Cases reported "Vitamin K Deficiency"

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11/29. Severe deficiency of vitamin K dependent coagulation factors in an infant.

    A severe deficiency of vitamin K dependent coagulation factors presenting 25 days after birth in an apparently healthy breast-fed infant is reported. The administration of antibiotics to the lactating mother, and lack of a vitamin K supplement to the new-born baby were possible predisposing factors.
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12/29. New insights on vitamin K.

    Vitamin K catalyzes the post-translational carboxylation of coagulation proteins C, S, and factors II, VII, XI, and X. Detection of the noncarboxylated forms allows an indirect and specific measure of the vitamin k deficiency found in early, classic, and late hemorrhagic disease of the newborn (HDN), malabsorption syndromes, and drug related (warfarin, anticonvulsants, and antibiotics) states. Idiopathic late HDN (CNS bleeding) occurs in exclusively breast-fed infants and is prevented by appropriate parenteral and oral vitamin K prophylaxis given at birth. All newborn infants and older infants with malabsorption syndromes should receive prophylactic vitamin K.
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13/29. Vitamin K-dependent clotting factor deficiency in pregnancy.

    A case of malabsorption of vitamin K, leading to a vitamin K-dependent clotting factor deficiency that developed during the eighth gestational month, is reported. Evaluation of the coagulopathy at term showed the cause to be an obstructive hepatobiliary disorder. Given the pathophysiologic relationship between the coagulation cascade and the hepatic and biliary systems, routine measurement of the prothrombin and partial thromboplastin times is advised for all patients with evidence of hepatobiliary dysfunction.
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14/29. Effects of N-methyl-thiotetrazole cephalosporin on haemostasis in patients with reduced serum vitamin K1 concentrations.

    Two patients with low random serum vitamin K1 concentrations but with normal prothrombin times and normal biological assays of the vitamin K dependent coagulation proteins were treated with an N-methyl-thiotetrazole cephalosporin (cefotetan) postoperatively. Four to six days later both patients developed a prolonged prothrombin time and a noticeable and specific lowering of the clotting activities of factors II, VII, IX and X, though the serum vitamin K1 concentrations remained unchanged. Crossed immunoelectrophoresis of prothrombin showed the appearance of a second peak corresponding to descarboxyprothrombin (PIVKA II). These abnormalities corrected after vitamin K administration. These data are consistent with the hypothesis that cephalosporins with an N-methyl-thiotetrazole side chain inhibit the hepatic utilisation of vitamin K but that this only causes hypoprothrombinaemia when liver reserves of vitamin K are low.
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15/29. association of congenital deficiency of multiple vitamin K-dependent coagulation factors and the phenotype of the warfarin embryopathy: clues to the mechanism of teratogenicity of coumarin derivatives.

    We have evaluated a boy who had excessive bleeding and bruising from birth and showed markedly prolonged prothrombin times, partially correctable by oral vitamin K administration. Additional laboratory studies demonstrated decreased activities of plasma factors II, VII, IX, and X; near normal levels of immunologically detected and calcium binding-independent prothrombin; undercarboxylation of prothrombin; excess circulating vitamin K epoxide; decreased excretion of carboxylated glutamic acid residues; and abnormal circulating osteocalcin. These results all are consistent with effects resulting from decreased posttranslational carboxylation secondary to an inborn deficiency of vitamin K epoxide reductase. This individual also had nasal hypoplasia, distal digital hypoplasia, and epiphyseal stippling on infant radiographs, all of which are virtually identical to features seen secondary to first-trimester exposure to coumarin derivatives. Therefore, by inference, the warfarin embryopathy is probably secondary to warfarin's primary pharmacologic effect (interference with vitamin K-dependent posttranslational carboxylation of glutamyl residues of various proteins) and may result from undercarboxylation of osteocalcin or other vitamin K-dependent bone proteins.
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16/29. Haemorrhage responsive to vitamin K in a 6-week-old infant.

    A 6-week-old breast-fed infant presented with vomiting, jaundice, and irritability. Haemorrhage occurred after lumbar puncture, and a coagulation abnormality which responded to vitamin K was found. It would seem prudent to estimate the prothrombin time before invasive procedures in breast-fed infants of this age, or to give vitamin K to such infants when doubt exists about previous vitamin K administration.
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17/29. Severe coagulation defect due to a dietary deficiency of vitamin K.

    A patient with multiple injuries developed a severe coagulation defect due to a deficiency of vitamin K. None of the usual predisposing factors was present and the patient's diet was very poor. Dietary deficiency of vitamin K and the importance of antibiotic therapy in its production are discussed.
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18/29. vitamin k deficiency presenting with hemarthrosis.

    A breast-fed 25-day-old infant was hospitalized because of swelling and tenderness of the left leg, developed after mild rotary motion of the leg by his brother. Radiographic examination showed widening of the left articular hip joint space. On the day of admission, a presumptive diagnosis of septic arthritis was entertained, and antibiotic therapy was instituted. Following profuse bleeding from sites of skin punctures, coagulation studies were performed. prothrombin time and partial thromboplastin time were prolonged. Administration of phylloquinone (vitamin K1) resulted in rapid normalization of coagulation. Differential diagnosis between hemarthrosis resulting from vitamin k deficiency and septic arthritis with disseminated intravascular coagulation is a matter of great importance in such patients.
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19/29. Congenital deficiency of vitamin K-dependent coagulation factors and protein c.

    A 15-month-old girl from Coimbra (portugal) had a history of numerous hemorrhagic episodes with multiple bruises, hematomas but not hemarthroses. On serial testing she showed deficiency of factors II, VII, IX, X and protein c. Malabsorption-induced vitamin k deficiency, liver disease or ingestion of a coumarin compound were excluded. An absence of detectable abnormalities was found among her relatives. consanguinity was not present. The immunologic assay, immunoelectrophoresis or antibody neutralization, revealed much higher levels of these factors than the clotting assay. The non-physiological activator (Echis carinatus venom) produced higher levels of prothrombin activation than those detected by physiological activation. Two-dimensional immunoelectrophoresis of the patient's plasma in calcium showed that prothrombin had the same mobility as acarboxyprothrombin. No significant response to large doses of intravenous vitamin K3 (6 mg) was observed. Transfusion of 120 ml of frozen fresh plasma led to an immediate increase in the procoagulant activities of vitamin K dependent protein, similar to that found after perfusion of plasma plus vitamin K3. The results obtained from this patient suggest a defect in the gammacarboxylation mechanism inside the hepatocyte.
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ranking = 0.8
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20/29. bulimia nervosa complicated by deficiency of vitamin K-dependent coagulation factors.

    A 28-year-old woman manifested a hemorrhagic tendency caused by a deficiency of vitamin K-dependent coagulation factors. Her condition was diagnosed as bulimia nervosa in view of a previous history of anorexia nervosa and episodes of self-induced vomiting and purging. There were no remarkable lesions in her alimentary system. In treatment of bulimia nervosa, attention should be given not only to the loss of body fluids and electrolytes, but also to the possibility of a deficiency of vitamin K-dependent coagulation factors.
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