Phenytoin, hemorrhage, skeletal defects and vitamin K in the newborn.
The vitamin K-dependent hemostatic factors are present in reduced quantities at birth and may decrease further in the first few days of life. Administration of vitamin K1 on day 1 prevents hemorrhagic disease of the newborn. Maternal ingestion of anticonvulsants puts the newborn at greater risk from hemorrhage, possibly as a result of induction of fetal microsomal enzymes with a resultant increased oxidative degradation of vitamin K which gives rise to a vitamin K deficiency and other concomitant clinical results, for example skeletal defects. Evidence for this sequence of events is presented and the widespread effect of vitamin K deficiency on the fetus is discussed.
D000014:Abnormalities, Drug-Induced / Q000209:etiology*; D000818:Animals; D001779:Blood Coagulation Factors / Q000502:physiology; D001842:Bone and Bones / Q000002:abnormalities*; D002642:Chick Embryo; D005260:Female; D006487:Hemostasis / Q000187:drug effects; D006801:Humans; D008431:Maternal-Fetal Exchange; D008862:Microsomes, Liver / Q000201:enzymology; D010084:Oxidation-Reduction; D010672:Phenytoin / Q000009:adverse effects*; D011247:Pregnancy; D010837:Vitamin K 1 / Q000627:therapeutic use; D014813:Vitamin K Deficiency / Q000139:chemically induced*; D006475:Vitamin K Deficiency Bleeding / Q000139:chemically induced* / Q000188:drug therapy; D014859:Warfarin / Q000494:pharmacology
D001779:Blood Coagulation Factors; D014859:Warfarin; D010672:Phenytoin; D010837:Vitamin K 1