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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To examine whether the gut is a source of infection in acute pancreatitis, bacterial translocation and alterations of intestinal microecology and morphology were studied in 16 dogs. Dogs were colonized with a strain of Escherichia coli (E. coli 6938K) bearing the plasmid pUC4K, which confers kanamycin resistance. In eight dogs (group I), pancreatitis was induced by sodium taurocholate/trypsin injection. Eight other dogs (group II) underwent laparotomy only. The pancreas, mesenteric lymph nodes, peritoneal fluid, liver, and spleen were harvested 7 days later for culturing and histologic analysis. Identification of E. coli 6938K was accomplished by plasmid DNA analysis. Group I dogs had severe pancreatitis and ischemic changes in small bowel mucosa. Group II dogs had no changes. Translocation to the pancreas occurred in five dogs and to mesenteric lymph nodes in six dogs with pancreatitis. No translocation occurred in group II dogs (p < 0.05). In addition to E. coli 6938K, other gram-negative kanamycin-resistant species were isolated, including E. coli (other than 6938K) and Enterobacter cloacae. Enteric origin of these strains was confirmed by antibiography and plasmid DNA analysis. No overgrowth of cecal gram-negative bacteria was found. This study suggests that the gut is a primary source of infection in pancreatitis and that ischemic damage of intestinal mucosa may promote bacterial translocation.
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PMID:Plasmid labeling confirms bacterial translocation in pancreatitis. 831 Nov 34

It has been suggested that the gut plays a role in the development of bacterial complications, which are important contributors to morbidity and mortality in patients with acute pancreatitis. The present study evaluated the enteric bacterial translocation, bacterial homeostasis, and reticuloendothelial system function in experimental acute pancreatitis induced by intraductal injection of 5% sodium taurodeoxycholate in the rat. The incidence of bacterial translocation from the gut to mesenteric lymph nodes (MLNs) and lungs significantly increased after 12 hours and to the systemic circulation, ascites, and pancreas at 24 hours. The number of anaerobic bacteria and lactobacilli decreased in the colon and distal ileum from 6 or 12 hours, whereas the number of Escherichia coli increased from 12 hours. The systemic uptake rate of radiolabeled bacteria decreased from 6 hours after induction of acute pancreatitis. The uptake of radiolabeled bacteria by Kupffer cells decreased from 6 hours, whereas the uptake by macrophages from blood, lungs, and the intestine increased. A decrease in macrophage killing capacity was noted, reflected by an increase in the number of cultured viable bacteria from isolated macrophages. The whole-body oxygen extraction rate increased 4 to 24 hours after induction of pancreatitis, whereas the gut oxygen extraction rate decreased at 2 and 4 hours, followed by an increase at 12 to 24 hours. These data show that translocation of enteric bacteria occurs during the early stage of acute pancreatitis and that the MLN-thoracic duct-circulation may be a major route of bacterial dissemination. Compromised gut oxygen metabolism, overexaggerated intestinal macrophages, and impaired host immune function may be involved in the development of infectious complications associated with acute pancreatitis.
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PMID:Gut origin sepsis, macrophage function, and oxygen extraction associated with acute pancreatitis in the rat. 866 35

Despite the array of new diagnostic and therapeutic tools, acute pancreatitis remains a critical condition with a high rate of septic morbidity and mortality. To date the main cause of death is still the occurrence of septic complications. In 80% the cases, the microorganisms responsible for infection are of enteric origin and in 30% of the patients with septic shock, no evident focus of infection is recognized. Bacterial translocation is increasingly accepted as the main cause of infection, sepsis and multiple organ failure in these critically ill patients. The mechanisms facilitating the loss of gut barrier function are overgrowth of enteric bacteria and damage to the intestinal mucosa. Pancreatitis-induced immunosuppression may allow the systemic spread of translocated organisms and subsequent severe septic sequelae.
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PMID:[The intestine: a central organ in the pathogenesis of septic complications in acute pancreatitis]. 876 82

Two-hundred Wistar rats were allocated to 4 groups. The groups, 3 representing our acute pancreatitis model induced by intrabiliary injection of a trypsin/enterokinase mixture, were studied as follows: (A) no treatment; (B) given a daily 30-ml enema with 20 mg/kg rifaximin; (C) given a daily 30-ml enema with 20 mg/kg rifaximin plus lactitol 0.5 g/kg, and (D) given a daily 30-ml enema with warm saline. A further group of healthy rats was given an intrabiliary injection of 0.15 ml saline. Sacrifices were made after 6, 12, 24, 48 and 72 h of observation. Serial blood samples were drawn to measure pancreatic enzymes and endotoxin. At sacrifice, ascites, lymph nodes, pancreas, spleen, portal vein blood, arterial blood and bile were obtained for bacteriological culture. Both enema treatments brought about a significant improvement in survival. Enema treatments did not affect the serum level of pancreatic enzymes. A time-course increase in endotoxin level was observed in untreated rats. However, significantly decreased levels were observed after both enema treatments. Overall, ascites was the sample most frequently infected. Lymph nodes contiguous to the gut were found to be infected more frequently than those close to major vessels. The histological pancreatic damage was of a significantly lesser degree in both enema treatment groups. Virtually all severe necrotico-hemorrhagic pancreatic lesions were associated with bacterial infection. These data suggest that bacterial translocation plays a relevant role in the outcome of experimental necrotizing pancreatitis. Intra-abdominal spread and lymphatics seem to be the pathways most likely involved in such processes. Colonic cleansing by non-absorbable antibiotics and lactitol seems to exert a beneficial effect on the supervening infection of experimental necrotizing pancreatitis.
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PMID:Bacterial translocation in the course of acute pancreatitis: beneficial role of nonabsorbable antibiotics and lactitol enemas. 891 7

Gastrointestinal tract failure may be involved in the development of systemic septic complications in acute pancreatitis. Systemic and intestinal circulation, intestinal permeability and absorptive function were evaluated in the early course of acute pancreatitis induced in rats by retrograde intraductal injection of 0.2 ml of 5 per cent sodium taurodeoxycholate and 0.4 nmol trypsin. A decrease in systemic arterial pressure and intestinal blood flow and an increase in intestinal permeability as measured by the leakage of 125I-labelled human serum albumin from blood to lumen were noted in the distal ileum and colon, reaching statistically significant differences 6 h after induction of pancreatitis. The transport of small molecular markers (sodium fluorescein and 51Cr-labelled ethylenediamine tetra-acetic acid) through the distal ileum and colon in vitro from the mucosal to the serosal site in Ussing chambers significantly increased in the early periodic (20-60 min) of incubation, while the passage of a macromolecular marker (ovalbumin) demonstrated a definite increase at 60-120 min of incubation. D-Xylose absorption from the gut lumen to the portal vein was significantly less in acute pancreatitis than after sham operation. Intravenous administration of the hydroxyl radical scavenger dimethylsulphoxide prevented the compromised intestinal permeability and gut absorptive capacity induced by acute pancreatitis, but did not affect the reduced arterial pressure and intestinal microcirculation. Cytotoxic oxygen-derived free radicals may contribute to the development of alterations in intestinal permeability and absorptive function found in the early stage of acute pancreatitis in the rat.
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PMID:Alterations in intestinal function in acute pancreatitis in an experimental model. 902 31

Bacterial translocation (BT) from the gastrointestinal tract to mesenteric lymph nodes (MLN) and other extraintestinal organs is an important source of infection in acute pancreatitis (AP). Epidermal growth factor (EGF), a peptide hormone with trophic effects on gut mucosa, has decreased intestinal mucosal injury in septic rats and decreased burn-induced BT in mice. The purpose of this study is to examine whether EGF could affect BT in acute necrotizing pancreatitis. Forty-eight male Sprague-Dawley rats (250-350 g) were studied. AP was induced in Group I and Group II by pressure injection of 3% taurocholate and trypsin into the biliopancreatic duct (1 ml/kg of body weight). Group III and Group IV underwent laparotomy without induction of acute pancreatitis. Group I rats received human recombinant EGF (100 micrograms/kg, subcutaneously twice daily) and Group II rats received a similar volume of 0.1% bovine serum albumin as a placebo postoperatively. Group III and Group IV received EGF and placebo, respectively. At 48 hr postoperatively, blood was drawn for culture and amylase determinations. Jejunum and ileum were obtained to measure mucosal protein content, mucosal thickness, villus height, and crypt depth. Specimens from MLN, spleen, liver, pancreas, and cecum were harvested for pathology and culture of gram positive (G+), gram negative (G-), and anaerobic bacteria. Ileal mucosal protein levels were increased significantly in Group I (1.96 +/- 0.14 mg/cm) compared to Group II (0.95 +/- 0.15 mg/cm intestinal segment) (P < 0.01). Jejunal and ileal mucosal thickness, villus height, and crypt depth in Group I were significantly increased when compared to Group II (P < 0.05). All 12 rats in Group II had BT to MLN compared to 58% (7 of 12 rats) in Group I (P < 0.05). Thirty-three percent (4 of 12 rats) had BT to distant sites such as pancreas, spleen, liver, and/or blood in Group I vs 83% (10 of 12 rats) in Group II (P < 0.05). EGF treatment minimizes intestinal damage, decreases BT to MLN and bacterial spread to distant sites, and may be beneficial in preventing septic complications in AP.
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PMID:The effect of epidermal growth factor on the septic complications of acute pancreatitis. 920 65

We report a new case of idiopathic hypereosinophilic syndrome with multivisceral digestive failure. After an erroneous diagnosis of pancreatic cancer, the pathological examination of pancreaticoduodenectomy specimen demonstrated pancreatic fibrosis with eosinophilic infiltration without gastritis or duodenitis. The diagnosis of idiopathic hypereosinophilic syndrome was made three months later upon the classical criteria: a) blood eosinophilia of 1.5 G/L or more, persisting for more than 6 months; b) lack of evidence for any other recognised cause of eosinophilia: c) multiple organ systemic involvement: rheumatologic, cutaneous and digestive (pancreatitis, ascites and diarrhoea): d) previous history of allergic disease and increased plasmatic IgE levels; e) absence of leukemic markers. This case emphasises the difficulty in classifying eosinophilic infiltration of the gut and the possibility of transitional forms between eosinophilic gastro-enteritis and idiopathic hypereosinophilic syndrome. We argue that in case of eosinophilic infiltration of the gut, systematic research of multiple organ systemic involvement is mandatory.
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PMID:[Pancreatic involvement, ascites and diarrhea in idiopathic hypereosinophilic syndrome]. 929 82

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

This is a study on the efficacy and mechanism of rhubarb therapy for necrotizing pancreatitis in rats induce by intraductal infusion of 2% deoxycholate 0.4 ml/kg. The rats with such pancreatitis were orally fed with 10% rhubarb decoction 1.5 ml (treatment group n = 8) or normal saline 1.5 ml (control group n = 9) per 8 hours. Sham operated rats (sham group n = 8) were given intraductal infusion of normal saline 0.4 ml/kg. 48 hours after infusion, the rats were killed for studies of intestinal motility, serum endotoxin and amylase levels as well as bacterial cultures in messentary lymph nodes (MLN) and pancreas tissues. 5 rats died in the control group (5/9) and 1 died in the treatment group (1/8). Remarkable inhibition of gut motility was observed in control group, but gut motility was significantly improved by administration of rhubarb in treatment group. No rat died in the sham group and the rate therein were all free from endotoxemia or positive cultures. Endotoxin level of control group is much higher (61.36 +/- 28.30 pg/L) than that of treatment group (5.41 +/- 3.58 pg/L), (P < 0.001). Positive cultures were noted in most of MLN (4/4) and pancreas (4/4) in control group, but only 1 in MLN and 1 in pancreas were noted in treatment group. It is concluded that in the treatment of necrotic pancreatitis in rats rhubarb decoction is effective for promoting gut motility and preventing intestinal bacterial translocation.
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PMID:[Rhubarb decoction prevents intestinal bacterial translocation during necrotic pancreatitis]. 938 17

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


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