D-dimer, plasminogen activator inhibitor-1, prothrombin fragments and protein C – role in prothrombotic state of colorectal cancer.

Neoplasma ◽  
2011 ◽  
Vol 58 (3) ◽  
pp. 235-238 ◽  
Author(s):  
M. MYTNIK ◽  
J. STASKO
Keyword(s):  
Colorectal Cancer ◽  
Plasminogen Activator ◽  
Protein C ◽  
Plasminogen Activator Inhibitor ◽  
Prothrombotic State ◽  
Plasminogen Activator Inhibitor 1 ◽  
Activator Inhibitor ◽  
D Dimer

scholarly journals THE FIBRINOLYTIC ALTERATION ASSOCIATED WITH DAILY ADMINISTRATION OF SILDENAFIL

2018 ◽  
Vol 11 (8) ◽  
pp. 107
Author(s):  
Fathelrahman M Hassan
Keyword(s):  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Daily Administration ◽  
Control Group ◽  
Average Weight ◽  
Plasminogen Activator Inhibitor 1 ◽  
Control Groups ◽  
Activator Inhibitor ◽  
Pai 1 ◽  
D Dimer

Objective: The objective of this study was to determine the fibrinolytic alteration associated with daily administration of sildenafil.Methods: A total of 12 adult male rabbits without mortality rate had been fed standard and subdivided into four groups; their average weight was 1.5, 2.5, 1.9, and 2 kg randomly selected during the period of March 2012–July 2013. Depending on weight, the control groups (2.25 mg/1.5 kg day) and sildenafil groups (3 mg/2 kg/day, 2.85 mg/1.9 kg/day, and 1.7 mg/2.5 kg/day) were injected by normal saline and sildenafil concentration, respectively to create four groups, every group was composed of three rabbits; saline rabbit (control group, n=3) and sildenafil rabbits (sildenafil group, n=9). All rabbit’s plasma samples have been investigated for prothrombin time, activated partial thromboplastin time, fibrinogen, plasminogen activator inhibitor-1 (PAI-1), prothrombin fragment 1+2, tissues plasminogen activator (tPA), plasmin antiplasmin (PAP), plasminogen, and D-dimer after 24 h of administration.Results: The PAP level was significantly (p<0.05) decreased following sildenafil injection. Sildenafil-injected (3 mg/ml) rabbits had decreased the means of PAI-1 and mean tPA, as early as 1-day post-injection, with a considerable lower PAP first determined 3 days after injection that continued into each rabbit 2 and 3.Conclusion: Better strategies are to initiate and manipulate this drug ought to reduce the chance of each thrombosis and hemorrhage, at the same time as minimizing the need for laboratory monitoring with the aid of the use of PAI-1, tPA, and PAP checks.

Vascular Thrombosis and Relation to Hemostatic Parameters in Omani Patients with Behcet’s Disease

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4090-4090
Author(s):  
Anil Pathare ◽  
Juma AlKaabi ◽  
Hamood AlHaddabi ◽  
Salam Alkindi
Keyword(s):  
Plasminogen Activator ◽  
Protein C ◽  
Factor V Leiden ◽  
Plasminogen Activator Inhibitor ◽  
Factor V ◽  
Plasminogen Activator Inhibitor 1 ◽  
Repeat Testing ◽  
Tissue Plasminogen ◽  
Thrombotic Tendency ◽  
Activator Inhibitor

Abstract Background: Behcet’s disease (BD) has been shown to be associated with increased mortality rate in several studies. A significant portion of this mortality (40%) was related to vascular thrombosis. The basis for the thrombotic tendency in BD is not fully understood and studies on hemostatic parameters have been controversial. Objectives: To determine the frequency of vascular events in Omani patients with BD and to study various hemostatic variables that might contribute to this vascular risk in BD. Methods: The study was started after approval by the institutional review board. Blood samples from 34 patients with BD, and 30 healthy controls after an informed consent and were analyzed for several hemostatic parameters including protein C, protein S, AT, factor VIII:C, factor V Leiden, von Willibrand factor antigen, ristocetin and collagen binding activity, Plasminogen, Alpha 2 antiplasmin, tissue plasminogen activator, and Plasminogen activator inhibitor-1. Additionally, anticardiolipin antibodies, anti-B2 glycoprotein antibodies, lupus anticoagulant, homocysteine, ESR, CRP, glucose and lipid profile were also studied. Results: Eight patients with BD had thrombotic events (26%). Of these, 50% were arterial, 25% were venous and 25% had mixed arterial and venous events. The mean values of factors VIII:C, vWF:Ag, Protein C and ATIII were significantly higher in the patient’s group compared to the controls (P&lt;0.05, Mann-Whitney). (Table) There were no deficiencies in protein C, S, or AT and factor V Leiden was absent in these patients. Six patients had elevated FVIII [&gt;150 iu/ml] [p&lt;0.01;Fisher’s exact test]. There were no differences in anti-cardiolipin antibodies, anti-b2-glycoprotein-1 antibodies, lupus anticoagulant, homocysteine, total cholesterol, triglycerides or blood glucose levels, between patients and controls. We found significant correlations between inflammatory markers [ESR, CRP] and factor VIII:C, Anti-thrombin, vWF:Ag;vWF:CBA, vWF:RiCof in the control group but not in the patient group. Furthermore, the elevated factor VIII levels were normalized on repeat testing after 3 months. Comparison of hemostatic parameters in BD patients with thrombosis v/s normal controls [Mean ± SD] Reference Range Patients Controls P value Plasma F VIII:C 50–150[iu/ml] 107 ± 48 78 ± 31 0.017 Functional Protein C Chromogenic 72–154[iu/ml] 125 ± 37 118 ± 25 NS Protein C Clotting 80–181[iu/ml] 139 ± 43 126 ± 32 NS Protien S Functional 52–118[iu/ml] 101 ± 28 83 ± 27 0.008 Antithrombin 83–118[iu/ml] 108 ± 12 100 ± 12 0.022 Plasminogen 73–127[iu/ml] 114 ± 15 114 ± 19 NS Alpha 2 Antiplasmin 89–112[iu/ml] 118 ± 15 116 ± 16 NS Tissue Plasminogen Activator 1–12[ng/ml] 7 ± 3 7 ± 2 NS Plasminogen Activator Inhibitor-1 4–43[ng/ml] 31 ± 21 38 ± 33 NS Plasma vWF:Ag 50–158[iu/ml] 102 ± 34 83 ± 25 0.008 Plasma vWF:RiCof 40–150[iu/ml] 100 ± 46 90 ± 30 NS Plasma vWF:CBA 50–400[iu/ml] 101 ± 38 94 ± 37 NS Plasma Homocystine 5–15 [mmol/L] 9 ± 2 9 ± 2 NS Conclusion: The elevated hemostatic parameters are likely to represent an acute phase phenomena as shown by their normalization in the repeat testing after 3 months. Thrombophillic factors do not seem to explain the thrombotic tendency in BD. Further work is needed to elucidate the basis for the thrombotic complication of BD. It is hypothesized that active BD causes endothelial damage and dysfunction leading to the increased propensity for thrombosis.

scholarly journals Continuous Active State of Coagulation System in Patients With Nonthrombotic Inflammatory Bowel Disease

2011 ◽  
Vol 17 (6) ◽  
pp. 600-604 ◽  
Author(s):  
Huseyin Alkim ◽  
Selime Ayaz ◽  
Canan Alkim ◽  
Aysel Ulker ◽  
Burhan Sahin
Keyword(s):  
Plasminogen Activator ◽  
Degradation Products ◽  
Plasminogen Activator Inhibitor ◽  
Protein S ◽  
Plasminogen Activator Inhibitor 1 ◽  
Inflammatory Bowel ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Activator Inhibitor ◽  
D Dimer

This study was planned for searching possible changes of the total coagulation and fibrinolysis system in inflammatory bowel disease (IBD) in order to obtain some clues for explaining the relation between IBD and hypercoagulability. A total of 24 patients with ulcerative colitis, 12 patients with Crohn disease, and 20 healthy controls were studied. Platelets; prothrombin time (PT); partial thromboplastin time (PTT); fibrinogen; d-dimer; fibrinogen degradation products; protein C; protein S; antithrombin; thrombin time; von Willebrand factor; coagulation factors V, VII, VIII, IX, XI, and XIII; plasminogen; antiplasmin; tissue plasminogen activator; plasminogen activator inhibitor 1; and prothrombin fragments 1 + 2 were studied. Most of the procoagulants (platelets, fibrinogen, von Willebrand factor, coagulation factor IX, and plasminogen activator inhibitor 1) were found increased together with decreases in some anticoagulants (protein S and antithrombin) in IBD. Also the activation markers of coagulation (d-dimer, fibrinogen degradation products, and prothrombin fragments 1 + 2) were all increased. The parameters of the total coagulation–fibrinolysis system were increased in IBD, regardless of the form and the activity of the disease.

scholarly journals Hemostatic Indices in Healthy Foals from Birth to One Month of Age

1995 ◽  
Vol 7 (3) ◽  
pp. 380-385 ◽  
Author(s):  
Michelle Henry Barton ◽  
Debra Deem Morris ◽  
Natalie Crowe ◽  
Chrysann Collatos ◽  
Keith W. Prasse
Keyword(s):  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Protein C ◽  
Antithrombin Iii ◽  
Degradation Products ◽  
Plasminogen Activator Inhibitor ◽  
Plasminogen Activator Inhibitor 1 ◽  
Fibrin Degradation Products ◽  
Tissue Plasminogen ◽  
Activator Inhibitor

Hemostatic indices were determined in 45 healthy light breed foals, from birth to 1 month of age, and in 20 healthy adult (>2 years of age) light breed horses. Blood samples were obtained from each foal at 4 ages: 1) < 24 hours, 2) 4-7 days, 3) 10-14 days, and 4) 25-30 days. The following hemostatic indices were determined: platelet count; prothrombin and activated partial thromboplastin times; activity concentrations of protein C, antithrombin III, plasminogen, alpha-2 antiplasmin, tissue plasminogen activator, and plasminogen activator inhibitor- 1; plasma protein C antigen and fibrinogen concentrations; and serum fibrin degradation products concentration. Prothrombin and activated partial thromboplastin times were significantly longer at birth than in older foals. The plasma concentrations of the following were significantly lower at birth than in older foals: antithrombin III, plasminogen and tissue plasminogen activator activities, protein C antigen, and fibrinogen. Concentrations of the following were significantly higher at birth than in older foals: protein C and plasminogen activator inhibitor-1 activities and fibrin degradation products. These results indicate that hemostatic indices of neonatal foals differ significantly from those of older foals and adults. With the exceptions of antithrombin III and tissue plasminogen activator activities, all hemostatic indices measured in foals at 1 month of age were equivalent to adult values.

scholarly journals Fibrin D-dimer impairs the accumulation and anticoagulant properties of heparan sulphate and stimulates secretion of plasminogen activator inhibitor-1 by rabbit coronary endothelial cells.

2003 ◽  
Vol 50 (1) ◽  
pp. 279-289 ◽  
Author(s):  
Natalia Yu Yevdokimova ◽  
Larisa D Veselovska ◽  
Genrietta K Gogolinska ◽  
Olexandra M Buchanevich ◽  
Galina V Kosyakova ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Plasminogen Activator ◽  
Heparan Sulphate ◽  
Plasminogen Activator Inhibitor ◽  
No Production ◽  
Plasminogen Activator Inhibitor 1 ◽  
Coronary Endothelial Cells ◽  
Activator Inhibitor ◽  
Pai 1 ◽  
D Dimer

Fibrin split product D-dimer (DD) is most probably involved in the development of vascular disorders. At 1.5 microM concentration DD inhibited the incorporation of D-[1-(3)H]glucosamine hydrochloride and [2-(14)C]acetate x Na into pericellular heparan sulphate (HS) of rabbit coronary endothelial cells without affecting other groups of glycosaminoglycans (GAGs). At the same time, DD reduced HS ability to bind antithrombin (AT) and suppressed NO production. The effect of DD on pericellular GAGs was similar to that of N(omega)-methyl-L-arginine, the competitive inhibitor of endothelial NO synthase (eNOS). L-Ascorbic acid, eNOS activator, increased the level of endogenous NO in the DD-treated cells, and restored HS accumulation and antithrombin binding. It is suggested that DD influence on endothelial HS may be mediated by NO production. Another effect of DD, namely, stimulation of plasminogen activator inhibitor-1 (PAI-1) secretion did not depend on the NO level. The decreased HS content, reduced anticoagulant properties of HS, and increased PAI-1 secretion disorganized the endothelial matrix, and promoted fibrin formation and vascular damage. This points to DD as an important factor in the development of vascular disorders.

Disseminated Intravascular Coagulation Is a Frequent Complication of Systemic Inflammatory Response Syndrome

1996 ◽  
Vol 75 (02) ◽  
pp. 224-228 ◽  
Author(s):  
Satoshi Gando ◽  
Takashi Kameue ◽  
Satoshi Nanzaki ◽  
Yoshimi Nakanishi
Keyword(s):  
Systemic Inflammatory Response Syndrome ◽  
Inflammatory Response ◽  
Plasminogen Activator ◽  
Disseminated Intravascular Coagulation ◽  
Protein C ◽  
Plasminogen Activator Inhibitor ◽  
Systemic Inflammatory Response ◽  
Plasminogen Activator Inhibitor 1 ◽  
Intravascular Coagulation ◽  
Activator Inhibitor

SummaryTo evaluate the role of disseminated intravascular coagulation (DIC) and to determine the influence of antithrombin, protein C, and plasminogen activator inhibitor 1 on multiple organ dysfunction syndrome (MODS) and outcome in patients with systemic inflammatory response syndrome (SIRS), we made a prospective cohort study. The study subjects consisted of thirty-five patients who exhibited two or more of the conditions of SIRS for more than three consecutive days. They were classified into subgroups of survivors (n = 13) and nonsurvivors (n = 22). The global coagulation and fibrinolytic markers, antithrombin, protein C, and plasminogen activator inhibitor 1 were measured on the day of the diagnosis of SIRS, and also on the 1st, 3rd, and 5th days. The results of these measurements, demographic data, criteria of severity, incidence of MODS were compared between the subgroups. For prediction of patient’s death, a receiver operating characteristic (ROC) curve analysis was made. DIC was frequently associated with SIRS patients (29/35, 82.9%). A significant decrease in the DIC score was found in the survivors (p = 0.0001). None of them suffered from DIC on the 5th day. In the nonsurvivors, low levels of protein C and antithrombin and markedly high values of plasminogen activator inhibitor 1 continued up to the 5th day, no improvement of the DIC was observed during the study period and the number of the dysfunctioning organs were significantly higher than in the survivors. Plasminogen activator inhibitor 1 on the 5th day had prognostic value for the prediction of death on the SIRS patients. In conclusion, DIC occurs commonly in patients with SIRS and may be the main determinant for the outcome of these patients. Changes in antithrombin, protein C, and plasminogen activator inhibitor 1 are one of the aggravating factors of MODS. Furthermore, plasminogen activator inhibitor 1 is a good predictor of death in these patients.

scholarly journals Thrombomodulin, Plasminogen Activator Inhibitor-1 and Protein C Levels, and Organ Dysfunction in Sepsis

2019 ◽  
Vol 1 (5) ◽  
pp. e0013 ◽  
Author(s):  
Shinshu Katayama ◽  
Kansuke Koyama ◽  
Jun Shima ◽  
Ken Tonai ◽  
Yuya Goto ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Organ Dysfunction ◽  
Protein C ◽  
Plasminogen Activator Inhibitor ◽  
Plasminogen Activator Inhibitor 1 ◽  
Activator Inhibitor
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