on the cardiovascular system of pregnant women. Oral magnesium supplementation reduces platelet-dependent thrombosis in patients with coronary heart disease by 35% [20, 21]. At the same time, a low level of magnesium in the blood corresponds to a 2-fold increase in the risk of developing cardiovascular complications (95% CI 1.2-3.4) [5]. The use of bioabsorbable magnesium-based shunts significantly reduces the incidence of postoperative thrombosis and chronic inflammation [8, 22]. Blood coagulation with too rapid hemodilution is apparently associated with instantaneous decreases in magnesium concentration [19].

There is increasing interest in magnesium as an antithrombotic agent in the management of pregnant women. Congenital and acquired thrombophilia leads to an increased risk of venous thrombosis during pregnancy and the risk of miscarriage. A study involving 289 pregnant women found that the most common causes of recurrent pregnancy loss were estrogen- and androgen-dependent endocrine abnormalities (28%), uterine disorders (10%), antiphospholipid syndrome (4.5%), and autoimmune diseases (1.4%). ), while the etiology of thrombophilias in the remaining patients was not established [3, 26].

Regardless of the specific etiology of thrombophilia, magnesium and other antithrombotic drugs are used to reduce the tendency to thrombosis in pregnant women. A clinical trial demonstrated the effectiveness of antithrombotic therapy with low molecular weight heparins during pregnancy [31]. A meta-analysis of 10 studies (n=627) showed that the combination of heparin with aspirin led to a significant reduction in the incidence of miscarriage compared with aspirin alone (OR = 0.46; 95% CI 0.29-0.71), while the combination of prednisone and aspirin had no such effect [7].

In the Department of Prevention and Therapy of Miscarriage of the Scientific Center for Obstetrics, Gynecology and Perinatology named after. acad. IN AND. Kulakova, Magne B6 has been used as a component of basic therapy since 1995, regardless of the pathogenetic mechanisms of recurrent miscarriage. It is possible to use the drug from early stages of pregnancy, especially in patients with severe pain and a high level of anxiety. We recently conducted a study that analyzed the effectiveness of including Magne B6 in complex therapy for patients with a history of early miscarriages and the threat of termination of this pregnancy [1]. The daily dose of the drug was 4 tablets per day (2 tablets 2 times a day or 1 tablet in the morning, 1 tablet in the afternoon and 2 tablets at night).

An analysis was made of the course of the first trimester, including the incidence of hematomas in the uterine cavity, the development of chronic disseminated intravascular coagulation syndrome, as well as the development of complications in the second and third trimesters of pregnancy with early initiation of therapy with an oral magnesium drug (Magne B6). The study group (main) included 120 married couples with a history of 2 early miscarriages or more. The average age of the patients was 32.1±1.8 years. In the anamnesis of married couples, from 2 to 8 spontaneous abortions were noted, on average 3.4 per patient.

In most married couples, the genesis of miscarriage was polyetiological. When analyzing the leading causes of miscarriage, it was found that hyperandrogenism as the main factor was identified in 36.6% of women, antiphospholipid syndrome and sensitization to hCG - in 40.0%, HLA compatibility - in 18.3%, uterine malformations - in 5 ,1%. Using the method of selecting pairs from the department's archival material for 1994, 120 patients with similar data on age, parity, reasons and timing of termination of pregnancy (control group) were selected.

When Magne B6 was included in the complex therapy of women with recurrent miscarriage in the first trimester, the following results were achieved:

— in 83.3% — rapid normalization of uterine tone;

- in 79.2% of observations - normalization of sleep, reduction of anxiety, restlessness;

- reduction in the incidence of hematoma formation in the uterine cavity in the first trimester - 17.5% in the main group compared to 29.2% in the control group (p<0.05);

— reduction in the need for antiplatelet therapy from 37.5 to 19.2% (p<0.05);

- the prescription of anticoagulants was required with almost the same frequency in the main and control groups - in 27.5 and 29.2% of patients, respectively, which is likely due to a significant percentage of patients with antiphospholipid syndrome.

The threat of late miscarriage and premature birth occurred in 18.3 and 30%, respectively—much less often in the group of patients taking magnesium. In addition, the use of Magne B6 allowed the majority of patients to avoid the use of β-mimetic and other tocolytic agents. The pregnancy rate in the main group of women was 96.7.

Thus, Magne B6 ensures an optimal level of cellular metabolism, adequately relaxes the muscles of the uterus, acting as an antiplatelet agent and a mild tranquilizer. Along with etiopathogenetic methods of treatment in women with habitual early miscarriage, it is an effective means of treating threatened miscarriage. In addition, when prescribed early in the first trimester of pregnancy, Magne B6 helps to promptly replenish magnesium deficiency and prevent the development of other complications in the second and third trimesters (such as placental insufficiency, intrauterine growth retardation, gestosis, threat of premature birth). Magne B6 can be used both in inpatient and outpatient settings and as an independent remedy. The use of magnesium as a drug that potentiates other treatment methods in patients with miscarriage is promising.

Pregnancy places special demands on the mother's health and often provokes secondary diseases (arterial hypertension, gestational diabetes, thromboembolism). However, secondary diseases can be effectively compensated for by proper nutrition, lifestyle and pharmacotherapy. Excessive thrombus formation not only leads to thrombosis in the maternal body (including deep vein thrombosis and thromboembolic complications), but also to spontaneous abortion. Therefore, thromboembolic and hypercoagulable conditions that occur during pregnancy require special attention from an obstetrician-gynecologist. Since the mother-placenta-fetus system is extremely sensitive to pharmacological influences, the safest thrombolytics, disaggregants and anticoagulants are needed. The molecular mechanisms of the effect of magnesium on the hemostatic system discussed in this article indicate disaggregant, anticoagulant, vasodilator and other positive effects. Evidence-based medicine data substantiate the advisability of using magnesium as part of complex therapy and prevention of spontaneous abortion. The material presented is also of some interest to therapists. The continuity of patient management from obstetricians-gynecologists to therapists will contribute to the early prevention of widespread “diseases of civilization”, i.e. cardiovascular, oncological, diabetes, obesity throughout the subsequent life of women.

This work was carried out with the support of the Russian Foundation for Basic Research (RFBR).

special instructions

Vitamin B6 is found in plants and animal organs, especially in unrefined cereal grains, vegetables, meat, fish, milk, cod and cattle liver, and egg yolk. Yeast is relatively high in vitamin B6. The need for vitamin B6 is satisfied by food: it is partially synthesized by the intestinal microflora. The daily requirement for pyridoxine for adults is 2-2.5 mg; for children from 6 months to 1 year - 0.5 mg, 1-1.5 g - 0.9 mg; 1.5-2 years - 1 mg; 3-4 years - 1.3 mg; 5-6 years - 1.4 mg; 7-10 years - 1.7 mg; 11-13 years - 2 mg; for boys 14-17 years old - 2.2 mg; for girls 14-17 years old - 1.9 mg. For women - 2 mg and additionally during pregnancy 0.3 mg, during breastfeeding - 0.5 mg. In case of severe liver damage, pyridoxine in large doses can cause deterioration of liver function. When determining urobilinogen using the Ehrlich reagent, it may distort the results.

Impact on the ability to drive vehicles and operate machinery

During the treatment period, it is possible to drive vehicles and engage in potentially hazardous activities that require increased concentration and speed of psychomotor reactions.

Pyridoxine

Pyridoxine is vitamin B6 in tablet or injectable form. Strictly speaking, vitamin B6 is represented by three different vitamers, transforming into one another - pyridoxine, pyridoxal and pyridoxamine, but only one of them is used as a drug - pyridoxine. Although, by and large, this is not so important: in any case, when passing through the liver, all pyridoxine vitamers are converted into pyridoxal, which, in turn, is phosphorylated to form pyridoxal phosphate. Putting aside all these biochemical nuances, let's move on to the main thing, namely: what role does vitamin B6 play in the human body. So, pyridoxine is an active participant in metabolic processes; it ensures the normal functioning of the central and peripheral nervous system. Pyridoxine (or rather, its phosphorylated form) is a coenzyme of a number of enzymes involved in non-oxidative amino acid metabolism (including the processes of transamination and decarboxylation). Without pyridoxine, it is difficult to imagine the exchange of methionine, cysteine, tryptophan, histamine, glutamic and some other amino acids. Vitamin B6 helps normalize lipid metabolism. The daily requirement for this vitamin is 2 mg (men) and 1,702.3 mg (women). Considering the fact that the biological role of pyridoxine is strongly associated with protein metabolism, its recommended amount is also calculated based on the daily intake of this macronutrient: 0.016-0.032 mg of vitamin per 1 g of food protein. Pyridoxine is widely distributed in both animal and plant foods. The richest foods in this vitamin are chicken breast, sunflower seeds, wheat bran, soybeans, walnuts, avocados, and potatoes. Pyridoxine is well absorbed both orally and when administered by injection, and its absorption in the small intestine occurs through passive diffusion, and this process is not saturable. In the blood, pyridoxine circulates in a close “embrace” with albumin and hemoglobin. The main storage site for the vitamin is striated muscles, which accumulate about 80-90% of all pyridoxine.

Hypovitaminosis B6 in isolated form practically does not occur in clinical practice: to date, only 3 such cases have been described. Meanwhile, pyridoxine preparations are in demand for a fairly wide range of diseases and deficiency conditions. Thus, vitamin B6 is used to treat sideroachristic anemia associated with a lack of α-aminolevulinic acid synthase. Its result is a disruption of the formation of the heme protoporphyrin ring, and therefore the latter cannot be integrated into the heme even against the background of a high iron content in the body, which deprives red blood cells of hemoglobin. Pyridoxine is used in pediatrics for the correction of pyridoxine-associated seizure syndrome. This is a genetically determined disease in which the process of decarboxylation of glutamic acid into gamma-aminobutyric acid is disrupted. In the presence of this pathology, children begin to have tonic-clonic seizures 2-4 hours after birth, which are practically uncontrollable with the help of classical anticonvulsants. Some drugs (for example, D-penicillamine, hydralazine, isoniazid, cycloserine) can inactivate pyridoxine in neurons of the central nervous system, resulting in neurotoxic reactions. To prevent such undesirable effects, vitamin B6 is prescribed at a rate of 1 to 10 (10 mg of vitamin for every 100 mg of the above drugs). Pyridoxine has another, rather specific area of application: it is indicated for women who do not tolerate oral contraceptives well in order to eliminate headaches, increased excitability, and sleep disturbances. Hypervitaminosis B6 is an extremely rare phenomenon, to say the least. In some cases, pyridoxine may be contraindicated, for example, it is incompatible with levodopa, used to treat Parkinson's disease. By activating decarboxylases in the gastrointestinal tract, the drug will destroy levodopa before it enters the central nervous system.

Directions for use and doses

Parenteral (subcutaneous, intramuscular or intravenous). The drug is administered by injection when it is impossible to take it orally (in case of vomiting or in case of impaired absorption in the intestine).

Prevention. Adults - 2 - 5 mg/day, children from 0 months - 2 mg/day.

Treatment. Adults - 50-100 mg/day in 1-2 doses, children from 0 months - 20 mg. The course of treatment for adults is 1 month, for children - 2 weeks.

With concomitant therapy with anti-tuberculosis drugs - 5-10 mg/day.

For the treatment of pyridoxine-dependent convulsive syndrome in adults - intravenously or intramuscularly - 30-600 mg; children from 0 months - 10-100 mg daily.

Vitamin B6 (pyridoxine, pyridoxal, pyridoxamine, etc.)

Vitamin B6

and its main forms:
pyridoxine
(or
pyridoxole
),
pyridoxal, pyridoxamine
, etc. - a group of biologically active compounds that are part of enzymes that catalyze the transamination and decarboxylation of amino acids.

Basic functions and intake rates of vitamin B6

According to Methodological Recommendations MP 2.3.1.2432-08 “Norms of physiological needs for energy and nutrients for various groups of the population of the Russian Federation”, approved by Rospotrebnadzor on December 18, 2008, vitamin B6 (pyridoxine) in the form of its coenzymes is involved in the transformation of amino acids and the metabolism of tryptophan , lipids and nucleic acids, participates in maintaining the immune response, processes of inhibition and excitation in the central nervous system, promotes the normal formation of red blood cells, maintaining normal levels of homocysteine in the blood.
Insufficient intake of vitamin B6 is accompanied by decreased appetite, impaired skin condition, and the development of homocysteinemia and anemia. The average consumption in different countries is 1.6-3.6 mg/day, in the Russian Federation - 2.1-2.4 mg/day. Insufficient supply of this vitamin is found in 50-70% of the population of the Russian Federation. The established level of requirement in different countries is 1.1-2.6 mg/day. The upper permissible level of consumption is 25.0 mg/day. The physiological need for adults is 2.0 mg/day. The physiological need for children is from 0.4 to 2.0 mg/day. The 2015–2020 Dietary Guidelines for Americans (official publication of the US Department of Health) recommend the following daily intakes of vitamin B6:

children under 3 years old - 0.5 mg
children from 4 to 8 years old - 0.6 mg
children from 9 to 13 years old - 1 mg
girls from 14 to 18 years old - 1.2 mg
women from 19 years to 50 years inclusive - 1.3 mg
boys and men from 14 to 50 years inclusive - 1.3 mg
women 51 years and older - 1.5 mg
men 51 years and older - 1.7 mg

Pyridoxine is the international nonproprietary name of the drug

In the ATC, pyridoxine is classified in the “A11 Vitamins” group, the “A11HA Other pure vitamins” subgroup. The code for pyridoxine (vitamin B6) is A11HA02. Pharmacological group “Vitamins and vitamin-like products”.

Pyridoxine

Pyridoxal

Pyridoxamine

Pyridoxal phosphate

Indications for use of vitamin B6 vitamin

Vitamin B6 is indicated for:

deficiency of vitamin B6 in the patient’s body
peptic ulcer of the stomach and duodenum
hepatitis
hypochromic and microcytic anemia
parkinsonism
chorea
toxicosis of pregnant women
dermatitis
exudative diathesis
neurodermatitis
psoriasis

Compatibility of pyridoxine with other drugs

Pyridoxine combines well with cardiac glycosides, asparkam, and glutamic acid.
Strengthens the effect of diuretics, weakens the effect of levopod. The effect of pyridoxine is weakened by corticosteroids, isoniazid, anticonvulsants, penicillamine, hydralysine, estrogen-containing oral contraceptives, cycloserine. Pyridoxine is pharmaceutically incompatible with vitamins B1 and B12, in powder with ascorbic and nicotinic acids.* *Instructions for medical use of the drug PYRIDOXINE, approved on January 15, 2004 by the Head of the Department of State Control of Medicines and Medical Equipment of the Ministry of Health of the Russian Federation V.E. Akimochkin.

Sources of Vitamin B6

Vitamin B6 (pyridoxine) is sold as a medicine or dietary supplement in the form of a single drug, as well as as part of many vitamin and mineral complexes: Bio-Max, Complivit, Vitrum, Selmevit, Hexavit, Multi-Tabs and others.
Pyridoxine is usually included in infant formula (Kozhevnikova E.N.). Neuromultivit multivitamins, approved for use in Russia, Benexol (approved in the European Union) and some others, contain three B vitamins: thiamine (B1), pyridoxine (B6) and cyanocobalamin (B12).

Vitamin B6 is produced by human intestinal bacteria, in particular bifidobacteria, lactobacilli and Escherichia coli.

Long-term use of B vitamins increases the risk of developing lung cancer in men

According to researchers from Ohio, Seattle and Taipei:**

Taking high doses of vitamins B6 or B12 by men for 10 years is associated with a 30-40% increase in the likelihood of developing lung cancer. Male smokers are even more likely to
There is no relationship in women or when taking B vitamins in foods

**Source: Brasky TM, White E, Chen CL.
Long-Term, Supplemental, One-Carbon Metabolism-Related Vitamin B Use in Relation to Lung Cancer Risk in the Vitamins and Lifestyle (VITAL) Cohort. J Clin Oncol. 2022 Aug 22 . doi: 10.1200/JCO.2017.72.7735. PMID: 28829668. Vitamin B6 has contraindications, side effects and application features; consultation with a specialist is necessary.

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Side effect

Allergic reactions, hypersecretion of hydrochloric acid, numbness, a feeling of constriction in the limbs - a symptom of “stockings” and “gloves”, decreased lactation (sometimes this is used as a therapeutic effect); convulsions (occur only with rapid administration).

Overdose

Symptoms Metabolic disorder, manifested by the accumulation of lactic acid in the myocardium, muscles, liver and kidneys with a simultaneous decrease in glycogen content in them.

There may be patches of baldness.

Possible inhibition of activity against the blood coagulation system.

Treatment. The drug is discontinued. Treatment is symptomatic. There is no special antidote.