Epithelial-myoepithelial carcinoma?

Vitamin K and metabolic bone diseaseThe report by Vermeer and colleagues 1 that vitamin K may be important in the causation of metabolic bone disease is interesting, but there is an alternative hypothesis that could also explain some of the apparently vitamin K mediated bone eVects.Vitamin B-6 is an essential cofactor for the enzyme ornithine decarboxylase which is the rate limiting enzyme in the formation of putrescine which regulates osteoblast glucose-6-phosphate dehydrogenase activity and thus osteoblast NADPH concentrations. [2]3][4][5] NADPH is essential for the vitamin K cycle in which the epoxide form of vitamin K is converted back to the naphthoquinone form which is required for -carboxylation of osteocalcin. 6 It is therefore possible that vitamin B-6 status could modulate the eVects of vitamin K on bone metabolism.Although the chain of events described above may seem excessively complicated there is evidence that vitamin B-6 deficiency in rats reduces bone healing 7 and that vitamin B-6, assayed by high performance liquid chromatography, 8 is lower in patients who spontaneously (traumatically) fracture their hips than in patients whose hip fracture is at the hands of an orthopaedic surgeon as an elective procedure. 9Further research into the interaction of these two vitamins may be indicated.