Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019087 (hemorrhagic diathesis)
 678 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vitamin K deficient hemorrhagic diathesis is well known as a cause of infantile intracranial hemorrhage. Its occurrence, however, as a post-surgical complication is rare and has never been reported previously. Two cases are presented here which illustrate the existence of such a hazard. Case 1. A 73-year-old woman admitted with subarachnoid hemorrhage (WFNS IV) underwent microsurgical exploration of a left internal carotid aneurysm, and neck clipping of the aneurysm was performed. She had an uneventful postoperative course, but her neurological condition deteriorated suddenly on the fifth postoperative day. CT scan revealed a large epidural hematoma. Case 2. A 6-year-old boy was admitted due to the dysfunction of a ventriculo-peritoneal shunt system that had previously been placed for hydrocephalus. This dysfunction was thought to be caused by meningitis. Twelve days after ventricular drainage and antibiotic therapy, sudden intraventricular hemorrhage occurred. In both cases, PT and APTT were markedly prolonged, FDP slightly increased and fibrinogen slightly decreased. SFMC was positive in case 2. After the administration of vitamin K, PT and APTT were immediately normalized. Recent reports emphasize the adverse effect of antibiotics that leads to vitamin K deficient hemorrhagic diathesis, especially, in patients in a cachectic state. In these two cases, such a cachectic condition was not observed. We presume that the cause of vitamin K deficiency would be, along with the administration of antibiotics, a preliminary condition of disseminated intravascular coagulation which is encountered in some neurological disorders including subarachnoid hemorrhage. We conclude that attention should be paid for these pitfalls in perioperative neurosurgical care.
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PMID:[Postoperative intracranial hemorrhage due to vitamin K deficiency: report of two cases]. 173 30

Two cats with intestinal malabsorption developed a hemorrhagic diathesis. Although unsubstantiated, the probable cause of bleeding was a chronic malabsorption of fat and the fat-soluble vitamin K. When treated with vitamin K1 per os, one cat's clotting times were only partially corrected. Since vitamin K1 is actively absorbed in the proximal small intestine, the incomplete response of this case to orally administered vitamin K1 was predictable. The infrequent occurrence of bleeding in animals with malabsorption is, in part, attributable to the ileal and colonic absorption of bacterially derived vitamin K2. For this reason, nonspecific use of antibiotics in these animals is contraindicated. Since long-chain, polyunsaturated fats impair vitamin K absorption, dietary fat given to animals with malabsorption should be restricted to medium- and short-chain, saturated fats. Vitamin K should be administered subcutaneously to these animals if prolonged clotting times or active bleeding is present, and routinely prior to surgery. Oral supplementation with vitamin K3, which is absorbed in the colon and less lipid soluble than vitamin K1, should be given to animals with malabsorption that are maintained as outpatients. Adequate dosage levels of vitamin K3, however, are yet to be established for the cat, and dose-dependent hemolytic anemia is a probable toxic manifestation.
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PMID:Probable vitamin K--deficient bleeding in two cats with malabsorption syndrome secondary to lymphocytic-plasmacytic enteritis. 350 99

The history of the antithrombotic agents--aspirin, heparin, warfarin, and the thrombolytics--is a rich and lively odyssey of serendipity, perseverance, vision, and conflict involving a number of striking personalities. The history of aspirin spans ages and continents from Hippocrates' analgesic for women in labor to the rediscovery of the white willow bark by English country scholar Reverend Edward Stone. Bayer chemist Felix Hoffmann reinvented aspirin for his ailing father; suburban physician L.L. Craven pioneered the prophylactic antithrombotic uses of aspirin; and Sir John Vane elucidated aspirin's mechanism of action as the inhibition of prostaglandin synthetase. Heparin was discovered by McLean, working as a medical student in 1915 in search of a pure procoagulant in dog liver. His original impure material differed somewhat from today's heparin, but purified heparin was rapidly accepted for a myriad of clinical uses; to this day, diverse new properties of this complex glycosaminoglycan continue to be elucidated. The oral anticoagulants emerged from veterinary research in the 1920s on a hemorrhagic disorder afflicting cattle that consumed spoiled sweet clover hay. Several chance encounters led Karl Link and his University of Wisconsin team to the identification of dicumarol as the offending agent in 1939 and its widespread therapeutic use by Wright and others in the 1940s. Link later developed warfarin as a rodenticide, but its use in humans soon followed in the 1950s. Vitamin K was discovered in the 1930s; its involvement in the mechanism of the anticoagulant agents was not delineated until the 1970s. The intrinsic ability of clotted blood to liquify and the fibrinolytic properties of normal urine were noted in the 1800s. Tillett and Sherry's group stumbled on the fibrinolytic properties of streptokinase in the 1930s and pioneered the therapeutic use of streptokinase in the 1940s and of urokinase in the 1960s. Several teams found tissue-type plasminogen activator in various body sites beginning in the 1940s, leading to its cloning and widespread use in the 1980s; anisoylated plasminogen-streptokinase activator complex is an example of rational drug design. The discoverers of these diverse agents have not only provided physicians with a potent armamentarium of antithrombotic drugs but also helped elucidate much basic science and vividly demonstrated the merits of perseverance, independent thought, and adherance to the scientific method.
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PMID:History of drugs for thrombotic disease. Discovery, development, and directions for the future. 828 78

Vitamin K is needed to synthesize coagulation factors II (prothrombin), VII, IX, and X through the carboxylation of glutamic acid in vitamin K-dependent proteins which results in the creation of effective calcium binding sites which, in turn, facilitates the coagulation process. Vitamin K exists as naturally occurring vitamin K-I (phylloquinone) in green leafy vegetables and vegetable oils, vitamin K-II (menaquinone) as produced in the gut by bacteroides fragilis and E. coli, and synthetic vitamin K-III (menadoine sodium bisulfite) which is water-soluble and capable of producing serious jaundice in newborns, especially those with instability of glutathione and deficiency of G6PD. Humans require about 5 mcg of vitamin K daily. Since it is indigenously produced in the gut by bacterial flora, dietary deficiency of vitamin K in healthy subjects is rare. Vitamin K is usually the first vitamin given at birth. Newborn babies, however, absorb only approximately 30% of ingested vitamin K, compared to 50-70% in adults. Hemorrhagic disease is a manifestation of vitamin K deficiency in newborn infants. Hemorrhagic disease of the newborn (HDN), early HDN, classical HDN, and late HDN are discussed. The American Academy of Pediatrics recommended in 1961 that all healthy term newborn babies receive 0.5-1.0 mg of vitamin K-I intramuscularly at birth. However, while the authors have not followed those recommendations in their neonatal unit for 15 years, they have experienced only a 0.1% incidence of classical HDN. High-risk newborns at the unit are routinely given the recommended dose of K-I at birth.
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PMID:Vitamin K during infancy: current status and recommendations. 949 99