scholarly journals High mobility group B1 levels in sepsis and Disseminated Intravascular Coagulation.

2012 ◽  
Vol 59 (4) ◽  
Author(s):  
Zeynep M Eskici ◽  
Şerefden Açıkgöz ◽  
Nihal Pişkin ◽  
Görkem Mungan ◽  
Murat Can ◽  
...  
Keyword(s):  
Tract Infection ◽  
Disseminated Intravascular Coagulation ◽  
Protein C ◽  
High Mobility ◽  
Protein S ◽  
High Mobility Group ◽  
Hmgb1 Protein ◽  
Intravascular Coagulation ◽  
The Difference ◽  
D Dimer

Cytokines trigger coagulant and fibrinolytic systems in sepsis to result in Disseminated Intravascular Coagulation (DIC) that is an important complication and leads to disseminated hemorrhages and multi-organ failure. High Mobility Group B1 DNA Binding (HMGB1) protein is a cytokine taking part in systemic inflammatory response. The objective of this study was to investigate HMGB1 levels in groups of septic patients with and without DIC.Twenty-one septic patients without DIC and 12 septic patients with DIC from the Intensive Care Unit (ICU) were included in the study. In addition, 20 patients admitted to the ICU without sepsis or DIC and 20 healthy volunteers served as controls. Levels of HMGB1, prothrombin time, activated partial thromboplastin time, fibrinogen, D-dimer, protein C, protein S, anti-thrombin III (ATIII), platelet (thrombocyte) and leukocyte count were determined. Levels of fibrinogen, protein C, ATIII and platelet count were significantly lower and D-dimer was significantly higher in the group with sepsis plus DIC compared to the group with sepsis without DIC. Levels of HMGB1 were higher in the group with sepsis and DIC compared to the group with sepsis; however, the difference was not statistically significant and the levels of HGMB1 of both groups were significantly higher compared to ICU and healthy control groups. HMGB1 levels were not significantly different in survivor and non survivor patients. HMGB1 levels did not differ in lower respiratory tract infection (LRTI) and urinary tract infection (UTI) in regard to the etiology of sepsis.

scholarly journals Endothelial Dysfunction Is Associated with Mortality and Severity of Coagulopathy in Patients with Sepsis and Disseminated Intravascular Coagulation

2019 ◽  
Vol 25 ◽  
pp. 107602961985216 ◽  
Author(s):  
Amanda Walborn ◽  
Matthew Rondina ◽  
Michael Mosier ◽  
Jawed Fareed ◽  
Debra Hoppensteadt
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Protein C ◽  
High Mobility ◽  
Severity Of Illness ◽  
Endothelial Activation ◽  
Endothelial Damage ◽  
Intravascular Coagulation ◽  
Angiopoietin 2 ◽  
Von Willebrand ◽  
Relationship Of

The role of the endothelium in sepsis-associated disseminated intravascular coagulation (DIC) is multifaceted and may contribute substantially to disease severity and outcome. The purpose of this study was to quantify measures of endothelial function, including markers of activation (endocan, Angiopoietin-2 [Ang-2], and von Willebrand Factor), endogenous anticoagulants (tissue factor pathway inhibitor and protein C), and damage-associated factors (High Mobility Group Box 1 [HMGB-1]) in the plasma of patients with sepsis and DIC, and to determine the relationship of these factors with severity of illness and outcome. Plasma samples were collected from 103 adult patients with sepsis within 48 hours of intensive care unit admission. Biomarker levels were measured using commercially available, standardized methods. Disseminated intravascular coagulation was diagnosed according to the International Society of Thrombosis and Hemostasis scoring algorithm. Twenty-eight-day mortality was used as the primary end point. In this study, endothelial damage and dysfunction were associated with the severity of coagulopathy and mortality in DIC patients. Loss of the endogenous anticoagulant protein C and elevation in the vascular regulator Ang-2 were associated with the development of overt DIC. In addition to Ang-2 and protein C, endocan, a biomarker of endothelial activation, and HMGB-1, a mediator of endothelial damage and activation, were significantly associated with mortality. This underscores the contribution of the endothelium to the pathogenesis of sepsis-associated DIC.

Plasma Levels of High Mobility Group Box Protein in Patients with Organ Failure, Disseminated Intravascular Coagulation or Poor Outcome.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 2142-2142
Author(s):  
Hideo Wada ◽  
Tsutomu Nobori ◽  
Shingo Yamada ◽  
Ikuro Maruyama
Keyword(s):  
Infectious Diseases ◽  
Organ Failure ◽  
Disseminated Intravascular Coagulation ◽  
Plasma Levels ◽  
High Mobility ◽  
High Mobility Group ◽  
Study Group ◽  
Chromosomal Protein ◽  
Intravascular Coagulation ◽  
Significant Difference

Abstract High Mobility Group Box chromosomal protein 1 (HMGB1) is a nuclear DNA-binding protein acting as a proinflammatory cytokine when released in the extracellular space from necrotic cells, activated macrophages and dendritic cells. HMGB1 acts on a specific receptor, RAGE (receptor for advanced glycation end-products), and induces prolonged inflammation, organ failure, septicaemia and death. The aim of the study was to determine the diagnostic value of plasma HMGB1 concentration and its role in the development of organ failure in patients with disseminated intravascular coagulation (DIC). Plasma HMGB-1 levels were measured in patients with suspected DIC by ELISA and their relationships with DIC, organ failure and clinical outcome were determined. The study group included 201 patients suspected of having DIC (79 females and 122 males, age; 52.1±16.5 years, mean±SD). The study group represented all such patients admitted to the Second Department of Internal Medicine and Intensive Care Unit (ICU) of Mie University Hospital between January 1, 2002 and December 31, 2003. The underlying diseases were infectious diseases (n=40), hematopoietic diseases (n=58), solid cancers (n=16), trauma (n=21), aneurysm (n=12), autoimmune diseases (n=8), liver diseases (n=7), post-operation (n=32) and other diseases (n=7). Results: Plasma HMGB1 was below the detection limit in normal subjects, but moderately elevated in patients with infectious diseases (4.54 ± 8.18 ng/ml, mean±SD), malignancies (2.15 ± 5.34 ng/ml), and traumas (6.47 ± 13.13 ng/ml). DIC was associated with significantly high plasma HMGB1 (14.05 ± 12.56 ng/ml) in these patients. The highest HMGBI levels were in patients with organ failure (8.29 ± 10.99 ng/ml) and non-survivors (16.58 ± 11.01 ng/ml). HMGB1 plasma levels correlated with the DIC score and sepsis-related organ failure assessment (SOFA) score. Plasma levels of HMGB1 were significantly higher in patients with PAI-I of >50 ng/ml (3.66 ± 6.36 ng/ml) than in those with PAI-I <50 ng/ml (1.38 ± 2.97 ng/ml) (p< 0.05) but there was no significant difference in HMGB1 levels between patients with TNF-a of >1.5 (3.04 ± 5,56 ng/ml) and those with less than 1.5 pg/ml (2.44 ± 5.36 ng/ml). Our data suggest that HMGB-1 is a potentially suitable prognostic marker of OF or DIC.

Plasma concentrations and importance of high mobility group box protein in the prognosis of organ failure in patients with disseminated intravascular coagulation

2005 ◽  
Vol 94 (11) ◽  
pp. 975-979 ◽  
Author(s):  
Tsuyoshi Hatada ◽  
Tsutomu Nobori ◽  
Kazuhiro Okabayashi ◽  
Kazuo Maruyama ◽  
Yasunori Abe ◽  
...  
Keyword(s):  
Organ Failure ◽  
Disseminated Intravascular Coagulation ◽  
Nuclear Dna ◽  
Advanced Glycation Endproducts ◽  
Plasma Concentrations ◽  
High Mobility ◽  
Care Facility ◽  
High Mobility Group ◽  
Chromosomal Protein ◽  
Intravascular Coagulation

SummaryHigh Mobility Group Box chromosomal protein 1 (HMGB1) is a nuclear DNA-binding protein acting as a proinflammatory cytokine when released in the extracellular space from necrotic cells, activated macrophages and dendritic cells. HMGB1 acts on a specific receptor, RAGE (receptor for advanced glycation endproducts), and induces prolonged inflammation, organ failure, septicaemia and death. The aim of the study was to determine the diagnostic value of plasma HMGB1 concentration and its role in the development of organ failure in patients with disseminated intravascular coagulation (DIC). Plasma HMGB-1 levels were measured in patients with suspected DIC and their relationships with DIC, organ failure and clinical outcome were determined. The study took place at the intensive care facility, Mie University School of Medicine and comprised 201 patients with suspected DIC. Plasma HMGB1 was below the detection limit in normal subjects, but moderately elevated in patients with infectious diseases (4.54 ± 8.18 ng/ml, mean±SD), malignancies (2.15 ± 5.34 ng/ml), and traumas (6.47 ± 13.13 ng/ml). DIC was associated with significantly high plasma HMGB1 (14.05 ± 12.56 ng/ml) in these patients. The highest HMGBI levels were in patients with organ failure (8.29 ± 10.99 ng/ml) and non-survivors (16.58 ± 11.01 ng/ml). HMGB1 plasma levels correlated with the DIC score and sepsis-related organ failure assessment (SOFA) score. In conclusion, our data suggest that HMGB-1 is a potentially suitable prognostic marker of OF or DIC.

Severe Acquired Protein C Deficiency in Purpura Fulminans Associated With Disseminated Intravascular Coagulation: Treatment With Protein C Concentrate

PEDIATRICS ◽  
1993 ◽  
Vol 91 (2) ◽  
pp. 418-422
Author(s):  
WILLIAM T. GERSON ◽  
JOSEPH D. DICKERMAN ◽  
EDWIN G. BOVILL ◽  
ELIZABETH GOLDEN
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Protein C ◽  
Purpura Fulminans ◽  
Protein S ◽  
Clinical Settings ◽  
Protein C Deficiency ◽  
Intravascular Coagulation ◽  
Hemorrhagic Necrosis ◽  
Protein C Concentrate ◽  
History Of

Purpura fulminans (PF) defines an acute, often lethal syndrome of disseminated intravascular coagulation (DIC) with rapidly progressive hemorrhagic necrosis of the skin due to dermal vascular thrombosis.1-7 It is indicative of a severe disturbance in hemostasis now recognized to involve the protein C system in many cases.1,2,5,8-12 Purpura fulminans is usually seen in three clinical settings: (1) in the newborn period as a manifestation of homozygous protein C deficiency, or rarely protein S deficiency13,14; (2) in individuals with acute, severe viral or bacterial infection where an acquired deficiency in protein C activity is documented1-3,5-8,10,12,15; and (3) as a rare, postinfectious syndrome with a history of an antecedent" preparatory disease," most commonly a viral or bacterial illness involving the skin (eg, varicella or scarlet fever), with the sudden development, during an otherwise unremarkable convalescence, of progressive purpura and necrosis.3-5,7,10,12

scholarly journals Activation and complexation of protein C and cleavage and decrease of protein S in plasma of patients with intravascular coagulation

Blood ◽  
1989 ◽  
Vol 73 (2) ◽  
pp. 455-461 ◽  
Author(s):  
MJ Heeb ◽  
D Mosher ◽  
JH Griffin
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Protein C ◽  
Activated Protein C ◽  
Protein S ◽  
Coagulation Test ◽  
Major Band ◽  
Intravascular Coagulation ◽  
Protein C Inhibitor ◽  
Dependent Protein

Abstract Activated protein C (APC) is inhibited by two major plasma inhibitors (PCIs). To find evidence for in vivo complexation of APC, immunoblotting studies were performed on plasmas of 85 patients with suspected disseminated intravascular coagulation (DIC). Samples from 62 of these patients contained 5% to 35% of protein C antigen in APC:inhibitor complexes, indicating that protein C activation and inhibition had occurred. In 24 normal plasmas, no detectable APC:PCI complexes were observed (less than 5%). Patients with higher levels of complexes had more abnormal coagulation test data for DIC. The major band of APC complexes detected by anti-protein C antibodies did not react with antibodies to the heparin-dependent protein C inhibitor (PCI- 1) previously described. Rather, APC was complexed with another recently described plasma protein C inhibitor, PCI-2. Immunoblotting studies for protein S, the cofactor for APC, revealed that the majority of the DIC patient plasmas contained a higher than normal proportion of protein S in cleaved form, suggesting that protein S may have been proteolytically inactivated. Protein S total antigen levels were also found to be low in DIC patients, excluding those with malignancy. These studies support the hypothesis that the protein C pathway is activated during DIC.

Role of plasma high mobility group box-1 in disseminated intravascular coagulation with leukemia

2015 ◽  
Vol 136 (2) ◽  
pp. 422-426
Author(s):  
Manzhi Wang ◽  
Heng Mei ◽  
Haiming Kou ◽  
Jun Deng ◽  
Huafang Wang ◽  
...  
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
High Mobility ◽  
High Mobility Group ◽  
Intravascular Coagulation

scholarly journals Activation and complexation of protein C and cleavage and decrease of protein S in plasma of patients with intravascular coagulation

Blood ◽  
1989 ◽  
Vol 73 (2) ◽  
pp. 455-461
Author(s):  
MJ Heeb ◽  
D Mosher ◽  
JH Griffin
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Protein C ◽  
Activated Protein C ◽  
Protein S ◽  
Coagulation Test ◽  
Major Band ◽  
Intravascular Coagulation ◽  
Protein C Inhibitor ◽  
Dependent Protein

Activated protein C (APC) is inhibited by two major plasma inhibitors (PCIs). To find evidence for in vivo complexation of APC, immunoblotting studies were performed on plasmas of 85 patients with suspected disseminated intravascular coagulation (DIC). Samples from 62 of these patients contained 5% to 35% of protein C antigen in APC:inhibitor complexes, indicating that protein C activation and inhibition had occurred. In 24 normal plasmas, no detectable APC:PCI complexes were observed (less than 5%). Patients with higher levels of complexes had more abnormal coagulation test data for DIC. The major band of APC complexes detected by anti-protein C antibodies did not react with antibodies to the heparin-dependent protein C inhibitor (PCI- 1) previously described. Rather, APC was complexed with another recently described plasma protein C inhibitor, PCI-2. Immunoblotting studies for protein S, the cofactor for APC, revealed that the majority of the DIC patient plasmas contained a higher than normal proportion of protein S in cleaved form, suggesting that protein S may have been proteolytically inactivated. Protein S total antigen levels were also found to be low in DIC patients, excluding those with malignancy. These studies support the hypothesis that the protein C pathway is activated during DIC.

APC Resistance and other Haemostatic Variables during Pregnancy and Puerperium

1999 ◽  
Vol 81 (04) ◽  
pp. 527-531 ◽  
Author(s):  
U. Kjellberg ◽  
N.-E. Andersson ◽  
S. Rosén ◽  
L. Tengborn ◽  
M. Hellgren
Keyword(s):  
Factor Viii ◽  
Plasminogen Activator ◽  
Protein C ◽  
Activated Protein C ◽  
Plasminogen Activator Inhibitor ◽  
Protein S ◽  
Reference Level ◽  
Soluble Fibrin ◽  
Prothrombin Fragment ◽  
D Dimer

SummaryForty-eight healthy pregnant women were studied prospectively and longitudinally. Blood sampling was performed at 10-15, 23-25, 32-34 and 38-40 weeks of gestation, within one week and at eight weeks postpartum. Classic and modified activated protein C ratio decreased as pregnancy progressed. In the third trimester 92% of the ratios measured with the classic test were above the lower reference level whereas all modified test ratios were normal. Slight activation of blood coagulation was shown with increased levels of prothrombin fragment 1+2, soluble fibrin and D-dimer. Fibrinogen, factor VIII and plasminogen activator inhibitor type 1 and type 2 increased. Protein S and tissue plasminogen activator activity decreased. Protein C remained unchanged. No correlation was found between the decrease in classic APC ratio and changes in factor VIII, fibrinogen, protein S, prothrombin fragment 1+2 or soluble fibrin, nor between the increase in soluble fibrin and changes in prothrombin fragment 1+2, fibrinogen and D-dimer.

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