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  • 1
    ISSN: 1432-1238
    Keywords: Key words Sepsis ; Hemostasis ; Organ failure ; Severity of disease ; IL-6 ; PAI-1 ; Neopterin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective: To find out whether changes within the hemostatic system are related to the severity of illness and organ failure in patients at the onset of clinically defined sepsis and to find some indications for the contribution of endothelial cell activation or perturbation to the patient‘s status. The following measurements were undertaken: Acute Physiology and Chronic Health Evaluation (APACHE) II score, multiple organ failure (MOF) score, plasma levels of thrombin–antithrombin III complexes (TAT), antithrombin III (AT III), protein C antigen, factor XII, and plasminogen activator inhibitor type 1 antigen (PAI-1), neopterin, and interleukin 6 (IL-6). Design: A prospective case series study. Setting: Intensive care unit (ICU) of the Department of Internal Medicine, Justus Liebig University, Giessen, Germany. Patients: 28 consecutive patients (11 females, 17 males; mean age 58 years) with clinically defined sepsis. Eleven patients were admitted from the surgical ICU (9 after elective surgery, 2 after trauma surgery). The operations were done 1–26 days (mean 14 days) prior to the onset of sepsis. Main results: At the onset of sepsis we found elevated plasma levels of TAT, PAI-1, neopterin, and IL-6, and lowered plasma levels of AT III, factor XII, and protein Cantigen. Neopterin, PAI-1, IL-6, and factor XII showed a statistically significant correlation with the APACHE II score. The MOF score is significantly correlated with IL-6 and neopterin. The extent of hemostatic abnormalities was related to increasing levels of IL-6. Conclusions: Clinical evidence of a septic process is most likely to be preceded by activation of the hemostatic system, the vascular endothelium, and the monocyte/ macrophage system. IL-6 may have a regulatory function for hemostasis in inflammation. Laboratory monitoring could be helpful in deciding whether to start early intensive therapy in patients at risk for sepsis.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1238
    Keywords: Sepsis ; Hemostasis ; Organ failure ; Severity of disease ; IL-6 ; PAI-1 ; Neopterin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective To find out whether changes within the hemostatic system are related to the severity of illness and organ failure in patients at the onset of clinically defined sepsis and to find some indications for the contribution of endothelial cell activation or perturbation to the patient's status. The following measurements were undertaken: Acute Physiology and Chronic Health Evaluation (APACHE) II score, multiple organ failure (MOF) score, plasma levels of thrombin—antithrombin III complexes (TAT), antithrombin III (AT III), protein C antigen, factor XII, and plasminogen activator inhibitor type 1 antigen (PAI-1), neopterin, and interleukin 6 (IL-6). Design A prospective case series study. Setting Intensive care unit (ICU) of the Department of Internal Medicine, Justus Liebig University, Giessen, Germany. Patients 28 consecutive patients (11 females, 17 males; mean age 58 years) with clinically defined sepsis. Eleven patients were admitted from the surgical ICU (9 after elective surgery, 2 after trauma surgery). The operations were done 1–26 days (mean 14 days) prior to the onset of sepsis. Main results At the onset of sepsis we found elevated plasma levels of TAT, PAI-1, neopterin, and IL-6, and lowered plasma levels of AT III, factor XII, and protein Cantigen. Neopterin, PAI-1, IL-6, and factor XII showed a statistically significant correlation with the APACHE II score. The MOF score is significantly correlated with IL-6 and neopterin. The extent of hemostatic abnormalities was related to increasing levels of IL-6. Conclusions Clinical evidence of a septic process is most likely to be preceded by activation of the hemostatic system, the vascular endothelium, and the monocyte/macrophage system. IL-6 may have a regulatory function for hemostasis in inflammation. Laboratory monitoring could be helpful in deciding whether to start early intensive therapy in patients at risk for sepsis.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Zeitschrift für Kardiologie 87 (1998), S. s026 
    ISSN: 1435-1285
    Keywords: Schlüsselwörter Koronare Mikrozirkulation – KHK – Myokardinfarkt – Angina pectoris ; Key words Coronary microcirculation – coronary artery disease – myocardial infarction – angina pectoris
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Disturbances of microcirculation in coronary artery disease can be seen in the presence of critical stenosis of epicardial coronary arteries, as a result of endothelial dysfunction in the absence of significant stenosis or during recovery of ischaemic myocardium after successful angioplasty of stenosed or occluded coronary arteries. Diagnostic methods are morphologic/morphometric analyses, measurement of the global coronary reserve, measurement of the regional coronary microcirculation (scintigraphy, positron emission tomography) and laboratory analysis of haemorheological alterations (plasma, erythrocytes, leucocytes). After successful angioplasty, normalisation of glutamate extraction rate takes three to six months. In patients with unstable angina, changes in plasma viscosity, erythrocyte aggregation and neutrophil activation occur. Neutrophils are activated after successful angioplasty in acute myocardial infarction and even after elective angioplasty (when measured in the coronary sinus). Therapeutic improvements of disturbed microvascular flow can be obtained by increasing perfusion pressure (by revascularisation, nitrates, calcium antagnoists, physical training), by improving the fluidity of the blood and by reducing the extravascular component of coronary vascular resistance (by antihypertensive treatment).
    Notes: Zusammenfassung Eine mikrovaskuläre Dysfunktion bei koronarer Herzkrankheit kann bei hämodynamisch relevanten Stenosen der epikardialen Koronararterien, bei Endotheldysfunktion in Abwesenheit signifikanter Lumeneinengungen oder in der Erholungsphase des Herzmuskels nach erfolgreicher Angioplastie einer stenosierten oder verschlossenen Koronararterie beobachtet werden. Diagnostisch läßt sie sich durch morphologische/morphometrische Analysen, Messung der globalen Koronarreserve, Erfassung der regionalen koronaren Mikrozirkulation (Myokardszintigraphie, Positronen-Emissions-Tomographie) oder laborchemische Analyse hämorheologischer Veränderungen (Plasma, Erythrozyten, Granulozyten) nachweisen. So findet sich nach erfolgreicher Angioplastie erst nach drei bis sechs Monaten eine Normalisierung der Glutamat-Extraktionsrate. Bei Patienten mit instabiler Angina pectoris sind eine Erhöhung der Plasmaviskosität, Veränderungen der Erythrozytenaggregation und -Verformbarkeit sowie eine Aktivierung von Granulozyten nachweisbar. Eine Aktivierung neutrophiler Granulozyten tritt auch nach erfolgreicher Angioplastie bei akutem Myokardinfarkt auf und läßt sich sogar bei elektiver Angioplastie im Koronarsinusblut nachweisen. Therapeutisch können Störungen der Mikrozirkulation durch Steigerungen des Perfusionsdruckes (Revaskularisation, Nitrate, Calcium-Antagonisten, körperliches Training), durch Verbesserung der Fließfähigkeit des Blutes und durch eine Verminderung der extravasalen Komponente des Koronarwiderstandes (antihypertensive Therapie) günstig beeinflußt werden.
    Type of Medium: Electronic Resource
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