scholarly journals Activated Factor XI is Increased in Plasma in Response to Surgical Trauma but not to Recombinant Activated FVII-Induced Thrombin Formation

2020 ◽  
Author(s):  
Heiko Rühl ◽  
Anne M. Friemann ◽  
Sara Reda ◽  
Nadine Schwarz ◽  
Franziska I. Winterhagen ◽  
...  
Keyword(s):  
Surgical Trauma ◽  
Factor Xi ◽  
Thrombin Formation

scholarly journals The Role of Factor XI in Thrombin Generation Induced by Low Concentrations of Tissue Factor

2001 ◽  
Vol 85 (06) ◽  
pp. 1060-1065 ◽  
Author(s):  
Irene Keularts ◽  
Ariella Zivelin ◽  
Uri Seligsohn ◽  
H. Coenraad Hemker ◽  
Suzette Béguin
Keyword(s):  
Tissue Factor ◽  
Thrombin Generation ◽  
Contact Activation ◽  
Factor Xi ◽  
Platelet Poor Plasma ◽  
Low Concentrations ◽  
Time Determination ◽  
Thrombin Formation

SummaryThrombin generation has been studied in the plasma of severely factor XI deficient patients under conditions in which contact activation did not play a role. In platelet-rich as well as platelet-poor plasma, thrombin generation was dependent upon the presence of factor XI at tissue factor concentrations of between 1 and 20 pg/ml i.e. ~ 0.01 to 0.20% of the concentration normally present in the thromboplastin time determination. The requirement for factor XI is low; significant thrombin generation was seen at 1% factor XI; at 10%, thrombin formation was nearly normalised. A suspension of normal platelets in severely factor XI deficient plasma did not increase thrombin generation. This implies that there is no significant factor XI activity carried by normal platelets, although the presence of factor XI and factor XI inhibitors in platelets cannot be ruled out.

Invasive therapeutic options in truncal varicosity of the great saphenous vein

VASA ◽  
2006 ◽  
Vol 35 (3) ◽  
pp. 157-166 ◽  
Author(s):  
Hach-Wunderle ◽  
Hach
Keyword(s):  
Minimally Invasive ◽  
Saphenous Vein ◽  
Venous Insufficiency ◽  
Great Saphenous Vein ◽  
Varicose Veins ◽  
Venous Pressure ◽  
Stage Iii ◽  
High Ligation ◽  
Surgical Trauma ◽  
Disease Stages

It is known from current pathophysiology that disease stages I and II of truncal varicosity of the great saphenous vein do not cause changes in venous pressure on dynamic phlebodynamometry. This is possibly also the case for mild cases of the disease in stage III. In pronounced cases of stage III and all cases of stage IV, however, venous hypertension occurs which triggers the symptoms of secondary deep venous insufficiency and all the complications of chronic venous insufficiency. From these facts the therapeutic consequence is inferred that in stages I and II and perhaps also in very mild cases of stage III disease, it is enough "merely" to remove varicose veins without expecting there to be any other serious complications in the patient’s further life caused by the varicosity. Recurrence rates are not included in this analysis. In marked cases of disease stages III and IV of the great saphenous vein, however, secondary deep venous insufficiency is to be expected sooner or later. The classical operation with saphenofemoral high ligation ("crossectomy") and stripping strictly adheres to the recognized pathophysiologic principles. It also takes into account in the greatest detail aspects of minimally invasive surgery and esthetics. In the past few years, developments have been advanced to further minimize surgical trauma and to replace the stripping maneuver using occlusion of the trunk vein which is left in place. Obliteration of the vessel is subsequently performed via transmission of energy through an inserted catheter. This includes the techniques of radiofrequency ablation and endovenous laser treatment. High ligation is not performed as a matter of principle. In a similar way, sclerotherapy using microfoam is minimally invasive in character. All these procedures may be indicated for disease stages I and II, and with reservations also in mild forms of stage III disease. Perhaps high ligation previously constituted overtreatment in some cases. Targeted studies are still needed to prove whether secondary deep venous insufficiency can be avoided in advanced stages of varicose vein disease without high ligation and thus without exclusion of the whole recirculation circuit.

Effects of Radiographic Contrast Agents on Thrombin Formation and Activity

1998 ◽  
Vol 80 (08) ◽  
pp. 266-272 ◽  
Author(s):  
Andrew Parker ◽  
William Fay
Keyword(s):  
Contrast Agents ◽  
Tissue Factor ◽  
Coronary Angioplasty ◽  
Molecular Mechanisms ◽  
Factor Viia ◽  
Minor Effect ◽  
Ionic Contrast ◽  
Radiographic Contrast ◽  
Inhibition Of Thrombin ◽  
Thrombin Formation

SummaryClinical trials suggest that the risk of thrombosis during coronary angioplasty is lower with ionic contrast agents than with nonionic contrast agents. However, the molecular mechanisms underlying this effect are unknown. This study examined the effects of contrast agents on thrombin formation and its interaction with substrates, inhibitors, and ligands to define potential mechanisms by which contrast agents affect thrombus formation. Two ionic agents, diatrizoate and ioxaglate, and one nonionic agent, ioversol, were studied. Ionic agents inhibited factor X activation by the tissue factor-factor VIIa complex more potently than ioversol (53 ± 3.7, 43.0 ± 1.9, and 26.5 ± 2.4% inhibition by diatrizoate, ioxaglate, and ioversol, respectively, at concentrations of 5%). Ionic contrast agents were potent inhibitors of prothrombinase function, inhibiting thrombin formation by >75% at contrast concentrations of 0.6% (p <0.005). Ioversol inhibited prothrombinase to a significantly lesser extent than ionic agents. Clotting assays suggested that ioxaglate was the most potent inhibitor of thrombin generation in plasma despite having the least effect on fibrin polymerization. Contrast agents inhibited binding of thrombin to fibrin, with ionic agents producing a more potent effect than ioversol (p <0.02). However, contrast agents did not inhibit thrombin-mediated platelet activation, had only a minor effect on inhibition of thrombin by antithrombin III, and did not affect thrombin-hirudin interactions. In summary, these studies identify specific mechanisms by which radiographic contrast agents inhibit thrombin formation and function – i.e. inhibition of tissue factor-dependent factor Xa generation, inhibition of the prothrombinase complex, and inhibition of thrombin binding to fibrin. These findings may help to explain the reduced risk of thrombosis during coronary angioplasty associated with ionic contrast agents.

Very Low Activated Factor VII and Reduced Factor VII Antigen in Familial Abetalipoproteinaemia

1998 ◽  
Vol 80 (08) ◽  
pp. 233-238 ◽  
Author(s):  
K. A. Mitropoulos ◽  
M. N. Nanjee ◽  
D. J. Howarth ◽  
J. C. Martin ◽  
M. P. Esnouf ◽  
...  
Keyword(s):  
Plasma Concentrations ◽  
Positive Association ◽  
Factor Ix ◽  
Factor Vii ◽  
Unesterified Fatty Acid ◽  
Factor Xii ◽  
Factor X ◽  
Factor Xi ◽  
Activated Factor Vii ◽  
Normal Mean

SummaryAbetalipoproteinaemia is a rare disorder of apolipoprotein B metabolism associated with extremely low plasma concentrations of triglyce-ride. To discover whether the general positive association between factor VII and triglyceride levels extends to this condition, 5 patients were compared with 18 controls. All patients had a triglyceride below 100 μmol/l. Plasma unesterified fatty acid concentration was normal. Although factor IX activity was only slightly reduced (mean 88% standard) and factor IX antigen was normal, mean activated factor VII in patients was strikingly reduced to 34% of that in controls, a level similar to that found in haemophilia B. The patients’ mean factor VII activity and factor VII antigen were also significantly reduced to 54% and 63% of those in controls, respectively. Mean factor XI activity and tissue factor pathway inhibitor activity were reduced in patients to 70% and 75% of control values respectively, while factor XII, factor XI antigen, factor X, prothrombin and protein C were normal.

The Lupus Inhibitor: A Study of Its Heterogeneity

1981 ◽  
Vol 46 (04) ◽  
pp. 734-739 ◽  
Author(s):  
M C Coots ◽  
M A Miller ◽  
H I Glueck
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Inhibitory Activity ◽  
Inhibition Test ◽  
Clotting Factor ◽  
Factor Xii ◽  
Factor V ◽  
Systemic Lupus ◽  
Factor Xi ◽  
Factor Specificity

SummaryThe plasmas of six patients with prolonged activated partial thromboplastin times were studied in detail. In five of the six, the Russell’s viper venom and prothrombin times were likewise prolonged. Five of the patients had documented systemic lupus erythematosus; one lacked the necessary criteria for this diagnosis. On quantitation, factor XI was decreased in all six; factors X and XII were diminished in five of the six. When tested for inhibitory activity, plasma from each of the patients prolonged the celite eluate inhibition test for factor XII and/or XI inhibition. In the formation of the Xa-V-phospholipid-Ca2+ complex (prothrombinase), factors X and Xa were inhibited to a greater degree than factor V or the phospholipid. Finally, each plasma was isofocused, the inhibitory fractions were identified and the clotting factor specificity of each inhibitory peak was determined.Fractions inhibitory against factors XI and XII isofocused with the IgG in each patient’s plasma. Based on the data presented from these six patients, the “lupus inhibitor” is in fact a heterogeneous collection of inhibitors directed against factors XII, XI and X rather than a homogeneous entity.

Acquired Factor XI Inhibitors in Two Patients with Hereditary Factor XI Deficiency

1984 ◽  
Vol 51 (03) ◽  
pp. 371-375 ◽  
Author(s):  
Kangathevy Morgan ◽  
Sandra Schiffman ◽  
Donald Feinstein
Keyword(s):  
Protein A ◽  
Lambda Light Chain ◽  
Factor Xi ◽  
Spontaneous Bleeding ◽  
Factor Xi Deficiency ◽  
Hereditary Factor ◽  
Coagulation Mechanism ◽  
Factor Xia ◽  
Polyclonal Igg ◽  
Glass Surfaces

SummaryTwo patients with hereditary factor XI deficiency developed inhibitors following plasma transfusions. Neither had severe spontaneous bleeding. The patients’ plasmas neutralized both factor XI in plasma, purified factor XI, and purified factor XIa. The inhibitor in both patients’ plasmas adsorbed to Protein A- Sepharose. The inhibitors eluted from Protein A-Sepharose were partially neutralized by kappa and lambda light chain antisera indicating that they were polyclonal IgG antibodies. Both inhibitors markedly decreased adsorption of factor XI to glass surfaces. The cleavage of factor XI by trypsin was unaffected by the inhibitors. The lack of severe spontaneous bleeding in both of these patients strongly suggests that an alternate coagulation mechanism bypassing factor XI must compensate for this severe defect.

Anticoagulant Activity of β2-Glycoprotein I Is Potentiated by a Distinct Subgroup of Anticardiolipin Antibodies

1992 ◽  
Vol 68 (03) ◽  
pp. 297-300 ◽  
Author(s):  
Monica Galli ◽  
Paul Comfurius ◽  
Tiziano Barbui ◽  
Robert F A Zwaal ◽  
Edouard M Bevers
Keyword(s):  
Human Plasma ◽  
Anticoagulant Activity ◽  
Factor Xa ◽  
Type A ◽  
Lipid Vesicles ◽  
Dependent Manner ◽  
Type B ◽  
Distinct Subgroup ◽  
Glycoprotein I ◽  
Thrombin Formation

SummaryPlasmas of 16 patients positive for both IgG anticardiolipin (aCL) antibodies and lupus anticoagulant (LA) antibodies were subjected to adsorption with liposomes containing cardiolipin. In 5 of these plasmas both the anticardiolipin and the anticoagulant activities were co-sedimented with the liposomes in a dose-dependent manner, whereas in the remaining cases only the anticardiolipin activity could be removed by the liposomes, leaving the anticoagulant activity (LA) in the supernatant plasma. aCL antibodies purified from the first 5 plasmas were defined as aCL-type A, while the term aCL-type B was used for antibodies in the other 11 plasmas, from which 2 were selected for this study.Prolongation of the dRVVT was produced by affinity-purified aCL-type A antibodies in plasma of human as well as animal (bovine, rat and goat) origin. aCL-type B antibodies were found to be devoid of anticoagulant activity, while the corresponding supernatants containing LA IgG produced prolongation of the dRVVT only in human plasma.These anticoagulant activities of aCL-type A and of LA IgG's were subsequently evaluated in human plasma depleted of β2-glycoprotein I (β2-GPI), a protein which was previously shown to be essential in the binding of aCL antibodies to anionic phospholipids. Prolongation of the dRVVT by aCL-type A antibodies was abolished using β2-GPI deficient plasma, but could be restored upon addition of β2-GPI. In contrast, LA IgG caused prolongation of the dRVVT irrespective of the presence or absence of β2-GPI.Since β2-GPI binds to negatively-charged phospholipids and impedes the conversion of prothrombin by the factor Xa/Va enzyme complex (Nimpf et al., Biochim Biophys Acta 1986; 884: 142–9), comparison was made of the effect of aCL-type A and aCL-type B antibodies on the rate of thrombin formation in the presence and absence of β2-GPI. This was measured in a system containing highly purified coagulation factors Xa, Va and prothrombin and lipid vesicles composed of 20 mole% phosphatidylserine and 80 mole% phosphatidylcholine. No inhibition on the rate of thrombin formation was observed with both types of aCL antibodies when either β2-GPI or the lipid vesicles were omitted. Addition of β2-GPI to the prothrombinase assay in the presence of lipid vesicles causes a time-dependent inhibition which was not affected by the presence of aCL-type B or non-specific IgG. In contrast, the presence of aCL-type A antibodies dramatically increased the anticoagulant effect of β2-GPI. These data indicate that the anticoagulant activity of aCL-type A antibodies in plasma is mediated by β2-GPI.

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