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

Three hundred patients with acute pancreatitis have been studied. Pancreatitis was associated with alcoholism in 207, biliary tract disease in 51 and other conditions in 42. Twenty-two patients died, and an additional 34 patients required more than one week of treatment in the intensive care unit. Retrospective analysis of the first 100 patients identified 11 objective findings which correlated with the occurrence of serious illness or death. They were, on admission, age over 55 years, blood glucose level over 200 milligrams per cent, white blood count over 16,000 per cubic millimeter, serum lactic dehydrogenase level over 350 International units per liter and serum glutamic-oxalacetic transaminase level over 250 Sigma Frankel units per cent. During the initial 48 hours of therapy, the findings were hematocrit value decrease over 10 percentage points, serum calcium level below 8 milligrams per cent, base deficit over 4 milli-equivalents per liter, a blood urea nitrogen level increase over 5 milligrams per cent, estimated fluid sequestration over 6 liters and arterial oxygen tension less than 60 millimeters of mercury. Prospective application of these signs in the latter 200 patients permitted the accurate early identification of those with severe pancreatitis. Only one of 162 patients with fewer than three of these early features was seriously ill or died, while 24 of 38 patients with three or more early positive findings were seriously ill or died. The objective early identification of patients with severe pancreatitis permits more vigorous management of this group and also provides a basis for the selection of patients for the evaluation of proposed improved therapies. Percutaneous peritoneal dialysis in severe pancreatitis was evaluated in ten patients, with three or more positive early signs, who were randomly assigned to dialysis or continued conventional care. Morbidity was strikingly reduced in patients who underwent dialysis, and while death or more than nine days of intensive care occurred in two of five patients who did not receive dialysis, all five patients having dialysis recovered after fewer than nine days of intensive care treatment. Serious illness or death occurred in 31 of the first 100 patients but in only 26 of the more recent 200 patients. There has been a similar fall in mortality from 15.0 to 3.5 per cent. Factors which may contribute to this improvment include the objective early identification of patients with severe disease, the avoidance of early laparotomy whenever practical, the prolongation of nasogastric suction until all evidence of pancreatic inflammation has resolved, careful monitoring of respiratory function and early treatment of pulmonary complications and peritoneal dialysis in patients with severe disease.
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PMID:Prognostic signs and nonoperative peritoneal lavage in acute pancreatitis. 94 Oct 75

Despite the potential utility of intraoperative manometry of the sphincter of Oddi, limited data are available validating its use. The current study was undertaken to validate the method of intraoperative sphincter of Oddi manometry by comparing the pressure tracings obtained at operation (transduodenal sphincteroplasty and transampullary septoplasty) and endoscopy (preoperative) in the same group of patients. Seventy-four patients with idiopathic pancreatitis or unexplained disabling pancreaticobiliary pain had sphincter of Oddi manometry performed endoscopically and intraoperatively within six weeks of each other. Thirty-five patients had manometric evaluation of the bile duct segment of the sphincter of Oddi. The mean basal sphincter pressure determined endoscopically and intraoperatively was 41.1 +/- 6.4 millimeters of mercury (mean plus or minus standard error of the mean) and 42.0 +/- 6.8 millimeters of mercury (not significantly different, p > 0.05), respectively. There was no significant difference between the biliary sphincter phasic pressure, phasic frequency and phasic duration, as recorded by the two techniques. Fifty-five patients had manometric evaluation of the pancreatic duct sphincter. The mean basal sphincter pressure determined endoscopically and intraoperatively (after biliary sphincteroplasty) was 111.9 +/- 9.9 millimeters of mercury and 102.7 +/- 8.7 millimeters of mercury, respectively (not significantly different, p > 0.05). There was no significant difference in the pancreatic sphincter phasic duration and phasic frequency determined by the two techniques. However, the pancreatic sphincter phasic pressure was significantly higher when measured endoscopically (p < 0.001). Overall, 70 percent of patients benefited from surgical sphincter ablation therapy. Patients with an elevated basal sphincter pressure determined intraoperatively were more likely to improve than those with a normal basal sphincter pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of intraoperative and endoscopic manometry of the sphincter of Oddi. 144 Jan 68

Vascular mechanisms play an important but controversial role in the pathogenesis of acute pancreatitis. In experimental animals, injection of wax, powder, air, mercury, and microspheres into the pancreatic artery causes pancreatitis by end artery occlusion with resulting cellular infarction. Larger microspheres do not cause pancreatitis because collateral blood flow is preserved. Clinical evidence, such as microthrombi and atheromatous emboli in the pancreatic artery of patients with pancreatitis, supports pancreatic infarction as an etiologic agent. Experimental and clinical studies have suggested that pancreatic ischemia may also cause pancreatitis, but these studies have not been conclusive. We have compared five hours of total occlusion of the pancreaticoduodenal artery along with four hours of reperfusion to bile injection into the pancreatic duct as causes of pancreatitis. Bile injection caused a significant increase in serum amylase, activation of trypsin in pancreatic exudate, and histologic evidence of necrotizing pancreatitis. Pancreatic blood flow decreased as pancreatitis developed. Ischemia for five hours did not cause a significant increase in serum amylase or activation of trypsin in pancreatic exudate. Only edema was seen histologically, but there was no necrosis. Pancreatic blood flow increased with reperfusion. We believe ischemia aggravates, but does not initiate pancreatitis. Ischemia does not induce inflammation and necrosis in the pancreas, although infarction does.
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PMID:Mechanisms of acute pancreatitis. Vascular etiology. 174 44