Evaluation of vitamin K deficiency in children with acute and intractable diarrhea
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Prothrombin time
Vitamin K deficiency
Gastrointestinal bleeding
Prothrombin time
Vitamin K deficiency
Gastrointestinal bleeding
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Vitamin K is generally regarded as a procoagulant drug with physicians, concerns have been raised about its effects on hemostasis in the healthy population. We aimed to investigate whether vitamin K2 affects activities of individual vitamin K dependent coagulation factors in healthy individuals without anticoagulation treatment. Forty healthy volunteers between 25 and 40 years old were recruited. They received 90 μg of vitamin K2 every day for 30 days. Prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT), international normalized ratio (INR), fibrinogen (FIB) levels and blood coagulation factors II, VII, IX, and X activity levels (F II : C, FⅦ : C, FⅨ : C,FⅩ : C), protein induced by vitamin K absence or antagonist-II (PIVKA-II), which is uncarboxylated prothrombin were measured at day 0, and day 30 after vitamin K2 administration. Plasma diluted 1:10 from vitamin K2 group and healthy control group were assayed for the activity of factors II, VII, IX, and X. PT, APTT, TT, and FIB did not show significant difference at day 30 when compared with baseline. The activities of coagulation factors II, VII, IX, and X was not significantly different with baseline (97.28 ± 12.42% vs. 99.96 ± 10.24%, P = 0.24 for F II: C; 76.12 ± 15.82% vs. 76.40 ± 12.33%, P = 0.92 for FⅦ: C; 97.65 ± 13.98% vs. 99.65 ± 13.30%, P = 0.47 for FⅨ: C; 89.18 ± 10.76% vs. 92.01 ± 10.46%, P = 0.1 for FⅩ: C) . PIVKA-II levels were not changed with 30 days vitamin K2 supplementation (21.62 ± 3.21 vs. 23.87 ± 2.65 mAU/ml, P = 0.16). After 30 days vitamin K2 administration, factor II, Ⅶ, Ⅸ, and Ⅹ activity of plasma diluted up to 10 times were proportionally decreased, and did not show significant difference with the healthy control without vitamin K2 exposure (10.32 ± 1.24% vs. 10.97 ± 1.55%, P = 0.38 for F II: C; 9.52 ± 2.94% vs. 9.14 ± 1.79%, P = 0.68 for FⅦ: C; 11.78 ± 2.12% vs.11.65 ± 1.54%, P = 0.87 for FⅨ: C; 8.22 ± 1.28% vs. 8.92 ± 1.13%, P = 0.21 for FⅩ: C). Vitamin K2 supplementation at recommended dosage does not affect vitamin K-dependent coagulation factors activity in healthy subjects. Uncarboxylated prothrombin (PIVKA-II) in healthy individuals is not decreased with vitamin K supplementation. None.
Prothrombin time
Vitamin K antagonist
Vitamin K deficiency
Thrombin time
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Vitamin K deficiency
Clotting factor
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Objective: To investigate the clinical applications of four coagulation tests and D-dimer test in patients with liver cirrhosis. Methods: Four coagulation tests and the D-dimer test were performed in 216 patients with liver cirrhosis(62 in Child-Pugh A group,88 in B group and 66 in C group) and 84 healthy individuals by Sysmex Cs-5100 auto blood coagulation analyzer. Results: Compared with the control group,the prothrombin time(PT),activated partial thromboplastin time(APTT) and thrombin time(TT) in liver cirrhosis group were significantly prolonged(P 0. 05),the fibrinogen(FIB) was significantly lower(P 0. 05),and the D-dimer level was significantly higher(P 0. 05). Conclusion: The four blood coagulation indexes and serum Ddimer level are correlated with disease status of liver cirrhosis. The combination detection of blood coagulation function and serum D-dimer may be significantly useful for the assessment of disease condition,the treatment and prevention of hemorrhage in upper digestive tract and the prediction of prognosis for cirrhosis patients.
Prothrombin time
Thrombin time
D-dimer
Coagulation testing
Liver disease
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Vitamin K has long been regarded as a procoagulant drug by physicians, and concerns have been raised with regard to its effects on hemostasis. Although many studies have shown that vitamin K supplementation is safe for thrombotic events, the effect of vitamin K supplementation on the activities of vitamin K dependent procoagulation factors in healthy individuals is not available.This study aimed to investigate whether vitamin K2 supplementation at recommended doses affects the activity of vitamin K dependent procoagulation factors in healthy individuals without any anticoagulation treatment.Forty healthy volunteers between 25 and 40 years of age were recruited. Menaquinone-7 (MK-7) was administrated at 90 μg for 30 days. Prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT), and blood coagulation factors II, VII, IX, and X activities and Protein induced by vitamin K absence or antagonist-II (PIVKA-II) were measured on days 0 and 30 after MK-7 administration.PT, APTT, and TT showed no significant differences on day 30 when compared with baseline. The activities of coagulation factors II, VII, IX, and X on day 30 showed no significant differences with those at baseline. PIVKA-II levels were unchanged after 30 days of MK-7 supplementation.MK-7 supplementation at recommended dosage does not affect vitamin K-dependent coagulation factors' coagulation activity, and does not enhance the carboxylation of prothrombin in healthy individuals. This indicated that MK-7 administration does not alter hemostatic balance in healthy populations without anticoagulation treatment.
Prothrombin time
Vitamin K antagonist
Vitamin K deficiency
Thrombin time
Factor VII
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Prothrombin time
Liver function
Thrombin time
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To summarize the clinical characteristics of secondary coagulation disorders caused by exposure to poison (raticide) in children and to investigate the diagnosis and corresponding treatment.The process of diagnosis, clinical characteristics, response to treatment and the prognosis were analyzed.The main clinical manifestation was mucosal bleeding (66.6%), including epistaxis, gingival bleeding, hematomas and so on. All these children were previously well and had no history of bleeding. Activated partial thromboplastin time (APTT) and prothrombin time (PT) were prolonged, factor II was undetectable and the levels of factors VII, IX, and X were lower. The fibrinogen was normal. A raticide was detected in blood and urine of 13 children although 12 of the patients had no definite history of raticide ingestion. Prothrombin complex, fresh frozen plasma and vitamin K(1) were effective in these cases. However, 2 - 3 weeks later, 6 patients presented with recurrent bleeding.For children with secondary coagulation disorders of unknown cause, intoxication of raticide should be considered. The administration of blood coagulation factors and vitamin K(1) are effective in early treatment, and the treatment period should be more than 2 months. The PT and APTT should be followed up. Vitamin K(1) should be stopped when PT and APTT are normal.
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Fresh frozen plasma
Coagulation testing
Factor IX
Vitamin K deficiency
Coagulation Disorder
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Feeding of vitamin K-deficient diets or fasting produced vitamin K deficient syndromes in both conventional and germ-free male rats in 3 days, increasing prothrombin time (PT), activated partial thromboplastin time (APTT), plasma and liver descarboxyprothrombin (PIVKA) levels and liver gamma-glutamylcarboxylase activities, but decreasing plasma clotting factor VII and prothrombin levels. These changes were not found when daily 30 micrograms/rat of vitamin K1 was injected during this period. The changes caused by fasting were comparable with those caused by a diet containing 20-30 ng/g of vitamin K1, while a diet containing less than 5 ng/g caused greater changes in both conventional and germ-free rats. Germ-free rats on a diet containing sufficient amounts of vitamin K1 showed PT and APTT values similar to those in conventional rats, but lower plasma clotting factor levels and higher PIVKA and microsomal gamma-glutamylcarboxylase activities. The values for PT, APTT, factor VII, prothrombin and PIVKA in the fasted germ-free rats were almost the same as those in the fasted conventional rats. These findings suggest that menaquinones synthesized in the large intestine are not utilized sufficiently to prevent vitamin K deficiency in rats.
Prothrombin time
Vitamin K deficiency
Factor VII
Clotting factor
Thromboplastin
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Feeding of a vitamin K-deficient diet caused the development of hypo-prothrombinemic changes in rats such as prolongation of prothrombin time (PT) and activated partial thromboplastin time (APTT), decreases in plasma prothrombin and clotting factor VII levels, and an increase in the descarboxyprothrombin (PIVKA) level in both plasma and liver. Successive administrations of latamoxef (LMOX) to the vitamin K-deficient rats resulted in the further enhancement of these changes. After the development of hypoprothrombinemia with LMOX, a single subcutaneous injection of vitamin K1 normalized most of these abnormalities in blood coagulation parameters within 6 hr. When vitamin Κ was given at 200 μg/kg, PT, APTT and the plasma PIVKA level showed normal values for at least 8 days even when the animals were fed a vitamin K-deficient diet and treated with LMOX during the recovery period. The amount of vitamin Κ required to maintain most of the blood coagulation parameters in the normal range was about 3 μg/kg/day. The plasma level of vitamin Κ was higher than 0.3-0.5 ng/ml when the blood coagulation parameters were maintained in the normal range.
Hypoprothrombinemia
Latamoxef
Prothrombin time
Vitamin K deficiency
Thromboplastin
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Hypoprothrombinemic changes were compared in rats fed various vitamin K-deficient diets. Changes such as prolongation of prothrombin time and activated partial thromboplastin time, decrease in plasma levels of prothrombin and clotting factor VII, and increase in plasma descarboxyprothrombin, appeared in rats maintained on vitamin K-deficient diet, but in rats on ordinary diet (vitamin K-sufficient diet). As the development of hypoprothrombinemia was not significanthly different among animals fed various vitamin K-deficient diets, the blood coagulation parameters were concluded to be regulated only by the vitamin K level. Following the development of hypoprothrombinemia, hemorrhaging in various organs was detected in vitamin K-deficient rats, with strain differences in the severity of hemorrhage ; Fischer and Wistar strains were more sensitive than the Sprague Dawley strain. Administration of a beta-lactam antibiotic, latamoxef (LMOX), to vitamin K-deficient rats led to enhancement of the hypoprothrombinemic conditions, but LMOX-associated changes in plasma enzyme levels were not detected.
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Vitamin K deficiency
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