Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The rate of clearance of technetium-99m labelled diethylene triamine pentacetic acid (99mTc DTPA) was measured in 32 patients with adult respiratory distress syndrome to determine if a more rapid clearance rate, possibly reflecting a more severe abnormality of pulmonary function, was associated with a reduced likelihood of recovery from pulmonary failure. Although the mean rate of clearance from lung to blood (T1/2LB) of 99mTc DTPA was more rapid in the patients (T1/2LB = 29 (SEM 3.2) min than in 42 normal subjects (T1/2LB = 59 (1.8)min), there was no difference between the clearance rate in the 18 patients who recovered from respiratory failure (T1/2LB = 31 (5) min) and the 14 who died (T1/2LB = 27 (4) min). Additionally, not all patients studied had abnormally rapid clearance rates. In 12 of the 32 patients the T1/2 fell within the range for normal individuals; this was found more commonly in patients who were predisposed to develop adult respiratory distress syndrome by pancreatitis or massive blood transfusion. These data suggest that a single measurement of 99mTc DTPA clearance in patients with established respiratory failure and adult respiratory distress syndrome is of no value in assessing the likelihood of recovery from this condition.
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PMID:Failure of aerosolised 99mTc DTPA clearance to predict outcome in patients with adult respiratory distress syndrome. 332 12

The adult respiratory distress syndrome (ARDS) is a frequent feature of acute pancreatitis. Amylase and lipase values were determined in samples of bronchial secretions in two patients with endotracheal intubation and under supportive ventilation for severe hypoxemia occurring during the course of acute pancreatitis. A pancreatico-bronchial fistula was suggested in both cases. In one case, an endoscopic retrograde pancreatography was performed and demonstrated a fistula between the pancreatic body and the left bronchial tree. Arterial pH values decreased following pancreatography. Splenopancreatectomy was performed in one case, and necrosectomy associated with left pulmonary lobectomy in the other. Documented cases of pancreaticobronchial fistulas have been rarely reported to date. A retrospective study of 10 patients with ARDS was made among 32 patients undergoing laparotomy for objectively recognized necrotizing pancreatitis. A pancreatico-bronchial fistula could be incriminated in three cases. This 30 p. 100 prevalence has to be re-evaluated in the light of serial determinations of amylase and lipase levels in patients with ARD and endotracheal intubation in the course of pancreatic disease. In these patients, high levels of amylase and lipase in bronchial secretions, the use of iso-osmolar X-ray colloids could be helpful in protecting the alveolar membrane against osmolar injury during pancreatography.
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PMID:[Acute respiratory distress caused by pancreatico-bronchial fistula in acute pancreatitis. Apropos of 2 cases]. 365 19

An experimental model of acute pancreatitis in rats has been used to study intrapulmonary 125I-fibrinogen and 111In-platelet deposition. Pancreatitis caused a significant increase in wet lung weight compared to normal, and this could be abolished by heparin or aspirin pretreatment. 125I-fibrinogen was deposited in the lungs of animals to a significantly greater degree than in controls (P less than 0.01). 125I-fibrinogen deposition was reduced to control levels by pretreatment with aspirin or heparin (P less than 0.05). The uptake of radiolabeled platelets was greater in pancreatitis than in controls (P less than 0.001). Pancreatitis appears to be responsible for platelet entrapment in the lungs. Platelet uptake was reduced by heparin treatment but unaffected by aspirin therapy.
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PMID:111In-platelet and 125I-fibrinogen deposition in the lungs in experimental acute pancreatitis. 369 53

Injection of infected human bile into a closed duodenal loop in the rat consistently produces lethal pancreatitis with severe pulmonary damage. Lung abnormalities, resembling the human adult respiratory distress syndrome (ARDS) are frequently seen in this model and are usually ascribed to the pancreatitis. Similar pulmonary problems are seen in the human form of acute pancreatitis. Recently, it has been suggested, that the lung changes in the experimental animal are more likely to be due to bacteremia than to the pancreatitis. The aim of this study was to determine whether bacteremia occurred in this model, and if so, to determine whether bacteremia alone, in the absence of pancreatitis could produce this lung damage. A group of rats underwent induction of acute pancreatitis by a closed duodenal loop method and were compared to two groups comprising a closed small bowel loop bile infusion preparation, isolated from the pancreas, and a control group of rats undergoing a "sham" gastrotomy. Both pancreatitis and closed small bowel groups of animals were found to be bacteremic when sacrificed at 6 hr. The lungs from the animals with pancreatitis were significantly heavier than those in the other groups and scanning electron micrographs of the lungs in pancreatitis showed gross abnormalities, with marked increases in the alveolar wall thickness. The lungs in the closed small bowel loop preparation were indistinguishable from a control sham gastrotomy group of non-bacteremic rats. These results indicate that although the closed duodenal loop model of pancreatitis produces bacteremia, pancreatitis is necessary for development of pulmonary abnormalities.
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PMID:Bacteriology of the closed duodenal loop model of acute pancreatitis and ultrastructural changes induced in the lungs. 378 44

The current study was designed to characterize toxic substances in hemorrhagic ascitic fluid by using in vivo dogs model and to examine the toxicity of hemorrhagic ascitic fluid by using an in vivo mice model injecting the fluid intraperitoneally. Our experiment showed that high levels of bradykinin, histamine and prostaglandin E were found in serum and in hemorrhagic ascitic fluid which reported as toxic substances during severe pancreatitis. A similar finding was also obtained clinically in four patients with severe acute pancreatitis. The mortality rate on 72 hours following the intraperitoneal injection of 2.0 and 3.0 ml of ascitic fluid were 66.0% and 89.7% respectively. Mice which died following the injection of ascitic fluid showed shock lung at autopsy. These results indicate that peritoneal lavage might be an effective method for the treatment of severe pancreatitis. We evaluated 25 patients with severe acute pancreatitis clinically. Laparotomy and drainage operations were performed in 16 patients of these patients. Twelve among 16 patient had good results. The cause of death were multiorgan failures.
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PMID:[Pathophysiology and treatment of severe pancreatitis]. 408 46

The adult respiratory distress syndrome has been associated with acute pancreatitis in 5-8% of patients. to determine, in a quantitative manner, the effects of acute, hemorrhagic pancreatitis on alveolar epithelial permeability, we studied two groups of dogs (group 1 - sham-operated, 7 dogs; group 2 - surgically induced pancreatitis, 7 dogs) and measured the flux of 10,000-20,000 molecular weight dextran and albumin (69,000 molecular weight), from the blood to the saline-filled lung. Following the surgical procedure (day 1), serum amylase levels increased significantly (397 +/- 70-1,268 +/- 95 dye units) in group 2 but not in group 1. Alveolar epithelial permeability (expressed as T1/2 time in minutes to 50% equilibration between blood and lung liquid) did not increase in either group for dextrans or albumin. We conclude that experimental acute pancreatitis does not cause an increase in alveolar epithelial permeability for molecular weight substances up to 69,000 daltons.
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PMID:Pulmonary alveolar epithelial permeability in surgically induced hemorrhagic pancreatitis in dogs. 616 83

With the purpose of studying the role of proteinases in the development of ARDS, plasma levels of immunoreactive trypsin (IRT) and amylase were measured in 43 intensive care patients at risk of developing ARDS (22 polytrauma, seven abdominal surgery, four burns, two DIC and eight pancreatitis). Twenty four of these 43 patients developed ARDS and 31 presented abnormal IRT values (above 70 micrograms/L). Twenty-one of these 31 patients had ARDS; a significant correlation thus appeared between ARDS and abnormal IRT values. In nine patients, IRT values were higher than 800 micrograms/L and remained high for 3 to 4 days. A statistically significant correlation also appeared between abnormal IRT and septic phenomena: 20 patients with high IRT values presented septic problems. When IRT values were high, amylase values were often also abnormal: 12 of 23 patients with high IRT had abnormal amylase levels (the eight patients with documented pancreatitis were excluded); no other clinical signs or symptoms of pancreatitis were present in these patients. IRT could be one of the mediators of ARDS in septic patients. It is not clear that the pancreas is the origin of IRT in all cases.
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PMID:Immunoreactive trypsin in the adult respiratory distress syndrome. 619 96

Pulmonary damage in acute tryptic pancreatitis is frequently a main contributory factor in death. Morphology shows a toxic pneumonosis with a course in stages. Various pathogenetic mechanisms may contribute towards its occurrence. Similar to the acute tryptic pancreatitis in the pancreas proper the pancreatitis-induced adult respiratory distress syndrome (ARDS) is probably not caused by a single enzyme or its reaction products but by a summation effect, i.e. the "concert of pancreatic enzymes".
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PMID:[Pulmonary damage in acute tryptic pancreatitis]. 670 96

Morphological changes of the lung occur frequently in fatal acute hemorrhagic pancreatitis. The pulmonary alterations are independent of mechanical ventilation and therefore not due to iatrogenic damage caused by high inspired oxygen concentrations. The histological findings are similar to those seen in the so-called shock lung syndrome. The pulmonary lesion develops progressively and three stages can be separated: early, late, and final phase. The pulmonary complications in acute hemorrhagic pancreatitis may be explained by the release of mediators such as pancreatic enzymes or free fatty acids into the blood stream. In acute hemorrhagic pancreatitis a close monitoring for shock parameters is necessary. A fall in arterial PO2 is an early indication for mechanical ventilation, including positive end-expiratory pressure.
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PMID:Pulmonary complications in fatal acute hemorrhagic pancreatitis. 682 33

Myocardial depression (measured by ventricular function curves on response to a fluid load) has been shown in 10 patients with acute hemorrhagic pancreatitis. Significant inadequate responses were found on evaluation of both the left and right heart. The increased pulmonary vascular resistance associated with adult respiratory distress syndrome (ARDS) of this disease was shown to correlate inversely with pulmonary wedge pressure, thereby excluding myocardial failure and pulmonary edema as mechanisms for the production of the ARDS.
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PMID:The myocardial depressant factor (MDF) in acute hemorrhagic pancreatitis. 724 73


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