Increased Levels of Activated Factor VII and Decreased Plasma Protein S Activity and Circulating Thrombomodulin during Use of Oral Contraceptives

1996 ◽  
Vol 76 (05) ◽  
pp. 729-734 ◽  
Author(s):  
Peter Quehenberger ◽  
Uta Loner ◽  
Stylianos Kapiotis ◽  
Sylvia Handler ◽  
Barbara Schneider ◽  
...  
Keyword(s):  
Blood Coagulation ◽  
Plasma Protein ◽  
Plasma Levels ◽  
Protein S ◽  
Factor Vii ◽  
Activation Markers ◽  
Treatment Groups ◽  
Activated Factor Vii ◽  
Inhibitory Components ◽  
Protein S Activity

SummaryIn the present study the effect of oral contraceptive (OC) treatment on selected factors involved in the activation, i.e. circulating activated factor VII (cFVIIa), and in the inhibition of blood coagulation, i.e. plasma protein S activity and circulating thrombomodulin (cTM), were for the first time measured in OC users in a prospective study. Beside other coagulation variables, these parameters were measured during treatment with three low estrogen formulations containing different gestagen components (norgestimate, gestodene). During OC treatment increases in the activation markers prothrombin fragment F1+2 and D-Dimer were found, suggesting an increased activation of blood coagulation and fibrinolysis. Along with elevated plasma levels of FVII antigen, cFVIIa was also found increased in all three treatment groups, while inhibitory components of blood coagulation, plasma protein S activity and cTM, significantly and similarily decreased during treatment in all three treatment groups. We conclude that low dose estrogen pills induce similar changes in the plasma levels of main regulatory components of blood coagulation, despite differences in their gestagen components. Increased levels of activators and decreased activities of inhibitors may contribute to arterial and venous thrombotic complications seen in predisposed OC users.

Chemotherapy for breast cancer decreases plasma protein C and protein S.

1988 ◽  
Vol 6 (2) ◽  
pp. 276-281 ◽  
Author(s):  
J S Rogers ◽  
A J Murgo ◽  
J A Fontana ◽  
P C Raich
Keyword(s):  
Breast Cancer ◽  
Plasma Protein ◽  
Plasma Levels ◽  
Protein C ◽  
Protein S ◽  
Factor Vii ◽  
C Protein ◽  
S Factor ◽  
Free Plasma ◽  
Thrombotic Tendency

An increased incidence of thromboembolic events has been described in women receiving chemotherapy for breast cancer. The etiology of this enhanced thrombotic state has not been defined. We performed serial coagulation studies in 15 women during 1 monthly cycle of cyclophosphamide, methotrexate, and fluorouracil (CMF) chemotherapy for breast cancer; seven adjuvant and eight metastatic. Plasma protein C levels were measured by anticoagulant, amidolytic, and antigenic techniques. Antigen levels of both total and free plasma protein S were quantitated by immunoelectrophoresis. Plasma levels of protein C, an important vitamin K-dependent inhibitor of blood coagulation and a profibrinolytic agent, and protein S, a cofactor for protein C, decreased 1 and 2 weeks after initiation of chemotherapy compared with pretreatment values. Plasma levels of factor VII and fibrinogen also decreased. The changes in protein C and protein S may contribute to the enhanced thrombotic tendency described in this setting. Possible mechanisms for the decreases in plasma protein C, protein S, factor VII, and fibrinogen are discussed.

BIOLOGICAL PRETHROMBOTIC MARKERS AND COAGULATION INHIBITORS IN NEPHROTIC SYNDROME

1987 ◽  
Author(s):  
P Picard ◽  
J Y Borg ◽  
M Vasse ◽  
D Boudhabhay ◽  
J Soria ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Acute Phase Proteins ◽  
Degradation Products ◽  
Protein S ◽  
Factor Vii ◽  
Activated Factor Vii ◽  
Prethrombotic State ◽  
At Iii ◽  
Coagulation Inhibitors

Nephrotic syndrome (NS) has long been recognized as a clinical prethrombotic state, because of severe thrombo-embolic complications. But underlying mechanisms are still poorly defined. In 56 untreated nephrotic adult patients (most of them without renal failure), we investigate in vivo coagulation activation by measuring 0 plasmatic specific fibrin degradation products (FbDP) (immuno-enzymological assay using a monoclonal anti D-neo antibody) and (2) the ratio of factor VII coagulant activity (V11c) to factor VII:Anti gen (VII;Ag) tested by an ELISA method. We examined coagulation inhibitors in plasmas and urines (antithrombin III—AT III, heparin cofactor II-HC II by amidolytic and laurell methods; protein C-PC by an ELISA assay ;free and bound protein S—PS:Ag by laurell assays). In few patients we also determinecjfribronectin and t-PA inhibitor.Results in plasma are submitted and expressed as mean ± DS and compared (t test) with controls (C) without nephropathySignificantly elevated activated factor VII and FbDP levels show an “in vivo activation” of coagulation in NS. Plasmatic fibronectin, HC II, PC:frg, and tPA-I levels are alsp significantly elevated and roughly paralleled fibrinogen (6,25 ± 2,9 g/1) and other acute-phase proteins measurements. Significant amounts of AT 111:Ag were present in about half tested urines, but in a degraded form with low or absent heparin cofactor activity. Mean plasmatic AT III concentration was in normal range, but three of the 4 patients with a thrombotic disease had the lowest values of AT III and the highest fibrinogen levels.We could demonstrate a biological prethrombotic state in NS and suggest the way of identifying patients with high risk of thrombosis.

scholarly journals Effect on Plasma Protein S Activity in Patients Receiving the Factor Xa Inhibitors

2021 ◽  
Author(s):  
Takako Terakami ◽  
Satomi Nagaya ◽  
Kenshi Hayashi ◽  
Hiroshi Furusho ◽  
Noboru Fujino ◽  
...  
Keyword(s):  
Plasma Protein ◽  
Factor Xa ◽  
Protein S ◽  
Factor Xa Inhibitors ◽  
Protein S Activity

scholarly journals Activation of the coagulation cascade after infusion of a factor XI concentrate in congenitally deficient patients

Blood ◽  
1994 ◽  
Vol 84 (4) ◽  
pp. 1314-1319
Author(s):  
PM Mannucci ◽  
KA Bauer ◽  
E Santagostino ◽  
E Faioni ◽  
S Barzegar ◽  
...  
Keyword(s):  
Plasma Levels ◽  
Factor Ix ◽  
Coagulation Cascade ◽  
Factor Vii ◽  
Factor Xi ◽  
Factor Xi Deficiency ◽  
Activated Factor Vii ◽  
Before And After ◽  
Post Infusion ◽  
Secondary Hyperfibrinolysis

Virally inactivated, high-purity factor XI concentrates are available for treatment of patients with factor XI deficiency. However, preliminary experience indicates that some preparations may be thrombogenic. We evaluated whether a highly purified concentrate produced signs of activation of the coagulation cascade in two patients with severe factor XI deficiency infused before and after surgery. Signs of heightened enzymatic activity of the common pathway of coagulation (elevated plasma levels of prothrombin fragment 1 + 2 and fibrinopeptide A) developed in the early post-infusion period, accompanied by more delayed signs of fibrin formation with secondary hyperfibrinolysis (elevated D-dimer and plasmin-antiplasmin complex). These changes occurred in both patients, but were more severe in the older patient with breast cancer when she underwent surgery, being accompanied by fibrinogen and platelet consumption. There were no concomitant signs of heightened activity of the factor VII-tissue factor mechanism on the factor Xase complex (plasma levels of activated factor VII and of factor IX and X activation peptides did not increase). The observed changes in biochemical markers of coagulation activation indicate that concentrate infusions increased thrombin generation and activity and that such changes were magnified by malignancy and surgery. Because some factor XI concentrates may be thrombogenic, they should be used with caution, especially in patients with other risk factors for thrombosis.

Activation of the coagulation cascade after infusion of a factor XI concentrate in congenitally deficient patients

Blood ◽  
1994 ◽  
Vol 84 (4) ◽  
pp. 1314-1319 ◽  
Author(s):  
PM Mannucci ◽  
KA Bauer ◽  
E Santagostino ◽  
E Faioni ◽  
S Barzegar ◽  
...  
Keyword(s):  
Plasma Levels ◽  
Factor Ix ◽  
Coagulation Cascade ◽  
Factor Vii ◽  
Factor Xi ◽  
Factor Xi Deficiency ◽  
Activated Factor Vii ◽  
Before And After ◽  
Post Infusion ◽  
Secondary Hyperfibrinolysis

Abstract Virally inactivated, high-purity factor XI concentrates are available for treatment of patients with factor XI deficiency. However, preliminary experience indicates that some preparations may be thrombogenic. We evaluated whether a highly purified concentrate produced signs of activation of the coagulation cascade in two patients with severe factor XI deficiency infused before and after surgery. Signs of heightened enzymatic activity of the common pathway of coagulation (elevated plasma levels of prothrombin fragment 1 + 2 and fibrinopeptide A) developed in the early post-infusion period, accompanied by more delayed signs of fibrin formation with secondary hyperfibrinolysis (elevated D-dimer and plasmin-antiplasmin complex). These changes occurred in both patients, but were more severe in the older patient with breast cancer when she underwent surgery, being accompanied by fibrinogen and platelet consumption. There were no concomitant signs of heightened activity of the factor VII-tissue factor mechanism on the factor Xase complex (plasma levels of activated factor VII and of factor IX and X activation peptides did not increase). The observed changes in biochemical markers of coagulation activation indicate that concentrate infusions increased thrombin generation and activity and that such changes were magnified by malignancy and surgery. Because some factor XI concentrates may be thrombogenic, they should be used with caution, especially in patients with other risk factors for thrombosis.

Treatment of Hereditary Protein C Deficiency with Stanozolol

1987 ◽  
Vol 57 (01) ◽  
pp. 020-024 ◽  
Author(s):  
A W Broekmans ◽  
J Conard ◽  
R G van Weyenberg ◽  
M H Horellou ◽  
C Kluft ◽  
...  
Keyword(s):  
Plasma Protein ◽  
Protein C ◽  
Protein S ◽  
Fold Increase ◽  
Factor Ix ◽  
Factor Vii ◽  
Type I ◽  
Factor V ◽  
Factor X ◽  
Protein C Deficiency

SummaryFive type I protein C deficient male patients received 5 mg stanozolol b.i.d. during 4 weeks. After four weeks of treatment plasma protein C activity increased from 0.42 to 0.74 U/ml and protein C antigen from 0.49 to 0.75 U/ml. This approximately 1.6 fold increase in plasma protein C was accompanied by an increase in factor II antigen (1.5 fold), factor V activity (1.6 fold), factor X antigen (1.1 fold), antithrombin III antigen (1.3 fold) and heparin cofactor II antigen (1.5 fold), while the concentration of factor VII, factor VIII, and factor IX activity, and of protein S antigen remained unchanged. Prothrombin fragment F1+2, measured in two patients, increased 1.3 fold. In addition to its effect on procoagulant and anticoagulant factors stanozolol had profibrinolytic effects, reflected in an increase in tPA activity and in the concentration of plasminogen. These data indicate that in type I protein C deficient patients stanozolol increases the concentrations of both procoagulant and anticoagulant factors and favours fibrinolysis. The efficacy of stanozolol in preventing thrombotic disease in type I protein C deficient patients, however, remains to be established. During the four weeks of stanozolol treatment no thrombotic manifestations were observed in the protein C deficient patients.

Impaired Procoagulant-anticoagulant Balance during Hormone Replacement Therapy?

2000 ◽  
Vol 83 (01) ◽  
pp. 29-34 ◽  
Author(s):  
W. van Baal ◽  
Jef Emeis ◽  
Marius J. van der Mooren ◽  
Hilda Kessel ◽  
Peter Kenemans ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Plasma Levels ◽  
Degradation Products ◽  
Hormone Replacement ◽  
Plasminogen Activator Inhibitor ◽  
Protein S ◽  
Tissue Type ◽  
Factor Vii ◽  
Negative Results ◽  
Increased Risk

SummaryIn this randomised, placebo-controlled 12-week study, sixty healthy postmenopausal women received either placebo (N = 16) or daily 2 mg micronised oestradiol, either unopposed (N = 16, E2 group) or combined with a progestagen for 14 days of each cycle (N = 28, E2+P group).As compared to placebo, plasma levels of AT III were reduced only in the E2 group (∼28%), plasma levels of protein C decreased only in the E2+P group (∼4%) and plasma levels of protein S decreased in both the E2 and E2+P group (∼21%). In both the E2 and E2+P groups, the plasma levels of factor VII (antigen and activity) showed a borderline significant increase (∼10%), whereas no significant change was observed in active factor VII. Plasma levels of tissue-type plasminogen activator (∼22%), urokinase plasminogen activator (∼25%) and plasminogen activator inhibitor type-1 (∼43%) decreased in the E2 and E2+P groups, whereas those of plasminogen increased (∼12%). Treatment was associated with an increase in levels of prothrombin fragment 1+2 (∼31%), but levels of thrombin-antithrombin III complexes, and of plasmin-α2-antiplasmin complexes and total fibrin(ogen) degradation products did not change significantly.Short-term E2 and E2+P treatment is associated with a shift in the procoagulant-anticoagulant balance towards a procoagulant state. A substantial proportion of women do not have a net increase in fibrinolytic activity. These data may be relevant in explaining the increased risk of venous thromboembolism associated with ERT and HRT, and possibly also in explaining the negative results of the Heart and Estrogen/progestin Replacement Study.

Heparin lowers plasma levels of activated factor VII

1999 ◽  
Vol 105 (4) ◽  
pp. 1127-1129 ◽  
Author(s):  
Thomas Pernerstorfer ◽  
Bernd Jilma ◽  
Hans-Georg Eichler ◽  
Susanne Aull ◽  
Sylvia Handler ◽  
...  
Keyword(s):  
Plasma Levels ◽  
Factor Vii ◽  
Activated Factor Vii
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