Tissue Factor Pathway Inhibitor and P-Selectin as Markers of Sepsis-Induced Non-overt Disseminated Intravascular Coagulopathy

Mosad, Eman; Elsayh, Khalid I; Eltayeb, Azza A.

doi:10.1177/1076029609344981

Cited by 29 publications

(17 citation statements)

References 53 publications

(60 reference statements)

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“…[13] The results of our study indicated that CD62P is not only involved in inflammatory response by its relationship with hs-CRP and TNF-α, but also involved in platelet activation and subsequent widespread microthrombosis in microvessels via its relationship with D-dimer, AT-III activity, PT and APTT and that CD62P is an important initiating factor for infl ammatory response and coagulation/fibrinolysis dysfunction in sepsis. Mosad et al [14] found in 176 sepsis patients complicated with DIC, CD62P level was positively correlated with the level of DIC, fi brinogen consumption, D-dimer, and markers of thrombin activation. CD62P can not only initiate the inflammatory cascade but also trigger the coagulation cascade.…”

Section: Discussionmentioning

confidence: 98%

Endothelial cell injury with inflammatory cytokine and coagulation in patients with sepsis

Ding¹,

Cao²,

Ma³

et al. 2013

World Journal of Emergency Medicine

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BACKGROUND: Current studies on CD62P have focused mainly on cardiovascular diseases, while only few studies have evaluated the effects of CD62P on the development of sepsis and the association between endothelial cell injury with infl ammation and coagulation. This study attended to explore the association between endothelial cell injury with infl ammation and coagulation by evaluating the expression of soluble CD62P (s-CD62P) in plasma and its mechanism in patients with sepsis, thus to provide the evidence of effective treatment of sepsis with anti-adhesion therapy targeted CD62P. METHODS: A total of 70 critically ill patients with systemic inflammatory response syndrome (SIRS) admitted to intensive care unit (ICU) between September 2009 and February 2010 were enrolled for a prospective and control study. According to the diagnostic criteria of sepsis/SIRS, the patients were divided into two groups: a sepsis group (n=38) and a SIRS group (n=32). Another 20 healthy volunteers served as a control group. Patients in the sepsis group and SIRS group were matched by clinical signs of high blood pressure, diabetes and its complications. The demographics of the patients including age, sex, body mass index (BMI), smoking and alcohol addict were compared among the groups. Six mL peripheral blood samples were collected within 24-hour admission in ICU for enzymelinked immunosorbent assay (ELISA) to detect the plasma levels of s-CD62P, TNF-α, and hs-CRP. And variables of coagulation function such as platelet (PLT), prothrombin (PT), activated partial thromboplastin time (APTT), D-dimer and antithrombin-III (AT-III) were analyzed during 24 hours after admission to ICU. Meanwhile sequential organ failure assessment (SOFA) score of critically ill patients was evaluated. Data were expressed as mean±standard deviation and were statistically analyzed by using SPSS 17.0 statistical software. The differences in plasma levels of s-CD62P of patients in each group were analyzed by ANOVA and the Kruskal-Wallis test. The relations between s-CD62P and infl ammatory cytokines as well as with coagulation were determined by Pearson's product moment correlation coeffi cient analysis. Changes were considered as statistically signifi cant if P value was less than 0.05. RESULTS: Compared with the control group and SIRS group, the sepsis group demonstrated signifi cantly higher levels of s-CD62P, TNF-α and highly sensitive C-reactive protein (hs-CRP) (P<0.05). The plasma levels of D-dimer, PT, and APTT in the sepsis and SIRS groups were signifi cantly higher than those in the control group, while the platelet count and the activity of AT-III were obviously lower (P<0.05). In the sepsis group, the plasma levels of hs-CRP and TNF-α were positively correlated with PT, APTT, and D-dimer, and negatively correlated with AT-III and PLT (P<0.05). The plasma levels of s-CD62P were signifi cantly correlated with the plasma levels of TNF-α, hs-CRP, D-dimer, PT, and APTT, whereas they were correlated negatively well with PLT and AT-III (P<0.05). CONCLUSIONS:...

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Section: Discussionmentioning

confidence: 98%

Endothelial cell injury with inflammatory cytokine and coagulation in patients with sepsis

Ding¹,

Cao²,

Ma³

et al. 2013

World Journal of Emergency Medicine

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“…Unfortunately, no association was searched between high levels of the biomarker and pneumonia. Several other clinical studies focusing on platelets as potential biomarkers for sepsis diagnosis and prognostication have been carried out but almost all concerned patients with sepsis as an inclusion criterion [32, 33]. …”

Section: Discussionmentioning

confidence: 99%

Sepsis prediction in critically ill patients by platelet activation markers on ICU admission: a prospective pilot study

Layios

Delierneux

Hego

et al. 2017

ICMx

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BackgroundPlatelets have been involved in both immune surveillance and host defense against severe infection. To date, whether platelet phenotype or other hemostasis components could be associated with predisposition to sepsis in critical illness remains unknown. The aim of this work was to identify platelet markers that could predict sepsis occurrence in critically ill injured patients.MethodsThis single-center, prospective, observational, 7-month study was based on a cohort of 99 non-infected adult patients admitted to ICUs for elective cardiac surgery, trauma, acute brain injury, and post-operative prolonged ventilation and followed up during ICU stay. Clinical characteristics and severity score (SOFA) were recorded on admission. Platelet activation markers, including fibrinogen binding to platelets, platelet membrane P-selectin expression, plasma soluble CD40L, and platelet-leukocytes aggregates were assayed by flow cytometry at admission and 48 h later, and then at the time of sepsis diagnosis (Sepsis-3 criteria) and 7 days later for sepsis patients. Hospitalization data and outcomes were also recorded.MethodsOf the 99 patients, 19 developed sepsis after a median time of 5 days. These patients had a higher SOFA score at admission; levels of fibrinogen binding to platelets (platelet-Fg) and of D-dimers were also significantly increased compared to the other patients. Levels 48 h after ICU admission no longer differed between the two patient groups. Platelet-Fg % was an independent predictor of sepsis (P = 0.0031). By ROC curve analysis, cutoff point for Platelet-Fg (AUC = 0.75) was 50%. In patients with a SOFA cutoff of 8, the risk of sepsis reached 87% when Platelet-Fg levels were above 50%. Patients with sepsis had longer ICU and hospital stays and higher death rate.ConclusionsPlatelet-bound fibrinogen levels assayed by flow cytometry within 24 h of ICU admission help identifying critically ill patients at risk of developing sepsis.Electronic supplementary materialThe online version of this article (doi:10.1186/s40635-017-0145-2) contains supplementary material, which is available to authorized users.

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“…First, platelet p-selectin expression results in increased monocyte TF expression and platelet adhesion to leukocytes and endothelium. [31, 32] Once adhered to leukocytes and endothelium, platelets serve as a surface for thrombin generation and cellular signaling of other coagulation factors. [8]…”

Section: Pathogenesis Of Thrombus Formation In Sepsismentioning

confidence: 99%

The coagulopathy of acute sepsis

Simmons¹,

Pittet

2015

Current Opinion in Anaesthesiology

232

190

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Purpose of Review Sepsis, defined by the presence of infection and host inflammation, is a lethal clinical syndrome with an increasing mortality rate worldwide. In severe disease, the coagulation system becomes diffusely activated, with consumption of multiple clotting factors resulting in Disseminated Intravascular Coagulation (DIC). When present, DIC portends a higher mortality rate. Understanding the mechanisms that tie inflammation and diffuse thrombosis will allow therapeutic interventions to be developed. The Coagulopathy of Acute Sepsis is a dynamic process that is time and disease burden specific. Whole blood testing of coagulation may provide more clinically useful information than classical tests. Natural anticoagulants that regulate thrombosis are down regulated in sepsis. Patients may benefit from modulation of the coagulation system when systemic inflammation and hypercoagulopathy exist. Proper timing of anticoagulant therapy may ultimately lead to decreased incidence of multisystem organ dysfunction (MODS). Recent Findings The pathogenesis of coagulopathy in sepsis is driven by an up-regulation of procoagulant mechanisms and simultaneous down-regulation of natural anticoagulants. Inflammation caused by the invading organism is a natural host defense than cannot be eliminated during treatment. Successful strategies to prevent MODS center on stratifying patients at high risk for DIC and restoring the balance of inflammation and coagulation. Summary The prevention of DIC in septic patients is a key therapeutic target in preventing death from multisystem organ failure. Stratifying patients for therapy using thromboelastometry, specific markers for DIC, and composite scoring systems is an area of growing research.

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Tissue Factor Pathway Inhibitor and P-Selectin as Markers of Sepsis-Induced Non-overt Disseminated Intravascular Coagulopathy

Cited by 29 publications

References 53 publications

Endothelial cell injury with inflammatory cytokine and coagulation in patients with sepsis

Endothelial cell injury with inflammatory cytokine and coagulation in patients with sepsis

Sepsis prediction in critically ill patients by platelet activation markers on ICU admission: a prospective pilot study

The coagulopathy of acute sepsis

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