Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Systemic inflammatory response syndrome (SIRS) is characterized by body temperature abnormalities, tachypnea or hyperventilation, tachycardia, and leukocytosis or leukopenia. Although it is typically associated with a serious infection and referred to as sepsis, SIRS can stem from noninfectious causes, as well. We report the cases of four patients with toxic serum levels of salicylate (33.5 to 67.6 mg/dL) and SIRS, and we discuss mechanisms responsible for SIRS. Our patients showed temperature disturbances (35.5 degrees C to 39.8 degrees C), noncardiogenic pulmonary edema, and mixed acid base disturbances. Other abnormalities included coagulopathy (disseminated intravascular coagulation), encephalopathy, and hypotension. All four patients recovered from SIRS, probably due to early recognition and treatment; only one patient did not survive the hospitalization. Chronic salicylate toxicity should be considered as a cause of SIRS in the absence of a source of infection, since survival appears to be dependent on prompt diagnosis and management.
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PMID:Systemic inflammatory response syndrome caused by chronic salicylate intoxication. 863 72

While infection is a consequence of invasion of microorganisms, sepsis is a phenomenon of the host. Systemic inflammatory response syndrome (SIRS), "severe sepsis", and "septic shock" may occur without infection, or persist, and lead to multiple organ dysfunction syndrome (MODS) after infection has been eradicated with antibiotics and surgery. The mechanisms responsible for these phenomena are increasingly being elucidated, but we cannot yet define when infective sepsis merges into non-infective sepsis. What do we know is they are just as lethal as each other.
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PMID:Duration of antibiotic treatment in surgical infections of the abdomen. At what point is infection cured but inflammation persists? 890 62

Emerging concepts of sepsis suggest that the host response to an infectious stimulus results in some cases of uncontrolled release of inflammatory cytokines leading to signs of sepsis. Systemic inflammatory response syndrome (SIRS) has been suggested as a diagnosis when no etiologic organism can be found. Infection may account for up to 30% of cases of pre-term labor, and may either be clinically-evident or sub-clinical. Inflammatory cytokines can be detected in elevated concentrations in the amniotic fluid and plasma of women with pre-term labor, and human gestational tissues are potentially rich sources of inflammatory cytokines, as found in in vivo and in vitro studies. Also, maternal decidua and fetal membranes produce mRNA for inflammatory cytokines in the setting of infection-associated pre-term labor and normal term labor. Notably, anti-inflammatory cytokines, such as interleukin-10 (IL-10) do not appear to be present in substantial quantities in these pathophysiologic and physiologic conditions. Animal models indicate that pre-term labor can be stimulated by bacteria, bacterial cell wall products, and inflammatory cytokines such as IL-1 and tumor necrosis factor. These findings suggest that: (1) infectious stimuli may result in the liberation of inflammatory cytokines from gestational tissues leading inevitably to pre-term labor and delivery; (2) inhibition of this process may either be overcome or abrogated, and (3) the mechanisms regulating cytokine production in maternal and fetal tissues are disturbed. Thus, pre-term labor associated with sub-clinical infection may result in a dysregulated local inflammatory response, in which the maternal host response causes an 'intra-uterine inflammatory response syndrome' leading to pre-term labor and delivery.
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PMID:Pre-term labor: an intra-uterine inflammatory response syndrome? 943 Jul 41

Systemic inflammatory response syndrome (SIRS) is one of the most common causes of death in intensive care unit patients. The detoxification plasma filtration (DTPF) system (HemoCleanse, Inc., West Lafayette, IN) combines the DT hemodiabsorption system in series with a push-pull pheresis PF system (a suspension of powdered sorbents surrounding 0.5 microm plasma filter membranes). Bidirectional plasma flow (at 80-100 ml/min) across the PF membranes provides direct contact between plasma proteins and powdered sorbents, as well as clearance of cytokines (tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6) at a rate of 15-25 ml/min, without evidence of saturation for 90 minutes. In a U.S. Food and Drug Administration approved study we treated eight patients with SIRS and organ failure with a single DTPF treatment, using powdered charcoal as sorbent in four patients and powdered charcoal and silica in four patients. Treatments proceeded for 6 hours with proper heparin anticoagulation (activated clotting time 250-300 sec) and appeared safe. All patients improved during the treatments and each had increased blood pressure and decreased need for pressor agents. Plasma cytokine levels stabilized or decreased during treatment and were significantly lower the morning after treatment. Multiple organ dysfunction (MOD) and Acute Physiology Chronic Health Evaluation II scores and organ function gradually improved in most patients, and two patients survived for more than 28 days and two for more than 14 days. The DTPF System may prove beneficial in treatment of patients with sepsis.
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PMID:Systemic inflammatory response syndrome treatment by powdered sorbent pheresis: the BioLogic-Detoxification Plasma Filtration System. 980 17

Systemic inflammatory response syndrome (SIRS) is typically associated with trauma, surgery, or acute pancreatitis. SIRS resembles sepsis, triggered by exogenous macromolecules such as LPS acting on Toll-like receptors. What triggers SIRS in the absence of infection, however, is unknown. In this study, we report that a SIRS-like response can be induced in mice by administration of soluble heparan sulfate, a glycosaminoglycan associated with nucleated cells and extracellular matrices, and by elastase, which cleaves and releases heparan sulfate proteoglycans. The ability of heparan sulfate and elastase to induce SIRS depends on functional Toll-like receptor 4, because mutant mice lacking that receptor or its function do not respond. These results provide a molecular explanation for the initiation of SIRS.
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PMID:Cutting edge: an endogenous pathway to systemic inflammatory response syndrome (SIRS)-like reactions through Toll-like receptor 4. 1468 4

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.
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PMID:[Evaluation of severity for systemic inflammatory response syndrome and sepsis]. 1559 98

Systemic inflammatory response syndrome (SIRS) and sepsis have been considered forms of hypercytokinemia in critically ill patients and immunocompromized hosts. It has been reported that some antimicrobial agents, including antifungal agents, not only have an antibiotic effect, but also they affect the host's immunological response. Immunofunctional cells, including monocytes and macrophages, were examined to determine whether they are influenced by the newly synthesized candin family antifungal agent micafungin (MCFG) using the human monocytic cell line THP-1 stimulated with lipopolysaccharide (LPS) as a model of hypercytokinetic conditions. LPS-induced production of TNF-alpha (tumor necrosis factor-alpha) and interleukin-8 (IL-8) in THP-1 cells was significantly suppressed dose-dependently by MCFG, although high concentrations of MCFG may reach toxic levels. It was clarified that MCFG inhibits the LPS-induced expression of TNF-alpha in THP-1 cells at the mRNA (messenger ribonucleic acid) level. In conclusion, administration of MCFG had an immunomodulatory effect on the host by reducing levels of TNF-alpha and IL-8. The effectiveness of MCFG in modulating hypercytokinemia is due not only to its direct antifungal effect, but also to the modulation of cytokine production in macrophages that regulates immunological activity and inflammation.
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PMID:Candin family antifungal agent micafungin (FK463) modulates the inflammatory cytokine production stimulated by lipopolysaccharide in THP-1 cells. 1700 23

The hypothalamic-pituitary-adrenal axis is an essential component for the maintenance of homeostasis following trauma. Major surgical trauma often induces overwhelming inflammatory responses leading to sepsis and organ dysfunction. This study was designed to evaluate the adrenal responses both before and after various degrees of surgical trauma and to determine the incidence of postoperative relative adrenal insufficiency resulting in the marked inflammatory response often associated with postoperative complications. Fifty-one surgical patients were divided into groups who underwent major, moderate, and minor surgeries. Before the operation and during resting conditions, a short corticotropin (ACTH) stimulation test was performed in each patient. The postoperative concentrations of serum cortisol, interleukin (IL)-6, IL-10, C-reactive protein (CRP), and plasma ACTH were measured. Fifty of 51 patients were identified as responders to ACTH. The postoperative cortisol levels were the same as those obtained by ACTH stimulation in highly and moderately stressful surgeries. The increases in postoperative IL-6 and CRP levels were greatest with major surgery, intermediate with moderate surgery, and least with minor surgery. Furthermore, plasma ACTH levels increased after major and moderate surgeries; however, there was no significant differences in postoperative serum IL-10 levels. Systemic inflammatory response syndrome (SIRS) was found in 11 of 17 patients (64.7%) who underwent major surgery and in 4 of 16 patients (25%) who underwent moderate surgery (p=0.037). The duration of SIRS was significantly longer in patients undergoing major surgery (62+/-20 hrs) than in patients undergoing moderate surgery (21+/-3 hrs, p=0.038). Postoperative complications were more frequent in patients undergoing major surgery (41.2%) than in patients undergoing moderate surgery (6.3%, p=0.039). Furthermore, there were significant differences in the length of the postoperative stay among the three groups (p<0.01). One nonresponder had serious postoperative inflammatory complications. These results suggest that a short ACTH stimulation test performed preoperatively is a helpful method for determining the maximal cortisol response to surgical trauma and to identify high-risk individuals and that a relative postoperative adrenal insufficiency may be closely related to the decreased cortisol secretion following major surgical trauma.
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PMID:Surgical trauma-induced adrenal insufficiency is associated with postoperative inflammatory responses. 1787 97

Systemic inflammatory response syndrome (SIRS), severe infection and sepsis are the problems of present interest in contemporary medicine. The specificity and sensitivity of widespread clinical and laboratory parameters are insufficient for diagnosing these diseases. A new marker for diagnosing of infective etiology of SIRS, severe infection and sepsis which allows early diagnosis and begin specific treatment is procalcitonin (PCT). In severe viral infections or inflammatory reaction of non-infective origin the level of PCT does not elevate or increases moderately. The level of PCT correlates with the severity of SIRS: the more severe the SIRS, the higher the level of PCT. The monitoring of PCT allows a rapid diagnosis of infective complications in patients after severe injuries or operations, in acute respiratory distress syndrome. PCT is considered as a marker of severe bacterial and parasitic infection. However, PCT should not be considered as the only marker we can rely upon in diagnosing of sepsis. The levels of PCT correlate with levels of TNF and IL-6. But the pathophysiological role of PCT in sepsis is not definitely clear yet. The indexes of PCT are most valuable for evaluating treatment efficiency and prognosis.
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PMID:[Procalcitonin - marker of severe infection and sepsis]. 1825 Apr 91

Systemic inflammatory response syndrome (SIRS) is a highly mortal inflammatory disease, associated with systemic inflammation and organ dysfunction. SIRS can have a sterile cause or can be initiated by an infection, called sepsis. The prevalence is high, and available treatments are ineffective and mainly supportive. Consequently, there is an urgent need for new treatments. The brain is one of the first organs affected during SIRS, and sepsis and the consequent neurological complications, such as encephalopathy, are correlated with decreased survival. The choroid plexus (CP) that forms the blood-CSF barrier (BCSFB) is thought to act as a brain "immune sensor" involved in the communication between the peripheral immune system and the CNS. Nevertheless, the involvement of BCSFB integrity in systemic inflammatory diseases is seldom investigated. We report that matrix metalloprotease-8 (MMP8) depletion or inhibition protects mice from death and hypothermia in sepsis and renal ischemia/reperfusion. This effect could be attributed to MMP8-dependent leakage of the BCSFB, caused by collagen cleavage in the extracellular matrix of CP cells, which leads to a dramatic change in cellular morphology. Disruption of the BCSFB results in increased CSF cytokine levels, brain inflammation, and downregulation of the brain glucocorticoid receptor. This receptor is necessary for dampening the inflammatory response. Consequently, MMP8(+/+) mice, in contrast to MMP8(-/-) mice, show no anti-inflammatory response and this results in high mortality. In conclusion, we identify MMP8 as an essential mediator in SIRS and, hence, a potential drug target. We also propose that the mechanism of action of MMP8 involves disruption of the BCSFB integrity.
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PMID:Matrix metalloprotease 8-dependent extracellular matrix cleavage at the blood-CSF barrier contributes to lethality during systemic inflammatory diseases. 2281 95


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