PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 2776313

Measuring tissue factor (factor III) activity in plasma.

C Fukuda·K Iijima·K Nakamura
View original source ↗Export metadata ↓

Abstract

This is a method for measuring tissue factor (TF, Factor III, tissue thromboplastin) activity in plasma by using a chromogenic substrate. As pretreatment, the euglobulin fraction of plasma was prepared by removing endogenous inhibitors and heated at 60 degrees C for 3 min to remove fibrinogen. This allowed us to measure the low TF activity in plasma that could not otherwise be measured. Neither phospholipids nor coagulation factors VII, IX, X, or Xa in the samples interfere. Within-run and day-to-day reproducibility were both good. The mean value obtained by this method for normal persons was 1.02 (SD 0.91) arbitrary units/L. A markedly high plasma TF activity of 20 arb. units/L or more was observed in patients with some types of disseminated intravascular coagulation.

Explore related subjects

Disseminated Intravascular CoagulationFibrinogenHumansHydrogen-Ion ConcentrationOligopeptidesSpecimen HandlingThromboplastinJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

C Fukuda, K Iijima, K Nakamura. 1989. Measuring tissue factor (factor III) activity in plasma.. https://pubmed.ncbi.nlm.nih.gov/2776313/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2003

Imbalances between the levels of tissue factor and tissue factor pathway inhibitor in ARDS patients.

INTRODUCTION: To evaluate the pathogenetic role of tissue factor (TF), tissue factor pathway inhibitor (TFPI), and neutrophil elastase in acute respiratory distress syndrome (ARDS), as well as to test the hypothesis that TFPI levels modified by neutrophil activation are not sufficient to prevent TF-dependent intravascular coagulation, leading to sustained systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS), which determine the prognosis of these patients. MATERIALS AND METHODS: The study subjects consisted of 55 patients with trauma and sepsis who were divided into three groups according to the Lung Injury Score. Ten normal healthy volunteers served as control. Plasma levels of TF, TFPI, and neutrophil elastase were measured on the day of injury or the day of diagnosis of sepsis (day 0) and days 1 through 4. The number of SIRS criteria that the patient met and the disseminated intravascular coagulation (DIC) score is determined daily. RESULTS: Patients (15) developed ARDS, 23 were at risk for but did not develop the syndrome, and 17 patients were without risk for ARDS. TF and neutrophil elastase levels in ARDS patients were persistently higher than those in other two groups and control subjects. However, the TFPI levels showed no difference among the three groups, which retained normal or slightly elevated levels compared to the control subjects. DIC scores did not improve and SIRS continued during the study period in patients with ARDS. The ARDS patients showed higher numbers of dysfunctioning organs and associated with poorer outcome than the other two groups. CONCLUSION: Systemic activation of the TF-dependent pathway not adequately balanced by TFPI is one of the aggravating factors of ARDS. High levels of neutrophil elastase released from activated neutrophils may explain the imbalance of TF and TFPI. Persistent DIC and sustained SIRS contribute to MODS, determining the prognosis of ARDS patients.

Disseminated Intravascular Coagulation↗
PubMed2003

Disseminated intravascular coagulation current concepts of etiology, pathophysiology, diagnosis, and treatment.

The pathophysiologic mechanisms and clinical and laboratory manifestations of DIC are complex, partly because of inter-relationships within the hemostasis system. Only by clearly understanding these extraordinarily complex pathophysiologic inter-relationships can the clinician and laboratory scientist appreciate the divergent and wide spectrum of often-confusing clinical and laboratory findings in patients with DIC. Many therapeutic decisions to be made are controversial and lack validation. Nevertheless, newer antithrombotic agents and agents that can block, blunt, or modify cytokine activity and the activity of vasoactive substances seem to be of value. The complexity and variable degree of clinical expression suggest that therapy should be individualized depending on the nature of DIC, the patient's age, etiology of DIC, site and severity of hemorrhage or thrombosis, and hemodynamics and other appropriate clinical parameters.

Disseminated Intravascular Coagulation↗