False Prolongation of Prothrombin Time in the Presence of a High Blood Concentration of Daptomycin

2016 ◽  
Vol 119 (4) ◽  
pp. 353-359 ◽  
Author(s):  
Tomoyuki Yamada ◽  
Ryuji Kato ◽  
Kazutaka Oda ◽  
Hidema Tanaka ◽  
Kaoru Suzuki ◽  
...  
Keyword(s):  
Prothrombin Time ◽  
Blood Concentration

Influence of Spironolactone and other Steroids on the Enzymatic Decay and Anticoagulant Activity of Bishydroxycoumarin

1970 ◽  
Vol 23 (03) ◽  
pp. 562-568 ◽  
Author(s):  
B Solymoss ◽  
S Varga ◽  
M Krajny ◽  
J Werringloer
Keyword(s):  
Prothrombin Time ◽  
Anticoagulant Therapy ◽  
Blood Concentration ◽  
Enzyme Inhibitor ◽  
Anticoagulant Activity ◽  
Subsequent Treatment ◽  
Supernatant Fraction ◽  
Great Care ◽  
Microsomal Enzyme ◽  
Do So

SummaryIn rats, pretreatment with spironolactone, norbolethone or ethylestrenol enhances the disappearance of bishydroxycoumarin from blood and restores prothrombin time to almost normal whereas triamcinolone or progesterone fail to do so.In itself SKF 525-A does not influence prothrombin time, but it markedly increases the blood concentration and the anticoagulant activity of bishydroxycoumarin. Furthermore, this microsomal enzyme-inhibitor suppresses the decrease of blood bishydroxycoumarin concentration elicited by ethylestrenol.Pretreatment with spironolactone or ethylestrenol (but not with progesterone) enhances the NADPH-dependent enzymatic decay of bishydroxycoumarin in liver microsomal + supernatant fraction.The elimination of bishydroxycoumarin from blood is reduced if its administration is followed by subsequent treatment with norbolethone, progesterone, ethylestrenol or triamcinolone.These findings suggest that great care should be exercised in patients on anticoagulant therapy and treated previously or conjointly with various steroids ; in dubious cases not only prothrombin time but also the blood concentration of the anticoagulant should be checked.

Recombinant Tissue Factor as Substitute for Conventional Thromboplastin in the Prothrombin Time Test

1992 ◽  
Vol 67 (01) ◽  
pp. 042-045 ◽  
Author(s):  
Armando Tripodi ◽  
Arnaldo Arbini ◽  
Veena Chantarangkul ◽  
Pier Mannuccio Mannucci
Keyword(s):  
Prothrombin Time ◽  
Tissue Factor ◽  
Oral Anticoagulant Therapy ◽  
Clotting Factor ◽  
Rabbit Brain ◽  
Sensitivity Index ◽  
Clotting Factors ◽  
Wide Range ◽  
Reference Preparation ◽  
Time Test

SummaryRelipidated recombinant tissue factor (r-TF) has been assessed in comparison with conventional rabbit brain thromboplastin (Manchester Reagent) for its suitability for measurement of prothrombin time (PT). The International Sensitivity Index (ISI) of r-TF calibrated against the International Reference Preparation BCT/253 (human plain) was found to be 0.96 and 1.12 with instrumental and manual techniques. Our study of plasmas from patients with congenital deficiencies of clotting factors covering a wide range of severity demonstrates that r-TF is able to detect even minor deficiencies of factors involved in the extrinsic and common coagulation pathways. Patients with liver diseases were correctly diagnosed with a prevalence of abnormal results comparable for both reagents. Between-assay reproducibility expressed as coefficient of variation was 2.3 % and 3.9 % at normal and abnormal PT levels.In conclusion, our evaluation shows that relipidated r-TF possesses the necessary requisites of sensitivity, diagnostic accuracy and reproducibility which make it a suitable candidate for PT determination both for monitoring oral anticoagulant therapy and diagnosing congenital and acquired clotting factor deficiencies. Moreover, being a highly defined reagent it may constitute a step forward in the standardization of PT testing.

The Effect of Several Tissue Thromboplastins on the Activation of the Abnormal Factor X (Factor X Friuli)

1972 ◽  
Vol 27 (03) ◽  
pp. 535-542 ◽  
Author(s):  
A Girolami ◽  
M Lazzarin ◽  
G Molaro
Keyword(s):  
Prothrombin Time ◽  
Rabbit Brain ◽  
Factor X ◽  
Dilution Curve ◽  
Human Origin ◽  
Rabbit Lung ◽  
Normal Ratio

SummaryThe effect of several tissue thromboplastins on the abnormal factor X (factor X Friuli) has been investigated.The prothrombin time varied between 33.6 and 69 sec. The prothrombin time percentile values (saline dilution curve and Quick’s formula for citrated plasma) varied between 6.6 and 22% and between 10.9 and 32.8%, respectively. The prothrombin time patient/normal ratio varied between 2.24 and 4.43.The factor X level varied between 3.5 and 20% of normal.Significant correlations were found to exist between the percentile factor X level and the prothrombin time in seconds, the percentile prothrombin time values and the prothrombin time patient/normal ratio. Thromboplastins of human origin yielded the lowest factor X values namely 5% thereby appearing to be practically “inert” with regard to the abnormal factor X. Thromboplastins obtained from rabbit lung on the contrary yielded the highest values, namely 15.3%. Thromboplastins obtained from simian or rabbit brain gave values intermediate between these two extremes.

The Reaction of Thiol Compounds with the Vitamin-K Dependent Clotting Factors

1969 ◽  
Vol 21 (03) ◽  
pp. 573-579 ◽  
Author(s):  
P Fantl
Keyword(s):  
Prothrombin Time ◽  
Vitamin K ◽  
Anaerobic Conditions ◽  
Clotting Factors ◽  
Thiol Compounds ◽  
Aerobic Conditions ◽  
One Stage ◽  
Factor Ii ◽  
Ph Dependent ◽  
The One

SummaryTreatment of human and dog oxalated plasma with 0.2 to 1.0 × 10−1 M 2.3-dithiopropanol (BAL) or dithiothreitol (DTT) at 2–4° C for 30 min results in the reduction of the vitamin-K dependent clotting factors II, VII, IX and X to the respective-SH derivatives. The reaction is pH dependent. Under aerobic conditions the delayed one stage prothrombin time can be partly reversed. Under anaerobic conditions a gradual prolongation of the one stage prothrombin time occurs without reversal.In very diluted plasma treated with the dithiols, prothrombin can be converted into thrombin if serum as source of active factors VII and X is added. In contrast SH factors VII, IX and X are inactive in the specific tests. Reoxidation to active factors II, VII, IX and X takes place during adsorption and elution of the SH derivatives. The experiments have indicated that not only factor II but also factors VII, IX and X have active-S-S-centres.

The Effect of Warfarin Sodium on the Duration of Platelet Aggregation

1967 ◽  
Vol 18 (03/04) ◽  
pp. 766-778 ◽  
Author(s):  
H. J Knieriem ◽  
A. B Chandler
Keyword(s):  
Platelet Count ◽  
Placebo Group ◽  
Platelet Aggregation ◽  
Prothrombin Time ◽  
Platelet Rich Plasma ◽  
Healthy Adults ◽  
Double Blind Study ◽  
Double Blind ◽  
Warfarin Sodium

SummaryThe effect of the administration of warfarin sodium (Coumadin®) on the duration of platelet aggregation in vitro was studied. Coumadin was given for 4 consecutive days to 10 healthy adults who were followed over a period of 9 days. The duration of adenosine diphosphate-induced platelet aggregation in platelet-rich plasma, the prothrombin time, and the platelet count of platelet-rich plasma were measured. Four other healthy adults received placebos and participated in a double-blind study with those receiving Coumadin.Although administration of Coumadin caused a prolongation of the prothrombin time to 2 or 21/2 times the normal value, a decrease in the duration of platelet aggregation was not observed. In most individuals who received Coumadin an increase in the duration of platelet aggregation occurred. The effect of Coumadin on platelet aggregation was not consistently related to the prothrombin time or to the platelet count. In the placebo group there was a distinct relation between the duration of platelet aggregation and the platelet count in platelet-rich plasma.The mean increase in the duration of platelet aggregation when compared to the control value before medication with Coumadin was 37.7%. In the placebo group there was a mean increase of 8.4%. The difference between the two groups is significant (p <0.001). Increased duration of platelet aggregation also occurred in two individuals who received Coumadin over a period of 10 and 16 days respectively.

Inhibition of Coagulation and Fibrinolysis by Aromatic Amidino Compounds

1971 ◽  
Vol 25 (03) ◽  
pp. 391-404 ◽  
Author(s):  
J.D Geratz
Keyword(s):  
Prothrombin Time ◽  
Human Plasma ◽  
Partial Thromboplastin Time ◽  
Inhibitory Effect ◽  
Clot Lysis ◽  
Similar Degree ◽  
Contact Activation ◽  
Plasma Clot ◽  
Human Thrombin ◽  
Canine Plasma

Summary1. Aromatic diamidines which are potent inhibitors of trypsin possess a marked inhibitory effect on the clotting activity of human thrombin and on the prothrombin time and partial thromboplastin time of human plasma. They also block the contact activation phase of the coagulation process. The strongest inhibitor among the compounds tested was M & B 4596 which was followed in second place by pentamidine.2. Pentamidine was 10 times more active than ε-ACA in impeding streptokinase-induced lysis of human plasma clots. It was 100-200 times stronger than ε-ACA in inhibiting the activation of bovine plasminogen by activators formed from the interaction between streptokinase and either human plasmin(ogen) or human plasma.3. The prothrombin time and partial thromboplastin time of canine plasma were less susceptible to inhibition by pentamidine than the same tests on human plasma. Clot lysis in the canine system was inhibited by pentamidine to a similar degree as in the human system. After intravenous injection of pentamidine in the dog there occurred the expected prolongation of the partial thromboplastin time and of the clot lysis time.

Two-Stage Procedure for the Quantitative Determination of Autoprothrombin III Concentration and Some Applications

1967 ◽  
Vol 18 (01/02) ◽  
pp. 198-210 ◽  
Author(s):  
Ronald S Reno ◽  
Walter H Seegers
Keyword(s):  
Prothrombin Time ◽  
Factor Vii ◽  
Two Stage ◽  
Pronounced Increase ◽  
One Stage ◽  
Assay Procedure ◽  
Bovine Plasma ◽  
The One ◽  
Autoprothrombin C

SummaryA two-stage assay procedure was developed for the determination of the autoprothrombin C titre which can be developed from prothrombin or autoprothrombin III containing solutions. The proenzyme is activated by Russell’s viper venom and the autoprothrombin C activity that appears is measured by its ability to shorten the partial thromboplastin time of bovine plasma.Using the assay, the autoprothrombin C titre was determined in the plasma of several species, as well as the percentage of it remaining in the serum from blood clotted in glass test tubes. Much autoprothrombin III remains in human serum. With sufficient thromboplastin it was completely utilized. Plasma from selected patients with coagulation disorders was assayed and only Stuart plasma was abnormal. In so-called factor VII, IX, and P.T.A. deficiency the autoprothrombin C titre and thrombin titre that could be developed was normal. In one case (prethrombin irregularity) practically no thrombin titre developed but the amount of autoprothrombin C which generated was in the normal range.Dogs were treated with Dicumarol and the autoprothrombin C titre that could be developed from their plasmas decreased until only traces could be detected. This coincided with a lowering of the thrombin titre that could be developed and a prolongation of the one-stage prothrombin time. While the Dicumarol was acting, the dogs were given an infusion of purified bovine prothrombin and the levels of autoprothrombin C, thrombin and one-stage prothrombin time were followed for several hours. The tests became normal immediately after the infusion and then went back to preinfusion levels over a period of 24 hrs.In other dogs the effect of Dicumarol was reversed by giving vitamin K1 intravenously. The effect of the vitamin was noticed as early as 20 min after administration.In response to vitamin K the most pronounced increase was with that portion of the prothrombin molecule which yields thrombin. The proportion of that protein with respect to the precursor of autoprothrombin C increased during the first hour and then started to go down and after 3 hrs was equal to the proportion normally found in plasma.

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