Let’s discuss the function of Vitamin K first:

• The most important function of vitamin K is that it acts as a cofactor for the post-translational γ-carboxylation of glutamate residues in clotting factors II (prothrombin), VII, IX, X, and proteins C and S, enabling calcium binding and proper blood coagulation. A decrease in plasma prothrombin level is seen in deficiency of vitamin K.
• It appears to have some role in the electron transport system, because its structure is similar to coenzyme Q. In the plant kingdom, vitamin K1 (phylloquinone) is an essential component of the photosynthetic electron transport process in Photosystem I.

Vitamin K exists in different forms:

• Vitamin K1 (phylloquinone) – found in green leafy vegetables
• Vitamin K2 (menaquinone) – produced by intestinal bacteria and found in fermented foods
• Vitamin K3 (menadione) – synthetic form, not commonly used clinically due to toxicity

Vitamin K cycle and mechanism:

Vitamin K functions through the vitamin K cycle, in which it is regenerated after participating in carboxylation reactions. This cycle involves vitamin K epoxide reductase (VKOR), which is also the target of anticoagulant drugs like warfarin.

Bone and vascular roles:

Vitamin K is also important for bone and vascular health, as it activates:

• Osteocalcin (important for bone mineralization)
• Matrix Gla protein (MGP) (prevents vascular calcification)

1. Effects of Deficiency of Vitamin K

These are due to lower levels of prothrombin and other factors needed for normal blood clotting mechanisms. There is an increase in prothrombin time showing a deficiency of clotting factors, and clotting time is prolonged, with a tendency to bleed profusely from minor wounds. Bleeding occurs mainly from the gastrointestinal tract, urinary tract, and uterus.

2. Additional points (clinical manifestations):

• The earliest laboratory abnormality is prolonged prothrombin time (PT) (due to factor VII having the shortest half-life)
• Platelet count remains normal (important distinguishing feature from thrombocytopenia)
• Severe deficiency may cause ecchymosis, epistaxis, hematuria, and intracranial hemorrhage

3. Condition associated with Vitamin K deficiency

Many conditions are associated with a deficiency of vitamin K and lead to bleeding tendencies by producing hypoprothrombinemia. These include the following:

• Faulty absorption of Vitamin K due to lack of bile, as occurs in obstructive jaundice and biliary fistula. Water-soluble preparations of Vitamin K can, however, be absorbed even in the absence of bile salts.
• Diarrheal diseases, e.g., sprue, celiac disease, and ulcerative colitis, interfere with absorption of Vitamin K. Administration of mineral oil (liquid paraffin) over prolonged periods also has the same effect.
• Administration of broad-spectrum antibiotics: These drugs kill the normal flora of the intestine and reduce the intestinal synthesis of vitamin K.
• In newborn babies, especially premature ones: Vitamin K does not easily cross the placental barrier. Moreover, the bowels of a newborn are sterile, and thus no vitamin K can be formed within them. This results in physiological hypoprothrombinemia of the newborn. However, Vitamin K is routinely given to newborn babies as prophylaxis, because deficiency can otherwise lead to serious bleeding (hemorrhagic disease of the newborn). Without supplementation, toxic effects such as hemolytic anemia, hyperbilirubinemia, hepatomegaly, and death have been reported with some older formulations (e.g., menadione in high doses).
• Administration of drugs having anti-vitamin K activity: The anticoagulant drug bishydroxycoumarin and large doses of salicylates exert an anti-vitamin K effect and produce hypoprothrombinemia. Vitamin K reverses the effects of these drugs. Vitamin K1 (phytonadione) is effective in reversing the effects of bishydroxycoumarin, whereas Vitamin K3 (menadione) is not used clinically due to toxicity and is not preferred for reversal therapy.

4. Additional risk factors

• Long-term therapy with warfarin (vitamin K antagonist anticoagulant)
• Severe malnutrition or very low dietary intake (rare alone)
• Fat malabsorption syndromes (chronic pancreatitis, cystic fibrosis, short bowel syndrome)

5. Liver disease association

In addition to the above-mentioned conditions in which hypoprothrombinemia is due to a lack of vitamin K, extensive liver disease will also result in a low plasma prothrombin level. Vitamin K will not improve this type of hypoprothrombinemia because liver cells themselves are diseased and cannot synthesize clotting factors.

In liver disease, both production of clotting factors and storage/utilization of vitamin K–dependent proteins are impaired, so response to vitamin K may be minimal or absent.

6. Human requirements

Not fully established historically, but modern estimates suggest a requirement of approximately 90–120 µg/day in adults, depending on sex and physiological status. Normally, there is sufficient vitamin K in the diet, which is also supplemented by intestinal bacterial synthesis. Its storage occurs to a limited extent only.

7. Additional points (nutrition):

• Vitamin K is found mainly in green leafy vegetables (K1) and fermented foods (K2)
• Gut microbiota contributes significantly to menaquinone (K2) production, but dietary intake is still important
• Deficiency from diet alone is rare in healthy adults
• Fat is required for optimal absorption since vitamin K is fat-soluble