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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fibronectin is a large-molecular-weight glycoprotein present on most cell surfaces, in extracellular fluids, and in plasma. Both cell-associated and soluble fibronectin are thought to have important roles in the inflammatory response and host defense and may contribute to the maintenance of microvascular integrity during septic episodes. Newborn infants have levels of fibronectin in plasma that are one-third to one-half those found in the healthy adult. In addition, neonates with respiratory distress syndrome, perinatal asphyxia, bacterial sepsis, intrauterine growth retardation, or postnatal malnutrition have a further depression in their plasma levels of fibronectin. The low plasma concentration of fibronectin in newborn infants may contribute to the hypofunction of the neonatal reticuloendothelial system and predispose to the development of sepsis. Rates of synthesis of plasma fibronectin are diminished in the neonate, and an inverse correlation between fibronectin half-life and gestational age exists. The role of fibronectin in treatment or prophylaxis of neonatal sepsis remains to be determined.
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PMID:Role of fibronectin in diseases of newborn infants and children. 219 69

We describe immunoluminometric assays for seven acute-phase proteins, which can be determined in minimal volumes of plasma, serum, sputum, and bronchioalveolar lavage. The theoretical volume of serum or plasma required to measure all seven analytes in duplicate is 130 nL, although in practice the smallest volume of sample was enough to fill a hematocrit tube (about 25 microL of blood), collected from neonates by the heel-prick method. The assays could be performed with 10 microL of sputum or with 100 microL of bronchioalveolar lavage. We measured alpha 1-antitrypsin, alpha 2-macroglobulin, alpha 1-acid glycoprotein, thyroxin-binding prealbumin, C-reactive protein, and total and secretory immunoglobulin A. The assays are rapid enough for all results to be returned to the ward on the same day and are suitable for monitoring neonatal sepsis. All coefficients of variation, derived from compound precision profiles, were less than 7% for clinically relevant analyte concentrations. Correlation with commercially available nephelometric assays was good.
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PMID:Luminometric assays of seven acute-phase proteins in minimal volumes of serum, plasma, sputum, and bronchioalveolar lavage. 242 43

We examined the pathogenicity of coagulase-negative staphylococci (CONS) in newborn infants by comparing presenting nonspecific signs of infection in infants with and without CONS bacteremia. During a 6-month period 799 blood cultures were obtained in a tertiary care nursery; 81 (10.1%) grew CONS and 25 (3.0%) grew other bacteria. A comparison group of 121 infants was selected randomly from ill patients whose blood cultures were negative. In addition 70 well infants were matched to CONS-positive cases. Abnormal clinical signs, complete blood cell counts, C-reactive protein, alpha-1-acid glycoprotein and prealbumin were determined at the time of culture. Signs that discriminated best between infants with and without CONS bacteremia were identified by logistic regression analysis. Infants with CONS bacteremia did not differ from infants with sepsis caused by recognized pathogens, except for lethargy, which was significantly more common in unequivocal infection. Infants with presumed infection but negative blood cultures, and noninfected control patients had abnormal signs significantly less often than CONS-positive infants. C-reactive protein, hyperthermia, increased oxygen requirements and lethargy were the most useful signs in identifying neonatal bloodstream infection. This cohort study provides objective evidence for the pathogenicity of CONS in newborn infants.
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PMID:Coagulase-negative staphylococci as true pathogens in newborn infants: a cohort study. 244 54

The mediator(s) and mechanism(s) of acute-phase protein synthesis in the liver following injury and sepsis are not fully known. Elevated plasma levels of the catabolic hormones cortisol, glucagon, and epinephrine have been reported in trauma and sepsis. In previous reports, when these hormones were infused simultaneously (triple hormone infusion), several, but not all, of the metabolic alterations characteristic of sepsis occurred. In the current investigation, the effect of triple hormone infusion on hepatic protein synthesis was studied. Rats were infused intravenously during 16 hours with a solution containing corticosterone (4.2 mg/kg/h), glucagon (2.5 micrograms/kg/h), and epinephrine (6 micrograms/kg/h). Control animals were infused with a corresponding volume of vehicle. Total hepatic protein synthesis in vivo was measured with a flooding dose technique using [14C]-leucine. The synthesis of total secretory proteins and of the individual proteins albumin, complement component C3, and alpha 1-acid glycoprotein was measured in isolated, perfused liver using [3H]-leucine and a recirculating technique. Urinary excretion of nitrogen and plasma concentration of glucose were higher and plasma total amino acid concentration was lower in hormone-infused than in control rats. Total hepatic protein synthesis in vivo, expressed as the proportion of the protein pool that was replaced each day, was increased from 39% +/- 2% per day to 48% +/- 3% per day (P less than .05) by hormone infusion, but synthesis of secretory proteins in perfused liver was not significantly altered. The results suggest that although total hepatic protein synthesis may be increased by catabolic hormones, other mediator(s) are probably responsible for the stimulation of acute-phase protein synthesis in sepsis.
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PMID:Protein synthesis in liver following infusion of the catabolic hormones corticosterone, epinephrine, and glucagon in rats. 247 64

To study the effect of intraabdominal sepsis on hepatic protein synthesis, male Sprague-Dawley rats underwent celiotomy with either cecal ligation and puncture (CLP) or sham operation. Eight and sixteen hours later total hepatic protein synthesis was measured by flooding dose technique. Specific synthetic rates of structural or secreted hepatic proteins were further studied 16 hr after CLP in an isolated perfused liver model. Total hepatic protein synthesis was significantly elevated at 16 hr (59 +/- 6%/day vs 37 +/- 6%/day, P less than 0.05), but not 8 hr post-CLP. Structural hepatic protein synthesis was unchanged after CLP; however, the synthetic rates of the acute-phase secretory proteins alpha 1-acid glycoprotein, transferrin and complement component C3 were significantly increased 16 hr after CLP. However, the albumin synthetic rate was not increased during sepsis. We conclude that sepsis causes augmentation of hepatic protein synthesis primarily to increase acute-phase proteins for host defense.
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PMID:Increased synthesis of secreted hepatic proteins during abdominal sepsis. 333 73

The usefulness of the neutrophil blood cell count, the ratio of band forms to total neutrophils, the platelet count, the quantitative determination of serum IgM, C-reactive protein, alpha-1-acid glycoprotein and haptoglobin for the early identification of the serious neonatal infections was evaluated in 70 preterm newborns: 15 with sepsis, 2 with serious infections, 53 without infections. None of these tests has proved sensitive and predictive enough to be used as a single measure. The combination of 2 or more of them had improve the sensitivity (76.4%) and the predictive value of negative test (91.6%). The authors suggest that the greatest potential value of the tests is to exclude infections, with a more than 90% probability, if they are negative.
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PMID:[Early diagnosis of sepsis in the preterm neonate]. 344 33

In a series of 135 patients with severe surgical infections, we determined the sepsis score and the plasma level of the acute-phase proteins alpha-1-acid glycoprotein, alpha 1-antitrypsin, complement factor B, and C3. The initial sepsis score was a strong determinant of survival: in survivors it was significantly lower than in nonsurvivors. Only 8% of patients with a sepsis score above 20 survived. At the onset of severe sepsis, the plasma levels of all four acute-phase proteins were significantly lower in nonsurvivors. A significant elevation of C3a levels in the plasma of both surviving and nonsurviving patients indicated marked consumption of complement components in all patients with severe sepsis. A linear equation was developed to predict survival: sepsis index of survival (SIS) % = 121 + 0.26 (complement factor B) + 0.36 (alpha-1-acid glycoprotein)-6 (sepsis score). Based on our analysis, at the onset of severe sepsis, an SIS of 50% or more can correctly predict 88% of survivors and an SIS less than 50% can correctly predict 86% of nonsurvivors several days in advance of clinical outcome.
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PMID:Sepsis score and acute-phase protein response as predictors of outcome in septic surgical patients. 349 85

von Willebrand factor (vWF), a large adhesive glycoprotein, is synthesized by vascular endothelial cells (EC). Plasma levels of vWF manifest a broad normal range, and are elevated during sepsis and in inflammatory states. Since the inflammatory mediator, interleukin 1 (IL1) and bacterial endotoxin (LPS) both initiate procoagulant changes in vascular endothelium, we investigated the effect of these substances on endothelial cell release and residual endothelial cell content of vWF-antigen (vWFAg). Cultured human EC exposed to either IL1 or LPS released greater amounts of vWFAg compared to control EC. The augmented release could be detected within 1-2 h after exposure to IL1 or LPS and was not inhibited by cycloheximide, suggesting that de novo protein synthesis was not required for release to occur. Residual cellular vWFAg was reciprocally lower in IL1- or LPS-treated EC at 24 and 48 h, indicating that compensatory increase in synthesis of vWFAg did not occur during this time interval. Released vWF contained the higher molecular weight multimers observed in normal endothelial cells, and it possessed ristocetin cofactor activity. We propose that release of functional vWF from EC exposed to inflammatory mediators may be at a mechanism for localization of platelets and enhanced thrombogenicity at inflammatory foci.
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PMID:Interleukin 1 or endotoxin increases the release of von Willebrand factor from human endothelial cells. 349 29

The gastromucosal barrier (GMB) can be disrupted by a number of aggressive factors or by a decrease in mucosal defense factors. If there is back diffusion of hydrogen ions into the mucosa, mucosal damage ranging from an erythematous gastro-duodenitis to erosive and ulcerative gastritis or life-threatening hemorrhage may ensue. The pathogenesis of stress-related mucosal damage seen in critically ill patients suffering from burns, sepsis, head trauma, respiratory insufficiency, or multisystem disease is also related to a decrease in mucosal resistance. Early studies of cimetidine in animals and in humans demonstrated its ability to increase gastric transmucosal potential difference, indicating an enhancement of the integrity of the GMB. Several studies show that cimetidine protects the stomach from aspirin-induced mucosal damage; increases gastric mucus production and mucus glycoprotein content, which contributes to the protective action of mucus; increases mucosal secretion of bicarbonate; increases gastric mucosal blood flow, which prevents mucosal hypoxia seen in patients in shock or otherwise critically ill patients; increases endogenous mucosal prostaglandin synthesis; and increases the rate of epithelial cell renewal, a factor important to mucosal healing. Since cimetidine suppresses acid secretion and enhances mucosal defense, it is an important therapeutic tool in the management of acid-related disorders, particularly stress-related mucosal damage.
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PMID:Gastric acid secretion and mucosal defense mechanisms with special reference to the role of cimetidine in critically ill patients. 353 48

1. Plasma fibronectin, a glycoprotein, is an opsonin of the reticuloendothelial system. 2. In ten healthy volunteers starved for 4.5 d, daily measurements showed a rapid reduction in plasma fibronectin, no alteration in either C3 or plasma transferrin and, at the end of the starvation period, an elevated serum albumin. 3. On refeeding, plasma fibronectin rapidly returned to its prestarvation level but plasma transferrin was significantly reduced and did not recover by the end of the study. 4. Changes in plasma fibronectin may be a sensitive index of nutritional status. The reduction of plasma fibronectin in short-term starvation may compromise host defence tolerance of injury and sepsis.
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PMID:Changes in plasma fibronectin during acute nutritional deprivation in healthy human subjects. 366 79


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