Post-transcriptional, post-translational and pharmacological regulation of tissue factor pathway inhibitor

Subramaniam, Saravanan; Kanse, Sandip M.; Kothari, Hema; Reinhardt, Carsten; Fletcher, Craig

doi:10.1097/mbc.0000000000000775

Cited by 7 publications

(1 citation statement)

References 155 publications

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“…TFPI is produced by microvascular endothelial cells and pooled in the endothelium (80%), plasma (10%-20%), and platelets (<2.5%). 4,5 The concentration of TFPI in plasma is very low, with the major component (80%) bound to lipoproteins (ie, high-density lipoprotein [HDL], 6,7 while the full length, minor component [20%], called free TFPI, is unbound and therefore has the main anticoagulant effect. The anticoagulant effect of TFPI can be attributed to two mechanisms: inhibition of tissue factor-activated coagulation factor VII [TF-FVIIa] and activated coagulation factor X [FXa] via the tissue factor-activated coagulation factor VII-tissue factor pathway inhibitor-activated coagulation factor X [TF-FVIIa-TFPI-FXa] complex, 8 and inhibition of prothrombinase as reported in a recent study.…”

Section: Introductionmentioning

confidence: 99%

The Impact of Anticoagulant Activity of Tissue Factor Pathway Inhibitor Measured by a Novel Functional Assay for Predicting Deep Venous Thrombosis in Trauma Patients: A Prospective Nested Case-Control Study

Cao

Zhang

et al. 2021

Clin Appl Thromb Hemost

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Objective Deep venous thrombosis (DVT) is a common complication in patients with traumatic injury. Tissue factor pathway inhibitor (TFPI) is a natural anticoagulant protein in the extrinsic coagulation pathway. However, the relationship between DVT after trauma and the anticoagulant activity of TFPI remains unclear. In this prospective study, we investigated the role of TFPI in trauma patients with DVT to evaluate whether the anticoagulant activity of TFPI measured by a new functional assay can be used to help predict the risk of DVT. Patients and methods: This prospective nested case-control study enrolled trauma patients and healthy volunteers. Forty-eight trauma patients diagnosed with DVT and forty-eight matched trauma patients without DVT were included in the study. 120 healthy volunteers were also included as controls. Blood samples and case information were collected at admission. Patients accepted angiography before surgery to diagnose DVT. The parameters examined included TFPI anticoagulant activity, free-TFPI antigen, blood cell counts, and routine clinical coagulation tests. Results: For the parameters of TFPI anticoagulant activity, three were markedly increased in the DVT group compared to the non-DVT group (TFPI initial anticoagulant time ratio, P = .022; TFPI whole anticoagulant time ratio, P = .048; and TFPI anticoagulant rate, P = .034). The free-TFPI antigen concentration also showed a significant increasing trend in trauma patients with DVT compared with trauma patients without DVT (P = .035). Multivariate logistic regression analysis identified four independent factors for the development of DVT (TFPI initial anticoagulant time ratio, free-TFPI antigen, prothrombin time, and red blood cell count). We calculated the TFPI correlation coefficient and found that the area under the receiver operating characteristic curve was .821. Conclusions: A novel functional assay was developed to measure the anticoagulant activity of TFPI. The anticoagulant activity of TFPI can be used as a potential biomarker for diagnosing DVT in trauma patients.

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