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Vitamin k levels 8th day


Scientific Evidence For Circumcision On The Eighth Day

Circumcision is the removing of the male foreskin and as a consequence, it is a rather bloody process. Therefore, here we provide scientific evidence for why circumcision has to be on the eighth day.

 

4 thousand years ago, Yahweh instructed Abraham to circumcise males on the eighth day:

 

This is My covenant, which you shall keep, between Me and you and your descendants after you: every male among you shall be circumcised. And you shall be circumcised in the flesh of your foreskin, and it shall be the sign of the covenant between Me and you. And every male among you who is eight days old shall be circumcised throughout your generations, a servant who is born in the house or who is bought with money from any foreigner, who is not of your descendants. (Genesis 17:10-12 NASB)

 

Abraham followed this prescription with his son Isaac:

 

Then Abraham circumcised his son Isaac when he was eight days old, as God had commanded him.  (Genesis 21:4 NASB; cf. Acts 7:8)

 

Some 600 years later Yahweh gave Moses the same instruction for the Israelites:

 

On the eighth day the flesh of his foreskin shall be circumcised. (Leviticus 12:3 NASB)

 

Why did Yahweh order circumcision on the 8th day for Abraham’s male descendants? Why not sooner or later? Why did it need to be on Day Eight?

 

Scientific Evidence For Circumcision On The Eighth Day

 

In the 1930s, Danish researcher Henrik Dam and American researcher Edward Doisy found that which was required for blood to clot. They shared the 1943 Nobel Prize in Medicine for this research.

 

The human body has 2 blood clotting elements. One of them is called Vitamin K. Vitamin K is not formed in the body up until the 5th to the 7th day.

 

The 2nd clotting factor which is essential is called Prothrombin. It surprisingly enough develops to 30% of normal by the 3rd day of life and after that with seeming in-consequence, peaks at 110% on the 8th day, just before leveling off at 100% of normal.

 

If vitamin K is not present when a baby boy is circumcised, the baby will bleed to death. The reason why Yahweh established Day Eight for circumcision is that vitamin K peaks in a newborn at 8 days of age. The 8th day is the optimum day for circumcision because of the highest presence of the clotting factor vitamin K.

 

Today when baby boys are circumcised within a couple of days of birth, they are administered vitamin K to help with blood clotting.

 

How did Abraham and Moses know to circumcise on the 8th day? Solely the Creator, who understands every intricate detail of human physiology (since He made it), could have disclosed this to them.

 

Return from “Scientific Evidence For Circumcision On The Eighth Day” to “Scientific Evidence For The Bible“

Vitamin K in neonates: facts and myths

Blood Transfus. 2011 Jan; 9(1): 4–9.

doi: 10.2450/2010.0034-10

1 and 2

Author information Article notes Copyright and License information Disclaimer

Vitamin K was first discovered in the early 1930s by the Danish biochemist Henrik Dam who observed – while studying cholesterol metabolism in chickens – that chicks fed with a diet free of sterols and low in fat tended to develop subcutaneous and intramuscular haemorrhages. Further studies on different foods led to the discovery of an "anti-haemorraghic factor", which was designated vitamin K (with the "K" standing for "Koagulations-Vitamin") given that it was essential for normal haemostasis1.

The term vitamin K actually denotes a group of lipophilic, hydrophobic vitamins that belong to the class of 2-methyl-1,4-naphthoquinone derivatives. All the members of the vitamin K group share a common methylated naphthoquinone ring structure, but have different aliphatic side chains attached at the 3-position. The naturally occurring compounds are vitamin K1 (also known as phylloquinone, phytomenadione or phytonadione), and vitamin K2 (also known as menaquinone or menatetrenone). The former compound is the primary source of vitamin K in humans. It is acquired through the diet and is prevalently present in leafy green vegetables such as spinach, Swiss chard, Brassica (e.g. cabbage, kale, cauliflower, turnip, and Brussels sprout), some fruits such as avocado, banana and kiwi, as well as in some vegetable oils, especially soybean oil. Interestingly, cooking does not remove significant amounts of vitamin K from these foods. Many bacteria that colonise the human intestine (especially Bacteroides) synthesise vitamin K2 or menaquinone, which is used as a redox reagent in electron transport and oxidative phosphorylation. There is, however, ongoing debate on whether bacterial synthesis of vitamin K in the intestine provides a significant supply of this vitamin in humans. The colon contains a large reservoir of bacterial vitamin K2 (~2 mg), but it is now undeniable that this pool represents only about 10% of normal human requirements and is, therefore, insufficient to satisfy these requirements. Furthermore, there is some evidence of poor bioavailability of this intestinal source of vitamin K. Bile salts are necessary for effective absorption of vitamin K, but are not present in the colon, and the intestinal synthesis of vitamin K is not sufficient to compensate for deficiency due to biliary obstruction. Moreover, intestinal menaquinones are enveloped within the bacterial membranes and are, therefore, poorly available for intestinal adsorption. Taken together, these data argue against the concept of the colon as a significant source of vitamin K for human use, so that patients at risk of deficiency remain those who cannot absorb vitamin K from the small intestine2.

Fasting vitamin K1 reference values in healthy adults range from 0.15 to 1.0 μg/L (median 0.5 μg/L)2. The average liver storage pool of phylloquinone in adults is around 9 μg, but might vary widely on an inter-individual basis. The liver, moreover, contains a larger pool of vitamin K2 (~90% of total liver vitamin K stores) which, therefore, represents a reservoir against vitamin deficiency when the more labile vitamin K1 stores are depleted. Other extra-hepatic tissues, especially the brain, kidney, and pancreas, store additional amounts of vitamin K2 (usually <2 pmol/g), which probably originates from endogenous synthesis through the metabolism of vitamin K13. Isotopic studies are consistent with a high turnover rate of vitamin K1, in that up to 70% of the oral dose is excreted in the bile and urine within a few days2.

According to the U.S. Institute of Medicine, the recommended dietary allowance (i.e., the daily intake sufficient to meet the requirements of nearly all healthy individuals) of vitamin K is 120 μg in adult men and 90 μg in adult women4, but it is much lower in other countries and Europe (including Italy), where, for example, a daily average of ~1 μg per kg of body weight is recommended5. The Third National Health and Nutrition Examination Survey set the thresholds of adequate vitamin K intake as 2 μg/die for infants in the first 6 months of life and 2.5 μg/die for infants aged 7–12 months6. After this age, the adequate intake progressively increases from 30 μg/die in children aged 1–3 years, up to 75 μg/die in adolescents (up to 18 years old).

While vitamin K1 is commercially manufactured for medicinal use under several brand names (Phylloquinone®, Phytonadione®, AquaMEPHYTON®, Mephyton®, Konakion® ), there are three additional synthetic forms of vitamin K (i.e., vitamin K3, K4, and K5), which are used in many areas including the pet food industry (vitamin K3) and to inhibit fungal growth (vitamin K5). A water-soluble preparation of vitamin K3 (menadione) is also available for adults.

The vitamins belonging to the K group are involved in the carboxylation of glutamate residues in proteins, to form gamma (γ)-carboxyglutamate residues (Gla-residues), typically located within Gla domains. These Gla-residues, which are usually involved in calcium binding, are essential for the function of most – if not all - known Gla-proteins 7. Vitamin K is essential for the function of several proteins involved in blood coagulation (prothrombin, also know as factor II, factors VII, IX, and X, protein C, protein S, and protein Z)8, bone metabolism (osteocalcin, periostin and matrix Gla protein), as well as vascular biology, cell growth, and apoptosis (growth-arrest-specific gene 6 protein)2,9. A poor vitamin K status is, therefore, currently regarded as a risk factor not only for bleeding, but also for increased postmenopausal bone loss and arterial calcification, especially in diabetics and in patients with chronic renal disease.

The pivotal importance of vitamin K in haemostasis arises from the fact that all vitamin K-dependent coagulation factors require γ-carboxylation of glutamic acid residues at their Gla domains to enable binding of calcium and attachment to phospholipid membranes. This enzymatic reaction is catalysed by a microsomal, vitamin K-dependent enzyme, γ-glutamyl carboxylase, which in turn is linked to a cyclic salvage pathway known as the vitamin K epoxide cycle. This carboxylation process necessarily requires a functional vitamin K cycle to produce the active vitamin K co-factor (vitamin K quinole) for the γ-carboxylase which post-translationally modifies the precursors of the vitamin K-dependent proteins (). When the cyclic inter-conversion of vitamin K to its 2,3 epoxide is blocked, as in the case of oral anticoagulant therapy with coumarin derivatives, the net effect is the appearance in plasma of coagulation factors called PIVKA (Protein Induced by Vitamin K Absence), which are virtually non-functional for the clotting process10.

As previously described, only a very small amount of vitamin K is necessary for blood coagulation in humans. Dietary deficiency of vitamin K is, therefore, extremely rare in adults, and, when it does occur, it is usually associated with profoundly inadequate dietary intake, intestinal disorders (e.g., regional enteritis, cystic fibrosis, intestinal resection), malabsorption and, to a lesser extent, decreased production by normal flora (e. g., during the use of a broad spectrum antibiotic) and renal failure2. Vitamin K deficiency is, however, much more frequent in neonates, due to both endogenous and exogenous deficiency. The former case, which is probably less clinically significant, has been attributed to insufficient intestinal colonisation by bacteria, whereas the latter case arises from poor placental transport of the vitamin and its low concentration in breast milk. The main exogenous source of vitamin K in neonates, which is almost exclusively milk, cannot adequately compensate for deficient endogenous production, since human breast milk contains between 1 and 4 μg/L of vitamin K1 (and a much lower concentration of vitamin K2).

As in other circumstances in science and medicine, there is an apparent paradox in haemostasis in neonates in that prolonged global coagulation tests (i.e., activated partial thromboplastin time and prothrombin time) do not translate into a particular bleeding phenotype. In fact, it is now clear that the physiology of haemostasis in childhood differs considerably from that in adults11,12. Studies in humans and animals clearly indicate that coagulation factors in neonates are qualitatively similar, in terms of molecular weights and degree of glycosylation, to those in adults. The greatest difference between the two age periods is quantitative, with plasma levels of many coagulation factors being different throughout childhood from those found in adults, with some of the deficits being attributed to vitamin K deficiency.

As previously highlighted, neonates are prone to vitamin K deficiency due to the limited stores at birth and insufficient intake13. Vitamin K deficiency-related bleeding (VKDB) is defined as a bleeding disorder in which the coagulation is rapidly corrected by vitamin K supplementation. The diagnosis is suggested by an international normalised ratio =4 or a prothrombin time =4 times the control value in the presence of a normal platelet count and normal fibrinogen level. Confirmation of the diagnosis requires measurement of the specific vitamin K-dependent factors (II, VII, IX, X) whose levels are rapidly corrected by the parenteral administration of 1 mg vitamin K14. VKDB is usually classified by aetiology (idiopathic and secondary) and by the age of onset (early, classical and late)14. In idiopathic VKDB no cause other than breast-feeding can be demonstrated. In secondary VKDB there is usually an underlying cause, such as the effect of drugs that have been given to the mother or infant or a hereditary hepatobiliary/malabsorption disease (e.g., biliary atresia, a-1-antitrypsin deficiency, cystic fibrosis)15. In addition, autosomal recessive vitamin K-dependent coagulation factor deficiencies (VKCFD), due to mutations in the gene encoding for g-glutamyl carboxylase (VKCFD type I) and in the gene encoding for vitamin K epoxide reductase (VKCFD type II), have been reported8.

According to the age of onset, early VKDB presents within 24 hours of birth and is almost exclusively seen in infants of mothers taking drugs which inhibit vitamin K. These drugs include anticonvulsants (carbamazepine, phenytoin and barbiturates), antituberculosis drugs (isoniazid, rifampicin), some antibiotics (cephalosporins) and vitamin K antagonists (coumarin, warfarin). The clinical presentation is often severe with cephalic haematoma and intracranial and intra-abdominal haemorrhages16. The incidence of early VKDB in neonates of mothers taking these drugs without vitamin K supplementation varies from 6% to 12%17,18.

Classical VKDB occurs between 24 hours and 7 days of life and is associated with delayed or insufficient feeding. The clinical presentation is often mild, with bruises, gastrointestinal blood loss or bleeding from the umbilicus and puncture sites. Blood loss can, however, be significant, and intracranial haemorrhage, although rare, has been described15. Estimates of the frequency vary from 0.25% to 1.5% in older reviews19 and 0–0.44% in more recent reviews20.

Late VKDB is associated with exclusive breast-feeding. It occurs between the ages of 2 and 12 weeks. The clinical presentation is severe, with a mortality rate of 20% and intracranial haemorrhage occurring in 50%. Persistent neurological damage is frequent in survivors. In fully breast-fed infants who did not receive vitamin K at birth, the incidence is between 1/15,000 and 1/20,000. Babies with cholestasis or malabsorption syndromes are at particular risk21.

Once the diagnosis of VKDB has been confirmed, intravenous vitamin K should be administered to correct the existing deficiency. In the presence of major bleeding, factor replacement therapy may also be required with fresh-frozen plasma or prothrombin complex concentrates15. As regards the prevention of VKDB, the best prophylactic method has been the subject of considerable debate in recent years and still remains to be completely resolved22. The dispute originated from the publication of two retrospective studies in the early 1990s, in which a possible association between vitamin K injections in neonates and the development of childhood leukaemia and other forms of cancer was suspected23,24. This alarming suspicion was, however, confuted by two large retrospective studies in the USA and Sweden, which failed to find any evidence of a relationship between childhood cancers and vitamin K injections at birth25,26. A further pooled analysis of six case-control studies, including 2,431 children diagnosed with childhood cancer and 6,338 cancer-free children, also confirmed the lack on any epidemiological association between vitamin K injections in neonates and an increased risk of leukaemia27. Although it might be concluded that there is no definitive evidence, the confirmed benefits of vitamin K prophylaxis seem to largely outweigh the hypothetical association with childhood cancer28,29.

In 2003 the American Academy of Pediatrics recommended that vitamin K1 should be given to all neonates as a single, intramuscular dose of 0.5 to 1 mg29, and this recommendation was recently reaffirmed in 200930. A similar recommendation was issued and reaffirmed in 2009 by the Canadian Paediatric Society and the Committee on Child and Adolescent Health, College of Family Physicians of Canada. Accordingly, it is recommended that vitamin K1 should be given as a single intramuscular dose of 0.5 mg (for babies weighing 1,500 g or less at birth) or 1.0 mg (for babies weighing more than 1,500 g at birth) to all neonates within the first 6 hours after birth following initial stabilisation of the baby and an appropriate opportunity for maternal (family)-baby interaction31. Several European countries are increasingly moving towards a uniform policy. Prophylaxis with 1 mg vitamin K was endorsed by the UK Department of Health in 1998, while no preference was stated for either administration route (i.e., intramuscular or oral), concluding that this is a matter for professionals and services to agree locally32. In the 2008 guidelines of the UK National Health System, it is, however, recommended that babies weighing less than 2. 5 kg should be administered 400 μg/kg, whereas the dose for babies weighing more than 2.5 kg is 1 mg. It is especially important that babies at extra risk receive vitamin K via the intramuscular route. When the intramuscular route is declined by the parent, two oral doses of 2 mg should be offered instead (the first dose within 6 hours of birth, and the second between 4 – 7 days of age)33. A consensus conference of the Italian Society of Neonatology held in 2004 established that 0.5 mg of vitamin K should be administered intramuscularly at birth, followed by 25 μg/die orally from the second to the fourteenth week of life. An alternative strategy accepted by the consensus conference is the administration of 2 mg of vitamin K at birth, followed by 25 μg/die from the seventh day to the fourteenth week of life34.

It should, however, be noted that Kumar et al. found extremely high plasma K levels on day 14 of life in premature infants (<28th gestational week) who received 1 mg of vitamin K intramuscularly shortly after birth35. In another study, by Costakos et al., preterm neonates who were given 0.5 to 1 mg vitamin K prophylaxis also showed vitamin K levels that were 1,900 to 2,600 times higher (2 days afterwards) and 550 to 600 times higher (10 days afterwards) than normal adult plasma values (0.5 ng/mL)36.

The haemostatic system is not fully mature until 3 to 6 months of age. It is, therefore, essential to acknowledge that the differences observed between adults and infants are probably physiological and do not always reflect an underlying pathological condition. Several clinical observations support the hypothesis that children have natural protective mechanisms that justify the existence of these broad variations, since they have both an increased capacity to inhibit thrombin and a decreased capacity to generate it11,12. Despite the presence of specific homeostatic mechanisms equilibrating the haemostatic balance in neonates and infants, the concentration and activity of vitamin K-dependent procoagulant factors might be dramatically reduced due to insufficient storage and poor transfer of vitamin K across the placental barrier. Although haemostasis might still be "appropriate" and the vast majority of neonates would not bleed, it is now universally accepted that all infants should be given prophylaxis with vitamin K at birth in order to prevent classical and late VKDB37,38. Although both intramuscular and oral administration of 1 mg of vitamin K protect against classical VKDB, a single oral dose does not protect all infants against late VKDB. The intramuscular route of administration of vitamin K prophylaxis has, therefore, been universally adopted, but oral administration should be continued subsequently, according to one of the available guidelines (). This approach seems to effective at preventing VKDB, but also has some drawbacks, the foremost being the fact that available commercial products cost a hundred times more than the basic cost of their one active ingredient, so that broadening this policy to developing countries might be challenging22.

Table I

Summary of the available recommendations about vitamin K administration in neonates.

OrganisationVitamin K dosage
American Academy of PediatricsSingle intramuscular dose of 0.5 to 1 mg
Canadian Paediatric Society, Committee on Child and Adolescent Health, College of Family Physicians of Canada.Single intramuscular dose of 0.5 mg (birthweight =1,500 g) or 1.0 mg (birthweight >1,500 g) within the first 6 h after birth
UK Department of Health in 1998Single intramuscular or oral dose of 400 μg/kg (babies <2.5 kg) or 1 mg (babies >2. 5 kg)
Italian Society of Neonatology (two alternatives)- Single intramuscular dose of 0.5 mg at birth, followed by 25 μg/die orally from the 2nd to the 14th week.
- Single intramuscular dose of 2 mg at birth, followed by 25 μg/die from the 7th day to the 14th week

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Vitamin K test with 30% discount at Lab4U in Moscow

Test description

Vitamin K (phylloquinone) - belongs to the group of fat-soluble vitamins necessary for the synthesis of proteins that provide a sufficient level of coagulation. In nature, fat-soluble vitamin K is represented by two forms: contained in plant foods K1 (phylloquinone) and synthesized by intestinal bacteria K2 (menaquinone). Vitamin K regulates the processes of blood clotting in the body, accelerates wound healing, it is necessary for the normal activity of liver cells.

Test Method - HPLC/MS (High Performance Liquid Chromatography with Mass Spectrometry)

Test Material — Venous blood with EDTA

Due date

The analysis will be ready in within 5 days, excluding Saturday, Sunday and the day of collection. The term can be extended by 1 day if necessary. You will receive results by email. email as soon as it's ready.

Deadline: within 5 days, excluding Saturday, Sunday and the day of sampling, excluding Saturday and Sunday (except for the day of taking the biomaterial)

How to prepare

In advance

Talk to your doctor about taking your medications the night before and on the day of your blood test, and any other additional preparations.

Do not take a blood test immediately after X-ray, fluorography, ultrasound, physiotherapy.

The day before

24 hours before blood sampling:

  • Limit fatty and fried foods, do not take alcohol.
  • Avoid strenuous exercise.

From 8 to 14 hours before donating blood, do not eat, drink only clean still water.

On the day of donation

Before blood sampling

  • Do not smoke for 60 minutes,
  • 15-30 minutes to be in a calm state.

Result

Analysis result example.pdf

Explanation of

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

Unit: µg/l

Reference values: 0.1 - 2.2 µg/l

Boost:

  • An overdose of vitamin K preparations.

Decline:

  • Chronic liver disease;
  • Chronic pancreatitis;
  • Crohn's disease;
  • Chronic infectious diseases;
  • Malabsorption syndrome;
  • Cystic fibrosis;
  • Celiac disease;
  • Haemorrhagic disease of the newborn;
  • Hypoprothrobinemia.

Vitamin K

Vitamin K (phylloquinone) belongs to the group of fat-soluble vitamins necessary for the synthesis of proteins that provide a sufficient level of coagulation, hence its name - K (from "coagulation factor"). In nature, fat-soluble vitamin K is represented by two forms: contained in plant foods K1 (phylloquinone) and synthesized by intestinal bacteria K2 (menaquinone). Vitamin K is not synthesized by intestinal bacteria in sufficient quantities to provide all the needs of the body, so a certain amount of vitamin K must be ingested with food. Foods high in vitamin K include: green leafy vegetables (cabbage, spinach, mustard, green lettuce), a number of other vegetables (turnips, radishes, broccoli, green onions, parsley, asparagus, Brussels sprouts), dairy products, cereals , vegetable oil and soybeans. Daily requirement for vitamin K - 90 mcg. Stocks of vitamin K, supplied with food and synthesized by the microflora of the large intestine, are stored in adipose tissues and the liver. Proper vitamin K metabolism is especially important for the elderly and people with gastrointestinal diseases due to an insufficiently nutritious diet and problems absorbing vitamins from food. For patients on anticoagulant therapy (for example, warfarin), a strict diet must be followed, since vitamin K is an antagonist of warfarin, it interferes with the action of the drug.

Vitamin K is a cofactor for the carboxylation of calcium-binding proteins. Vitamin K is involved in the conversion of glutamic acid residues into gamma-carboxyglutamic acid residues (abbreviated as Gla radicals). Gla-radicals, thanks to two free carboxyl groups, are involved in calcium binding and play an important role in the biological activity of proteins.

Currently, 14 human Gla proteins have been identified that play a key role in the regulation of a number of physiological processes:

  • synthesis of blood coagulation proteins: prothrombin (factor II), proconvertin (factor VII), Christmas factor (IX), Stewart factor (X), protein C and protein S;
  • synthesis of osteocalcin;
  • synthesis of a vascular protein that destroys and promotes the removal of calcium crystals deposited on the walls of blood vessels.

Vitamin K regulates the processes of blood clotting in the body, accelerates wound healing, it is necessary for the normal activity of liver cells. Vitamin K deficiency can lead to impaired blood clotting, external and internal bleeding, and a decrease in the activity of a number of enzymes. In newborns, vitamin K deficiency manifests itself in the form of hemorrhagic disease. Decreased vitamin K levels are associated with an increased risk of cardiovascular disease. The most common causes of vitamin K deficiency are: inadequate diet, chronic liver disease, intestinal dysbacteriosis, chronic infectious diseases, malabsorption syndrome, cystic fibrosis, celiac disease, chronic pancreatitis, Crohn's disease. Reduces the level of vitamin K in the blood and taking certain drugs: antibiotics, salicylates, coumarin anticoagulants.

Even with large doses of vitamin K, toxic side effects are very rare.

Vitamin K (phylloquinone): laboratory studies KDLmed

Vitamin K (phylloquinone) is a fat-soluble vitamin essential for blood clotting and bone mineralization.

Synonyms Russian

Antihemorrhagic vitamin, 2-methyl-3-wick-1,4-naphthoquinone, coagulation vitamin, antihemorrhagic vitamin, phytonadione.

Synonyms English

Phytonadione, menaphthone, vitamin K j , Vit K.

Method

Units

Ng/mL (nanograms per milliliter).

Which biomaterial can be used for research?

Venous blood.

How to properly prepare for an examination?

  • Do not eat for 2-3 hours before donating blood, you can drink pure non-carbonated water.
  • Do not smoke for 30 minutes before donating blood.

General information about the study

Vitamin K is a fat-soluble vitamin and exists in three structural variants: vitamin K 1 (phylloquinone), K 2 (menaquinone) and K 3 . In addition to differences in the structure of the molecule, phylloquinone and menaquinone differ in the source of entry into the body.

Phylloquinone is found in foods of plant and animal origin. A large amount of phylloquinone is found in green vegetables (Brussels and white cabbage, lettuce, spinach, parsley) and vegetable oils (olive and sunflower oils). Phylloquinone is the main form of vitamin K that comes from food.

Unlike phylloquinone, menaquinone does not come from outside, but is produced in the intestines by microflora. In the ileum, under the influence of bile acids and salts, both forms of vitamin K are absorbed, and the main organ where they are stored is the liver. Less lipophilic phylloquinone is easily mobilized from the liver tissue and is actively consumed in metabolic processes. Accordingly, phylloquinone is also the predominant form of vitamin K present in serum.

Some factors, such as age, gender, menopause, affect vitamin K metabolism. Phylloquinone stores in people over 60 years of age are lower than in younger people (under 40 years of age). In addition, there are genetic features of vitamin K metabolism. Thus, in patients with the E2 polymorphic variant of the ApoE gene, it is slower. This should be taken into account when prescribing coumarin preparations for the treatment of hypercoagulable conditions (characterized by increased blood clotting).

Vitamin K was originally called k oagulations vitamin - this is how the Danish scientist called the substance he discovered, which is necessary for blood coagulation, namely for gamma-carboxylation of blood coagulation factors II, IV, IX and X, as well as natural anticoagulants of protein C and protein S. Gamma-carboxylated factors have a unique ability to bind blood coagulation factor IV - calcium ions. The process of gamma-carboxylation is carried out by hepatocytes. In the absence of vitamin K, there is a deficiency of these coagulation factors, which is manifested by increased bleeding.

Although about 60-70% of dietary phylloquinone is excreted daily in the urine or bile, vitamin K deficiency is rare. This is due primarily to the presence of this vitamin in many foods and the reserves of the vitamin in the liver. Vitamin K deficiency in the vast majority of cases is caused by impaired absorption in the small intestine. Such disorders accompany diseases such as celiac disease, Crohn's disease, Whipple's disease, cystic fibrosis, as well as the condition after resection of the terminal ileum. In chronic pancreatitis, a lipase deficiency leads to a disruption in the breakdown of fats into fatty acid molecules and monoglycerides, which greatly complicates the absorption of fat-soluble vitamins, including vitamin K. A similar situation occurs with hypergastrinemia: in this case, an excess of gastrin stimulates the production of a large amount of hydrochloric acid in the stomach, which inactivates pancreatic lipase. Therefore, in patients with duodenal ulcer, antral gastritis and Zollinger-Ellison syndrome, the absorption of vitamin K is reduced. In diseases of the liver and gallbladder, the production and secretion of bile necessary for the absorption of vitamin K is impaired, so that in chronic hepatitis and cirrhosis of the liver, chronic cholangitis and cholecystitis, the absorption of vitamin K is also reduced. The lack of bile acids and salts is also observed in intestinal dysbacteriosis. At the same time, microorganisms use bile acids to carry out their own metabolic processes before bile enters the terminal ileum. The lipid-lowering drug cholestyramine binds excess cholesterol and bile acids in the intestine, which also impedes the absorption of vitamin K. A rare genetic disease, abetalipoproteinemia, is accompanied by a violation of the transport of fats from the intestine to the lymph, and then into the systemic circulation, while the transport of vitamin K is also impaired.

Vitamin K deficiency can be suspected with frequent epistaxis, meno- and metrorrhagia, ecchymosis, late bleeding in the postoperative period (for example, after tooth extraction), spontaneous or developed against a background of minimal trauma, hemorrhage into the joint, muscle and retroperitoneal cavity. It should be noted that such symptoms are characteristic not only of vitamin K deficiency. On the contrary, these manifestations occur in all diseases accompanied by a qualitative or quantitative change in blood coagulation factors and fibrinolysis. For the differential diagnosis of coagulopathy in clinical practice, tests for prothrombin time and activated partial thromboplastin time (APTT) are most often performed. Their disadvantage lies in the fact that they are indirect methods for assessing the deficiency of certain factors, suggesting, but not confirming, vitamin K deficiency as the cause of increased bleeding. To confirm vitamin K deficiency, directly measuring the concentration of phylloquinone in blood serum is used.

With the help of vitamin K, bone tissue protein osteocalcin matures. Osteocalcin is synthesized by osteoblasts and is able to bind calcium ions, which ensures calcification of the newly formed bone. For the synthesis of active osteocalcin, as well as for the synthesis of blood coagulation factors, a gamma-carboxylation reaction is necessary, which occurs only in the presence of vitamin K. In vitamin K deficiency, gamma-carboxylation of osteocalcin does not occur, which is accompanied by a decrease in bone tissue mineralization. Therefore, vitamin K deficiency contributes to the development of osteoporosis. High prepubertal phylloquinone levels are associated with high bone density in healthy girls. During the period of active growth and formation of bone tissue, adequate intake of vitamin K is necessary for the prevention of osteoporosis. In old age, vitamin K deficiency increases the rate of bone resorption. For example, a dietary intake of vitamin K of less than 109mcg/day increases the risk of hip fracture. Conversely, more than 250 mcg/day lowers the risk of hip fracture. In the daily diet of a young person, on average, there is about 80 micrograms of vitamin K, which is generally in line with accepted dietary recommendations (the recommended amount is 1 microgram/kg/day). The content of phylloquinone in the diet of older people who consume a lot of starchy foods and few green vegetables is often at the lower limit of the norm. Despite the fact that at this level of vitamin K intake, clinically detectable coagulopathy does not develop, this amount is not enough for the full mineralization of bone tissue. This condition is considered as subclinical vitamin K deficiency. Timely diagnosis and treatment of subclinical vitamin K deficiency improves bone health. Therefore, determining the concentration of vitamin K is used to assess the nutrient status, in a comprehensive assessment of the state of bone tissue and the development of individual dietary recommendations.

What is analysis used for?

  • To determine the cause of increased bleeding.
  • For the prevention, timely diagnosis and treatment of osteoporosis, especially in the prepubertal period and in old age.
  • For a comprehensive assessment of the content of vitamins and trace elements.
  • To develop individual dietary recommendations based on age, gender, hormonal status, and certain genetic metabolic characteristics.

When is the test ordered?

  • In diseases of the gastrointestinal tract - the small intestine and pancreas, as well as the liver and gallbladder - accompanied by malabsorption of fats and fat-soluble vitamins.
  • With symptoms of increased bleeding: frequent nosebleeds, meno- and metrorrhagia, ecchymosis, late bleeding in the postoperative period, spontaneous or developed against a background of minimal trauma, hemorrhage into the joint, muscle and retroperitoneal cavity.
  • In the presence of risk factors for osteoporosis: postmenopause, older age, drinking large amounts of alcohol and coffee, sedentary lifestyle, deficiency of calcium salts and vitamin D, etc.
  • For vertebral compression fractures, "fracture of the radius in a typical location", fracture of the femoral neck, as well as spontaneous or caused by minimal trauma fractures of any other location.
  • When developing individual dietary recommendations.

What do the results mean?

Reference values: 0.1 - 2.2 ng/ml.

Reasons for high vitamin K levels:

  • high intake of green vegetables in the diet;
  • high fat diet;
  • hypertriglyceridemia due to alcohol use, oral contraceptives, diabetes mellitus, chronic renal failure, hypothiazide and beta-blockers.

Reasons for low vitamin K levels:

  • low content of green vegetables in the diet;
  • bowel diseases affecting the small intestine - celiac disease, Crohn's disease, Whipple's disease, cystic fibrosis - as well as the condition after resection of the terminal ileum;
  • liver diseases: chronic hepatitis, post-infectious and alcoholic cirrhosis;
  • diseases of the gallbladder: chronic cholangitis and cholecystitis;
  • chronic pancreatitis;
  • duodenal ulcer, antral gastritis, Zollinger-Ellison syndrome;
  • intestinal dysbiosis;
  • use of cholestyramine;
  • abetalipoproteinemia;
  • elderly and senile age, postmenopause;
  • use of coumarin preparations (warfarin).

What can influence the result?

  • Concentration of phylloquinone transporting lipoproteins: in patients with a high concentration of chylomicrons and VLDL, the level of phylloquinone is increased.
  • Age: the lowest rates were found in men and women aged 30-40 and the elderly.
  • The level of phylloquinone is higher in carriers of the polymorphic variant E2 of the gene ApoE .
  • The result of the study depends on the intake of phylloquinone with food: the absence of green vegetables in the diet for 3 weeks is accompanied by a decrease in the concentration of phylloquinone by 50%.

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