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)

Cefpiramide (CPM) was given to 4 patients with respiratory tract infection (H. influenzae 3 cases, P. aeruginosa 1 case), 1 patient with enteritis (enteropathogenic E. coli) and 1 patient with sepsis (E. cloacae). Bacteriological eradication was observed in 5 cases (83.3%), and clinical effectiveness was 66.7%. Serum concentration of CPM at a dose of 15 mg/kg after intravenous drip-infusion for 30 minutes was 105 micrograms/ml at the end of infusion and 67 micrograms/ml at 1 hour. Bacteriological eradication by the administration of CPM was rapidly occurred in 3 strains of H. influenzae including 1 strain of beta-lactamase producing ABPC-resistant one, and 1 strain of P. aeruginosa in the sputum. One patient aged 2 years and 5 months with pneumonia was cured by the treatment of CPM as an outpatient. No side effects were observed except 1 case of vascular pain. It was concluded that CPM is a useful drug for the treatment of bacterial infections in children.
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PMID:[Clinical evaluation of cefpiramide in 6 cases of infection in children]. 665 37

Ecthyma gangrenosum caused by Escherichia coli (E. coli) occurred in a decompensated alcoholic cirrhotic patient with spontaneous bacterial peritonitis due to the same organism. Ecthyma is usually associated with systemic sepsis from Pseudomonas aeruginosa. Isolated instances due to other bacteria have been reported, but its occurrence in spontaneous bacterial peritonitis, of which the predominant causative organism is E. coli, is unique. The frequency, varied etiology, and pathogenesis of ecthyma are briefly reviewed.
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PMID:Spontaneous bacterial peritonitis with ecthyma gangrenosum due to Escherichia coli. 704 96

Endotoxin-induced cytokines such as interleukin-1 (IL-1) and tumor necrosis factor (TNF) are thought to contribute to the proinflammatory effects of endotoxin in gram-negative infections. Using a conscious rat model of sepsis, induced by intravenous challenge with LD95 doses of endotoxin (n = 24) or live Escherichia coli (E. coli) (n = 24), we examined frozen sections of kidney at various intervals for evidence of IL-1 alpha and TNF alpha expression. A transient glomerular endothelial IL-1 alpha expression was demonstrated at 30 and 90 min after initiation of the sepsis in both endotoxin and E. coli-treated animals using immunohistochemistry. The endothelial IL-1 alpha expression as determined by immunohistochemistry occurred at the same time as IL-1 alpha mRNA expression, as determined by Northern blot analysis. The glomerular endothelial IL-1 alpha expression coincided with a slight but significant increase in the number of the glomerular polymorphonuclear leukocytes as identified by naphthol AS-D chloroacetate esterase enzyme histochemical reaction. Glomerular endothelial IL-1 alpha expression was virtually absent by 180 and 360 min. No TNF alpha expression was detected in the renal tissues at any time interval. Neither alpha-naphthyl acetate esterase-positive nor acid phosphatase-positive monocytes/macrophages were identified in the glomeruli. Our findings provide direct in vivo evidence that the IL-1 alpha gene product is expressed locally in the kidney by glomerular endothelial cells in this septic rat model.
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PMID:Renal interleukin-1 expression during endotoxemia and gram-negative septicemia in conscious rats. 785 Sep 31

Gram negative sepsis causes changes in oxygen supply-demand relationships. We have used a primate model of hyperdynamic gram negative sepsis produced by intravenous infusion of Escherichia coli (E. coli) to evaluate sepsis-induced alterations in mitochondrial oxidation-reduction (redox) state in muscle in vivo. The redox state of cytochrome a,a3, the terminal member of the intramitochondrial respiratory chain, was assessed in the intact forearm by near-infrared (NIR) spectroscopy. The muscle NIR data were compared to routine measures of oxygen delivery (DO2) and oxygen consumption (VO2). After E. coli infusion and fluid resuscitation, DO2 and VO2 showed minimal changes through 24 hr of sepsis. In contrast, changes in cytochrome a,a3 redox state evaluated by NIR occurred within a few hours and were progressive. Mitochondrial functional responses were correlated with structural changes observed on serial muscle biopsies. Gross morphological changes in muscle mitochondria were present in some animals as early as 12 hr, and, in most animals, by 24 hr. The morphologic changes were consistent with decreases in oxidative capacity as suggested by NIR spectroscopy. The NIR data also suggest that two mechanisms are operating to explain abnormalities in oxygen metabolism and mitochondrial function in lethal sepsis. These mechanisms include an early defect in oxygen provision to mitochondria that is followed by a progressive loss in functional cytochrome a,a3 in the muscle.
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PMID:Altered mitochondrial redox responses in gram negative septic shock in primates. 798 71

Gram-negative bacterial sepsis is associated with endotoxemia and a high mortality rate. In previous studies, we demonstrated the therapeutic benefit of an anti-lipopolysaccharide factor isolated from amebocytes of Limulus polyphemus, and of a recombinant version of this protein, termed endotoxin neutralizing protein (ENP), in rabbits challenged with purified lipopolysaccharides. To assess the benefit of ENP in treating a live bacterial infection, we established a rabbit model of Escherichia coli (E. coli) peritonitis and bacteremia with high mortality despite gentamicin treatment. Twenty-four pairs of New Zealand white rabbits were challenged intraperitoneally (IP) with E. coli O18ac K1 in 5% porcine mucin (mean bacteria per dose = 2.5 x 10(8)). The animals were treated with intravenous (i.v.) gentamicin (2.5 mg/kg), and with either ENP (5 mg/kg) or saline i.v. at 1 hr after E. coli challenge. All rabbits were bacteremic 1 hr after challenge (geometric mean 4.1 +/- 1.2 x 10(4) cfu/mL). Peak geometric mean serum endotoxin (2.62 v 10.54 EU/mL, P = .013) and tumor necrosis factor (TNF) (2540 v 6438 TNF units/mL, P = .046) concentrations were lower in ENP-treated animals as compared to control animals. Seven of 24 animals treated with ENP survived 24 hr compared with 4 of 24 controls (Kaplan-Meier analysis, P = .19). However, in the subgroup of 13 paired animals in whom bacteremia was eliminated by gentamicin treatment, 5 of 13 ENP-treated animals survived 24 hr, compared with 1 of 13 controls (Kaplan-Meier analysis, P = .032).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Efficacy of a recombinant endotoxin neutralizing protein in rabbits with Escherichia coli sepsis. 801 61

We studied retrospectively the clinical records of 291 hospital patients with liver cirrhosis, 95% of which was alcohol related. Within this group, 114 patients presented 155 episodes of infection in 144 separate hospital admissions. In a previous communication, we pointed out that although infection was the fourth cause of admission, it was the main cause of death in this group. The main incidence of infection was among the female group. The most common infections episodes were respiratory and bacterial spontaneous peritonitis (BSP). On admission, 57% of the patients were diagnosed as belonging to the C Child group; 38% presented sepsis and 22% were hospitalary infections. The most frequent infections were respiratory and BSP. We obtained bacteriologic documentation in 55% of the episodes with prevalence of Gram negative bacilli (E. coli), with high relative frequency of neumoccocus. The most frequent complications were related to hepatic insufficiency. Global death rate was 27.1%, while nosocomial death rates were 42.1% and 40.9% for patients with Child C. We observed the highest incidence of mortality in patients with SBP and non localized bacteriemia. Survival rates were 42% for 2 years and 18% for 5 years. In summary, we stress the relevancy of checking the presence of infection systematically in every cirrhotic patient with encephalopathy and/or renal insufficiency without justifiable cause.
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PMID:[Infections during the hospitalization of patients with liver cirrhosis]. 829 12

The case of a patient with abdominal crisis and shock without any discernible origin who died 36 hours after hospital admission despite maximal therapy is described. Gram-negative sepsis, peritonitis and haemochromatosis with hepatic siderosis was the post-mortem diagnosis. We consider spontaneous peritonitis arising from translocation of normal intestinal flora (E. coli) through the intact wall of the gut combined with the impaired ability of the reticulo-endothelial system to remove endotoxin to be the causative factors. It is unknown whether the adrenal insufficiency due to siderophilic adrenal hypophysis and adrenal glands contributed to the fulminant course of the disease. Undiagnosed liver cirrhosis and especially haemochromatosis should therefore be included in the differential diagnostic considerations in patients presenting with these symptoms, and in whom no obvious cause for a septic focus can be found.
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PMID:[Septic shock with acute abdomen in idiopathic hemochromatosis]. 835 6

The role of free radicals in septic-shock-associated tissue injury and the mechanisms underlying the generation of free radicals in sepsis was investigated in a primate model using electron spin resonance (ESR) spectroscopy and spin-trapping techniques paired with physiological measurements. Baboons were administered the spin trap, 5,5-dimethyl-1-pyrroline N-oxide (DMPO) during infusions of live Escherichia coli (E. coli) with or without challenge with tumor necrosis factor (TNF). ESR spectra suggesting the trapping of carbon-centered and oxygen-centered radicals were detected in liver lipid extracts of E. coli infused animals which exhibited pathophysiological changes indicative of sepsis. In animals demonstrating a toxic response to E. coli. TNF challenge appeared to intensify the ESR signal observed. These data provide evidence of free radical production during sepsis and suggest a role for TNF in the production of these radicals.
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PMID:Free radicals and septic shock in primates: the role of tumor necrosis factor. 838 84

Alcohol, consumed as 36% of the caloric intake for 8-10 wk, causes a potentiation of cardiac dysfunction induced by a second insult, sepsis. Because chronic alcoholism may attenuate the responsiveness of the myocardium to catecholamine stimulation, and because catecholamine support seems to be essential for the myocardium to generate an adequate cardiac output in sepsis, we hypothesized that the heart from the alcoholic septic rat would show a compromised inotropic responsiveness to catecholamines compared with the heart from the nonalcoholic septic rat. To test this hypothesis, rats were fed an ethanol-containing or control liquid diet for 8-10 wk and were then made septic with live Escherichia coli (10(10) E. coli) through a dorsal subcutaneous catheter. The next day, hearts were removed and perfused at a constant hydrostatic pressure, and a compliant balloon was placed in the left ventricule for measurement of pressure (LVP). Hearts were paced at 350-360 beats/min. Hearts were allowed to stabilize for 15 min, and then the response to a submaximal dose of isoproterenol (Iso) was measured. Hearts recovered for 30 min, at which time the response to a maximum dose of Iso was recorded. Basal (pre-Iso) LVP was lower in the control septic and alcoholic septic groups than in the control and alcohol groups. However, the maximum increase in LVP in response to Iso was greater in the two septic groups than in the two nonseptic groups. The peak LVP in response to Iso was similar in the control, septic, and alcoholic septic groups, and was significantly greater than in the alcohol group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocardial responses to isoproterenol are altered by chronic alcoholism and infection. 844 52

To investigate whether the inhibition of protein kinases including protein kinase C can antagonize endotoxicosis, the in vivo effects of K252a, a potent inhibitor of protein kinases, on endotoxin-induced lethality and glucose dyshomeostasis were determined in conscious rats. Sprague-Dawley rats (260-340 g) were divided into the following four groups: Group DS, 2.5% dimethyl sulfoxide (DMSO), 6 ml/kg iv + 0.9% saline, 2 ml/kg iv; group KS, K252a in 2.5% DMSO, 4 mg/kg iv + 0.9% saline; group DE, 2.5% DMSO + endotoxin (E. coli), 15 mg/kg iv; and group KE, K252a in 2.5% DMSO + endotoxin. A quarter of DMSO or K252a solution was continuously infused over a 15 min period before a bolus injection of either saline or endotoxin. The remaining dose was administered over a 180 min period after saline or endotoxin. All animals in the DS and KS groups survived for 24 hrs. K252a significantly improved endotoxic lethality. It attenuated the initial hyperglycemia, and late hypoglycemia, hyperlactacidemia, and base deficit after endotoxin. However, K252a had no influence on the endotoxic alterations of blood pressure, PaCO2 or PaO2. These results suggest that the activations of protein kinases, particularly protein kinase C, are involved in the pathogenesis of lethal endotoxicosis and sepsis.
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PMID:K252a, a potent protein kinase inhibitor, improves endotoxic lethality and glucose dyshomeostasis. 846 75


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