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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bacterial infectious complications are the most common cause of morbidity and mortality associated with acute pancreatitis. Most pathogens are common gastrointestinal flora, indicating that the gut is the source of pancreatitis-related infections. However, the route whereby the microorganisms reach distant organs remains speculative. We tested the hypothesis that spread of bacteria occurs via a transperitoneal pathway. Acute interstitial pancreatitis (AIP) was induced in antibiotic (gentamicin, bacithracin, neomycin)-decontaminated rats by intravenous infusion of cerulein. Effects of pancreatic necrosis (PN) were studied in rats that received additional injections into the peritoneal cavity of pancreatic tissue obtained from donor rats. The rats were inoculated with Escherichia coli (O2:KN:H18) resistant to the antibiotics used for decontamination either orally (10(12) microorganisms; experiment I) or intraperitoneally (10(8) microorganisms; experiment II). Moreover, the rat peritoneal cavity wash was inoculated with 10(8) E. coli in vitro (experiment III). In rats with AIP and PN, recovery of the bacteria from liver, spleen, pancreas, lung, and blood following oral inoculation demonstrated that acute pancreatitis promotes bacterial translocation from the gut. The absence of E. coli in these organs following intraperitoneal inoculation showed that the bacteria do not spread from the peritoneal cavity. Rats with PN cleared E. coli from the peritoneal cavity in a shorter period than rats with AIP and controls (5 vs. 7 and 8 days; p < 0.05). The multiplication rate of E. coli in peritoneal cavity wash was lower in rats with PN than in rats with AIP and controls (p < 0.01). We conclude that (1) translocation of E. coli from the gut during cerulein-induced acute pancreatitis occurs via nonperitoneal pathways, (2) the peritoneal cavity acts as a trap for the bacteria rather than a source of bacterial seeding, and (3) PN impairs survival of E. coli in the peritoneal cavity via inhibition of the bacterial multiplication in this model.
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PMID:Cerulein-induced acute pancreatitis in rats--does bacterial translocation occur via a transperitoneal pathway? 933 94

Patients with severe pancreatitis, characterized by multiple organ failure and pancreatic necrosis on CT scan (identified by an Acute Physiology and Chronic Health Evaluation II score of > or = 10 with > or = 3 Ranson criteria), most likely require aggressive nutritional support. Use of the enteral route of feeding may help contain the hypermetabolic stress response, reduce morphologic change and atrophy of the gut, and theoretically decrease late complications of nosocomial infection and organ failure. Evidence that decreasing degrees of stimulation of the pancreas occur as the site of feeding descends in the gastrointestinal tract and evidence from perspective, randomized trials suggest that jejunal feeding appears at least as safe and well tolerated as total parenteral nutrition in acute pancreatitis.
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PMID:Nutritional management in acute and chronic pancreatitis. 965 25

Platelet-activating factor (PAF) may play a critical and primary role in the pathogenesis of acute pancreatitis and pancreatitis-associated distant organ injury. The present study evaluated the effect of a PAF antagonist, lexipafant (an (S)-4-methyl-2[methyl-imidazo[4,5-c]pyridin-1-ylmethyl)-benzene sulphonyl]-amino]pentanoic acid ethyl ester, BB-882; British Biotech Ltd.), on the potential prevention of gut barrier dysfunction, by measuring gut origin sepsis, bidirectional permeability of the intestinal barrier, and pancreatic capillary endothelial barrier integrity, in acute pancreatitis induced by intraductal infusion of 5% sodium taurodeoxycholate. Pancreatic endothelial permeability significantly increased in animals with acute pancreatitis, whereas pretreatment with lexipafant had a preventive effect (p < 0.05 vs. pancreatitis with saline). Similarly, alterations noted in hematocrit and plasma levels of lipase and calcium were counteracted by the PAF antagonist. It also prevented the increase in albumin leakage from blood to the mucosal interstitium and from blood to the intestinal lumen in acute pancreatitis. Albumin passage from the gut lumen to blood in animals with pancreatitis pretreated with saline increased from 3 h and on, and lexipafant prevented alterations in mucosal epithelial permeability. Bacterial translocation was commonly seen in pancreatitis, whereas only a few positive cultures were observed in pancreatitis animals given lexipafant. Microthrombosis in intestinal villi seemed less frequent after lexipafant pretreatment. We conclude that (a) PAF may play a role in the pathogenesis of pancreatitis-associated intestinal dysfunction, (b) PAF may be involved in the development of distant organ dysfunction by triggering endothelial barrier dysfunction, and (c) PAF antagonists may provide potential agents for preventing pancreatitis-associated gut barrier dysfunction.
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PMID:Effect of a platelet-activating factor antagonist on pancreatitis-associated gut barrier dysfunction in rats. 970 Sep 40

Bowel rest during treatment of acute pancreatitis deprives the gut of nutrients and affects its structure and function. Enteral feeding is usually performed late in the course of acute pancreatitis and therefore cannot prevent intestinal barrier dysfunction and possible bacterial translocation. To assess the effect of early enteral nutrition we performed a prospective study on 21 patients (11 males/10 females) presenting with severe acute pancreatitis (13 biliary, 6 alcoholic, and 2 miscellaneous). Severity was established by a mean Ranson score of 3.57. All but one patient could be fed through a double-lumen nasogastrojejunal tube within 60 h after admission. No significant complication of the technique was observed. We conclude that early jejunal feeding can be used safely in severe acute pancreatitis. Further comparative studies are necessary to demonstrate any superiority to total parenteral nutrition.
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PMID:Is early enteral nutrition in acute pancreatitis dangerous? About 20 patients fed by an endoscopically placed nasogastrojejunal tube. 970 Sep 52

Intestinal barrier failure and subsequent translocation of bacteria from the gut play a decisive role in the development of systemic infections in severe acute pancreatitis. Glutamine (GLN) has been shown to stabilize gut barrier function and to reduce bacterial translocation in various experimental settings. The aim of this study was to evaluate whether GLN reduces gut permeability and bacterial infection in a model of acute necrotizing pancreatitis. Acute necrotizing pancreatitis was induced in 50 rats under sterile conditions by intraductal infusion of glycodeoxycholic acid and intravenous infusion of cerulein. Six hours after the induction of pancreatitis, animals were randomly assigned to one of two groups: standard total parental nutrition (TPN) or TPN combined with GLN (0.5 g/kg(-1)/day(-1)). After 96 hours, the animals were killed. The pancreas was prepared for bacteriologic examination, and the ascending colon was mounted in a Ussing chamber for determination of transmucosal resistance and mannitol flux as indicators of intestinal permeability. Transmucosal resistance was 31% higher in the animals treated with GLN- supplemented TPN compared to the animals given standard TPN. Mannitol flux through the epithelium was decreased by 40%. The prevalence of pancreatic infections was 33% in animals given GLN-enriched TPN as compared to 86% in animals receiving standard TPN (P < 0.05). Adding GLN to standard TPN not only reduces the permeability of the colon but decreases pancreatic infections in acute necrotizing pancreatitis in the rat. This confirms previous reports that GLN decreases bacterial translocation by stabilizing the intestinal mucosal barrier. The present findings provide the first evidence suggesting that stabilizing the intestinal barrier can reduce the prevalence of pancreatic infection in acute pancreatitis and that GLN may be useful in preventing septic complications in clinical pancreatitis.
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PMID:Glutamine stabilizes intestinal permeability and reduces pancreatic infection in acute experimental pancreatitis. 983 29

Translocation of intestinal bacteria from the gut into pancreatic necrosis is an important factor in the development of septic complications in acute pancreatitis. Bacterial translocation is promoted by an impaired intestinal mucosal barrier, which can be attributed to the reduced oxygen and substrate supply of the intestine. A rat model of severe acute pancreatitis has been used to confirm the hypothesis that an impaired mucosal barrier can be stabilized by supplying certain nutrients, vitamins, and trace elements. A reduction in secondary pancreas infections with intestinal bacteria and improved survival was achieved under intravenous glutamine substitution, an essential amino acids in stress situations for enterocytes, colonocytes and immunocompetent cells. The positive experimental results are currently being investigated in a controlled randomized multicenter trial. Comparable studies need to be performed for verifying the effect of other nutritive factors on bacterial translocation and the disease course in acute pancreatitis.
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PMID:[Pancreatitis and translocation--approaches for nutritional strategies]. 993 85

Based on the literature dysfunction of splanchnic circulation may be assumeol in the development of severe acute pancreatitis. Abnormal gut functions investigated by routinely used clinical examination is not available. Gastric tonometry indirectly gives information about gut function. Authors followed prospectively 12 patients who suffered from acute pancreatitis. Four patients recovered without complications, 4 patients had different complications and 4 patients died. Gastric intramucosal pH (pHi) was measured by TRIP NGS catheter and Tonocap monitor. Measurements were started at the time of hospitalisation and repeated every six hours on the first 3 days. Intramucosal acidosis (pHi < 7.3) could be measured independently from aetiology. Gastric pHi showed strong correlation with Acute Physiology and Chronic Health Evaluation II. (APACHE II) score (p = 0.02). APACHE II scores were significantly higher in-group pHi < 7.2 (13.9 +/- 1.7) compared to group pHi > 7.2 (7.33 +/- 1.06) (p = 0.002). 24-hour changes in APACHE II scores were significantly greater in the cases of pHi < 7.2 (3.3 +/- 1.47) versus pHi > 7.2 (-0.6 +/- 0.97) (p = 0.03). Changes of pHi in the early phase of acute pancreatitis indicate that splanchnic circulation is already involved and the pHi may have a prognostic value.
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PMID:[Calculated gastric intramucosal pH changes in the early phase of acute pancreatitis]. 1034 41

Bacterial infections, frequently caused by bacteria of enteric origin, are often seen during the progression of severe acute pancreatitis, concomitant with the potential development of multiple organ dysfunction. In the present paper, the complex mechanisms of gut barrier dysfunction and gut origin sepsis in acute pancreatitis are discussed. The individual parts of the gut barrier, e.g. the immunological, bacteriological and morphological (mucus, epithelium, endothelium and interstitium) components, seem to interact and depend on each other. Pancreatitis-induced hypovolaemia due to endothelial barrier leakage and gut arteriovenous shunting causes intestinal ischaemia and reperfusion injury with concomitant gut barrier dysfunction. Gut endothelial barrier dysfunction probably plays a central role. Potential molecular mechanisms could, among others, be associated with alterations in intracellular signal transduction, intercellular signalling and expression of adhesion molecules on endothelial cells. The mechanisms underlying gut barrier dysfunction in acute pancreatitis are thus complex and still not fully elucidated. Knowledge about the regulating events will probably allow future pharmacological therapy for prevention and treatment of the severe complications of acute pancreatitis, including gut barrier dysfunction.
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PMID:Gut barrier dysfunction in experimental acute pancreatitis. 1037 40

Severe acute pancreatitis is in its first stage characterized by the syndrome of systemic inflammatory response (SIRS). The extent of activation of the mediator defense cascade of the organism depends on a hitherto unknown primary insult which cannot be influenced by therapeutic care. The cause of the development of sepsis or multiorgan failure is the supraliminal action of secondary insults (ischaemic reperfusion syndrome, hypoxia, impaired physiological function of the gut). By early and aggressive therapeutic action the effect of these adverse factors can be markedly reduced. Then also better therapeutic results in severe acute pancreatitis may be expected.
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PMID:[Preventing the development of secondary infections in severe acute pancreatitis]. 1037 76

Acute respiratory distress syndrome (ARDS) and multiple organ failure (MOF) are the most common causes of death in surgical intensive care units. A variety of stimuli, such as major surgery, trauma, shock, thermal injury, acute pancreatitis, and ischemia-reperfusion injury, initiate a systemic inflammatory response that contributes to the development of these complications. Splanchnic hypoperfusion is a common clinical event in critically ill patients. Recently, measurement of the adequacy of gut circulation has been demonstrated as an excellent tool for prediction of outcome in these patients. The emphasis of this review is on events associated with intestinal ischemia-reperfusion and subsequent distant organ injury.
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PMID:[Splanchnic hypoperfusion and distant organ injury]. 1041 57


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