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

Diagnostic cholangiopancreatography is a useful procedure which is attended by a relatively low incidence of immediate or delayed complications. Perforation of the esophagus or gut, myocardial infarction, hemorrhage, cholangitis, and pancreatitis are the most commonly reported morbid or fatal events. This paper reported a case of retropharyngeal abscess which led to tracheal compression requiring an emergency tracheostomy and antibiotic therapy after a routine ERCP procedure. This dramatic case pointed out an unusual but potentially fatal complication of diagnostic ERCP.
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PMID:Retropharyngeal abscess after endoscopic retrograde cholangiopancreatography: an uncommon but potentially fatal complication. 62 36

The plasma gastric inhibitory polypeptide (GIP), pancreatic glucagon-like immunoreactivity (PGLI), and gut glucagon-like immunoreactivity (GGLI) responses to oral glucose have been measured in five patients with chronic pancreatitis (with diabetic glucose tolerance tests) and in matched nondiabetic controls. Plasma GIP levels rise rapidly after glucose ingestion before changes in circulating glucose and insulin concentration. Patients with pancreatitis have a greater than normal GIP response to oral glucose, which may account for the relatively unimparied insulin response to oral glucose in these patients compared with that to iv glucose, as has been previously found. Patients with pancreatitis also have a paradoxical rise in PGLI and an exaggerated rise in GGLI concentration following oral glucose.
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PMID:Gastric inhibitory polypeptide (GIP) in chronic pancreatitis. 127 May 74

To investigate the possible secretion of lysosomal enzymes into pancreatic juice during stimulation with a pancreatic secretagogue under both physiological and pathological conditions, we measured the amount of cathepsin B, a lysosomal enzyme, in the pancreatic juice during the infusion of 6 different concentrations of caerulein (0.02, 0.05, 0.2, 0.5, 1.0, and 2.0 micrograms/kg. hr). In one group of rabbits the pancreatic duct was only cannulated (free-flow group); in others the pancreatic duct was obstructed for 7 hours and secretin was infused at 0.2 CU/kg. hr (obstructed group). In addition, we evaluated the effect of the intraduodenal instillation of a liquid meal (2 g/kg) on the secretion of lysosomal enzymes into pancreatic juice. Caerulein stimulated the secretion of cathepsin B into pancreatic juice in a dose-dependent manner, as it did that of amylase, and at higher concentrations of caerulein (1.0 and 2.0 micrograms/kg. hr), both cathepsin B output and amylase output were decreased. There was a significant positive correlation between cathepsin B output and amylase output into pancreatic juice during stimulation with caerulein. Blockage of the pancreatic duct for 7 hours caused a significant rise in serum amylase levels and a redistribution of cathepsin B activity in the pancreatic subcellular fractions, as a result of which an increased amount of cathepsin B was recovered in the pellet obtained by 1000 x g centrifugation for 15 min, which contained many zymogen granules. These changes noted after short-term pancreatic duct obstruction are very similar to those previously noted in the early stage of diet-and caerulein-induced experimental pancreatitis, suggesting the colocalization of lysosomal enzyme and digestive enzymes. In the duct-obstructed animals, the secretion of cathepsin B stimulated by caerulein was significantly greater than in the free-flow group. Furthermore, the intraduodenal instillation of a liquid meal caused the secretion of cathepsin B into the pancreatic juice along with amylase. These results indicate that under physiological conditions, such as food intake, lysosomal enzymes are secreted into the pancreatic juice in response to stimulation by gut hormones in the same manner as classical pancreatic digestive enzymes. Moreover, zymogen colocalized with lysosomal enzymes in duct-obstructed animals is secreted into pancreatic juice in increased amounts together with digestive enzymes; this finding suggests that lysosomal enzymes play important pathophysiological roles in pancreatic juice and that acinar cells are altered to maintain cellular organization by secreting the potentially dangerous lysosomal enzymes. This pancreatic duct-obstructed rabbit model should be useful in clarifying the early events of acute pancreatitis.
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PMID:Secretion of lysosomal and digestive enzymes into pancreatic juice under physiological and pathological conditions in rabbits. 138 3

This study was performed to elucidate the role of bacterial infection in acute pancreatitis in young female mice fed a choline-deficient diet supplemented with 0.5% DL-ethionine (CDE diet). Mice were randomly classified into two groups: one had been fed CDE diet alone (nonantibiotic group), the other was fed a CDE diet with oral administration of antibiotics (antibiotic group). Survival rates at 96 and 144 h after introduction of the CDE diet were significantly improved in the antibiotic group, 25.0 and 19.4%, respectively, as compared with 3.6 and 0% in the nonantibiotic group (p, 0.05). Aerobic and anaerobic bacterial cultures of blood, ascites, spleen, and pancreas were taken from living mice 72 h after introduction of the CDE diet. Positive bacterial growth from one or more of the specimens occurred in 29.4% of the nonantibiotic group, and in 10.0% of the antibiotic group. Mice with pancreatic necrosis had a higher positive culture rate, 62.5% in the nonantibiotic group vs 20.0% in the antibiotic group. These results suggest that reduction of intestinal flora in mice inhibits secondary infection caused by bacterial translocation and improves survival in diet-induced hemorrhagic pancreatitis. We believe the development of bacterial infection of gut origin may be a factor influencing mortality in severe pancreatitis.
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PMID:Role of bacterial infection in diet-induced acute pancreatitis in mice. 158 55

In 76 male wistar rats with a median weight of 340 g acute pancreatitis was induced by injection of 2% sodium taurocholate into a temporarily closed duodenal loop. 40 animals received an additional cecostomy (group B), the others served as controls (group A). The postoperative figures for amylase, leucocyte count, and hemoglobin were nearly identical in both groups. According to histologic criteria acute pancreatitis was comparable in both groups, too. In nine rats endotoxin was found elevated postoperatively (13.4%). Seven animals belonged to the control (22.6%) and only two to the cecostomy group (5.6%). The difference was statistically significant (p less than 0.05). Also the differences between the median serum endotoxin levels reached statistic significance (79 ng/l in group B vs. 219 ng/l in group A). Mortality was significantly increased in endotoxin-positive animals (42.9% vs. 19.4%). Additionally, among the animals of the control group alterations of the colonic mucosa were observed more frequently than in the cecostomy group. The results are in favour of a translocation of endotoxin from the gut lumen into the circulation during acute experimental pancreatitis.
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PMID:[Effect of cecostomy on the pathophysiology and prognosis of acute experimental pancreatitis]. 161 79

Eight cases of extensive colonic necrosis or colonic fistula secondary to gastric surgery or surgical drainage of necrotic pancreatitis were seen over a 2-year period. Four of the patients died, and all the survivors had fistula only. Diagnosis of such lesions is often difficult, and fistulography is recommended when a pancreatic abscess is drained. Resection of the gut is not mandatory in cases of fistula.
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PMID:Colonic necrosis or fistula following pancreatitis or gastric surgery. 167 8

The metabolic response to injury occurs after a diverse group of surgical injuries including major surgical intervention, shock, infection, and sources of inflammation such as pancreatitis. The response is mediated by the macroendocrine system, the autonomic nervous system, and the cell-cell communication system. The clinical manifestations include now well-described clinical, physiologic, and metabolic characteristics. The approach of aggressive source control, invasive circulatory resuscitation, and nutrition/metabolic support has been associated with an overall reduction in morbidity and mortality. In those patients who do not respond to this approach, the disease process progresses to multiple organ failure syndrome with its associated high mortality. Altering the route of feeding, preventing single nutrient and generalized nutrient deficiency, and reducing nosocomial infections with selective gut decontamination have not significantly altered the course or outcome of the disease process in this latter group of patients with persistent hypermetabolism. The available data support the position that this persistent hypermetabolism represents abnormal metabolic regulation resulting in persistence of the inflammatory response with associated suppression of the immune defenses. A number of research approaches are being taken to understand and modulate this abnormal state of regulation. Because of the role of specific nutrients in these regulatory processes, beyond their role in classic nutrition support, nutrients such as arginine n-3 polyunsaturated fatty acids, and RNA are being evaluated for their ability to modulate inflammation and to improve immune function. Preliminary results are encouraging.
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PMID:Nutrient modulation of inflammatory and immune function. 170 26

Acute pancreatic duct obstruction causes hyperamylasemia and mild pancreatic inflammation. We hypothesized that bile exclusion from the gut, which stimulates pancreatic secretion, exacerbates acute pancreatitis caused by pancreatic duct obstruction. Rats were surgically prepared with gastric, duodenal, bile, and pancreatic fistula catheters and a jugular vein catheter. After a 4-day recovery, groups of rats (a) served as controls, (b) had complete pancreatic duct obstruction for 6 h, or (c) had bile excluded from the gut for 24 h and then, during the final 6 h, complete pancreatic duct obstruction. Plasma amylase was measured, and all rats were euthanized at the end of experiments. Each pancreas was excised and weighed, and portions were fixed in formalin and glutaraldehyde. In blind fashion, each pancreas was examined under light microscopy and assigned a pancreatitis score based on presence of edema and severity of acinar cell changes and inflammation. Acute pancreatic duct obstruction was associated with increased pancreas weight, hyperamylasemia, and elevated pancreatitis score; moderate acinar cell vacuoles, which were observed in the cytoplasm near the basolateral membrane, and loss of microvilli were noted with electron microscopy. Bile exclusion from the gut exacerbated the acute pancreatitis caused by pancreatic duct obstruction; acinar cell distortion and destruction, as well as marked inflammation, were seen microscopically. These observations suggest that the absence of intestinal bile contributes to the pathogenesis of acute pancreatitis associated with pancreatic duct obstruction.
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PMID:Bile exclusion from the gut exacerbates acute pancreatitis caused by pancreatic duct obstruction in rats. 171 90

52 patients with normal pancreas, pancreatitis and pancreatic tumors were examined by magnetic resonance imaging (Magnetom 0.5 T). Using T1-, proton density- and T2-weighted spin-echo sequences images were obtained before and after oral administration of Gadolinium-DTPA (Gd-DTPA, 1 mM, 15 g/l Mannit, 5-13 ml/kg). Gd-DTPA resulted in hyperintense labeling of small bowel in all sequences and improved visualization of pancreatic head, body and tail in 15, 14 and 7 of 27 patients with normal pancreas and in 17, 8 and 6 of 25 patients with diseased pancreas. Better delineation of pseudocysts and tumorous gut wall invasion were diagnostically profitable. With regard to motion artifact reduced MRI of the intestine using fast sequences Gd-DTPA may be a suitable oral contrast agent to improve the imaging of the pancreas.
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PMID:[Gadolinium-DTPA as an oral contrast medium for magnetic resonance tomography of the pancreas]. 184 93

Between October 1987 and July 1990 a prospective, nonrandomized, preliminary study was carried out to assess the efficacy of Sandostatin in treating complex pancreatic and gastrointestinal disorders. The study group consisted of 18 women and 12 men, ranging in age from 23 to 80 years (mean 50 years), in whom conventional medical or surgical therapy, or both, had failed. Nineteen patients had pancreatic disease (5 had chronic pancreatitis, 8 acute necrotizing pancreatitis and 6 pancreatic fistula). Thirteen patients had disorders of the small intestine (7 had enterocutaneous fistula and 6 diarrhea-associated short-gut syndrome). Sandostatin was found to be effective in the closure of pancreatic (five of six cases) and enterocutaneous fistulas (five of seven cases), of benefit in controlling the pain associated with chronic pancreatitis (three of five cases) and of some use in achieving short-term control of intractable diarrhea in patients with short-gut syndrome (five of six cases). It was of particular benefit in the management of acute necrotizing pancreatitis. The standard principles of surgical management must be adhered to when using Sandostatin to treat patients with these disorders. Sandostatin can not correct underlying problems such as pancreatic-duct obstruction, malignant disease or unresolved sepsis. These preliminary results justify more widespread use of Sandostatin as part of a prospective randomized and controlled multicentre trial.
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PMID:Sandostatin in the management of nonendocrine gastrointestinal and pancreatic disorders: a preliminary study. 205 54


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