Vitamin K

In the human, vitamin K deficiency commonly occurs in the newborn and is named hemorrhagic disease. The deficiency is not due to poor nutrition of the mother, but to poor placental transfer, absence of bacterial synthesis in the newborn’s gut, low plasma concentrations of plasma clotting factors, and low vitamin K concentrations in human milk.4 The deficiency is characterized by low plasma prothrombin concentrations resulting from the lack of biosynthesis of prothrombin by the immature liver and the lack of vitamin K. Hemorrhagic disease produces bleeding in the skin, subcutaneous tissue, gastrointestinal (GI) tract, umbilical cord, and intracranium. Central nervous system damage occurs and the deficiency is often fatal.5 Hemorrhagic disease is prevented by intramuscular injection or oral administration4,6,7 of vitamin K1 within 6 h of birth. Breast-fed infants are more likely to develop hemorrhagic disease than formula-fed infants because human milk is low in vitamin K content. Infant formula is fortified at a minimum level of 4 mg per serving specified by the Infant Formula Act of 1980.8

Deficiency of vitamin K in the adult is rare. When it does occur, the deficiency is defined as a “vitamin K-responsive hypoprothrombinemia,”9 resulting from fat malabsorption syndromes, liver disease, and antibiotic therapy that inhibits microbial vitamin K2 synthesis in the gut. Anticoagulant treatment with coumarin and related compounds produces a functional or secondary vitamin K deficiency through disruption of the vitamin K cycle and inhibition of the synthesis of vitamin K-dependent blood clotting proteins in the liver. Defective coagulation of the blood measured by a one-stage prothrombin time (PT) is still used to assess vitamin K status; however, the test is not a sensitive indicator of vitamin K status.8 Coagulation assays are not useful to assess subclinical deficiencies.10 Direct measurement of gamma-carboxylation status of gamma-carboxyglutamate (Gla) proteins that are

vitamin K-dependent provides a biochemical marker to assess vitamin K status.9,10 Analytes include undercarboxylated prothrombin proteins (hepatic vitamin K status) and osteocalcin (bone vitamin K status).8,9 Serum and urinary levels of vitamin K do not reflect tissue status.10