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

Cholescintigraphy with technetium-labeled biliary agents has great value in evaluation of the patient with suspected acute cholecystitis. Visualization of the gall bladder virtually excludes acute cholecystitis and obstruction of the cystic duct. Nonvisualization of the gall bladder, however, is not specific for acute cholecystitis and may also occur in some patients with chronic cholecystitis or pancreatitis. Interpretation of gall bladder nonvisualization, therefore, must be correlated with the clinical presentation. Biliary tract imaging is also useful in evaluation of some focal abnormalities within the liver, neonatal jaundice, detection of bile leaks or bile reflux, and biliary-enteric shunts. The role of technetium-labeled biliary agents in the evaluation of patients with jaundice is less clear. Excretion of tracer into the gut excludes complete biliary tract obstruction, but the test may be nonconclusive at higher serum bilirubin levels. If persistent common bile duct activity is observed with delayed excretion into the gut, the diagnosis of partial obstruction may be made, but this procedure will be inconclusive if the common bile duct is not visualized and/or significant hepatocellular disease is present. Ultrasonography and abdominal CT are the preferred tools for the diagnosis of biliary tract obstruction at present, but newer biliary tract agents which achieve better hepatic extraction and greater bile concentration at high serum bilirubin levels may improve the diagnostic efficacy of cholescintigraphy.
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PMID:Radionuclide imaging of the biliary tract. 703 71

A mass associated with the gastrointestinal tract was detected by sonography in 33 patients. Etiologies included primary or metastatic tumor; intussusception; inflammation secondary to bowel infarction, pancreatitis, or irradiation; and a dilated, fluid-filled gut related to retained gastric contents, obstruction, ileus, or an ileal bypass. Mesenteric or omental changes were identified with inflammation and frequently with metastatic disease. The diagnosis was confirmed by repeat sonography, abdominal radiography, barium examination of the small bowel, computed tomography, surgery, or autopsy. Ultrasound patterns are characteristic in tumor, intussusception, and inflammation; specific features allowing differentiation between tumor and inflammation are described. Colonic haustra, valvulae conniventes, or bowel contours and peristalsis on real-time sonography are helpful in identifying fluid-filled bowel loops.
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PMID:Ultrasound patterns of disorders affecting the gastrointestinal tract. 736 Sep 50

To examine the possible secretion of lysosomal enzymes into the pancreatic juice in rats stimulated with pancreatic secretagogues under both physiological and pathological conditions, we investigated the changes in the secretion of cathepsin B, as a lysosomal enzyme, into pancreatic juice with stimulation of 5 different doses (0.1, 0.2, 0.5, 1.0, and 1.5 micrograms/kg.hr) of caerulein. Control rats had only pancreatic duct cannulation. In other rats, the pancreatic duct was obstructed for 3 hours and secretin was infused (0.2 CU/kg.hr). Caerulein stimulated the secretion of cathepsin B into the pancreatic juice in a dose-dependent manner, as in amylase secretion, and caerulein in higher doses (1.0 and 1.5 microgram/kg.hr) inhibited cathepsin B output as it did amylase output. There was a significantly high positive correlation between cathepsin B output and amylase output after stimulation with caerulein. The secretion of several other lysosomal enzymes was also stimulated by caerulein. Blockage of the pancreatic duct for 3 hours caused a significant but moderate rise in serum amylase levels. Redistribution of cathepsin B activity in the pancreatic subcellular fractions was noted with an increase in the amount of cathepsin B recovered from zymogen-rich pellets after 15 min of centrifugation at 1300 x g. These changes after temporary pancreatic duct obstruction are very similar to those previously noted during the early stage of diet-and caerulein-induced experimental pancreatitis and suggest colocalization of lysosomal enzymes and digestive enzymes. In addition, in duct obstructed rats, the secretion of cathepsin B and other lysosomal enzymes stimulated by caerulein was significantly greater than in animals with free-flowing pancreatic juice. These results indicate that lysosomal enzymes are secreted into pancreatic juice after stimulation by gut hormones in the same manner as classical pancreatic digestive enzymes such as amylase. Moreover, lysosomal enzymes which colocalize with zymogen granules in rats with short-term pancreatic duct obstruction are also secreted into pancreatic juice together with digestive enzymes after stimulation with gut hormones. These findings suggest that lysosomal enzymes are present in zymogen granules under normal conditions and that they may play pathophysiological roles in pancreatic juice. They also contribute to an understanding of the pathogenesis of pancreatitis, since cathepsin B can activate trypsinogen.
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PMID:Lysosomal enzyme secretion into pancreatic juice in rats injected with pancreatic secretagogues and augmented secretion after short-term pancreatic duct obstruction. 752 87

Pancreatic infection from gut-derived bacteria has emerged as the major cause of death in necrotizing pancreatitis. Bacterial overgrowth of indigenous enteric organisms as a consequence of guts stasis (ileus) represents a potential initial event in this process. The present study was designed to examine the interrelationships between intestinal transit, enteric bacteriology, and the translocation of bacteria from the gut lumen to mesenteric lymph nodes and splanchnic viscera during experimentally induced acute pancreatitis. Male rats underwent pancreaticobiliary duct ligation (PBDL) or sham surgery and were sacrificed after 24, 48, or 96 hr. Severity of pancreatitis was assessed with histology, tissue water content, and amylase and lipase levels. Intestinal transit was measured with fluorescent tracers. Blood, mesenteric lymph nodes (MLNs), splanchnic organs, and gut luminal contents were subjected to bacteriologic analysis. PBDL was followed by biochemical and histologic evidence of progressive pancreatic injury at each time interval. Enteric bacteria within the gut and in adjacent MLNs increased as intestinal transit decreased after PBDL-induced pancreatic inflammation. Surprisingly, all parameters returned to control levels by 96 hr in spite of progression of pancreatic inflammation.
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PMID:Intestinal transit and bacterial translocation in obstructive pancreatitis. 764 83

In the absence of causative therapy of acute pancreatitis the management of the disease focus on treatment and prevention of complications and symptoms. In mild acute pancreatitis intravenous fluid administration, analgetics and avoidance of oral fluid or food intake is sufficient in most cases. The treatment of severe pancreatitis involves identification of pancreatic and peripancreatic necroses, best demonstrated and evaluated by contrast-enhanced computerized tomography (CT). Infection of such necroses is the most common cause of death from acute pancreatitis. Recent data suggest that antibiotic prophylaxis is worthwhile and it should therefore always be instituted in the severe form of the disease. Careful monitoring of vital functions is mandatory and early treatment with assisted ventilation and renal dialysis is advised. Adequate volume replacement and nutritional support is important. The role of the gut in the development of infected necroses is becoming increasingly obvious. Also, the absence of food in the intestine may increase the intestinal barrier damage. Therefore, enteral nutrition is discussed as a logical step in pancreatitis treatment. However, the food should be delivered below the ligament of Treitz (below the area of the cholecystokinin (CCK) cells) as CCK stimulation probably worsen the course of the disease.
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PMID:Conservative treatment in acute pancreatitis. 766 93

Multiple organ system failure (MOSF) is a severe clinical process that causes progressive renal and liver failure. Acute pancreatitis (AP) can cause MOSF. Several series document high mortality rate from necrotizing forms is associated with MOSF. The authors observed 199 cases of acute necrotizing pancreatitis in 10 years, with a mortality rate of 14.1%. MOSF occurred in 14 cases, resulting in death in 100% of affected patients. In AP, MOSF follows hemodynamic abnormalities suspected to be secondary to activation of kinins system and other vasoactive peptides that are responsible for pathogenetic mechanism of disease. Similar hemodynamic abnormalities can be observed in septic shock. Then many authors suppose causes of MOSF in AP are local (abscess, infection of pancreatic necrosis) and systemic septic complications or translocation of enteric bacteria or their endotoxins from the gut lumen. So it is important to provide prophylactic use of antibiotics that are effective against expected bacteria and also achieve a therapeutic concentration in pancreatic tissue and juice. Fluid replacement, nutritional support and other therapeutic strategies must be employed to prevent MOSF. When the MOSF is clearly developed, medical and surgical measures are unuseful and the mortality rate is very high also in an intensive care unit.
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PMID:[The multiple-organ failure syndrome in acute pancreatitis. Its pathogenesis and treatment]. 775 79

This chapter reviews the therapeutic use of octreotide in a variety of pancreatic disorders, including acute pancreatitis, in the prevention of postoperative and post-ERCP pancreatitis, in the control of postoperative pancreatic fistulae, and in chronic pancreatitis for the control of pain and of pseudocysts and ascites. The review also discusses the use of octreotide in intestinal disorders of motility, gastrointestinal bleeding, intestinal fistulae and refractory diarrhoea, including the diarrhoeas of AIDS, diabetes, short gut, chemotherapy, ileostomy and gastric surgery. The use of octreotide in neuroendocrine tumours, both for therapy and diagnostic imaging, is reviewed briefly. The paucity of adequately controlled studies in many of these situations is indicated and the potential usefulness of octreotide estimated.
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PMID:Expanding uses of octreotide. 794 61

Intestinal pseudo-obstruction is a rare and heterogeneous syndrome caused by severe disorders of gastrointestinal motility. It affects the entire gastrointestinal tract or only segments, giving rise to symptoms and physical signs of a mechanical obstruction of the gut despite negative results of all imaging procedures. The disease may occur in an acute or chronic form. The acute and some of the chronic forms develop as complication of other gastrointestinal or extragastrointestinal diseases, e.g. pancreatitis or systemic sclerosis. The primary forms of chronic intestinal pseudo-obstruction are most often caused by genetic neuromuscular disorders of the gastrointestinal tract, e.g. familial visceral neuropathies. The diagnosis of intestinal pseudo-obstruction is based on the exclusion of a mechanical obstruction of the gut by fluoroscopy and endoscopy. Manometric studies may disclose the underlying disorder of gastrointestinal motility. In a few patients, results of all imaging procedures as well as motility studies are inconclusive, and laparatomy (with full thickness biopsy of the gut wall) has to be performed to exclude mechanical obstruction of the gut. Acute intestinal pseudo-obstruction is treated by elimination of the underlying intestinal or extraintestinal disease. In case of extensive colonic dilatation with imminent colonic perforation endoscopic decompression should be evaluated. Treatment of chronic pseudo-obstruction aims to correct the underlying motility disorder. Usually, restoration of normal gastrointestinal motility is attempted by prokinetic drugs, but often their effect is limited. Surgery may be helpful in the few patients in whom the disease is confined to small segments of the gut, leaving all other parts unaffected. Some patients with otherwise intractable disease may need long-term parenteral nutrition.
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PMID:[Intestinal pseudo-obstruction]. 816 Jan 67

A woman ingested 400 ml of leather tanning solution containing 48 g of basic chromium sulphate (CrOHSO4). This substance forms hydrogen ions and trivalent chromium when it reacts with tissue proteins. The patient died of cardiogenic shock, complicated by pancreatitis and gut mucosal necrosis and haemorrhage. There are no reported cases of toxicity due to oral ingestion of trivalent chromium. Toxicity of hexavalent and trivalent chromium is discussed and suggestions made for management of future cases.
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PMID:Death by tanning--a case of fatal basic chromium sulphate poisoning. 820 Oct 96

Infections from enteric bacteria are a major cause of morbidity and mortality during acute pancreatitis (AP), but the pathways by which these organisms reach distant organs remains speculative. Experiments were conducted to determine if bacterial translocation could be a mechanism for infection during this disease. AP was induced in Lewis rats by i.v. infusion of caerulein (experiment I) or ligation of the head of the pancreas (experiment II). In a third experiment, rats were gavaged with 1 x 10(8) 14C-radiolabeled Escherichia coli and pancreatitis was induced with caerulein. Results in all three experiments showed that AP increased the number of viable bacteria recovered in peritoneal fluid, mesenteric lymph nodes (MLN), liver, lungs, and pancreas. Radionuclide counting indicated that AP enhanced the gut permeability to 14C E. coli. To estimate the impact of AP on the magnitude of translocation and on the ability of the host to clear bacteria, the nuclide and colony-forming units (CFU) ratios were calculated between animals with and without AP. Blood, peritoneal fluid, and MLN had the highest nuclide ratio. During AP, these tissues may be the principal routes for bacterial spreading from the gut lumen. Peritoneal fluid, pancreas, and lung were the tissues with the highest CFU ratio. Bacterial killing ability of these tissues is likely impaired during AP.
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PMID:Bacterial translocation: a potential source for infection in acute pancreatitis. 830 91


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