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Query: UMLS:C0036690 (sepsis)
59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe a case of a 38-year-old female accident victim who was admitted to the trauma hospital with an ISS of 66. Successful emergency treatment (including amputation of the left leg) and 4 weeks of intensive care led to an overall improvement so that the patient was extubated on day 29. Throughout this period neopterin was measured routinely 3 times a week and correlated well with the clinical course. At the end of the fifth week massive lung impairment and all clinical signs of sepsis appeared. Neopterin values increased dramatically up to 200 nmol/L. However, no abnormal findings were revealed by X-ray, contrast fluoroscopy, or sonographic imaging. To examine the amputation site more closely, simultaneous determination of neopterin in samples from the vena and arteria femoralis was performed. We found a 50% higher level in the venous blood (300 vs. 200 nmol/L). This was regarded as evidence for a hidden focus. Immediate surgical intervention revealed an abscess, which proved to be Pseudomonas aeruginosa positive. After adequate treatment the patient recovered quickly. In this case neopterin was not only helpful in monitoring the septic episodes of the patient, but proved essential for the detection of a septic focus and the risk of explorative relaparotomy could be omitted.
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PMID:Septic focus localized by determination of arterio-venous difference in neopterin blood levels. 129 86

The relation of (multiple) organ failure (OF) to the release of inflammatory mediators and the incidence of infection and sepsis was studied prospectively in 100 patients with multiple trauma (injury severity score = 37). Sixteen patients died of OF, 47 patients survived OF, and 37 patients had no OF. Fifteen (24%) of the patients with OF showed no signs of infection. In patients with early onset of OF (n=45), infection followed with a lag of 2 or more days. In 16 (44%) of these patients, infection led to a deterioration in organ function. With late onset of OF (n=18), infection preceded OF in nine patients. Polymorphonuclear leukocyte-elastase, neopterin, C-reactive protein, lactate, antithrombin III, and phospholipase A discriminated significantly among the three outcome groups. Of all factors, only polymorphonuclear leukocyte-elastase showed a difference between patients with and without infection or sepsis, respectively. These data indicate that infection might not play a crucial role in the pathogenesis of posttraumatic OF in a substantial portion of patients with trauma. Early OF, especially, seems to be mainly influenced by the direct sequelae of tissue damage and shock (eg, the release of inflammatory mediators). Since infection and sepsis did not lead to an augmented release of mediators in patients with trauma, the role of both entities remains unclear.
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PMID:Inflammatory mediators, infection, sepsis, and multiple organ failure after severe trauma. 134 12

Burn victims have severely depressed cellular immunity and despite careful hygiene, antibiotics and early surgical therapy the infection rate remains high. The assessment of plasma neopterin levels can be considered as an indirect measurement of macrophage function, because activation of macrophages is accompanied by the release of D-erythro-neopterin. The influence of burn trauma on neopterin levels was investigated to determine whether neopterin estimations might have a prognostic or diagnostic value. Twenty patients with a mean age of 36 +/- 16 years and a TBSA of 45.5 per cent +/- 23 were studied. During the whole hospital treatment daily blood samples were analysed for neopterin levels using radioimmunoassay. Starting from normal levels (9 +/- 1.6 nmol/l), neopterin content increased continuously until day 10 (30-40 nmol/l), then fluctuated around these high levels for several weeks. There were no differences between patients with TBSA less than 35 per cent or greater than 35 per cent, and between survivors and non-survivors. Burn injury caused a constant increase of plasma neopterin indicating an intact reaction by macrophages. It can be used as an additional parameter for the diagnosis of sepsis: high values being a sign of adequate reaction by macrophages, whereas low neopterin values in the presence of bacteraemia and clinical symptoms of sepsis show a deleterious impairment of immune functions.
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PMID:Neopterin plasma levels in burn patients. 164 64

PMN elastase, a proteolytic enzyme, is a biochemical marker for pathologic granulocyte stimulation. In the presence of sepsis, excessive neutrophil stimulation occurs and significant amounts of PMN elastase are released into the plasma and serve as an indicator for the severity of the disease and the prognosis. PMN elastase is also a useful parameter for preoperative diagnostic management and postoperative follow-up of bone and joint infections. In patients with osteomyelitis and joint empyema (n = 48) PMN elastase had a sensitivity of 77%, which was only exceeded by that of the unspecific erythrocyte sedimentation rate (sensitivity 89%). Sensitivities of other inflammation parameters were lower: C-reactive protein (CRP) 67%, fibrinogen 50%, neopterin 32% and leukocyte count 21%. Determination of PMN elastase levels was also helpful in postoperative follow-up of patients with bone and joint infections. In the early postoperative period PMN elastase levels normalized more quickly than the other parameters unless patients actually developed complications. At the first postoperative determination (day 2-4 after surgery) 38% of the patients (n = 24) already had PMN elastase levels within the normal range (less than or equal to 40 micrograms/l) (CRP 13%). After 10 days PMN elastase was normal in 57% and CRP in 30% of the patients. Later on both parameters reacted similarly: by the time of discharge from hospital levels of PMN elastase were normal in 70% and CRP levels in 74%.
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PMID:[PMN-elastase as a marker in diagnosis and follow-up of bone and joint infections]. 171 43

Tumor necrosis factor (TNF) has been implicated as a proximal mediator of the septic syndrome. To evaluate the possible role of TNF in leukocyte activation in septicemia, we performed a cross-over saline-controlled study in six healthy men who were intravenously injected with recombinant human TNF (50 micrograms/m2), and analyzed changes in circulating white blood cells and parameters for neutrophil and monocyte activation. TNF elicited a very rapid neutropenia, reaching a nadir after 15 minutes, followed by a neutrophilia. Lymphocytes showed a sustained decrease, whereas monocytes declined transiently. TNF injection was also associated with neutrophil activation, as reflected by a mean fivefold increase in the plasma concentrations of elastase-alpha 1-antitrypsin complexes and a mean sevenfold increase in plasma lactoferrin levels. Serum neopterin, a marker of monocyte activation, was significantly increased 24 hours after the administration of TNF. These changes occurred in the absence of detectable complement activation, as indicated by unchanged C3a-desarg plasma values. Serum interleukin-6 showed a nearly 40-fold increase after TNF injection, whereas interleukin-1 remained undetectable throughout. We conclude that the systemic release of TNF, triggered early after invasive infection, may be involved in the alterations in circulating leukocyte numbers and in the activation of leukocytes, during the development of the septic syndrome.
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PMID:Effects on leukocytes after injection of tumor necrosis factor into healthy humans. 173 11

A hyperdynamic sepsis model was set up in seven adult baboons to evaluate neutrophil-activating peptide-1/interleukin (IL)-8 (NAP-1/IL-8), IL-1 beta, IL-6, tumor necrosis factor-alpha (TNF alpha), and IFN-gamma in plasma. By continuous intravenous administration of 10(10) cfu/kg live Escherichia coli over 8 h with additional infusion therapy (less than or equal to 50 ml/kg/h), endotoxin plasma levels of 2.7-22.3 ng/ml were observed. In plasma the kinetics of NAP-1/IL-8 and IL-6 were similar to those of IL-1 at the end of the experiment (8 h) (peak median values, 34, 4197, and 230 ng/ml, respectively). Differences were greatest for IL-6. Monocyte activation during sepsis was confirmed by elevated plasma neopterin levels (91-139 mumol/mmol of creatine). Granulocyte activation was evident from both incipient neutropenia and the massive release of neutrophil elastase into the plasma as measured by a new immunoassay (peak level, 374 ng/ml). Thus, in primate bacteremia, early TNF release is followed by a concomitant increase of NAP-1/IL-8 with plasma kinetics similar to those of IL-6 and IL-1 and accompanied by massive activation of neutrophils.
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PMID:Plasma neutrophil-activating peptide-1/interleukin-8 and neutrophil elastase in a primate bacteremia model. 190 12

Inventarising the inflammatory capacities of the three types of inflammatory cells, PMN, macrophages and mast cells, each type seems able to induce a lethal whole body reaction. This whole body inflammation has hitherto largely escaped our attention, as in clinical studies inappropriate methods have been used such as counting peripheral leucocytes, and as monitoring key-mediators (IL-1, TNF, PGE-2, leukotrienes) and key-cells (activated PMN, macrophages and mast cells) hitherto was impossible. Presently a new set of methods is available, allowing a closer look at this whole body inflammation, such as elastase (monitoring PMN activity), neopterin (monitoring macrophage activity) and hopefully clinically practicable methods to monitor cytokines as well as endotoxin-levels. Only after such comprehensive studies have been performed, it might be concluded that--as in the experimental animal--sepsis and MOF may not necessarily be caused by bacteria or their endotoxins, but by an untoward autodestructive and self-sustaining activation of angry leucocytes and mad macrophages.
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PMID:Multiple organ failure: whole body inflammation? 265 70

In a series of 56 patients (24 uncomplicated postoperative and 32 septic patients), neopterin and elastase alpha 1 protease inhibitor complex (E-alpha 1 PI) plasma levels were measured daily. The clinical course of each patient was evaluated with the Multiple Organ Failure (MOF) score according to Goris. Neopterin could differentiate between septic and nonseptic patients (p less than .001), and E-alpha 1 PI between septic nonsurvivors and nonseptic patients only (p less than .01). In septic patients, acute pulmonary insufficiency was indicated by elevated E-alpha 1 PI values (greater than or equal to 400 micrograms/L) 1 day before mechanical ventilation was performed with a sensitivity of 81% and a specificity of 82%. Defining a patient with MOF whose score was greater than or equal to 5 as a high-risk septic patient, a comparison neopterin greater than or equal to 40 nmol/L and E-alpha 1 PI greater than or equal to 400 micrograms/L, measured 1 day before the evaluation of an MOF score of greater than or equal to 5 yielded a sensitivity of 91% and a specificity of 99% when patients fulfilled both criteria. We conclude that neopterin and E-alpha 1 PI might be useful parameters for the diagnosis of septicemia and monitoring of the clinical course in septic patients. Moreover, they might indicate the possible central role of macrophage and PMN activation in the development of MOF.
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PMID:Relationship between neopterin and granulocyte elastase plasma levels and the severity of multiple organ failure. 278 90

Inflammatory mediators involved in the pathogenesis of the adult respiratory distress syndrome (ARDS) are products of the humeral cascade systems like the complement cascade and substances released from neutrophil granulocytes and macrophages like proteases, O2-radicals and arachidonate products. Phospholipase A2 (PLA) was shown by Vadas et al. to be correlated with circulatory shock in the sepsis syndrome, the probably most important underlying disease of ARDS. In a clinical study in 48 patients at risk for ARDS after trauma and sepsis we found plasma PLA elevated (52 +/- 5 U/l) in sepsis, with a positive correlation to the complement split product C3a (r = 0.42, p less than 0.01) and neopterin (r = 0.49, p less than 0.05), which serves as a marker of macrophage stimulation. Elastase-alpha 1PI and C3a showed higher plasma levels in patients with ARDS compared with non-ARDS patients, whereas the neopterin and PLA concentrations were not different with regard to ARDS. The relation between PLA and neopterin shown in the study is consistent with the possibility of macrophages being a source of the plasma PLA, as reported in experimental studies.
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PMID:Phospholipase A in acute lung injury after trauma and sepsis: its relation to the inflammatory mediators PMN-elastase, C3a, and neopterin. 278 15

Traumatology deals with two different types of shock - the early hypovolemic-traumatic, and the late, so called septic shock, which is often associated with multi-organ failure. Both types of shock are triggered by several mediator systems of humoral and cellular origin, with numerous interactions between each other. In hypovolemic-traumatic shock central events are a perfusion deficit (ischemia with reperfusion injury via the xanthine-xanthine oxidase system) and activation of the humoral axis - of coagulation, of fibrinolysis, of the complement and kallikrein-kinin system by injured tissue. Coagulation and complement are responsible for the activation of platelets and granulocytes respectively. These cells further interact with each other e.g. via platelet activation factor, which finally causes tissue damage. Granulocytes play a central role because of their ability to release oxygen radicals and neutral proteinases, which can be monitored (elastase) and probably used to predict organ failure. The gut area is less resistant to the events of shock and therefore is a "locus minoris resistentiae" for further development of endotoxemia, bacteremia, septic shock and multi-organ failure without a typical septic focus. By this "septic challenge" further mediator systems get involved, especially those of macrophages like interleukin-1 or cachectin. Similar to the activation marker of PMN-elastase, we could demonstrate that it was possible to use neopterin for monitoring macrophage activation in sepsis and organ failure. By the action of these cellular elements in microcirculation at the endothelial and interstitial level tissue damage occurs, which finally leads to individual and multi-organ failure.
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PMID:[Current findings in the pathogenesis of the shock process in traumatology]. 328 34


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