[Sepsis--sepsis syndrome--systemic inflammatory response syndrome].
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Acute-Phase Reaction↗
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Results for “Systemic Inflammatory Response Syndrome”
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An argument for Vitamin E supplementation in the management of systemic inflammatory response syndrome.
The systemic inflammatory response syndrome results from an uncontrolled, overexpression of the normal host inflammatory response, leading to destruction of host tissue and subsequent organ failure. Oxidant stress has been implicated in this process both as a mechanism for direct cellular injury, as well as activation of intracellular signaling cascades within inflammatory cells resulting in progression of the inflammatory response. Vitamin E is an inexpensive, nontoxic, chain-breaking antioxidant that has therapeutic potential in regulating this process. This review seeks to evaluate the current literature regarding the use of Vitamin E in controlling the excessive inflammation seen in systemic inflammatory response syndrome and argues for further study of its therapeutic potential for these critically ill patients.
Acute Disease↗
Circulating complement proteins in patients with sepsis or systemic inflammatory response syndrome.
The systemic inflammatory response of the body to invading microorganisms, termed sepsis, leads to profound activation of the complement system. Pathophysiological concepts suggest that complement activation occurs very early in this syndrome. Thus, we discuss whether the determination of concentrations of the complement components C3a, C5a, and C3 in plasma as well as of the C3a/C3 ratio might be helpful to diagnose sepsis early. For this purpose, 33 patients from an intensive care unit were monitored for 10 days. In comparison with healthy donors, C3a levels and the C3a/C3 ratio of intensive-care-unit patients were significantly elevated (P < 0.0001) on admission. In contrast, C3 levels were significantly reduced (P < 0.0001) but increased during the study. C5a levels in the plasma of healthy donors and patients were identical. Twenty-two of 33 patients fulfilled microbiological and clinical criteria of sepsis. Eleven patients had signs of systemic inflammatory response syndrome but no microbiological evidence of sepsis. The groups could be differentiated from each other by their C3a levels or their C3a/C3 ratios during the first 24 h after the clinical onset of sepsis (P < 0.05). Septic patients in shock had higher C3a levels than normotensive septic patients, although the differences were not significant. Nonsurvivors had significantly higher C3a levels on admission than survivors (P = 0.0185). No differences were found between septic patients who developed adult respiratory distress syndrome and those who did not. Thus, determination of C3a concentrations in plasma may prove useful (i) to diagnose sepsis early, (ii) to differentiate between patients with sepsis and those with systemic inflammatory response syndrome, and (iii) to assess prognosis.
Adolescent↗
The systemic inflammatory response syndrome.
The systemic inflammatory response syndrome (SIRS) is the body's response to an infectious or noninfectious insult. Although the definition of SIRS refers to it as an "inflammatory" response, it actually has pro- and anti-inflammatory components. This review outlines the pathophysiology of SIRS and highlights potential targets for future therapeutic intervention in patients with this complex entity.
Biomarkers↗
Polymorphisms in Toll-like receptor 4 and the systemic inflammatory response syndrome.
The systemic inflammatory response syndrome (SIRS) is a major cause of morbidity and mortality, and is thought to be due to an over-amplification of an inflammatory response. The Toll-like receptor 4 ( TLR4 ) Asp-299-->Gly polymorphism has been shown to reduce lipopolysaccharide responsiveness. We examined whether this TLR4 polymorphism is associated with severity of SIRS. A trend was found between the minor allele and mortality in SIRS (odds ratio of 4.3; P =0.076), suggesting a role for TLR4 signalling in the severity of SIRS.
APACHE↗
Anti-inflammatory response of IL-4, IL-10 and TGF-beta in patients with systemic inflammatory response syndrome.
The systemic inflammatory response syndrome (SIRS) is an inflammatory process seen in association with a large number of clinical infective and non-infective conditions. The aim of this study was to investigate the role of anti-inflammatory cytokines such as interleukin-4 (IL-4), interleukin-10 (IL-10), and transforming growth factor-beta (TGF-beta). Serum levels of IL-4, IL-10 and TGF-beta were determined in 45 patients with SIRS: 38 patients had SIRS of infectious origin, whereas seven patients had non-infectious SIRS. Twenty healthy subjects were used as controls. Serum levels of IL-4, IL-10 and TGF-beta were determined by an immunoenzyme assay. A significant increase of IL-4 was observed in these patients at the time of diagnosis and 5 days later. In contrast, serum levels of IL-10 were not increased at the time of diagnosis, but a slight decrease was noted after 5 days. Serum levels of TGF-beta were not increased at time of diagnosis, and a slight increase was observed after 5 days. Serum levels of IL-4 were significantly higher in patients with infectious SIRS at the time of diagnosis, whereas no significant difference between infectious and non-infectious SIRS was noted for serum levels of IL-10 and TGF-beta at the time of diagnosis and 5 days later. During SIRS, serum levels of IL-4 were significantly increased with a significant correlation between IL-4 and mortality, and only levels of IL-4 were significantly increased in the SIRS caused by infectious stimuli.
Adult↗
Redox regulation of neutrophil apoptosis and the systemic inflammatory response syndrome.
SIRS (systemic inflammatory response syndrome) may result from a wide variety of non-infective insults. Surgery is a recognized cause of SIRS, the onset of which can have adverse prognostic significance. Neutrophil activation is a key histopathological feature of SIRS, and neutrophil clearance through programmed cell death or apoptosis is an essential step in its resolution. Increasingly, it is recognized that ROS (reactive oxygen species), such as those generated by activated neutrophils during cardiac surgery, may have a regulatory role, influencing neutrophil lifespan and thus inflammation. In this review, we discuss the continuing importance of SIRS as a herald of inflammation and the role of neutrophil longevity in the resolution of inflammation, and we consider recent evidence for the regulation of neutrophil apoptosis by ROS.
Apoptosis↗
Anticytokine strategies in the treatment of the systemic inflammatory response syndrome.
The systemic inflammatory response syndrome (SIRS) is an acute illness characterized by generalized activation of the endothelium. The most severe form of the syndrome is found in patients with shock due to gram-negative sepsis. We examined both animal and limited human data for the contribution of cytokines to this syndrome. Cytokines are endogenously produced proteins of small molecular weight and multiple biological effects. The cytokines interleukin 1 (IL-1) and tumor necrosis factor (TNF), as well as interferon-gamma and interleukin 8, are discussed. Laboratory investigations suggest that these cytokines play a critical role in SIRS by promoting the biochemical and clinical characteristics of SIRS. The biochemical changes induced by TNF and IL-1 include increased synthesis of nitric oxide, prostaglandins, platelet-activating factor, and endothelial cell adhesion molecules. Specific blockade of TNF using neutralizing antibodies or soluble receptors to TNF in animal models of SIRS reduces mortality and severity of disease. Similar results have been observed blocking IL-1 using soluble IL-1 receptors or IL-1 receptor antagonists. Preliminary clinical studies suggest that blockade may be useful in treating human SIRS. The various strategies for blocking IL-1 and TNF are presented; in addition, their mechanism(s) of action and safety in humans are discussed. We conclude that based on animal studies and preliminary clinical trials, strategies to block IL-1 or TNF may benefit patients with the syndrome, although thorough clinical trials have not been completed.
Animals↗
CCL2 as a trigger of manifestations of compensatory anti-inflammatory response syndrome in mice with severe systemic inflammatory response syndrome.
Patients with compensatory anti-inflammatory response syndrome (CARS) are at a higher risk for infection with various opportunistic pathogens. CARS develops commonly in association with the manifestation of systemic inflammatory response syndrome (SIRS). In the present study, the role of SIRS-associated soluble factors on the CARS development was examined in mice with pancreatitis, a carrier of typical SIRS. Following the production of SIRS-related cytokines [tumor necrosis factor alpha and interleukin (IL)-1beta], CC chemokine ligand 2 (CCL2), IL-4, and IL-10 (typical CARS cytokines) were detected in the sera of mice with pancreatitis. CCL2 has been described as an essential chemokine for the T helper cell type 2 manifestation. CARS effector cells (cells with an ability to produce IL-4 and IL-10) were not generated from normal T cells after stimulation with SIRS-related cytokines. However, these cells were generated from normal T cells after cultivation with peripheral blood neutrophils (PMN) from SIRS mice in a dual-chamber transwell. Normal T cells did not convert to CARS effector cells after transwell cultures with PMN from normal mice. CCL2 was detected in culture fluids of PMN from SIRS mice, and PMN from normal mice did not produce CCL2 into their culture fluids. CARS effector cells did not appear in PMN-depleted SIRS mice or SIRS mice treated with anti-CCL2 monoclonal antibody, and these cells were demonstrated in PMN-depleted SIRS mice after treatment with recombinant murine CCL2. These results indicate that CCL2 produced by PMN from SIRS mice is an active molecule on the SIRS-associated CARS manifestation.
Animals↗
Gene expression pattern in human monocytes as a surrogate marker for systemic inflammatory response syndrome (SIRS).
BACKGROUND: Systemic inflammatory response syndrome (SIRS) is a mild inflammatory episode which, in a minority of patients, may deteriorate into septic shock. In the mouse, injection of bacteria or bacterial endotoxin induces systemic inflammation through the activation of blood monocytes, which leads to lethal shock. A number of intervention strategies have been shown to prevent progression to shock in mouse model systems. However, recent clinical trials of a number of these therapeutic strategies in patients have been uniformly disappointing. In contrast to the situation in the mouse models, there may be many different ways to initiate systemic inflammation in patients and not all of them need necessarily involve activation of blood monocytes. If there is no unifying mechanism behind the induction of systemic inflammation in patients and no common rules governing its development, then it is unlikely that generally applicable therapeutic strategies will be found that can prevent progression into shock. MATERIALS AND METHODS: We used differential display to compare gene expression patterns in monocytes of recent-admission multi-trauma patients with clinically diagnosed SIRS to the patterns in monocytes of healthy controls. RESULTS: Of seven differentially displayed bands that were recovered and sequenced, five were associated with SIRS and two were preferentially expressed in the monocytes of healthy controls. CONCLUSION: The data show that monocytes of SIRS patients are in an activation state that is different from that of monocytes from the healthy controls, that monocytes from many individual patients share similar patterns of differentially expressed sequences, and that by this criterion, the multi-trauma SIRS patients are a remarkably coherent group.
Adolescent↗
[Systemic inflammatory response syndrome: new concepts].
Systemic inflammatory response syndrome is secondary to several insults whose purpose is to limit and reverse the injury. The outcome and intensity of the inflammatory response is determined by injury extension and balance between inflammatory and compensatory antiinflammatory responses. The interaction of the several soluble and cellular mediators of inflammatory and antiinflammatory responses determine the next evolutive phases: a) local inflammatory response; b) systemic inflammatory response; c) massive systemic inflammatory response; d) immunologic paralysis; and e) immune dissonance. If the last three phases do not control, cell damage can be amplified and thus perpetuating the infectious process and leading the patient to multiple organ dysfunction. Gamma interferon and steroids as modulators of the inflammatory response, in stages of paralysis and immune dissonance has been studied in clinical and experimental trials with promising results, but more studies to are needed validate their usefulness.
Humans↗
[Evaluation of severity for systemic inflammatory response syndrome and sepsis].
Systemic inflammatory response syndrome (SIRS) is defined by four simple clinical and laboratory indices and now widely accepted for diagnosing sepsis. However, since the SIRS criteria include patients with a wide range of severity, other parameters are necessary to evaluate the severity and outcome of the patients. In this review, we discussed several methods to estimate the severity of SIRS, such as number of positive SIRS indices among four, duration of SIRS, plasma IL-6 and procalcitonin, etc.
Humans↗
Measurements of total plasma nitrite and nitrate in pediatric patients with the systemic inflammatory response syndrome.
OBJECTIVES: The systemic inflammatory response syndrome (SIRS) is typified by the presence of fever, hemodynamic changes, and end organ dysfunction. Endothelial cell activation leads to overproduction of nitric oxide, which results in sustained vasodilation and hypotension. This study was undertaken to determine the sensitivity, specificity, and positive and negative predictive values of plasma nitrite/nitrate measurements in identifying patients with clinical characteristics of SIRS, as defined by criteria based on physician diagnosis. DESIGN: Prospective cohort study with consecutive sampling of patients. SETTING: Tertiary, multidisciplinary, pediatric intensive care unit (ICU) at Children's Hospital of Wisconsin. PATIENTS: Patients were divided into five groups. There were 16 pediatric controls undergoing elective surgery and 177 pediatric ICU patients without and 46 pediatric ICU patients with physician-diagnosed sepsis, septic shock, SIRS, or sepsis syndrome documented in the medical record (all considered physician-diagnosed sepsis). The 223 pediatric ICU patients included 195 pediatric ICU patients not meeting and 28 pediatric ICU patients meeting predetermined physiologic criteria for SIRS (considered criteria-based sepsis). INTERVENTIONS: Blood samples were obtained for quantitative nitrite/nitrate analysis at the time of admission to the pediatric ICU and daily until discharge. MEASUREMENTS AND MAIN RESULTS: Mean plasma nitrite/nitrate concentrations in the controls were 34.5 +/- 12 microM (95th percentile 54 microM). In pediatric ICU patients without and with physician-diagnosed sepsis, mean plasma nitrite/nitrate concentrations were 39 +/- 24 microM (p > .05 compared with controls) and 127 +/- 91 microM (p < .0001 compared with both controls and patients without physician-diagnosed sepsis), respectively. In pediatric ICU patients without and with criteria-based sepsis, the mean total plasma nitrite/nitrate concentrations were 56 +/- 59 microM (p = .008 compared with controls) and 80 +/- 64 microM (p = .003 compared with patients without criteria-based sepsis), respectively. The ability of plasma nitrite/nitrate > 54 microM to identify patients with physician-diagnosed sepsis is characterized as follows: 87% sensitivity, 77% specificity, 50% positive predictive value, and 96% negative predictive value. The ability of plasma nitrite/nitrate > 54 microM to identify patients with criteria-based sepsis is characterized as follows: 61% sensitivity, 68% specificity, 21% positive predictive value, and 92% negative predictive value. CONCLUSIONS: Clinical diagnosis of SIRS is strongly associated with increased total plasma nitrite/nitrate concentrations in pediatric patients in the pediatric ICU. Many patients with increased nitrite/nitrate concentrations have inflammation without having a clinical diagnosis of SIRS. Our data suggest that increased plasma nitrite/nitrate concentrations are the standard for identifying patients with inflammation in the pediatric ICU.
Child, Preschool↗
Systemic inflammatory response syndrome without systemic inflammation in acutely ill patients admitted to hospital in a medical emergency.
Criteria of the systemic inflammatory response syndrome (SIRS) are known to include patients without systemic inflammation. Our aim was to explore additional markers of inflammation that would distinguish SIRS patients with systemic inflammation from patients without inflammation. The study included 100 acutely ill patients with SIRS. Peripheral blood neutrophil and monocyte CD11b expression, serum interleukin-6, interleukin-1beta, tumour necrosis factor-alpha and C-reactive protein were determined, and severity of inflammation was evaluated by systemic inflammation composite score based on CD11b expression, C-reactive protein and cytokine levels. Levels of CD11b expression, C-reactive protein and interleukin-6 were higher in sepsis patients than in SIRS patients who met two criteria (SIRS2 group) or three criteria of SIRS (SIRS3 group). The systemic inflammation composite score of SIRS2 patients (median 1.5; range 0-8, n=56) was lower than that of SIRS3 patients (3.5; range 0-9, n=14, P=0.013) and that of sepsis patients (5.0; range 3-10, n=19, P<0.001). The systemic inflammation composite score was 0 in 13/94 patients. In 81 patients in whom systemic inflammation composite scores exceeded 1, interleukin-6 was increased in 64 (79.0%), C-reactive protein in 59 (72.8%) and CD11b in 50 (61.7%). None of these markers, when used alone, identified all patients but at least one marker was positive in each patient. Quantifying phagocyte CD11b expression and serum interleukin-6 and C-reactive protein concurrently provides a means to discriminate SIRS patients with systemic inflammation from patients without systemic inflammation.
Acute Disease↗
Relationships of circulating nitrite/nitrate levels to severity and multiple organ dysfunction syndrome in systemic inflammatory response syndrome.
Excessive nitric oxide (NO) production has been implicated to be responsible for the development of septic shock. To determine whether plasma nitrite/nitrate (NOx) levels are related to the severity of systemic inflammatory response syndrome (SIRS) and the degree of multiple organ dysfunction, we studied plasma NOx levels in 70 patients with SIRS consisting of noninfectious SIRS (n = 32), sepsis (n = 23), and septic shock (n = 15). Infection is a microbial phenomenon characterized by an inflammatory response to the presence of microorganism. Positive culture for microorganism is regarded as infectious SIRS (sepsis and septic shock) and negative culture is regarded as noninfectious SIRS. Plasma samples collected from each patient within 24 h from admission to the intensive care unit were subjected for measurement of NOx levels, the stable end products of NO, by the high performance liquid chromatography-Greiss system. Mean plasma NOx levels in patients with SIRS were 52.8 +/- 44 microM/L, ranging from 8.1 to 186.2 microM/L. Plasma NOx levels were positively correlated with Acute Physiology, Age, and Chronic Health Evaluation (APACHE) III score (r = 0.414, P < 0.01) and sequential organ failure assessment (SOFA) score (r = 0.433, P < 0.01). Plasma NOx levels in patients with sepsis (51.0 +/- 38.5 microM/L) and septic shock (94.5 +/- 53.7 microM/L) were significantly (P < 0.01) higher than those in patients with noninfectious SIRS (25.8 +/- 16.9 microM/L) and healthy subjects (29.6 +/- 8.9 microM/L). Our study shows that plasma NOx levels are increased in patients with infectious, but not noninfectious SIRS, which increase as the severity of SIRS and the development of multiple organ dysfunction syndrome, suggesting its possible pathogenic role in SIRS.
APACHE↗
Vesnarinone and amrinone reduce the systemic inflammatory response syndrome.
OBJECTIVE: The systemic inflammatory response is an important cause of organ dysfunction. The present study tested the hypothesis that 2 clinically used agents, amrinone and vesnarinone, would decrease inflammation and cardiac dysfunction in a relevant model of systemic inflammatory response activation. METHODS: Rabbits received intravenous endotoxin, alone or in conjunction with amrinone or vesnarinone. Systemic effects were assessed by death, fever, behavior, and acidosis. Measures of inflammatory signaling were (1) plasma tumor necrosis factor-alpha and interleukin-1 beta production, (2) lung tissue myeloperoxidase activity, and (3) myocardial inducible nitric oxide synthase activity. Indices of systolic and diastolic myocardial function were measured in Langendorff-perfused hearts. RESULTS: Vesnarinone, in particular, reduced mortality rates (19% vs 61% for lipopolysaccharide alone, P =.01) and acidosis in lipopolysaccharide-treated rabbits. Both agents markedly reduced systemic tumor necrosis factor and interleukin-1 concentrations, lipopolysaccharide-mediated effects on myocardial systolic and diastolic function and on myocardial inducible nitric oxide synthase activity. Vesnarinone, but not amrinone, (1) decreased fever and lethargy, consistent with decreased central nervous system effects of endotoxin, and (2) decreased lung leukocyte infiltration. CONCLUSIONS: Vesnarinone and amrinone, which are used clinically for their inotropic and vasodilating properties, may be useful to limit inflammatory activation and consequent organ dysfunction. Structure-activity and/or pharmacokinetic between the compounds may be important, particularly in preventing inflammatory signaling within certain tissues.
Adjuvants, Immunologic↗
Sepsis and the systemic inflammatory response syndrome.
Sepsis and the systemic inflammatory response syndrome are common and represent a major factor in morbidity and mortality in intensive care units and the critically ill. The pathogenesis of these syndromes is becoming increasingly understood and it is hoped that this will result in improved outcome. However, novel treatments have so far failed to live up to the expectations following extensive and promising in vitro and in vivo animal studies. The aim of this review is to detail the currently used definitions of systemic inflammatory response syndrome, sepsis and septic shock and to present an overview of our current understanding of the pathophysiology which underline these conditions.
Biomarkers↗
Multiple organ failure, multiple organ dysfunction syndrome, and systemic inflammatory response syndrome. Why no magic bullets?
The concept of multiple organ failure and related abnormalities was first developed in the 1970s. Multiple organ failure became evident when the support systems in intensive care units were able to keep patients alive long enough for multiple organ problems to develop in them. The high mortality of patients with multiple organ failure provided a focus for the problems that ultimately led to death for many patients in the intensive care unit. The frequency of infection, sepsis, or inflammation in producing multiple organ failure led to clinical trials of so-called magic bullets for the treatment of patients with sepsis. These trials have had either limited success or negative results, despite considerable evidence for efficacy or protection by such agents in experimental animals and in studies of normal human volunteers. I believe a major reason for these negative results has been the use of general entry criteria for the trials rather than the treatment of specific diseases or injuries.
Humans↗