Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.21.6 (thromboplastin)
13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two spectrophotometric assays for prothrombin have been developed and compared with a one stage coagulant and an immunological assay. One of these assays (called the XAPC assay) uses a combination of factor Xa, phospholipid, Ca2+ and factor V as activator of prothrombin, and measures only normal prothrombin. The second (the ECAR assay) uses Echis carinatus venom as activator. This assay measures both normal prothrombin and PIVKA II (protein induced by vitamin K antagonists/absence). Combination of the results obtained by the XAPC and ECAR assays provides rapid and reliable information on the degree of "subcarboxylation" of prothrombin (oral anticoagulation, vitamin K deficiency). For patients on long term anticoagulant treatment the prothrombin time (Thrombotest) shows better correlation with the ratio prothrombin/prothrombin plus PIVKA II (XAPC/ECAR) than with the factor II concentration. For patients starting the anticoagulant treatment there is no correlation between the Thrombotest time and the XAPC/ECAR ratio. It seems doubtful that (a) spectrophotometric factor II assay(s) will be as useful as the prothrombin time in the control of oral anticoagulation.
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PMID:Spectrophotometric assays of prothrombin in plasma of patients using oral anticoagulants. 54 35

Cephalosporin antibiotics with N-methyl-thio-tetrazole (NMTT) side chains have been known to be associated with the development of hypoprothrombinemia. However, it has not been fully established whether these symptoms are induced by an inhibition of vitamin K production by intestinal microorganisms or by an inhibitory action of these antibiotics on endogenous vitamin K metabolism. Therefore, an attempt has been made to clarify the above-mentioned ambiguity by using germfree mice in which primary vitamin K deficiency can be established within a short experimental period. Germfree (GF) and conventional (CV) ICR male mice, 8-13 weeks old were used in this experiment. Vitamin K deficient (Def) and menaquinone-4 supplemented diet (MK-4) were fed to the mice in both rearing conditions. In the antibiotic-treated group, sodium latamoxef (LMOX, 300 mg/kg B.W./day) was intraperitoneally administered once a day, and in the control group the same volume of saline (Saline) was administered. Severe vitamin K deficient symptoms were observed in the GF-K-Def-LMOX group, and both prothrombin time (PT) and activated-partial thromboplastin time (APTT) values were prolonged on the 8th day of the experimental period compared with the GF-K-Def-Saline group. Furthermore the mortality rate of GF-K-Def-LMOX group was comparatively higher than that of the Saline group. This study has provided evidence that vitamin K deficiency is amplified by an administration of LMOX even in the absence of intestinal flora.
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PMID:Antibiotic-induced vitamin K deficiency and the role of the presence of intestinal flora. 227 82

Chemical modification of gamma-carboxyglutamic acid (Gla) residues in human prothrombin to gamma-methyleneglutamic acid (gamma-MGlu) residues elicited a conformation similar, if not identical, to that of des-gamma-carboxy prothrombin or PIVKA-II, i.e., prothrombin molecules induced by vitamin K antagonists or vitamin K deficiency states. The reaction seems to proceed sequentially by preferentially modifying a Gla at residue 32 that is located innermost among 10 Gla residues of human prothrombin. The initial modification resulted in nearly 50% losses of barium salt adsorption, the procoagulant activity and thrombin generation by the prothrombinase complex. The subsequent modification of two Gla residues at positions 6 and 16 gave rise to the immunoreactivity to an established monoclonal antibody that specifically recognizes the des-gamma-carboxy prothrombin. Further modification of Gla residues increased the reactivity to the antibody, indicating that the conformation recognized by the antibody was stabilized so as to more readily fit the recognition site of the antibody. The appearance of the immunoreactivity was obviously related to the modification of Gla residues in prothrombin, since all other similarly treated derivatives of prothrombin lacking the Gla-domain failed to react with the antibody. Such chemically modified prothrombins may serve as models for studying abnormal des-gamma-carboxy prothrombin produced in vitamin K deficiency states.
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PMID:Chemical modification of gamma-carboxyglutamic acid residues in prothrombin elicits a conformation similar to that of abnormal (des-gamma-carboxy)prothrombin. 227 30

We conducted a prospective study to determine (1) the maternal-fetal vitamin K1 transport in premature infants after vitamin K1 was given to the mothers antenatally and (2) the vitamin K1 effects on blood coagulation in the babies. Women in labor at less than or equal to 34 weeks of gestation were randomly selected to receive antenatal vitamin K1, 5 mg given intramuscularly (vitamin K1 group), or no vitamin K1 (control group). Eight infants, including one set of twins, were in the vitamin K1 group and six in the control group. Vitamin K1 concentrations were higher in the vitamin K1 group than in the control group (p = 0.06). Activated partial thromboplastin time was prolonged, and factor II coagulation activity and factor II antigen were proportionately decreased in cord plasma in both groups. The average ratio of factor II coagulation activity to antigen was not decreased in either group. Protein induced by vitamin K absence-II (PIVKA-II) was not detectable in any cord plasma sample in either group. These findings support previous reports that the decreased vitamin K-dependent coagulation activity in premature infants is the result of reduced synthesis of precursor proteins, rather than the result of vitamin K deficiency, and suggest that additional vitamin K1 is not likely to improve coagulation activity. Among those infants who underwent cranial ultrasonography, all four in the vitamin K1 group and one of five in the control group had mild intraventricular hemorrhage. Studies of a larger number of patients are necessary before it can be established that maternal antenatal administration of vitamin K1 results in improvement of coagulation and the prevention of intraventricular hemorrhage in premature infants.
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PMID:Maternal-fetal transport of vitamin K1 and its effects on coagulation in premature infants. 258 15

Most causes of abnormal bleeding can be determined from a complete blood count including platelet count and bleeding, prothrombin, activated partial thromboplastin, and thrombin times. Occasionally, further evaluation is necessary, such as tests of factor XIII function, fibrinolysis, and vascular integrity. Possible diagnoses include disseminated intravascular coagulation, thrombotic thrombocytopenic purpura, vitamin K deficiency, von Willebrand's disease, heparin-induced thrombocytopenia, acquired inhibitors of factor VIII, lupus anticoagulants, and coagulation disorders related to the acquired immunodeficiency syndrome.
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PMID:Laboratory evaluation of a bleeding patient. 266 Apr 7

Clinical and laboratory evaluation of severe bleeding can detect the presence of an intrinsic or acquired coagulation disorder. The three most common inherited coagulation disorders are factor VIII deficiency (hemophilia A), factor IX deficiency (hemophilia B), and von Willebrand's disease. Vitamin K deficiency, liver disease, and disseminated intravascular coagulation are the most common acquired disorders. A thorough clinical history is crucial to diagnosis. Screening tests that measure prothrombin time, partial thromboplastin time, thrombin time, and platelet count permit initial classification and guide selection of more specific tests. Results can then be used to determine appropriate therapy.
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PMID:Potentially catastrophic bleeding disorders. Approach to diagnosis and management. 267 67

Male and female rats were fed an ordinary diet which contained about 500 ng vitamin K/g or a vitamin K-deficient diet containing less than 5 ng vitamin K/g. Hypoprothrombinemic changes such as prolongation of the prothrombin time (PT) and activated partial thromboplastin time (APTT) were detected in male rats within 4-6 days after feeding of the vitamin K deficient diet. Blood clotting factor VII and descarboxy prothrombin (PIVKA) levels changed rapidly, with maximum alteration at 2-4 days. Similar changes in factor VII and PIVKA levels were observed in female rats, but they appeared only after feeding of the K deficient diet for a long period. PT and APTT in female rats showed slight or no alteration even after 10 day feeding of the K-deficient diet. These results indicate that male rats are more susceptible to vitamin K deficiency than female rats. Administration of latamoxef led to a dose-dependent development of hypoprothrombinemia in vitamin K-deficient female rats. The hypoprothrombinemia in vitamin K-deficient female rats was caused by beta-lactam antibiotics with N-methyltetrazolethiol, thiadiazolethiol and methyl-thiadiazolethiol as the 3'-position substituent of the cephem nucleus.
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PMID:Vitamin K-reversible hypoprothrombinemia in rats. I. Sex differences in the development of hypoprothrombinemia and the effects of beta-lactam antibiotics. 337 37

The authors administered cefotaxime to 20 children and studied laboratory parameters concerning peripheral blood: hemoglobin count, blood platelet count, red blood cell count, and hematocrit value, and the coagulation system: protein induced by vitamin K deficiency or by the presence of a vitamin K antagonist II (PIVKA II), hepaplastin test (HPT), prothrombin time (PT) and active partial thromboplastin time (APTT). The results obtained are summarized as follows: 1. Peripheral blood No abnormal values were observed. 2. Coagulation system (1) PIVKA II: In all cases, PIVKA II was negative. (2) HPT, PT and APTT: In all cases, no significant changes of these values which would suggest the tendency for prolonged bleeding were observed.
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PMID:[Effects of cefotaxime on the coagulation system, especially their dependence on vitamin K-related factors]. 344 28

Mouse Lewis lung (LL) carcinoma cells possess a factor X activator (procoagulant) that is inhibited in vivo by warfarin treatment or diet-induced vitamin K deficiency. This inhibition suggests that vitamin-K-dependent proteins are involved in LL cell activation of factor X. A LL primary tumor clone (LL13) was isolated which contained a warfarin-sensitive vitamin-K cycle of metabolism and expressed factor X procoagulant activity. LL13 cells exposed to media containing warfarin or deficient in vitamin K grew as well as cells in normal media, and activated factor X to similar extents. In contrast, administration of warfarin to mice bearing LL13 cells inhibited factor X procoagulant activity as well as the vitamin K cycle of metabolism in the primary tumors. In relation to LL13 cells grown in media containing fetal bovine serum, those incubated for 20 hr in media containing mouse serum or the sera from LL13-bearing mice exhibited 9- to 10-times higher levels of factor X procoagulant activity. However, LL13 cells exposed to media containing the sera of warfarin-treated LL-13-bearing mice or to barium-sulfate-adsorbed normal mouse serum activated factor X much less efficiently. Collectively, these data suggest that inhibition of vitamin K function in LL cells does not affect the extent of factor X activation and thus the intrinsic factor X procoagulant is not a vitamin-K-dependent protein. They further suggest that both a warfarin-sensitive (vitamin-K-dependent) protein present in normal mouse serum and a LL13 cell component participate in factor X procoagulant activity.
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PMID:Evidence for a warfarin-sensitive serum factor that participates in factor X activation by Lewis lung tumor cells. 357 May 55

A Cobas Bio centrifugal analyzer was used in a clinical laboratory for the performance of chromogenic clotting assays. Three commercially available photometric clotting tests--prothrombin time (PT), activated partial thromboplastin time (aPTT) and fibrinogen--were compared with the traditional clotting assays during 3 months. No great discrepancies were found between the traditional assays and the new photometric assays. The chromogenic PT could replace the traditional thrombotest, PT and Normotest, because it was sensitive and accurate over a broad range of clotting factor activity. Furthermore the chromogenic PT could be used to discriminate between a decreased clotting activity due to vitamin K deficiency or to a decreased protein synthesis by the liver. A decreased protein synthesis was confirmed by measuring a decrease in the serum cholinesterase activity. The chromogenic aPTT could be used for the assay of heparin concentrations in the therapeutic range and turned out to be more sensitive for deficiencies of factor VIII and factor IX than a traditional clotting aPTT. We conclude that the accuracy and practicability of clotting assays are improved by the new assays without diminishing the clinical value of the results.
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PMID:Use of a centrifugal analyzer for a chromogenic prothrombin time, a chromogenic activated partial thromboplastin time and a kinetic fibrinogen assay in a routine hospital laboratory. 366 83


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