Two-stage response to endotoxin infusion into normal human subjects: Correlation of blood phagocyte luminescence with clinical and laboratory markers of the inflammatory, hemostatic response

Taylor, Fletcher B.; Haddad, Phillip A.; Hack, Erik; Chang, Alvin; Peer, G.; Morrissey, James H.; Li, Anguo; Allen, Robert C.; Wada, Hideo; Kinasewitz, Gary T.

doi:10.1097/00003246-200102000-00020

Cited by 40 publications

(31 citation statements)

References 32 publications

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“…It has been reported that plasma TF antigen levels remain persistently elevated between 8 and 48 hours after endotoxin administration, 54 although we were unable to confirm these findings. 27 Since only one third to one half of plasma TF antigen can be sedimented by high-speed centrifugation, it has been proposed that the assay may in fact measure 2 forms of TF antigen in plasma: Figure 5.…”

Section: Discussioncontrasting

confidence: 86%

Induction of microparticle- and cell-associated intravascular tissue factor in human endotoxemia

Aras

Shet

Bach

et al. 2004

Blood

270

221

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The precise role of intravascular tissue factor (TF) remains poorly defined, due to the limited availability of assays capable of measuring circulating TF procoagulant activity (PCA). As a model of inflammation-associated intravascular thrombin generation, we studied 18 volunteers receiving an infusion of endotoxin. A novel assay that measures microparticle (MP)-associated TF PCA from a number of cellular sources (but not platelets) demonstrated an 8-fold increase in activity at 3 to 4 hours after endotoxin administration (P < .001), with a return to baseline by 8 hours. TF antigen-positive MPs isolated from plasma were visualized by electron microscopy. Interindividual MP-associated TF response to lipopolysaccharide (LPS) was highly variable. In contrast, a previously described assay that measures total (cell and MP-borne) wholeblood TF PCA demonstrated a more modest increase, with a peak in activity (1.3-fold over baseline; P < .000 01) at 3 to 4 hours, and persistence for more than 24 hours. This surprisingly modest increase in whole-blood TF activity is likely explained by a profound although transient LPS-induced monocytopenia. MP-associated TF PCA was highly correlated with whole-blood TF PCA and total number of circulating MPs, and whole-blood TF PCA was highly correlated with TF mRNA levels. (Blood. 2004;103:4545-4553)

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Section: Discussioncontrasting

confidence: 86%

Induction of microparticle- and cell-associated intravascular tissue factor in human endotoxemia

Aras

Shet

Bach

et al. 2004

Blood

270

221

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“…4), reflecting a decrease in total plasma FVII. Similar decreases in FVIIa have been reported after bolus infusions of endotoxin (36) and in sepsis (37). Because tissue factor is the principal ligand for FVIIa, we believe that the decrease in plasma FVII levels reflect accelerated clearance as a result of binding to an increased number of available tissue factor sites.…”

Section: Discussionsupporting

confidence: 85%

Effects of Hyperglycemia and Hyperinsulinemia on Circulating Tissue Factor Procoagulant Activity and Platelet CD40 Ligand

et al. 2006

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Individuals with chronically elevated glucose and/or insulin levels, i.e., most patients with type 2 diabetes, have accelerated atherosclerosis and are prone to acute vascular events. We have tested the hypothesis that hyperglycemia and/or hyperinsulinemia singly or combined may increase tissue factor, the primary initiator of blood coagulation. We have determined changes in circulating tissue factor procoagulant activity (PCA) and other procoagulation proteins in healthy volunteers exposed to 24 h of selective hyperinsulinemia, selective hyperglycemia, or combined hyperinsulinemia and hyperglycemia. Combined elevations of plasma insulin and glucose levels for 24 h produced a ninefold increase in tissue factor PCA, which was associated with an increase in monocyte tissue factor protein (flow cytometry) and mRNA (RT-PCR), increases in plasma thrombin-antithrombin complexes, prothrombin fragment 1.2, factor VIII coagulant activity, and platelet CD40 ligand as well as decreases in factor VIIa, factor VII coagulant activities, and factor VII antigen. Effects of selective hyperinsulinemia and selective hyperglycemia were less striking but appeared to be additive. We conclude that hyperinsulinemia and hyperglycemia but particularly the combination of both create a prothrombotic state and in addition may be proinflammatory and proatherogenic because of the proinflammatory actions of CD40 ligand and tissue factor. Diabetes 55: [202][203][204][205][206][207][208] 2006

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“…Because TF is the principal ligand for FVIIa and FVIIc, we believe that the decrease in plasma FVII activity reflected an accelerated clearance from plasma as a result of its binding to an increased number of available TF binding sites on cells/membranes (18). Similar decreases in FVII have been reported after bolus infusions of endotoxin (27) and in sepsis (28), and an inverse relationship between plasma FVII and TF-PCA has been observed by us in other studies (17).…”

Section: Tf-pca Fviic Fviii and Tat Are Elevated In T2dmsupporting

confidence: 74%

Circulating Tissue Factor Procoagulant Activity and Thrombin Generation in Patients with Type 2 Diabetes: Effects of Insulin and Glucose

Boden

Vaidyula

Homko

et al. 2007

The Journal of Clinical Endocrinology &Amp; Metabolism

123

112

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Context: Type 2 diabetes mellitus (T2DM) is a hypercoagulable state. Tissue factor (TF) is the principal initiator of blood coagulation.Objective: Our objective was to examine the effects of hyperglycemia and hyperinsulinemia on the TF pathway of blood coagulation in T2DM.Design: Three study protocols were used: 1) acute correction of hyperglycemia (with iv insulin) followed by 24 h of euglycemia, 2) 24 h of selective hyperinsulinemia, and 3) 24 h of combined hyperinsulinemia and hyperglycemia. Setting:The study took place at a clinical research center.Study Participants: Participants included 18 T2DM patients and 22 nondiabetic controls.Results: Basal TF-procoagulant activity (TF-PCA), monocyte TF mRNA, plasma coagulation factor VII (FVIIc), and thrombin-antithrombin complexes were higher in T2DM than in nondiabetic controls, indicating a chronic procoagulant state. Acutely normalizing hyperglycemia over 2-4 h resulted in a small (ϳ7%) but significant decline in TF-PCA with no further decline over 24 h. Raising insulin levels alone raised TF-PCA by 30%, whereas raising insulin and glucose levels together increased TF-PCA (by 80%), thrombin-antithrombin complexes, and prothrombin fragment 1.2. Plasma FVIIa and FVIIc declined with increases in TF-PCA. Conclusion:We conclude that the combination of hyperglycemia and hyperinsulinemia, common in poorly controlled patients with T2DM, contributes to a procoagulant state that may predispose these patients to acute cardiovascular events.

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Two-stage response to endotoxin infusion into normal human subjects: Correlation of blood phagocyte luminescence with clinical and laboratory markers of the inflammatory, hemostatic response

Cited by 40 publications

References 32 publications

Induction of microparticle- and cell-associated intravascular tissue factor in human endotoxemia

Induction of microparticle- and cell-associated intravascular tissue factor in human endotoxemia

Effects of Hyperglycemia and Hyperinsulinemia on Circulating Tissue Factor Procoagulant Activity and Platelet CD40 Ligand

Circulating Tissue Factor Procoagulant Activity and Thrombin Generation in Patients with Type 2 Diabetes: Effects of Insulin and Glucose

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