Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.6 (thromboplastin)
13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During the last three years we have analyzed, in 94 patients with chronic arterial occlusive disease, in order to assess the hemorheological and hemocoagulative balance, the following parameters: prothrombin time, partial thromboplastin time, antithrombin III, antiplasmin, fibrinogen, factor VIII, erythrocyte sedimentation rate, platelet aggregation, erythrocyte filterability and hematocrit values. The main findings were: in 56 patients the hematocrit value was higher than 44%; Katz index was above normal values in 61.7% of the cases; ATIII showed a trend to lower values; platelet aggregation was increased; no significant variations in comparison to normal values were found in FVIII, antiplasmin levels, prothrombin time and partial thromboplastin time. Erythrocyte filterability values were decreased at a level as lower as more advanced was the clinical stage of the disease. These findings show, in agreement with those of other authors, the presence of hyperviscosity and hypercoagulative state in patients with chronic arterial occlusive disease.
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PMID:[Hemorheologic and blood coagulation studies in 94 patients with chronic obstructive peripheral arterial disease]. 392 68

The plasma values for factors (F)VII, FVIII:C, FVIIIR:Ag, FIX, FX, and FXI and the thrombin clotting time (TCT) were determined for 28 dogs with naturally occurring hepatic disease. The major morphologic type of hepatic disease present in a given dog, as determined by hepatic biopsy and histopathologic examination, was degeneration (12 dogs), inflammation (9 dogs), cirrhosis (3 dogs), or neoplasia (4 dogs). A specific morphologic diagnosis also was made for each dog in the study. Plasma coagulation factor values and screening tests were consistently abnormal in greater than 50% of the dogs with each type of hepatic disease as follows: degeneration--decreased FXI; inflammation--increased FVIIIR:Ag; cirrhosis--shortened TCT, decreased FIX, FX, and FXI, and increased FVIIIR:Ag; and neoplasia--shortened TCT, decreased FVIII:C, and increased FVIIIR:Ag. The plasma coagulation factor values were compared with serum alanine aminotransferase (ALT) and alkaline phosphatase (ALP) activities, fibrinogen-fibrin degradation product (FDP) concentration, and the prothrombin time (PT) and activated partial thromboplastin time (APTT) to determine the sensitivity and specificity of each test in detection of hepatic disease. Of all dogs with hepatic disease, 93% had at least 1 abnormal coagulation test value. The PT and APTT were abnormal in 50% and 75%, respectively, of these same dogs. Increased serum ALT and ALP activities were present in 61% and 50%, respectively, and FDP concentrations were increased in 14% of dogs with hepatic disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma coagulation factor abnormalities in dogs with naturally occurring hepatic disease. 666 Jun 23

Intravenous adrenalin infusion (5 micrograms/kg, at most 160 micrograms in 10 min) normalized partial thromboplastin time (PTT) and ristocetin induced platelet aggregation (RIPA) in 4 of the 14 patients with von Willebrand's disease (VWD) in a short period of time. Although mean factor VIII (F-VIII) procoagulant activity was almost doubled 5 min following infusion, this was mainly observed in patients with relatively high baseline (> 2%) AHF activity. Mean F-VIII procoagulant activity rose by more than 100% following 10 days of corticosteroid treatment (deltacortil 2 mg/kg/day, at most 60 mg/day). PTT became normal in 6 of the 11 patients, but RIPA normalized only in 2. The improvement of RIPFA did not correspond to bleeding time in every patient. These results may suggest that if the baseline AHF activity is relatively high (greater than or equal to 9.5%), corticosteroid could be tried before schedule surgical intervention in patients with VWD.
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PMID:Effect of intravenous adrenalin infusion and corticosteroid treatment in patients with von Willebrand's disease. 677 88

Effects of partial hepatectomy on blood coagulation factors were investigated in rats. Analysis were performed 24, 48 and 72 hours after surgery. Howell's time was significantly higher after 24 and 48 h compared to the control value. Prothrombin time was significantly prolonged after 24 h. Partial thromboplastin time did not differ significantly in any time. FII values were significantly reduced after 24 and 48 h, but FV values only after 24 h. FVII showed significant decrease after 24 h, but significant increase at 48 h. FVIII and ATIII average values were significantly lower after 24, 48 and 72 h. Plasma fibrinogen increased. Significant differences were observed 48 and 72 h after surgery. Differences in normalization time of these coagulation factors are most probably the consequence of their synthesis in various cell types, regenerated at different periods after partial hepatectomy.
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PMID:Blood coagulation factors changes during liver regeneration in rats. 751 28

A wide variety of haemostatic variables were measured in healthy male subjects predominantly blood donors residing in Riyadh, the capital city of Saudi Arabia. Subjects were divided according to ethnic origin: Saudi Arabs n = 487, Westerners (Europeans and Americans) n = 300, South East Asians (Koreans and Filipinos) n = 360, and West Africans n = 82. There were no significant differences in prothrombin time, partial thromboplastin time, thrombin time, reptilase time, plasma fibrinogen, antithrombin, plasminogen and platelet count between Saudis, Westerners and Asians. Africans exhibited significantly lower plasma levels of fibrinogen, platelet count and plasminogen than other ethnic groups. Arabs and Africans had higher levels of FVIII:C and vWF:ristocetin cofactor than Westerners. On the other hand, FX was significantly higher in Westerners than in other ethnic groups. Smokers had higher fibrinogen levels than non-smokers. These variations, which could not be related to blood group distribution, physical parameters of height and weight, may be due to genetic and/or dietary habits. In conclusion, this study established the existence of racially determined variations in haemostatic variables, with Black Africans showing changes consistent with a lesser tendency towards atherosclerosis and cardiovascular disease than other ethnic groups. These variations should be taken into account when investigating the haemostatic system in patients.
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PMID:Ethnic variations in the haemostatic system: comparison between Arabs, Westerners (Europeans and Americans), Asians and Africans. 757 95

The procoagulant subcellular matrix of stimulated endothelial cells that contains tissue factor (TF) was used to investigate the mechanism by which TF pathway inhibitor (TFPI) inhibits thrombin formation initiated by TF/factor VIIa (FVIIa) under flow conditions. Purified coagulation factors VII, X, and V and prothrombin were perfused at a wall shear rate of 100 s-1 through a flow chamber containing a coverslip covered with matrix of cultured human umbilical vein endothelial cells. This resulted in a TF- and FVII-dependent FXa and thrombin generation as measured in the effluent at the outlet of the system. Inhibition of this TF/FVIIa-triggered thrombin formation by TFPI purified from plasma was dependent on the amount of TF present on the endothelial cell matrix. The rate of prothrombinase assembly and steady-state levels of thrombin formation were decreased by TFPI. Because persistent albeit decreased steady-state levels of thrombin formation occurred in the presence of TFPI, we conclude that plasma-TFPI does not inhibit FXa present in the prothrombinase complex. The addition of FIX and FVIII to perfusates containing FVII and FX increased the FXa generation on endothelial matrices, and counteracted the inhibition of thrombin formation on endothelial cell matrices by TFPI. Our data provide further evidence for the hypothesis that the rapid inactivation of TF/FVIIa by TFPI in combination with the absence of either FVIII or FIX causes the bleeding tendency of patients with hemophilia A or B.
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PMID:Activated factor X and thrombin formation triggered by tissue factor on endothelial cell matrix in a flow model: effect of the tissue factor pathway inhibitor. 804 29

Low-molecular-weight heparin (LMWH) (Fragmin) vs heparin was studied in vitro in order to investigate its antithrombotic efficacy in the isolated thrombogenic link of cardiopulmonary bypass (CPB). Fresh human blood (400 ml) with various dosages of the anticoagulant was recycled in a CPB circuit for 120 min. The standard dosage of heparin (1,500 IU, n = 6) was compared with a lower dosage (1,000 IU, n = 3) and several dosages of Fragmin (IU anti-FXa): 750 (n = 1), 1,500 (n = 3), 2,100 (n = 4) and 2,500 (n = 3). Clotting occurred in three Fragmin experiments at dosages of 750, 1,500 and 2,100 IU. This was associated with short activated clotting time (ACT) and activated partial thromboplastin time (aPTT) but was independent of the levels of anti-FXa, FVIII, von Willebrand factor and prothrombin complex. It was concluded that at least twice the dose of Fragmin (anti-FXa), compared with heparin, was required, suggesting that thrombin inhibition is crucial for the antithrombotic efficacy of heparin in CPB circuits. Absence of fibrinolytic markers suggests that the well known enhancement of fibrinolysis often seen during CPB, is not due to heparin interaction with normally circulating blood components, but rather to interaction with the vessel walls or to the surgical trauma itself.
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PMID:Fragmin (LMWH) vs heparin for anticoagulation during in vitro recycling of human blood in cardiopulmonary bypass circuits: dose-dependence and mechanisms of clotting. 805 61

We are reporting on a 47-year-old man who presented with a prolongation of the activated partial thromboplastin time (APTT) prior to orthopedic surgery. An evaluation suggested an inhibitor when his plasma prolonged a normal control APTT upon 50:50 solution of patients with normal plasma. The platelet-neutralizing procedure (PNP), anticardiolipin antibody, and antinuclear antibody (ANA) were positive. Further studies revealed decreased von Willebrand factor ristocetin cofactor (vWF:RCoF), von Willebrand factor antigen (vWF:Ag), an inhibitor to vWF, and absent high-molecular-weight vWF multimeters. Assays of FVIII:C, FIX, and FXI were nonparallel to the standard curve. Intravenous immunoglobulin (IVIG) corrected the APTT, multimeric pattern, and FVIII:C by the 7th day postinfusion. This case demonstrates the efficacy of IVIG for acquired von Willebrand's syndrome (vWS) and also represents a unique combination of a lupus-like anticoagulant and acquired vWS in a patient without the full serological requirement for systemic lupus erythematosus (SLE). Whether patients with acquired vWS and lupus inhibitors are more or less susceptible to either a thrombotic complication or hemorrhage is not established. Prospective studies for the incidence of lupus inhibitor/antiphospholipid syndromes and vWF deficiencies are needed to assess this question.
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PMID:Acquired von Willebrand's syndrome in association with a lupus-like anticoagulant corrected by intravenous immunoglobulin. 817 82

Cimex lectularius salivary gland homogenate delayed the recalcification time of human citrated plasma. Separation of the salivary gland homogenate by molecular sieving HPLC chromatography resulted in a single major peak of anticlotting activity with an apparent molecular mass of 17,000. The anticoagulant principle inhibited the activation of factor X to factor Xa in the tenase complex (FVIII, FIXa, FX, phospholipids, and calcium). However, it did not directly inhibit already activated factor Xa, suggesting that the anticlotting activity is not an anti-factor Xa. Additionally, this salivary gland anticoagulant further retarded the recalcification time of factor VIII- and factor IX-deficient plasmas, suggesting that the anticlotting principle is not directly inhibiting either the coagulation factor VIII or factor IXa. Altogether these data suggest that the anticlotting activity is an inhibitor of the activation of factor X to factor Xa in the tenase complex.
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PMID:A novel inhibitor of factor X activation from the salivary glands of the bed bug Cimex lectularius. 868 87

Twenty-five young subjects were divided into experimental (n = 13) and control (n = 12) groups in order to examine the acute and chronic effects of exercise on blood coagulation and fibrinolysis. Blood coagulation and fibrinolysis variables were ascertained in both groups before and after a physical conditioning programme both at rest and following maximal exercise. The experimental group exercised for 12 weeks [30 min, 3 x week at 70% (6 weeks) and 80% (6 weeks) of maximum heart rate]. The control group maintained normal activity patterns. Significant activation (P < 0.05) of blood coagulation was observed in response to maximal exercise before and after the conditioning programme in both groups in activated partial thromboplastin time (APTT), thrombin clotting time (TCT), factor VIII procoagulant activity (FVIII PA) and factor VIII antigen (FVIII A). Likewise, blood plasminogen activator showed a significant increase (P < 0.05) in response to maximal exercise before and after conditioning in both groups. Although VO2 max following the conditioning programme was significantly increased in the exercise group versus control, no significant changes (P > 0.05) were observed in either group in blood coagulation and fibrinolysis parameters at rest or in response to maximal exercise. It is concluded that maximal exercise transiently accelerates blood coagulation and activates blood fibrinolytic activity, however physical conditioning appears not to influence the haemostatic and fibrinolytic systems at rest or in response to maximal exercise.
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PMID:Blood coagulation and fibrinolysis at rest and in response to maximal exercise before and after a physical conditioning programme. 882 26


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