Increased Plasma Levels of Free Tissue Factor Pathway Inhibitor in Patients with Graves’ Disease

1998 ◽  
Vol 79 (05) ◽  
pp. 919-923 ◽  
Author(s):  
Eriko Morishita ◽  
Takuma Hashimoto ◽  
Hidesaku Asakura ◽  
Masanori Saito ◽  
Masahide Yamazaki ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Tissue Factor ◽  
Tissue Factor Pathway Inhibitor ◽  
Plasma Concentrations ◽  
Free Form ◽  
Control Group ◽  
Graves Disease ◽  
Thyroid State ◽  
Significant Difference ◽  
Tissue Factor Pathway

SummaryTissue factor pathway inhibitor (TFPI) is present in a free-form and in lipoprotein-associated forms in plasma. In this study, the plasma concentrations of total TFPI (tTFPI) and free-form TFPI (fTFPI) were measured in 25 patients with Graves’ disease and 25 age-matched healthy subjects, and the relationship between thyroid state and plasma TFPI was examined. Plasma concentrations (median) of tTFPI and fTFPI in Graves’ patients who were hyperthyroid were significantly increased compared with Graves’patients who were euthyroid (152 ng/ml versus 124 ng/ml, p <0.01 and 41.3 ng/ml versus 20.2 ng/ml, p <0.0001, respectively), and control subjects (152 ng/ml versus 96 ng/ml, p <0.0001 and 41.3 ng/ml versus 18.7 ng/ml, p <0.0001, respectively). There was no significant difference in plasma fTFPI concentrations between the euthyroid group and the control group. Plasma fTFPI concentrations correlated closely with thyroid hormone (T3) levels in the patients (r = 0.559, p <0.005). Serial measurement of individual patients revealed that plasma concentrations of fTFPI and tTFPI were significantly decreased, reaching normal control values upon attainment of euthyroidism. In conclusion, the close correlation between plasma fTFPI and serum thyroid hormone levels suggests that thyroid hormones might influence the synthesis or metabolism of TFPI on the surface of endothelial cells in patients with Graves’ disease. This is the first report concerning high concentrations of plasma fTFPI in patients with hyperthyroidism.

Tissue Factor and Tissue Factor Pathway Inhibitor in the Wound-Healing Process After Neurosurgery

2015 ◽  
Vol 18 (2) ◽  
pp. 207-212 ◽  
Author(s):  
Robert Ślusarz ◽  
Mariola Głowacka ◽  
Monika Biercewicz ◽  
Ewa Barczykowska ◽  
Beata Haor ◽  
...  
Keyword(s):  
Wound Healing ◽  
Tissue Factor ◽  
Research Group ◽  
Tissue Factor Pathway Inhibitor ◽  
Healing Process ◽  
Control Group ◽  
Wound Healing Process ◽  
Significant Difference ◽  
Tissue Factor Pathway ◽  
Subject Difference

Objectives: The aim of the study was to assess the concentrations of tissue factor (TF) and tissue factor pathway inhibitor (TFPI) in the blood of patients with a postoperative wound after neurosurgery. Method: Participants included 20 adult patients who underwent neurosurgery because of degenerative spine changes. The concentration of TF and TFPI in the patients’ blood serum was measured 3 times: before surgery, during the first 24 hr after surgery, and between the 5th and 7th days after surgery. The control group comprised 20 healthy volunteers similar to the patient group with respect to gender and age. Results: A statistically significant difference was observed between TF concentration at all three measurement time points in the research group and TF concentration in the control group ( p = .018, p = .010, p = .001). A statistically significant difference was found between TFPI concentration at the second time point in the research group and TFPI concentration in the control group ( p = .041). No statistically significant within-subject difference was found between TF concentrations before and after surgery. A statistically significant within-subject difference was found between TFPI concentrations within 24 hr after surgery and 5–7 days after surgery ( p = .004). Conclusion: High perioperative concentrations of TF indicate not only the presence of thrombophilia but also the importance of TF in the wound-healing process. Perioperative changes in TFPI concentrations are related to its compensatory influence on hemostasis in thrombophilic conditions.

Effect of Depolymerized Holothurian Glycosaminoglycan (DHG) on Tissue Factor Pathway Inhibitor: In Vitro and In Vivo Studies

1997 ◽  
Vol 78 (02) ◽  
pp. 864-870 ◽  
Author(s):  
Hideki Nagase ◽  
Kei-ichi Enjyoji ◽  
Yu-ichi Kamikubo ◽  
Keiko T Kitazato ◽  
Kenji Kitazato ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Tissue Factor Pathway Inhibitor ◽  
Factor Xa ◽  
Free Form ◽  
Initial Reaction ◽  
Extrinsic Pathway ◽  
Factor Xa Inhibition ◽  
Tissue Factor Pathway

SummaryDepolymerized holothurian glycosaminoglycan (DHG) is a glycosaminoglycan extracted from the sea cucumber Stichopus japonicusSelenka. In previous studies, we demonstrated that DHG has antithrombotic and anticoagulant activities that are distinguishable from those of heparin and dermatan sulfate. In the present study, we examined the effect of DHG on the tissue factor pathway inhibitor (TFPI), which inhibits the initial reaction of the tissue factor (TF)-mediated coagulation pathway. We first examined the effect of DHG on factor Xa inhibition by TFPI and the inhibition of TF-factor Vila by TFPI-factor Xa in in vitro experiments using human purified proteins. DHG increased the rate of factor Xa inhibition by TFPI, which was abolished either with a synthetic C-terminal peptide or with a synthetic K3 domain peptide of TFPI. In contrast, DHG reduced the rate of TF-factor Vila inhibition by TFPI-factor Xa. Therefore, the effect of DHG on in vitroactivity of TFPI appears to be contradictory. We then examined the effect of DHG on TFPI in cynomolgus monkeys and compared it with that of unfractionated heparin. DHG induced an increase in the circulating level of free-form TFPI in plasma about 20-fold when administered i.v. at 1 mg/kg. The prothrombin time (PT) in monkey plasma after DHG administration was longer than that estimated from the plasma concentrations of DHG. Therefore, free-form TFPI released by DHG seems to play an additive role in the anticoagulant mechanisms of DHG through the extrinsic pathway in vivo. From the results shown in the present work and in previous studies, we conclude that DHG shows anticoagulant activity at various stages of coagulation reactions, i.e., by inhibiting the initial reaction of the extrinsic pathway, by inhibiting the intrinsic Xase, and by inhibiting thrombin.

87 Evaluating Endothelial Dysfunction in Thermally-injured Patients with syndecan-1, Tissue Factor Pathway Inhibitor, and Thrombomodulin as Predictors of Mortality

2020 ◽  
Vol 41 (Supplement_1) ◽  
pp. S57-S58
Author(s):  
John W Keyloun ◽  
Saira Nisar ◽  
Kathleen Brummel-Ziedins ◽  
Maria Bravo ◽  
Matthew Gissell ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Tissue Factor Pathway Inhibitor ◽  
Burn Injury ◽  
Endothelial Damage ◽  
Inhalation Injury ◽  
Burn Patients ◽  
Mixed Effect ◽  
Significant Difference ◽  
Tissue Factor Pathway ◽  
Injured Patients

Abstract Introduction Endotheliopathy in burn patients is largely uncharacterized. Syndecan-1 (SDC-1), thrombomodulin (TM), and tissue factor pathway inhibitor (TFPI) are components of the vascular endothelial glycocalyx. Proteolytic cleavage of these moieties may yield biomarkers for endothelial damage. The aim of this study is to evaluate endotheliopathy after burn injury by monitoring plasma levels of these biomarkers over time to investigate potential relationship to mortality. Methods Burn injured patients presenting to a regional burn center from 2012 to 2017 were prospectively enrolled. Blood samples were collected at 0, 2, 4, 8, 12, 24, 36, 48, 60, and 72 hours from admission. Plasma SDC-1, TM, and TFPI levels were quantified by ELISA. Demographic data and injury characteristics were obtained from the medical chart. Patients with concomitant inhalation injury, trauma, or &lt; 10% total body surface area (TBSA) burns were excluded. Statistical analysis was performed using mixed-effect models with Sidak’s correction for multiple comparisons. Significance was set at p =0.05. Data are presented as mean ± standard deviation. Results A cohort of 22 patients was identified with an average age of 45±14 years, TBSA of 30±15%, with 6 patients who died from their injuries. The deceased group was older (59±13 vs. 40±10 years, p = 0.01), and there was no significant difference in burn size. Mean SDC-1 levels were higher in the deceased group at all time points (p=0.0004) and this difference was significant at hour 12 (106±11 vs. 41±31 ng/mL, p = 0.0002), hour 24 (160±39 vs. 35±20 ng/mL, p = 0.04) and hour 72 (100±3 vs. 35±38 ng/mL, p = 0.01). Mean soluble TM levels were higher in the deceased group after hour 12 (p = 0.04) and there was a trend towards higher TFPI levels after hour 12 in the deceased group. Conclusions Biomarkers are elevated in patients following burn injury who die, when inhalation injury and trauma are excluded. Given equivalent TBSA, older patients appear more sensitive to thermally induced glycocalyx degradation. SDC-1 shows the greatest promise as a prognostic indicator as levels tend to be higher among deceased patients on admission and are significantly higher as early as hour 12. Applicability of Research to Practice Reliable assessment of the patient’s endothelial damage may hold predictive value for clinicians and could assist in clinical decision making. Further research must investigate endotheliopathy in burn patients.

Tissue Factor Pathway Inhibitor in Tetracycline-induced Pleuritis in Rabbits

1998 ◽  
Vol 79 (03) ◽  
pp. 649-655 ◽  
Author(s):  
Usha Pendurthi ◽  
Siegfried Pueblitz ◽  
Kathleen Koenig ◽  
Todd Williams ◽  
Vijay Mohan Rao ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Pleural Fluid ◽  
Tissue Factor Pathway Inhibitor ◽  
Factor Viia ◽  
Plasma Concentrations ◽  
Coagulation Factors ◽  
Lung Fibroblasts ◽  
Fibrin Deposition ◽  
Tissue Factor Pathway ◽  
Pleural Injury

SummaryPleural fibrin deposition that promotes loculation and fibrosis after pleural injury is initiated by tissue factor (TF). In this study, we sought to determine if tissue factor pathway inhibitor (TFPI), an inhibitor of the TF-factor VIIa complex, was likewise expressed in tetracycline (TCN)-induced pleural injury and, if so, whether TFPI was locally elaborated. Pleural fluid TFPI activity approximated that of plasma by 24 h and doubled by 3 days after intrapleural TCN. By contrast, pleural fluid coagulation factors VII and V remained below plasma concentrations at these intervals. Immunohistochemical studies demonstrated TF, TFPI and fibrin localized in pleural and subpleural tissues and within intrapleural adhesions. TFPI activity and mRNA were also elaborated by rabbit pleural mesothelial cells and lung fibroblasts. TFPI is locally expressed and pleural fluid TFPI exceeds plasma levels during TCN-induced pleural injury. Resident cells as well as extravasation likely contribute to intrapleural TFPI. TFPI expression temporally and anatomically approximates that of TF and may limit TF-induced fibrin deposition in evolving TCN-induced pleuritis.

Regulation of monocyte procoagulant activity in acute myocardial infarction: role of tissue factor and tissue factor pathway inhibitor-1

Blood ◽  
2001 ◽  
Vol 97 (12) ◽  
pp. 3721-3726 ◽  
Author(s):  
Ilka Ott ◽  
Martin Andrassy ◽  
Dominik Zieglgänsberger ◽  
Stefanie Geith ◽  
Albert Schömig ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Tissue Factor ◽  
Tissue Factor Pathway Inhibitor ◽  
Polyclonal Antibodies ◽  
Venous Blood ◽  
Surface Expression ◽  
Procoagulant Activity ◽  
Control Group ◽  
Tissue Factor Pathway

In acute myocardial infarction (AMI), monocyte procoagulant activity is increased and may contribute to the risk for recurrence and other thrombotic events. This study sought to investigate the role tissue factor (TF) and tissue factor pathway inhibitor-1 (TFPI-1) in the regulation of monocyte procoagulant activity in AMI. Serial venous blood samples were obtained from 40 patients with AMI undergoing revascularization by stent placement. Twenty patients with elective stenting for stable angina served as control subjects. TF proteolytic activity was measured with spectrozyme factor Xa (FXa), TF and TFPI-1 surface expression on monocytes by flow cytometry, RNA expression in whole blood by reverse transcription–polymerase chain reaction, and concentrations of plasma prothrombin fragments F1 + 2 by immunoassay. Forty-eight hours after AMI, an increase was found in TF RNA, followed by an increase in TF surface expression by 24% ± 4% and in plasma concentration of F1 + 2 by 103% ± 17% (P &lt; .05). These changes could not be attributed to the intervention because they did not occur in the control group. TFPI-1 RNA and binding to the monocyte surface remained unchanged. FXa generation by monocytes of patients with AMI increased 53.6% ± 9% in the presence of polyclonal antibodies to TFPI-1, indicating that cell-associated TFPI-1 inhibits monocyte TF activity. The increased monocyte procoagulant activity in AMI was caused by an up-regulation of TF that was partially inhibited by surface-bound TFPI-1. Anticoagulant therapy by direct inhibition of TF activity may, thus, be particularly effective in AMI.

Tissue Factor Pathway Inhibitor Causes Unresponsiveness to Activated Prothrombin Complex Concentrates for Hemophilia A Patients with Inhibitors.

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 3663-3663
Author(s):  
Kenichi Ogiwara ◽  
Keiji Nogami ◽  
Ichiro Tanaka ◽  
Katsumi Nishiya ◽  
Nobuyuki Tsujii ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Tissue Factor Pathway Inhibitor ◽  
Hemophilia A ◽  
Poor Response ◽  
Free Form ◽  
Prothrombin Complex Concentrates ◽  
Tissue Factor Pathway ◽  
Bypassing Agents ◽  
Activated Prothrombin Complex Concentrates

Abstract Abstract 3663 Bypassing agents such as activated prothrombin complex concentrates (APCC, FEIBA®) and recombinant activated factor VII (rFVIIa, NovoSeven®) are effective for most hemophiliac patients with inhibitors. While, some patients exhibit unresponsiveness to the treatment with APCC and/or rFVIIa, but their mechanisms remain unknown. We had a severe hemophilia A patient with inhibitor whose bleeding worsened despite of consecutive infusion of APCC. Switching from APCC to rFVIIa was very effective for his bleeding symptoms, and one-week cessation of bypassing agents had restored good response for APCC. Comprehensive coagulation assay such as thromboelastometry and thrombin generation test (TGT) provided us clear evidence of unresponsiveness to APCC. In particular, tissue factor (TF)-triggered TGT showed two significant features, the prolonged lag time and reduced peak thrombin level even after APCC infusion. Although FII, FVII(a), FIX, FX(a) and protein C contained in APCC were elevated in his plasmas after APCC infusion, increased amounts of these factors did not affect the parameters of TGT described above in vitro. We focused on a natural anticoagulant, tissue factor pathway inhibitor (TFPI), since the prolonged lag time in TF-triggered TGT might result from the impairment of FVII/TF-induced initial reaction of blood coagulation. In vitro experiment on the addition of TFPI to FVIII-deficient plasma with APCC showed similar inhibitory pattern in TGT. TFPI antigen levels (total and free forms) in his plasma actually increased above normal range after APCC infusion, whilst these levels unchanged after rFVIIa infusion and returned to the normal range after one-week cessation, speculating that TFPI might contributes to unresponsiveness to APCC. To confirm this, plasmas from several hemophiliac patients with APCC and/or rFVIIa infusion, including 4 patients with poor response pattern in TGT, were prepared. Among 12 pairs of plasmas (a pair; pre and post bypassing agents), each of 4 pairs were for APCC-poor response (APCC-PR), APCC-good response (APCC-GR), and rFVIIa-good response (FVIIa-GR). Free form TFPI antigen levels (normal; 15–35 ng/ml) increased after infusion in APCC-PR (pre/post; 38±4/51±3 ng/ml, p<0.05) and APCC-GR (28±4/37±4 ng/ml, p<0.05), but not increased in FVIIa-GR (23±3/21±3 ng/ml, p>0.05). Post-infusion levels in APCC-PR were significantly higher than those in APCC-GR (p<0.05). By adding anti-TFPI antibody, plasmas in APCC-PR showed marked increase of peak thrombin levels than those in APCC-GR in TGT, supporting that APCC-PR possessed more TFPI activity. Unexpectedly, ELISAs revealed that total TFPI were contained in APCC at 24±4 ng/unit (corresponded to 25≂f50% of physiological concentration), and 34% of them were free form, speculating that APCC infusion with ≂f90 units/kg appeared to increase free TFPI by ≂f15 ng/ml in plasma. Taken together, our results supported that TFPI contained in APCC attenuated the potentials of thrombin generation in hemophilia A patients with inhibitors, and some patients exhibited APCC-resistance due to TFPI accumulated by the consecutive use of APCC. Disclosures: Ogiwara: Baxter Hemophilia Scientific Research and Education Fund in Japan 2009: Research Funding. Nogami:Bayer Hemophilia Award Program 2009: Research Funding.

scholarly journals Initiation of the tissue factor pathway of coagulation in the presence of heparin: control by antithrombin III and tissue factor pathway inhibitor

Blood ◽  
1996 ◽  
Vol 87 (6) ◽  
pp. 2301-2307 ◽  
Author(s):  
J Jesty ◽  
A Lorenz ◽  
J Rodriguez ◽  
TC Wun
Keyword(s):  
Tissue Factor ◽  
Tissue Factor Pathway Inhibitor ◽  
Antithrombin Iii ◽  
Plasma Concentrations ◽  
Factor X ◽  
Tissue Factor Pathway ◽  
Factor X Activation

Activation of factor X by both the unactivated tissue factor:factor VII complex (TF:VII) and the activated tissue factor:factor VIIa complex (TF:VIIa) has been studied in the presence of tissue factor pathway inhibitor (TFPI), antithrombin III (ATIII), and heparin. At near-plasma concentrations of TFPI, ATIII, and factor X, factor X activation that occurs in response to TF:VII is essentially abolished in the presence of heparin (0.5 micromol/L). This effect requires both inhibitors, acting on different targets: (1) ATIII, which in the presence of heparin blocks the activation of TF:VII, and (2) TFPI, which inhibits the TF:VIIa that is generated. In the absence of ATIII, TFPI alone with heparin reduces but does not abolish factor X activation. Conversely, in the absence of TFPI, ATIII + heparin reduces but does not abolish TF:VIIa generation and allows continuing activation of factor X. These results indicated that when the unactivated TF:VII complex is the initiating stimulus, heparin-dependent reduction in the rate and extent of factor X activation requires both ATIII and TFPI. In contrast, if TF:VIIa is used to initiate activation, only TFPI is involved in its regulation.

Tissue Factor Pathway Inhibitor (TFPI) May be Another Important Factor in the Coagulopathy in Acute Promyelocytic Leukemia (APL)

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 2278-2278 ◽  
Author(s):  
Sarah C Bassi ◽  
Eduardo Magalhães Rego
Keyword(s):  
Tissue Factor ◽  
Acute Promyelocytic Leukemia ◽  
Murine Model ◽  
Tissue Factor Pathway Inhibitor ◽  
Plasma Concentrations ◽  
Promyelocytic Leukemia ◽  
Procoagulant Activity ◽  
Factor X ◽  
Nb4 Cells ◽  
Tissue Factor Pathway

Abstract The characteristic coagulopathy in Acute Promyelocytic Leukemia (APL) is unique among the leukemias and thrombotic and bleeding complications remain the major causes of early deaths. APL promyelocytes express tissue factor (TF) which, after activation by phospholipids, forms a complex with factor VII and converts factor X to activated factor X. TF plays a central role in the pathogenesis of APL coagulopathy, for the procoagulant activity of lysates from freshly isolated APL cells is mainly attributed to TF. During periods of increased apoptosis of promyelocytes, the procoagulant activity is correspondingly intensified. In addition, APL cells may also induce TF procoagulant activity of endothelial cells through their secretion of IL-1b. The activity of the complex FVIIa-TF can be inhibited by the tissue factor pathway inhibitor (TFPI), but its role in the APL-associated coagulopathy remains unknown. This study aimed to determine the time-course of TFPI levels in patients with APL at diagnosis and during the first two-weeks of treatment with ATRA and anthracyclines. Twenty patients with de novo APL (12 males, age ranging from 17 to 72 years) and 20 healthy blood donors (age and sex matched) were included in this study. Peripheral blood (PB) samples were collected at diagnosis, and at D3, D7 and D15 of the induction therapy with ATRA and daunorubicin. The following plasma concentrations were determined: Thrombin-Antithrombin complex (TAT) (Enzygnost¨ TAT micro, Dade Behring/Siemens, IL, EUA), total TFPI (Asserachrom¨ total TFPI, Diagnostica Stago, Frana) and free TFPI (Asserachrom¨ free TFPI, Diagnostica Stago, Frana). The plasma concentrations of TAT were significantly higher in APL patients at presentation, D3 and D7 compared to controls, suggesting that the pathologic activation of coagulation was reversed by D15 of treatment Figure 1). The concentrations of free-TFPI were significantly higher in APL samples compared to controls in all time-points (Figure 2). In contrast, the concentrations of the truncated form of TFPI (estimated by subtracting the free-TFPI values from total-TFPI concentration) did not vary significantly between the groups. Since, free-TFPI (intact form) has been proven to present higher capacity to inhibit the activated factor X and VIIa-TF proteases than truncated-TFPI (bound to lipoprotein), we hypothesized that our findings confirm the relevance of free-TFPI in APL coagulopathy. To test whether the administration of rh-TFPI may revert aberrant activation of coagulation in APL patients, we developed a murine model using the IV infusion of NB4 cells. Similarly to the reported in APL patients, we observed an increase on TAT levels in mice injected with 5x106 NB4 cells [(60.7 ng/ml (24 - 116 ng/ml) vs 11.5 ng/ml (2.2 - 27.8 ng/ml), p<0.05)]. In contrast, murine TFPI levels decreased 30 minutes after the infusion of NB4 cells [30 ng/ml (5.8 - 217 ng/ml) vs 202 ng/ml (46 - 354 ng/ml)], suggesting that it was rapidly consumed. Unfortunately, it was not possible to distinguish between truncated and intact TFPI forms in mice. Intravenous infusion of recombinant human (rh) TFPI at the dose of 10mg/Kg significantly decreased the TAT levels (Figure 3) and increased TFPI levels in the murine model. In conclusion, our data on clinical samples and pre-clinical data using a murine model suggest that treatment with rh-TFPI may be a strategy to counteract APL-associated coagulopathy. Disclosures No relevant conflicts of interest to declare.

Acute Release of Tissue Factor Pathway Inhibitor after In Vivo Thrombin Generation in Baboons

1999 ◽  
Vol 82 (12) ◽  
pp. 1652-1658 ◽  
Author(s):  
Egbert Kruithof ◽  
Vijay Kakkar ◽  
Florea Lupu ◽  
Cristina Lupu
Keyword(s):  
Tissue Factor ◽  
Thrombin Generation ◽  
Tissue Factor Pathway Inhibitor ◽  
Plasma Concentrations ◽  
Factor Xa ◽  
Treatment Groups ◽  
Tissue Factor Pathway ◽  
Positive Correlations

SummaryTissue factor pathway inhibitor (TFPI), the major downregulator of the procoagulant activity of tissue factor (TF), is synthesised by endothelial cells (EC) and acutely released in vitro after thrombin stimulation. Expression of TF on EC and subsequent thrombin generation occurs in vivo during sepsis or malignancy, inducing disseminated intravascular coagulation (DIC). The present study investigates the changes in plasma TFPI in relation to markers of in vivo thrombin generation induced by injection of factor Xa (FXa)/phospholipids in baboons at dosages leading to partial (48%) or complete fibrinogen depletion. The plasma concentrations of thrombin-antithrombin III (TAT) and fibrinopeptide A (FpA), as markers of in vivo generation of thrombin, were strongly enhanced after injection of FXa/phospholipids. TFPI levels, whether measured as antigen or activity, increased significantly in both treatment groups within few minutes, and were dependent on the dose of FXa/phospholipids. Significant positive correlations between plasma levels of TFPI and of TAT or FpA were observed. Altogether, our results indicate that experimentally induced in vivo generation of thrombin causes the acute release of TFPI, high-lighting a possible novel function of thrombin in downregulation of the coagulation process, potentially relevant for the outcome of DIC.

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