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

Translocation of bacteria from the intestine causes local and systemic infection in severe acute pancreatitis. Increased intestinal permeability is considered a promoter of bacterial translocation. The mechanism leading to increased gut permeability may involve impaired intestinal capillary blood flow. The aim of this study was to evaluate and correlate early changes in capillary blood flow and permeability of the colon in acute rodent pancreatitis of graded severity. Edematous pancreatitis was induced by intravenous cerulein; necrotizing pancreatitis by intravenous cerulein and intraductal glycodeoxycholic acid. Six hours after induction of pancreatitis, the permeability of the ascending colon was assessed by the Ussing chamber technique; capillary perfusion of the pancreas and colon (mucosal and subserosal) was determined by intravital microscopy. In mild pancreatitis, pancreatic capillary perfusion remained unchanged (2.13 c 0.06 vs. 1.98 +/-0.04 nl x min(-1) x cap(-1) [control]; P = NS), whereas mucosal (1.59 +/-0.03 vs. 2.28 +/-0.03 nl x min(-1) x cap((-1))[control]; P <0.01) and subserosal (2.47 +/-0.04 vs. 3.74 +/-0.05 nl x min(-1) x cap((-1))[control]; P <0.01) colonic capillary blood flow was significantly reduced. Severe pancreatitis was associated with a marked reduction in both pancreatic (1.06 +/-0.03 vs. 1.98 +/-0.04 nl x min(-1) x cap(-1) [control]; P <0. 01) and colonic (mucosal: 0.59 +/-0.01 vs. 2.28 +/-0.03 nl x min(-1) x cap((-1))[control], P <0.01; subserosal: 1.96 +/-0.05 vs. 3.74 +/-0.05 nl x min(-1) x cap(-1) [control], P <0.01) capillary perfusion. Colon permeability tended to increase with the severity of the disease (control: 147 +/-19 nmol x thr(-1) x cm(-2); mild pancreatitis: 158 +/-23 nmol x hr(-1) x cm(-2); severe pancreatitis: 181 +/-33 nmol x hr(-1) x cm(-2); P = NS). Impairment of colonic capillary perfusion correlates with the severity of pancreatitis. A decrease in capillary blood flow in the colon, even in mild pancreatitis not associated with significant protease activation and acinar cell necrosis or impairment of pancreatic capillary perfusion, suggests that colonic microcirculation is especially susceptible to inflammatory injury. There was no significant change in intestinal permeability in the early stage of pancreatitis, suggesting a window of opportunity for therapeutic interventions to prevent the later-observed increase in gut permeability, which could result in improved intestinal microcirculation.
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PMID:Intestinal microcirculation and gut permeability in acute pancreatitis: early changes and therapeutic implications. 1045 30

Failure of intestinal barrier function and subsequent translocation of bacteria from the gut are believed to play a decisive role in the development of systemic septic complications, for example, following major trauma or major abdominal surgery. This study evaluated: (a) the effect of glutamine on colonic microcirculation and electrophysiological parameters reflecting gut barrier function, (b) the translocation of live bacteria to extraintestinal organs, and (c) disease outcome in two animal models with impaired gut barrier function. Severe acute pancreatitis or colitis was induced in rats randomized for therapy with or without glutamine (0.5 g/kg daily). After 48 h one animal group was prepared for intravital microscopy of colonic capillary blood flow and electrophysiological measurement of gut permeability; another was killed after 96 h for histological and microbiological examination. In animals with pancreatitis, glutamine (Gln) supplementation significantly improved gut permeability, i.e., Gln increased colonic transmucosal resistance from 67+/-7 to 92+/-3 Omega/cm(2) and decreased mannitol flux through the epithelium by 53%. Capillary blood flow in the colonic mucosa was improved by 25%. The prevalence of pancreatic infections was reduced from 86% in animals on standard parenteral nutrition to 33% in animals given the Gln-enriched diet (P<0.05); mortality decreased by 32%. In colitis, Gln had no significant effect on these parameters except for improving colonic capillary blood flow in colon segments not adjacent to the major injury site. Glutamine supplementation improves colonic capillary blood flow, stabilizes gut permeability, and reduces secondary pancreatic infections and mortality in severe rodent pancreatitis, but it is not helpful in colitis. This confirms previous reports that glutamine stabilizes gut barrier function only in certain diseases. Our experimental data strongly suggest that acute pancreatitis (rather than colitis) is one of the diseases with gut barrier dysfunction in which glutamine substitution may be helpful to reduce bacterial translocation and should therefore be tested in a controlled clinical trial.
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PMID:Does glutamine reduce bacterial translocation? A study in two animal models with impaired gut barrier. 1046 Sep 4

Acute pancreatitis is a disease process that begins with an initial injury to the pancreatic acinar cell due to the erroneous premature activation and intracellular release of digestive enzymes. The local injury is amplified through the induction of a systemic inflammatory response, mediated by the generation and release of cytokines and an aggressive inflammatory cell recruitment. Failure to maintain gut integrity may exacerbate the stress response and the systemic inflammatory reaction associated with this process, worsening the overall clinical severity of the pancreatitis and contributing further to complications of organ failure and nosocomial infection. Emphasis in the clinical nutritional management of these patients has shifted from efforts to minimize stimulation of the gland, to attaining enteral access, starting tube feeds low in the gastrointestinal tract, and monitoring tolerance. While clinical guidelines help identify those patients with acute pancreatitis at greatest need for aggressive nutritional support, the proper timing to initiate feeding, the optimal composition of the enteral formula, and whether or not enteral feeding is better than no nutritional therapy is still not clear from the current literature.
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PMID:Artificial nutrition in pancreatic disease: what lessons have we learned from the literature? 1070 May 27

Infection is the most common cause of death in acute pancreatitis. Earlier studies have demonstrated that early enteral nutrition decreases microbial translocation, upregulates the immune function and reduces septic complications and mortality. Lactobacillus plantarum (Lp) has been shown to be effective in reducing egress of endotoxin and microbial strain that showed very high adherence power to gut mucosa. We adopted a model of acute pancreatitis induced by isolation and ligation of biliopancreatic duct in adult Lewis rats. Three groups were studied: A. control group (sham operation); B. induced pancreatitis, no further treatment; C. Induced pancreatitis + gavage with 5 ml/day of a suspension of Lp 299 v in a dose of 0.5-1.0 x 10(9)/ml during 4 days before and 4 days after induction of pancreatitis. All animals were sacrificed after 96 hours. Histological studies and microbiological analyses were performed. Forty out of 55 animals showed signs of severe pancreatitis on sacrifice after 96 hours. Only these animals were further studied. In group A, we found only 1/20 bacteria in mesenteric nodes (MN). Pathogenic microrganisms were found in the non-treated group in MN in 14/20 and in the pancreatic tissue in 10/20. In contrast, when kept on an umbrella of Lp 299 v, only 4/20 animals demonstrated growth of enteric bacteria in MN and 3/20 in pancreatic tissue. All of these results showed a significant reduction of infection in the treated groups. In our model, Lp 299 v is effective in preventing microbial translocation in experimental pancreatitis. Treatment with probiotic bacteria, such as Lactobacillus spp, seems to be a promising alternative as problems with antibiotic-resistant bacteria seem to accumulate.
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PMID:[A probiotic as an antagonist of bacterial translocation in experimental pancreatitis]. 1079 68

Interleukin (IL)-11 has anti-inflammatory activity in animal models of gut inflammation, endotoxemia, and radiation-induced thoracic injury. The aim of the present study was to investigate the protective role of IL-11 in a model of acute necrotizing pancreatitis in mice. Acute pancreatitis was induced by administration of seven intraperitoneal injections of cerulein (50 microg/kg) at hourly intervals. Lipopolysaccharide (LPS) was injected 5 hours after the first cerulein injection. Treatment with recombinant human IL-11 (rhIL-11) was started 30 minutes before the first cerulein injection and repeated 4 hours later. Serum levels of amylase, lipase, and tumor necrosis factor (TNF)-alpha were measured at the end of the experiments. The severity of pancreatitis was evaluated by histological scoring using a semiquantitative analysis of hematoxylin and eosin-stained sections of the pancreas. Competitive reverse transcription-polymerase chain reaction (RT-PCR) was performed to quantify the intrapancreatic TNF-alpha mRNA levels. Serum amylase and lipase levels progressively increased with a maximum reached between 8 and 11 hours. Treatment with rhIL-11 significantly decreased amylase and lipase levels at 6 and 8 hours. Serum TNF-alpha peaked at 6 hours and rapidly decreased thereafter. The elevation of serum TNF-alpha was markedly inhibited by treatment with rhIL-11. Histologically, treatment of rhIL-11 reduced the severity of pancreatic injury including edema, inflammatory cell infiltration, and hemorrhage at 6 hours. Intrapancreatic TNF-alpha mRNA levels were reduced by >50% in the rhIL-11-treated group at 6 hours. In conclusion, rhIL-11 decreased the severity of experimental pancreatitis early on but not later and inhibited the intrapancreatic TNF mRNA expression in vivo, suggesting that the protective effect of IL-11 during the early stage of acute pancreatitis may be mediated, at least in part, through modulation of TNF production.
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PMID:Recombinant human interleukin-11 decreases severity of acute necrotizing pancreatitis in mice. 1097 6

The results of several controlled clinical trials, published during the last 5 years, provide evidence of a beneficial role for early antimicrobial prophylaxis in severe acute pancreatitis. Pancreatic infections, especially gram-negative, which are of major importance with regard to morbidity and mortality, are gut-derived. Early enteral administration of antibiotics therefore seems the most logical measure to nip the danger in the bud. Intravenous antibiotics should adequately penetrate (peri)pancreatic tissues, i.e. necrotic tissues, and should be effective against the prevalent flora in infected necrotic tissues. However, the optimal route of administration is still a matter of debate. In contrast to one clinical trial using selective decontamination (SD) (i.e. enteral antibiotics combined with short systemic prophylaxis until SD is established), no clinical trial using intravenous antibiotics has been reported in which both pancreatic infections as well as mortality were reduced. Although the evidence supporting enteral administration, i.e. SD, is not unimpressive, further controlled clinical trials, in which the different ways of administration are compared, are warranted.
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PMID:Antimicrobial prophylaxis in acute pancreatitis: selective decontamination versus antibiotics. 1103 Jun 9

Conventional wisdom has previously dictated that, in order to avoid stimulation of pancreatic secretion during acute pancreatitis, and thus avoid the perpetuation of the enzymatic activation from which the pancreatitis originated, enteral feeding should be avoided. With greater understanding of the potential role of the gastrointestinal tract in the development of a systemic inflammatory response within a number of scenarios, this dogma has recently been challenged. Moreover, there is some evidence to suggest that starving the gastrointestinal tract and providing nutritional support via the parenteral route may be associated with an increased incidence of septic complications. Experimental and clinical evidence suggests that feeding the gut may diminish intestinal permeability to endotoxin and diminish bacterial translocation, thus reducing the cytokine drive to the generalized inflammatory response and preventing organ dysfunction. Preliminary experience suggests that the institution of jejunal (but not gastric or duodenal) nutrition within 48 hours of the onset of severe acute pancreatitis diminishes endotoxic exposure, diminishes the cytokine and systemic inflammatory responses, avoids antioxidant consumption and does not cause the radiological appearances of the pancreas to deteriorate. These observations are paralleled by improvements in clinical outcome measures such as intensive care unit stay, septic complications and mortality. Whist parenteral nutrition continues to have a role in the management of acute pancreatitis particularly when complicated by fistulae or prolonged ileus, the early introduction of jejunal nutrition merits further investigation in acute pancreatitis.
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PMID:Enteral versus parenteral nutrition in acute pancreatitis. 1103 Jun 11

Sepsis continues to account for a second peak in mortality in patients with severe acute pancreatitis. The prevention of these septic complications and subsequent development of multiple organ dysfunction syndrome remains a major focus for investigators, yet despite considerable clinical and experimental work addressing its etiology, septic complications remain high. Several studies have been designed to demonstrate the mechanism of origin of these septic complications with an attempt to define strategies for their prevention to improve patient outcomes. There is clear evidence that the origin of this secondary bacterial infection arises from enteric bacterial translocation secondary to disruption of the gut mucosal barrier during acute pancreatitis. Strategies designed to prevent secondary pancreatic infection include aggressive fluid resuscitation to maximize organ perfusion, early systemic antibiotic treatment or selective gut decontamination, and recently attempts to block mediators of the systemic inflammatory response. This discussion will summarize our present understanding of the etiopathogenesis of secondary bacterial 'superinfection' of necrotizing pancreatitis and how the initiation of enteral feeding early in the course of acute pancreatitis may prove to be an effective means of preventing and/or reversing the breakdown of the gut mucosal defense barrier.
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PMID:Early enteral feeding in severe acute pancreatitis: can it prevent secondary pancreatic (super) infection? 1115 1

This retrospective study describes 4 cases of canine babesiosis with histologically confirmed acute pancreatitis. In addition, 16 dogs with babesiosis are reported with serum amylase (>3500 U/l) and/or lipase (>650 U/l) activity elevations of a magnitude that would support a diagnosis of probable acute pancreatitis, although extra-pancreatic sources of the enzymes could not be excluded in these cases. Median time of pancreatitis diagnosis was 2.5 days post-admission, with primarily young (median age 3 years), sexually intact dogs affected. The development of pancreatitis was unrelated to the degree of anaemia at time of admission. In addition to pancreatitis, 80% of cases suffered from other babesial complications, namely icterus (13), acute respiratory distress syndrome (6), immune-mediated haemolytic anaemia (6), renal failure (3), haemoconcentration (2) and cerebral syndrome (2). Acute respiratory distress syndrome, renal failure and cerebral syndrome were associated with a poor prognosis, with 4 of the 5 dogs included in the overall 26% mortality rate having at least 1 of these complications. Haemolytic anaemia with ischaemia-reperfusion injury to the pancreas is proposed as a possible primary pathophysiological mechanism in babesial pancreatitis. Hypotensive shock, immune-mediated haemolytic anaemia, haemoconcentration and possibly altered lipid metabolism in babesiosis may also be involved. The previously postulated pro-inflammatory cytokine milieu of complicated babesiosis may underlie the progression, if not the primary initiation, of pancreatic pathology. Acute pancreatitis may represent the previously reported 'gut' form of babesiosis.
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PMID:Acute pancreatitis: a newly recognised potential complication of canine babesiosis. 1121 34

Septic complications are an important factor for the morbidity and mortality of acute pancreatitis. The gut has been identified as a source of infection early in the course of the disease allowing intestinal bacteria to translocate into pancreatic necrosis and other organs. Bacterial translocation is promoted by an impaired intestinal mucosal barrier which can be attributed to the reduced oxygen and substrate supply of the intestine during the early systemic response to the pancreatic injury. 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 nutritients, vitamins and trace elements. Following a discussion of the many aspects of bacterial translocation and gut derived sepsis, the role of the gut and nutrition for the development of septic complications in acute pancreatitis is summarized as follows: Early in the course of acute pancreatitis the gut is a target organ of the primary systemic inflammatory response (SIRS) to pancreatic injury. SIRS-induced gut barrier dysfunction promoting bacterial translocation makes the gut the motor for secondary (septic) complications. As a septic focus the gut becomes a target for therapeutic measures aimed at stabilizing the impaired gut barrier. Nutritive factors demonstrated to improve impaired gut barrier function include early enteral feeding and specific factors like glutamine which are essential for enterocytes and colonocytes in stress. Experimental data are presented to underline the significance of these nutritive factors and subsequent randomized multicenter trials performed to verify the positive experimental results are introduced. The effect of other nutritive factors (e.g. omega-3-fatty acids) has not yet been systemically investigated. Thus, experimental and clinical studies need to be performed for evaluating their effect on bacterial translocation and the disease course in acute pancreatitis.
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PMID:[Pancreatitis and nutrition. Significance of the gastrointestinal tract and nutrition for septic complications]. 1122 93


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