Vitamin K is a fat-soluble vitamin and exists in different forms. The main form vitamin K₁ (Phylloquinone), is transported primarily by chylomicrons. Consequently, serum vitamin K concentrations are influenced by plasma triglycerides concentration and reflect recent dietary intake. It is also associated with serum lipoproteins.

It is essential for synthesis of vitamin K dependent clotting factors (Prothrombin II, VII, IX and X). It is also required for the synthesis of other vitamin K dependent proteins such as protein C, protein S (anti-coagulant activity), osteocalcin (bone formation), and protein Z. Vitamin K acts as a cofactor in the carboxylation of glutamic acid. This step confers calcium and phospholipid binding properties to the vitamin K dependent proteins and so is essential for their functional activity.

Vitamin K deficiency, although rare, is not uncommon. Patients who are at risk of developing vitamin K deficiency are those on long-term broad-spectrum antibiotics or long-term hyperalimentation; also patients with chronic liver disease, biliary obstruction, or fat malabsorption. Poor vitamin K status is associated with low bone mineral density. Oral anticoagulants such as warfarin act by antagonizing the metabolism of vitamin K.

No toxic manifestations have been noted on ingestion of large amounts of vitamin K over extended period of time. However administration of Menadione (not phylloquinone) may cause hyperbilirubinaemia and kernicterus in newborn.

Vitamin K analysis is currently restricted to cystic fibrosis patients, those on home parenteral nutrition or on consultation.

Sample Requirements and Reference Ranges for Vitamin K

* This is the absolute minimum volume; these volumes are insufficient to carry out a repeat analysis in the event of an analytical problem.