Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neisseria meningitidis infection may present as meningitis or as severe, fulminant sepsis. In order to classify individual patients early according to the expected course of the disease, we developed a score named Neisseria sepsis index [NESI]. The NESI was defined using the parameters heart rate, mean arterial blood pressure, base excess and presence of acute subcutaneous bleeding and/or skin necroses (minimal value [= no evidence for sepsis] NESI 0; maximum value [= most severe sepsis] NESI 8). Seventeen patients with documented, systemic N. meningitidis infection were prospectively assessed for the terminal complement complex (TCC), serum tumour necrosis factor alpha (TNF alpha) levels (as laboratory parameters for severity of sepsis) and NESI score. The evaluation was immediately performed when the patients were admitted to the hospital. The 17 patients showed the following distribution of data: NESI 0 (n = 4), NESI 1 (n = 6), NESI 2 (n = 0), NESI 3 (n = 1), NESI 4 (n = 2), NESI 5 (n = 2), NESI 6 (n = 0), NESI 7 (n = 1), NESI 8 (n = 1). Mortality was 4/17 patients, all had NESI > or = 5. TCC values ranged from 647-6461 ng/ml (normal range: 130-360 ng/ml); and was not correlated to NESI. TNF alpha values ranged from 10-910 pg/ml and were correlated to NESI (r2 = 0.71, n = 17, P < 0.001). In patients with fatal outcome, TNF alpha was 600 +/- 160 pg/ml (mean +/- SEM) and in surviving patients 130 +/- 50 pg/ml (mean +/- SEM). TNF alpha was increased in 15/17 patients when compared to normal controls (< 27 pg/ml). CONCLUSION. The NESI is based on few clinical, objective data, that are available in every hospital. NESI appears to offer an instrument: (1) for making decisions in regard to appropriate monitoring and treatment of vital organ function; and (2) for assessing the quality of care for this life-threatening infection.
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PMID:Definition of a new score for severity of generalized Neisseria meningitidis infection. 858 2

We have studied cerebral autoregulation and vasoreactivity to carbon dioxide in 10 patients with the sepsis syndrome receiving intensive therapy. All patients were sedated with infusions of midazolam and fentanyl, and their lungs were ventilated mechanically with oxygen-air to maintain normoxia and normocapnia. Inotropic support and antibiotics were administered as necessary. During a period of constant level of sedation and stable haemodynamics, cerebral autoregulation was tested by increasing mean arterial pressure (MAP) by 23 (SD 2) mm Hg from baseline with an infusion of phenylephrine and simultaneously recording middle cerebral artery blood flow velocity (vmca) using transcranial Doppler ultrasonography. Carbon dioxide reactivity was tested by varying PaCO2 between 3.0 and 7.0 kPa and simultaneously recording vmca. There was no significant change in vmca (57 (22) and 59 (23) cm s-1) during the increase in MAP (75 (11) to 98 (10) mm Hg). The mean index of autoregulation (IOR) was 0.92 (SEM 0.03), which was not significantly different from 1, indicating near perfect autoregulation. Although absolute carbon dioxide reactivity was lower than reported previously in awake subjects, relative carbon dioxide reactivity was within normal limits for all patients (11.6 (SEM 0.8) cm s-1 and 20.3 (3) % kPa-1, respectively). We conclude that cerebral carbon dioxide reactivity and pressure autoregulation remained intact in patients with the sepsis syndrome, providing indirect evidence that at least in the early stages of the syndrome, the widespread sepsis-induced vasoparalysis does not involve the cerebral vasculature.
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PMID:Sepsis-induced vasoparalysis does not involve the cerebral vasculature: indirect evidence from autoregulation and carbon dioxide reactivity studies. 867 51

Elevated serum levels of the prohormone of calcitonin (CT), procalcitonin (ProCT), have been documented in illnesses such as inhalational burn injury, in several sepsis syndromes, and in endotoxemia. In this study, we measured and characterized the circulating precursor forms of CT during the course of infectious pneumonitis. The initial (mean +/- SEM) serum total multiform CT level in 12 patients with acute infectious pneumonia was 1,019 +/- 430 pg/mL. In comparison, the mean level of total CT for 19 age-matched control patients without lung disease was 32 +/- 6 pg/mL (P < 0.001). The mean serum total CT level on initial examination was greater in the 6 patients with bacterial isolates, at 1,793 +/- 752 pg/mL, than in those with nonbacterial infectious pneumonia, at 242 +/- 109 pg/mL (P = 0.018). After admission to the hospital, patients' serum total CT progressively declined concomitantly with the clinical resolution of the pneumonia; at discharge, mean serum level was 121 +/- 34 pg/mL. On discharge, the patients who had persistent radiographic abnormalities had significantly higher levels than did those who had complete resolution. Both the mean serum calcium and phosphate were significantly lower at the initial time of study than at discharge (P < 0.002 and P < 0.0004, respectively). Gel filtration chromatography of sera obtained during the acute pneumonitis phase revealed increased levels of precursor forms of CT, including ProCT; these levels diminished with clinical resolution. In an additional three patients, the serum total CT increased very rapidly after aspiration (within 6 to 12 hours); the peak levels were several times greater than the upper limits of normal. In these patients, the principal serum CT components were ProCT and other precursor forms. These results show that both infectious and aspiration pneumonitis are associated with a rapid increase in circulating ProCT and other precursor forms of CT.
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PMID:Pneumonitis-associated hyperprocalcitoninemia. 868 24

Hypoperfusion of the gut mucosa is thought to be a factor in the development of gut barrier failure during sepsis and septic shock. Dopamine stimulates DA-1 receptors which mediate regional vasodilatation in the gut. Therefore, we have investigated the effect of low-dose dopamine (3 micrograms kg-1 min-1) on the intestinal villus microcirculation during endotoxaemia in a rat model of normotensive endotoxaemia, using in vivo videomicroscopy. Blood flow in and the diameters of central villus arterioles were measured before, immediately after and 60 min after a 1-h continuous infusion of endotoxin 1.5 mg/kg body weight. After baseline measurements were obtained, rats received either an infusion of 0.9% saline (group A; n = 7) or a volume-equivalent infusion of dopamine 3 micrograms kg-1 min-1 (group B; n = 7) throughout the study. Control animals (group C; n = 7) received no endotoxin or dopamine. In group A, villus blood flow (mean baseline 8.4 (SEM 0.9) nl min-1) decreased by 29.7 (8.9)% to 5.9 (0.9) nl min-1 immediately after endotoxin challenge and by a total of 43.1 (7.3)% to 4.7 (0.7) nl min-1 after another 60 min. Simultaneously, villus arteriolar diameters decreased from 7.8 (0.2) to 6.9 (0.3) microns and to 6.5 (0.3) microns, respectively. In group B, villus blood flow (baseline 8.7 (0.4) nl min-1) was unchanged immediately after the 1-h infusion of endotoxin (8.3 (0.4) nl min-1). However, another 60 min later blood flow decreased by 28.8 (8.0)% to 6.1 (0.7) nl min-1. In contrast with group A, the diameters of the central villus arterioles were unchanged despite administration of endotoxin (7.9 (0.2) microns; 8.1 (0.4) microns; 8.2 (0.5) microns). In group C, there were no changes in villus blood flow or arteriolar diameters throughout the study. Our results indicated that low-dose dopamine did not prevent, but delayed and attenuated, the decrease in intestinal villus blood during normotensive endotoxaemia.
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PMID:Effect of low-dose dopamine on intestinal villus microcirculation during normotensive endotoxaemia in rats. 868 74

Serum levels of human hepatocyte growth factor (HGF) were determined in 38 patients with acute pancreatitis by an enzyme-linked immunosorbent assay. The mean value of serum HGF levels on admission in the 38 patients was 1.69 +/- 0.40 (SEM) ng/ml. In 35 patients, serum HGF levels were found to be positive (> 0.39 ng/ml), with an incidence of 92.1%. In 17 patients, they were > 1.0 ng/ml, which was the cutoff value for fulminant hepatic failure. Serum HGF levels in the patients with severe acute pancreatitis (2.30 +/- 0.61 ng/ml; mean +/- SEM) were significantly higher than those in the patients with mild and moderate acute pancreatitis (0.63 +/- 0.06 ng/ml). Sixteen of seventeen patients whose serum HGF levels were > 1.0 ng/ml were evaluated as severe acute pancreatitis. Serum HGF levels were significantly elevated in the patients with higher Ranson scores, higher APACHE II scores, or higher computed tomography grades. Serum HGF levels in the patients with organ dysfunction (liver, kidney, or lung) were significantly higher than those in the patients without organ dysfunction. Moreover, serum HGF levels on admission in the nonsurvivors (3.17 +/- 1.30 ng/ml) were significantly higher than those in the survivors (1.22 +/- 0.33 ng/ml). The mortality rate of the patients showing serum HGF levels > 2.0 ng/ml on admission was 50%. In the patients with a lethal outcome, the mean serum HGF level remained constantly > 2.50 ng/ml during hospitalization. The serum HGF level reflected the clinical course of the disease rapidly and distinctly. Serum HGF levels increased with complications such as organ failure, infected pancreatic necrosis, and sepsis and decreased with successful intensive and surgical treatments. These results suggest that serum human HGF levels may reflect the severity, organ dysfunction, and prognosis in acute pancreatitis.
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PMID:Significant elevation of serum human hepatocyte growth factor levels in patients with acute pancreatitis. 892 23

Critical illness polyneuropathy (CIP) is a recognized cause of muscle weakness and failure of weaning from a ventilator. In order to characterize the features of CIP, we have examined 28 consecutive surgical patients with severe sepsis using bedside electrophysiology. Of the 28 patients (median APACHE II score 31), 20 developed moderate to severe CIP, as shown by the presence of moderate to severe denervation activity on resting EMG. The median nerve compound muscle action potential (CMAP) amplitudes were reduced to 3.24 (SEM 0.48) mV, while sensory nerve action potential (SNAP) amplitudes obtained from the same nerve were normal (13.1 (1.9) microV). In approximately 50% of these patients, the reduction in CMAP exceeded 50% of the lower limit of normal. Similar results were obtained from stimulation of the ulnar nerve. We conclude that CIP is a major complication in patients with severe sepsis and prolonged artificial ventilation. It predominantly involves motor fibres and thus markedly interferes with weaning from the ventilator.
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PMID:Predominant involvement of motor fibres in patients with critical illness polyneuropathy. 938 83

In vitro pretreatment of human monocytes (MO) with low-dose lipopolysaccharide (LPSp) inhibits TNF release in response to subsequent LPSa activation. Septic patients are often indistinguishable from patients with systemic inflammatory response syndrome (SIRS). We hypothesized that in vivo exposure to "septic" stimuli impairs subsequent LPSa-stimulated MO TNF production in vitro. Human peripheral MO were obtained after informed consent from controls or patients with sepsis, SIRS, or posttrauma [ACCP/SCCM definitions]. Cells were plated in vitro, incubated 24 hr, and then stimulated with 0-1000 ng/ml LPSa for 4 hr. Parallel control MO were incubated in vitro with 100 ng/ml LPSp for 24 hr and then stimulated with 1000 ng/ml LPSa for 4 hr. Supernatant TNF (mean U/ml +/- SEM) was measured by bioassay. ANOVA was used to determine statistical significance. In vitro LPSp pretreatment markedly inhibited subsequent LPSa-stimulated TNF release. In vitro LPSa-stimulated TNF release was likewise significantly inhibited with MO from septic patients compared to controls. Inhibition was more profound in septic patients with shock (not shown). No impaired TNF release was seen with MO from SIRS or trauma patients. In conclusion, in vivo preexposure to inflammatory stimuli in septic patients alters monocyte regulation in a manner similar to in vitro endotoxin tolerance. Provocative in vitro monocyte LPS stimulation may distinguish patients with sepsis and SIRS.
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PMID:In vivo endotoxin tolerance: impaired LPS-stimulated TNF release of monocytes from patients with sepsis, but not SIRS. 920 54

Many systems and techniques for continuous vascular access in small animals have been described. Problems with these systems have included (1) insufficient free movement, (2) sepsis, (3) high cost, (4) complicated construction, (4) thrombosis, and (5) dislocations of the intravenous catheter. The described operative techniques and a new experimental setup overcome these complications. The apparatus involves a swivel that is connected with an intravenously placed polyurethane catheter. A leather harness on the back of the animal is connected with the end of the swivel joint via a silicone tube in which the intravenous catheter runs to the swivel. The swivel, a modified conventional glass syringe, is positioned in ball bearings and a Johnson joint. The swivel, ball bearings, and Johnson joint are counterbalanced and can move up and down. When this system was used, the catheters functioned well for as long as 28 days, with a mean duration of 24.4 +/- 1.8 days (n = 420). Five catheter dislocations resulted from harness failure, and three dislocations were caused by animals twisting. All animals gained weight (3.53 +/- 0.37 gm/day (mean +/- SEM)). The rotary portion of the swivel and the Johnson joint secure stressless movement of the animal, avoiding twisting and dislocation of the catheter, which overcomes typical problems of existing methods. The low thrombogenicity of the polyurethane catheter also reduces complications. A further advantage is low cost, because prefabricated, reusable materials are used.
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PMID:Technical and surgical aspects of continuous vascular access in freely moving small animals. 935 81

Our aim was to evaluate gastric emptying and orocecal transit in patients with end-stage liver disease and portal hypertension undergoing evaluation for liver transplantation. Although gastric emptying half-times for both liquid and solid emptying were similar in patients with chronic liver disease and control subjects, orocecal transit, as measured by a scintigraphic technique, was significantly prolonged in the patients with liver disease (transit time, minutes, mean +/- SEM, patients versus controls: 127 +/- 10.5 versus 80 +/- 9.5, P < .003). Serum levels of progesterone and estradiol were similar in patients and controls. We conclude that small intestinal transit is delayed in patients with advanced liver disease and portal hypertension and may contribute to gastrointestinal symptoms and promote sepsis of enteric origin in this patient population.
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PMID:Gastric emptying and orocecal transit in portal hypertension and end-stage chronic liver disease. 937 56

The protective efficacy of immunisation with heat-killed Pseudomonas aeruginosa on murine gut-derived sepsis was evaluated. Mice were immunised intraperitoneally six times with heat-killed bacteria. This induced mean (SEM) serum IgG and IgM antibodies of 1792 (374.7) and 37.3 (8.9) ELISA units, respectively. Specific pathogen-free mice given P. aeruginosa strain D4 orally died of bacteraemia after administration of cyclophosphamide. Immunisation with heat-killed bacteria significantly increased the survival rate compared with that of control mice immunised with bovine serum albumin. Macroscopic observation revealed marked production of liver abscesses in mice immunised with bovine serum albumin but not in those immunised with heat-killed bacteria. Only low titres of antibody against the exoenzymes alkaline protease, elastase and exotoxin A were observed, and no significant difference between antibody titres to boiled and unboiled suspensions of sonicated P. aeruginosa was detected. This suggests that the main protective antibodies might be those specific to the heat stable antigen (lipopolysaccharide). Immunisation with heat-killed bacteria provided complete protection against death from gut-derived P. aeruginosa sepsis.
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PMID:Effect of immunisation with Pseudomonas aeruginosa on gut-derived sepsis in mice. 956 94


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