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)

Coagulation factors evaluated in a group of patients with borderline hypertension. The following tests were carried out: prothrombin time (PT) and partial thromboplastin time (PTT), Factor VIII coagulant activity, Factor VIII antigen and Factor VIII ristocetin cofactor, Factor XII and Factor XI activities. These tests were selected for their relationship to the contact coagulative activation near the vascular wall. Comparing the results with those of normal controls, Factor VIII coagulant activity, Factor XII and PTT levels were significantly higher. Other tests were all within normal limits in both groups. High Factor VIII and Factor XII levels associated with PTT shortening suggest that an increased synthesis and/or release of these coagulation factors was present in our patients. Activated coagulation seems to be present in borderline hypertension before the appearance of clinical signs of vascular lesions.
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PMID:Clotting changes in borderline hypertension. 350 21

Factor VIII Leiden is a genetic variant of coagulation factor VIII which has been detected in the plasma of a patient with mild haemophilia A. In this patient's plasma factor VIII procoagulant antigen was in 5-fold excess over factor VIII procoagulant activity, indicating the presence of an abnormal factor VIII molecule. The variant factor VIII was isolated from the patient's plasma, and its functional properties were studied in a factor X-activating system consisting of purified components. The isolated factor VIII Leiden was normally activated by factor Xa and by thrombin, but the activity of the factor VIIIa was about 3% of normal. The defect of factor VIIIa Leiden was studied by comparison with normal factor VIIIa in kinetic experiments of factor Xa formation. The results support the hypothesis that factor VIIIa Leiden has a reduced affinity for phospholipid-bound factor IXa in the intrinsic factor X-activating complex.
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PMID:The functional defect of factor VIII Leiden, a genetic variant of coagulation factor VIII. 393 62

The role of factor VIII in the activation of human factor X by factor IXa, Ca2+ and phospholipid has been investigated. Factor VIII stimulated the factor Xa formation after activation by factor Xa or thrombin; the activity of thrombin-activated factor VIII was about 4-fold that of factor Xa-activated factor VIII. The isolated procoagulant moiety of the factor VIII complex behaved identically to the complete complex, whereas the von Willebrand factor moiety did not participate in the factor Xa formation. Thrombin-activated factor VIII complex (factor VIIIa) was used to study the effect of factor VIIIa in kinetic experiments. The results revealed a complex kinetic behaviour, including substrate inhibition and non-linearity of the reaction rate with the enzyme concentration. Using previously obtained insight into the kinetics of factor X activation in the absence of factor VIII, the results were found to support the hypothesis that factor VIIIa participates in the factor Xa formation in a complex with phospholipid-bound factor IXa; the formation of the factor VIIIa-factor IXa complex then increases the catalytic efficiency of the factor IXa by 500-fold.
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PMID:The role of factor VIII in the activation of human blood coagulation factor X by activated factor IX. 393 63

Three activated partial thromboplastin time (APTT) reagent test systems, General Diagnostics Automated APTT, American Dade Actin FS, and Pacific Hemostasis (Thromboscreen KAPTT) reagent, containing different activators for the APTT assay, were evaluated for their precision and sensitivity to factor deficiencies in the intrinsic coagulation system. The data suggest that micronized silica and ellagic acid reagent systems were similar in sensitivity to Factor VIII, X, and XII deficiencies, whereas, the micronized kaolin reagent was significantly less sensitive to these deficiencies. Factor XI deficiency was detected equally well with the use of all three reagent systems. The ellagic acid reagent was somewhat more sensitive to Factor IX deficiency than the micronized silica reagent, and the micronized kaolin reagent was again least sensitive. Both the micronized silica and ellagic acid based reagents were insensitive to all but severe deficiencies in prekallikrein, whereas the micronized kaolin reagent was unable to detect this deficiency. All three reagents were insensitive to all but severe deficiencies in high-molecular-weight kininogen. The authors conclude that the reagent systems tested, containing micronized silica or ellagic acid as activators, are similar in sensitivity when used in a routine activated partial thromboplastin time to screen for factor deficiencies, whereas the reagent system containing micronized kaolin as an activator is less sensitive.
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PMID:Sensitivity of three activated partial thromboplastin time reagents to coagulation factor deficiencies. 394 Apr 20

Low-molecular-weight (LMW) heparin has been compared to standard unfractionated (UF) heparin in a total of 49 patients on hemodialysis and hemofiltration in order to determine the necessary therapeutic dose and its effect on the coagulation system. A LMW heparin dose corresponding to 50% of the normal UF heparin dose was found to produce similar plasma heparin levels (anti-FXa-U/ml) in particular on minimal heparinization. At higher doses, UF heparin produced a more marked increase in plasma-heparin than did LMW heparin. Highly significant differences were found between UF and LMW heparin in their effects on PTT and thrombin time. Partial thromboplastin time (PTT) increased under UF heparin by an average of 120 s whereas LMW heparin only produced an increase of 5-7 s. Thrombin time was increased by 250-280 s under UF heparin and by 5-8 s under LMW heparin. With this LMW heparin dose of 50% of the UF heparin dose, no thrombosis of the extracorporal system occurred and no macroscopic detectable thrombotic material was found in the dialyzers or filters. No significant differences were observed between the effects of UF and LMW heparin on Factor VIII activity and fibrin monomers, so that a difference in coagulation activation between the two heparins can be excluded. Furthermore, there were no changes in thromboplastin time according to Quick, fibrinogen, antithrombin III, plasminogen, and a2-antiplasmin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Use of low molecular-weight heparin in hemodialysis patients]. 398 50

To evaluate the effects of chlormadinone acetate upon the coagulation of blood and fibrinolysin systems, 35 healthy, young women voluntarily using some form of birth control were studied. 10 women who served as controls used intrauterine devices; 25 women took either a progestin-estrogen (1 mg norethindrone acetate and 1 mg mestranol) combination or a synthetic progestational agent (0.5 mg chlormadinone acetate) on a coded, double-blind basis. Platelet counts, thrombelastograms, and plasma assays were performed prior to and after 3 and 6 months of treatment. After 3 months, those taking progestin-estrogen showed a highly significant increase toward hypercoagulability in Quick time, Factors II, VII, and X, and increased levels in the thromboplastin generation time (TGT), Factors V and IX, and plasminogen. At 6 months all levels remained elevated except for TGT. Those on chlormadinone acetate had only a slightly significant change toward hypercoagulability in Quick time and Factor VIII, an increase in Factor IX, and a decrease in Factor X. In the control group only TGT was elevated. The progestin alone induced only minimal changes in comparison to the marked rises accompanied with progestin-estrogen therapy.
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PMID:Progestational agents and blood coagulation. IV. Changes induced by progestogen alone. 411 4

An 85 year old woman was studied because of severe bleeding. Acquired inhibitors to factor VIII and to phospholipid procoagulants were demonstrated. Platelet factor 3 (Pf3) assay was prolonged with both kaolin and Russell's Viper Venom (Stypven-R). It was normal with patient's washed platelets and normal plasma, but abnormal when normal platelets were incubated with patient's plasma. The inhibitor also blocked the coagulant action of Bell and Alton thromboplastin, inosithin, phosphatidyl ethanolamine and phosphatidyl choline, but not that of tissue thromboplastin or cardiolipin. All other platelet functions were normal. The inhibitors were purified by Al (OH3) absorption, heating at 56degrees, precipitation by 50% ammonium sulfate, followed by dialysis and DEAE-cellulose chromatography. A partial separation of the two inhibitors was achieved. Cyclophosphamide treatment resulted in cessation of bleeding and dissappearance of the inhibitors. This seems to be the first instance of an acquired circulating inhibitor specifically directed against phospholipid procoagulants in a patient who also had an inhibitor to Factor VIII.
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PMID:Hemostatic defect due to acquired circulating inhibitors against lipid procoagulant and factor VIII. 454 47

To assess the effect of a hypertonic saline infusion abortion upon the coagulation mechanism, 39 women from Roosevelt and Harlem Hospitals in New York were studied prior to and at 3 and 24, or 24 and 48 hours after the abortion. The prothrombin and partial thromboplastin times were unaffected at 24 and 48 hours when compared with the pre-infusion data. The platelet counts were decreased at 24 hours by 22% of their pre-abortion levels (246,000 vs. 193,000). Profibrinolysin was lower than pre-infusion levels at 24 and 48 hours by 21 and 17% respectively. Fibrinolytic inhibitors were lower at 24 hours by 22% of their pre-infusion levels, while fibriogin levels were not significantly changed. The plasma protamine paracoagulation test showed a change in 40, 68, and 40% of the women at 3, 24, and 48 hours respectively, from a clear plasma to one with a fine or coarse precipitate. The addition of protamine sulfate to plasma showed evidence of fibrin monomer in 60% of the patients at 3 hours, 20% at 24 hours, and 35% at 48 hours. This suggests the incomplete early activation of the coagulation mechanism. The results from the 6 patients studied at 3 and 24 hours showed a small decrease in Factor VIII at 3 hours and a more pronounced decrease at 24 hours. Results suggest changes in the coagulation mechanism begin at 3 hours, become more intensive at 24 hours, and are returning to normal at 48 hours.
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PMID:Coagulation changes after hypertonic saline infusion for late abortions. 501 99

Plasma coagulation factors were measured in twelve male insulin-dependent diabetics with no retinopathy, ten with background and ten with proliferative retinopathy and ten non-diabetics. Factor VIII pro-coagulant activities (VIII:C), ristocetin cofactor activities and factor VIII-related antigen concentrations (VIIIR:ag) were significantly related to the severity of diabetic retinopathy (P less than 0.025, trend test). The mean ratio of VIII:C/VIIIR:ag was lower in the diabetics with proliferative retinopathy than in the other groups of diabetics (P less than 0.05) or the controls (P less than 0.02). Concentrations of alpha 2 macroglobulin and alpha 1 antitrypsin were highest in diabetics with proliferative retinopathy (0.1 greater than P greater than 0.05, trend test) but mean prothrombin and activated partial thromboplastin times and mean concentrations of alpha 2 antiplasmin, plasminogen activator and antithrombin III were similar in all groups. Concentrations of the platelet-specific protein beta thromboglobulin, though higher in diabetics than controls (P less than 0.005), were not related to retinopathy. The plasma concentrations of coagulation factors did not correlate with creatinine clearance and there were no significant differences between groups in concentrations C-reactive protein; this suggests that the raised concentrations of coagulation factors in diabetics with retinopathy were not a result of associated nephropathy or an 'acute phase protein' response to diabetic tissue damage. Increased coagulation activity in diabetics may contribute to the development of retinopathy.
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PMID:Plasma haemostatic factors and diabetic retinopathy. 619 95

Factor VIII (FVIII) procoagulant activity is the function of a plasma glycoprotein that is missing or inactive in patients with classic hemophilia. Numerous studies have shown that trace thrombin causes rapid enhancement followed by gradual inactivation of FVIII procoagulant activity. Recent evidence suggests that thrombin activation of the FVIII/von Willebrand factor (vWF) protein is required for inactivation to occur. All of these studies have used the one-stage partial thromboplastin time to assay FVIII activity. Other investigators have used the two-stage assay of FVIII activity and have been unable to demonstrate thrombin-induced enhancement of FVIII activity, although inactivation has consistently occurred. We performed experiments designed to help resolve this disagreement, using the two-stage assay specifically modified to detect thrombin potentiation of FVIII activity. The length of the first-stage incubation time was found to be critical in demonstrating the initial effect of thrombin on FVIII activity. Taking advantage of this finding we were able to show a 4.1 +/- 0.5-fold enhancement of FVIII activity upon incubating purified FVIII/vWF with 0.04 NIH unit thrombin per ml. The apparent enhancement of FVIII activity declined with increasing thrombin concentration. Incubation with 0.08, 0.16, and 0.32 NIH unit thrombin per ml resulted in only 3.2 +/- 0.5, 2.6 +/- 0.5 and 1.5 +/- 0.3-fold enhancement, respectively, of FVIII activity. As with results from the one-stage assay, activation was followed by slow inactivation of FVIII/vWF. Using the two-stage assay we also showed 100% inactivation and 100% inhibition of FVIII activity by plasmin and human anti-FVIII IgG, respectively. Plasmin inactivation of FVIII activity showed a dose-response effect. Thrombin was unable to activate plasmin-degraded FVIII/vWF. Our results show that thrombin potentiation of FVIII activity is easily demonstrable in the two-stage assay. These findings support the contention that activation of FVIII activity by thrombin is prerequisite for inactivation and underscore the importance of thrombin activation of FVIII/vWF in the intrinsic clotting system.
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PMID:Thrombin potentiation of factor VIII procoagulant activity: assessment by the two-stage assay. 621 66


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