View clinical trials related to SIRS.
Filter by:Procalcitonin is a protein consisting of 116 amino-acids which can rapidly rise under inflammatory conditions and sepsis. More than 20 years ago it has been shown that dipeptidylpeptidase-4 (DPP-4) cleaves procalcitonin from the n-terminus, resulting in a truncated procalcitonin-variant which consists of 114 aminoacids. Within our workgroup we found that the truncated procalcitonin-variant had deleterious effects on vascular integrity during sepsis in mice. However, it is unknown if this applies also in humans. By using an ELISA-assay we want to examine the ratio between native and truncated human procalcitonin during diseases accompanied with hyperprocalcitoninemia and correlate the results with clinical data.
Advanced stages of the response to life-threatening infection, severe trauma, or other physiological insults often lead to exhaustion of the homeostatic mechanisms that sustain normal blood pressure and oxygenation. These syndromic presentations often meet the diagnostic criteria of sepsis and/or the acute respiratory distress syndrome (ARDS), the two most common syndromes encountered in the intensive care unit (ICU). Although critical illness syndromes, such as sepsis and ARDS, have separate clinical definitions, they often overlap clinically and share several common injury mechanisms. Moreover, there are no specific therapies for critically ill patients, and as a consequence, approximately 1 in 4 patients admitted to the ICU will not survive. The purpose of this observational study is to identify early patient biologic factors that are present at the time of ICU admission that will help diagnose critical illness syndromes earlier, identify who could benefit most from specific therapies, and enable the discovery of new treatments for syndromes such as sepsis and ARDS.
A case-control cohort study to develop and validate the performance of a whole blood gene expression test to distinguish sepsis infection from uninfected systemic inflammatory response syndrome cases in symptomatic adults and children without comorbidities.
A prospective observational cohort study investigating physiological parameters vs biological markers of whole blood in septic and non-septic pregnant woman to predict systemic immune health
Cytokine hemoadsorption is a novel therapy used to improve outcome in critically ill patients with a dysregulated cytokine response and hemodynamic instability. Patients on extracorporeal membraneous oxygenation (ECMO) often develop severe systemic inflammatory response syndrome (SIRS). Cytokine removal using different types of hemoadsorption devices is believed to block the vicious circle of inflammation dysregulation when other basic therapeutic measures fail. To date there are very limited reports on ECMO and cytokine hemoadsorption combination therapy. The aim of this retrospective study is to evaluate feasibility and effectiveness of hemoadsorption in veno-arterial and veno-venous ECMO patients.
Traditional management of community-acquired pneumonia (CAP) relies on the prompt administration of antimicrobials that target the most common causative pathogens. Retrospective analysis of observational clinical studies in CAP showed that the addition of macrolides to standard antibiotic therapy conferred a significant survival benefit. The proposed benefit of macrolides is coming from their anti-inflammatory mode of action. An RCT that proves the attenuation of the high inflammatory burden of the host with CAP after addition of clarithromycin in the treatment regimen is missing. This RCT is aiming to prove that addition of oral clarithromycin to a β-lactam rapidly attenuates the high inflammatory burden of the host in CAP.
Background: Sepsis (blood poisoning) is a clinical syndrome characterised by a dysregulated host response to infection causing life-threatening organ dysfunction which results in admission to an intensive care unit. It typically shows an initial harmful inflammation resulting from the immune system's overreaction to a severe infection. It is a major healthcare problem, affecting millions of people worldwide. In the UK, it kills over 37,000 people/year, costing the NHS £2.5 billion a year, and is increasing in incidence. Despite extensive efforts to tackle this burden, at present, however, there are no specific and effective therapies for this illness. Sepsis is a potentially life-threatening condition caused by a severe infection. When someone develops sepsis, inflammation occurs not just at the site of the infection but throughout the whole body. This widespread inflammation can be very harmful. It is known that similar responses occur in other conditions, not relating to infection. The investigators are recruiting patients with severe infections causing organ failure (also known as severe sepsis/ septicaemia and septic shock) and also patients where widespread inflammation, not related to infection, causes organ failure. In this study the investigators hope to find out whether certain groups of genetic and blood based protein markers of sepsis can forewarn the clinicians to this condition and also highlight patients who are responding well to the treatment. Although it is known that the majority of the patients suffering from sepsis will survive their ICU stay and leave the hospital alive, there is insufficient data how these patients do on a longer term, i.e. after some time at home. To date there is little information on the ability of the observed genetic and blood based protein markers to predict the functional status of the patients surviving these conditions.
Systemic inflammatory response syndrome (SIRS) is frequently observed in children after open-heart surgery and has been associated with both cardiopulmonary bypass and surgical trauma. Children with congenital cyanotic heart disease (CCHD) have complex changes in all blood values and clotting profiles due to chronic hypoxemia. Increased erythrocyte count decreases plasma and coagulation factors, platelet count and function. Therefore, blood and blood products transfusion may increase during intraoperative and postoperative periods. In addition, durations of cardiopulmonary bypass may prolong due to the complex defects of children with CCHD. The aim of this study is to investigate postoperative SIRS rates and risk factors in cyanotic and acyanotic children undergoing open heart surgery for congenital heart disease.
Surgical trauma elicits an immune response aiming to initiate healing and remove debris and damaged tissue locally at the wound site (1). This local reaction includes a considerable production of cytokines and chemokines that enters the circulation and initiate a systemic inflammatory response mediated by circulating cytokines and chemokines. This response is called systemic inflammatory immune response (SIRS) and is an aseptic systemic inflammation. Postoperative inflammation produces proinflammatory cytokines, mainly IL-6, IL1 beta, and tumor necrosis factor alfa (2). Neutrophils and emergency granulopoesis Polymorphonuclear neutrophils constitute the most abundant population of white blood cells. Their main task is to provide innate immune protection of the host from microbial attack, migrating to the site of infection, engulfing the microbes by phagocytosis, and killing the prey through attack by reactive oxygen species (ROS) and antimicrobial granule pro¬teins (22). Upon systemic infection or inflammation, e.g., sepsis or trauma, the bone marrow enters a state of emergency granulopoiesis, drenched in cytokines that augment production and survival of neutrophils for rapid delivery to the blood (23-25). Recently, advanced techniques have evolved that al¬low the isolation of different developmental stages of steady-state and emergency neutrophils, and characterization of these has just begun (26). Glycans Glycans (polysaccharides) attached to proteins and lipids on the surfaces on immune cells serve as ligands for glycan-binding proteins, lectins. Several neutrophil processes are directed by gly¬can - lectin interactions; selectin-directed rolling on the endothelium, siglec-mediated in¬hibitory signals, and activation of effector function by galectins. Many of the proteins that end up in neutrophil intra-cellular granules are highly glycosylated, but not much is known about if and how the neutrophil glycome evolves during the 'targeting-by-timing' process of differentiation and how this is affected by emergency granulopoiesis during systemic infection and inflammation. Here is a clear knowledge gap.
This observational nation-wide study is focused on evaluation of the new possible biomarkers for pediatric sepsis and their specificity/sensitivity in combination with usual diagnostic markers for sepsis in the terms of early identification of sepsis, severe sepsis, and septic shock.