nutritional disorders
Vitamin K Toxicity
Introduction
Vitamin K1 (phylloquinone) is not toxic when consumed orally, even in large amounts. However, menadione (a synthetic, water-soluble vitamin K precursor) can cause toxicity (infants have developed hemolytic anemia, hyperbilirubinemia, jaundice, and kernicterus) and should not be used to treat vitamin K deficiency. Vitamin K1 (phylloquinone) is dietary vitamin K. Sources include green leafy vegetables (especially collards, spinach, and salad greens), soy beans, and vegetable oils. Dietary fat enhances its absorption. Infant formulas contain supplemental vitamin K. After the neonatal period, bacteria in the gastrointestinal tract synthesize vitamin K, which is absorbed and used by the body. Vitamin K2 refers to a group of compounds (menaquinones) synthesized by bacteria in the intestinal tract; the amount synthesized does not satisfy the vitamin K requirement. Vitamin K controls the formation of coagulation factors II (prothrombin), VII, IX, and X in the liver (see table). Other coagulation factors dependent on vitamin K are protein C, protein S, and protein Z; proteins C and S are anticoagulants. Metabolic pathways conserve vitamin K. Once vitamin K has participated in formation of coagulation factors, the reaction product, vitamin K epoxide, is enzymatically converted to the active form, vitamin Khydroquinone. The actions of vitamin K–dependent proteins require calcium. The vitamin K–dependent proteins, osteocalcin and matrix gamma-carboxy-glutamyl (Gla) protein, may have important roles in bone and other tissues. Forms of vitamin K are common therapy for osteoporosis in Japan and other countries. Vitamin K toxicity is rare but is most common in formula-fed infants. The effects of vitamin K toxicity can include Overview of Hemolytic Anemia and (See also Overview of Vitamins .) 