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)

We evaluated the diagnostic utility of measuring pancreatic isoamylase (P-AMY) with a double-monoclonal antibody technique in a population of 43 consecutive hospitalized hyperamylasemic patients in comparison with serum pancreatic lipase (LPS) activity. In 27 cases (62.8%), the final diagnosis was acute pancreatitis. Predictive values were calculated for P-AMY and LPS activities, and a P-AMY percentage was calculated for selected decision levels. The maximal diagnostic efficiency was 0.930, 0.814, and 0.767 for LPS, P-AMY activity, and P-AMY percentage, respectively, indicating that serum LPS measurement was clinically superior to P-AMY for distinguishing patients with or without pancreatitis. Measurement of both P-AMY activity and percentage in serum did not significantly improve diagnostic accuracy.
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PMID:Diagnostic value of measuring pancreatic isoamylase with a double-monoclonal antibody immunoassay in serum of hospitalized hyperamylasemic patients. 228 65

Experiments performed on 71 Wistar rats confirm that preexisting interruption of lymph drainage by ligation of the ductus thoracicus can have a major influence on the development of pancreatitis. The effect of a ductus hepatopancreaticus blockade in experimental group A (32 animals) was greatly exacerbated by previous ligation of the ductus thoracicus (experimental group B; 34 animals). Edema of the interstitial pancreatic tissue led to lipolytic necrotizing pancreatitis with a slight hemorrhagic component, increasing ascites after the 12 th hour of the experiment, and numerous abdominal fat necroses after about 19 hours, but only relatively minor necroses of acinar parenchyma cells in the pancreas. Fat tissue necroses were only found in almost 20% of the animals in group A, and these probably resulted from manipulation of the duodenum during the implantation of a shunt to divert the bile, whereas they were found in all animals of group B after the 19th hour of the experiment, usually in large numbers. The sometimes considerable increases in serum amylase and particularly lipase activity were caused by obstruction of the efferent ducts, but did not increase appreciably after disturbance of the lymph drainage systems. On the contrary, under these circumstances, drainage of the salivary edema via the peritoneal mesothelium and into retroperitoneal fat tissue must be considered responsible for ascites and the initiation of fat cell necroses by lipase and other enzymes.
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PMID:[Lymph drainage disorder as a pathogenetic co-factor in acute pancreatitis?]. 228 56

We examined the biological and histologic characteristics of a new experimental model of acute necrotizing pancreatitis induced by excessive doses of arginine in rats. Rats were given a single intraperitoneal injection of 500 mg/100 g body weight of L-arginine. At 12-24 hr after the arginine injection, serum levels of amylase, lipase, and anionic trypsin(ogen) reached respective peak values 2, 5, and 20 times those of control rats without arginine and returned to control levels after 24-48 hr. The contents of pancreatic protein, DNA, and digestive enzymes were markedly reduced after the arginine injection and reached their nadirs at 72 hr. After 14 days these levels were almost normal. Histologic examination revealed a number of small vesicles within acinar cells at 6 hr, which were identified as markedly swollen mitochondria by the electron microscope. Other intracellular organelles and nuclei also showed degenerative changes. At 12 hr interstitial edema appeared, and acinar cell necrosis was seen after 24 hr. The extent and severity of necrotic changes of pancreatic exocrine tissue with inflammatory cell infiltration were maximal at 72 hr. At seven days, pancreatic acinar cells began to regenerate, and pancreatic architecture appeared almost normal after 14 days. The present study has demonstrated that the administration of excessive doses of arginine induces a new, noninvasive experimental model of acute necrotizing pancreatitis.
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PMID:New model of acute necrotizing pancreatitis induced by excessive doses of arginine in rats. 230 82

The possible association of pancreatitis with primary sclerosing cholangitis was studied in 17 patients. At endoscopic retrograde cholangiopancreatography (ERCP) four patients (24%) were found to have pancreatic changes in addition. The secretin test was abnormal in one patient, who also had morphological signs of pancreatitis at ERCP. One patient had raised basal serum concentrations of amylase and lipase, and another had decreased pancreatic amylase; these two patients had normal findings on ERCP and normal secretin tests. The findings suggest that pancreatic changes are present in a proportion of patients with primary sclerosing cholangitis despite the lack of clinical suspicion of pancreatitis. The pancreatic damage, however, seems to be confined to alterations in ductal morphology rather than including functional impairment.
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PMID:Pancreatic ductal morphology and exocrine function in primary sclerosing cholangitis. 236 50

A 48-year-old patient presented with a 24 hour history of diffuse abdominal pain and diarrhea. Based on elevated serum amylase and lipase levels, a CT-scan, and a history of chronic alcohol intake, acute alcoholic pancreatitis was diagnosed. The patient clinically improved under conservative therapy, but after restarting enteral nutrition on the fourth day, he developed full blown mechanical ileus. Intraoperatively, an adhesive band and acute edematous pancreatitis and fat necrosis was found. Retrospectively, the initial clinical symptoms and plain abdominal x-ray findings suggest coincidence of obstructive ileus and acute pancreatitis. We hypothesize that obstructive ileus had triggered pancreatitis.
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PMID:Obstructive ileus and acute pancreatitis. 239 51

Thirty patients with leukemia and lymphoma have been treated at our institution with high doses of cytosine arabinoside (Ara-C). Gastrointestinal symptoms were frequent after therapy, and 6 of the 30 patients had severe abdominal pain. Of the six, two had pancreatitis; two had normal amylase and lipase determinations; and in two, neither amylase nor lipase levels were determined. The two patients with pancreatitis are presented because this complication of high-dose Ara-C therapy has not been described. The authors conclude that pancreatitis can follow high-dose Ara-C chemotherapy and that patients with abdominal pain following this treatment be evaluated for pancreatitis.
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PMID:High-dose cytosine arabinoside-associated pancreatitis. 241 82

In this experimental study, we investigated pathophysiology of respiratory failure with acute pancreatitis. Pancreatitis was induced by injection of 15% Na-taurocholate 1 ml/kg into the main pancreatic duct of the dogs. Experimental dogs were divided into two groups based on the value of Respiratory Index (R-Index). Group A included 9 dogs in whom respiratory failure was not recognized (R-Index less than 0.5) and Group B included 9 dogs with respiratory failure (R-Index less than 0.5). All the dogs were sacrificed 12 hours after induction of pancreatitis, and histological findings were examined. Quantity of water in the lung (Qwl) was also measured by gravimetric method. Group B showed severe hypoxia with hypocapnia, and increase of A-aDO2, R-Index, and decrease of a/A PO2. Qwl in Group B increased significantly comparing with Group A. In biochemical study, increase of serum lipase, triglyceride, free fatty acid, and angiotensin converting enzyme were observed in Group B. These results indicate that respiratory failure with acute pancreatitis is due to lung edema following injury of the capillary of the lung. The role of free fatty acid liberated by lipolysis was suggested in the mechanism of pulmonary damage with acute pancreatitis.
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PMID:[Experimental study of respiratory failure with acute pancreatitis in dogs]. 241

The diagnostic value of a new enzyme immunoassay for lipase (IRL) was evaluated in controls (n = 65), in acute pancreatitis (n = 11) and in extrapancreatic hyperamylasemia (n = 15) by comparing IRL with serum amylase (TA), pancreatic isoamylase (PA) and lipase (turbidimetrically: TL). IRL and immunoreactive trypsin (IRT) of 60 patients with alcoholic chronic calcified pancreatitis were also studied and correlated with duration of disease and degree of pancreatic insufficiency (based on fecal chymotrypsin test: FCT). IRL was constantly elevated in patients with acute pancreatitis. In extrapancreatic hyperamylasemia IRL was mainly normal, in contrast to PA, which was elevated in 7 patients with macroamylasemia. In 56.7% of all patients with chronic pancreatitis, IRL was pathologically low; in association with advanced insufficiency (FCT less than 20 micrograms/g) this figure was 74%, and after duration of disease of greater than or equal to 15 years 77%. For IRT comparable results were found in 79% and 77% respectively. This new lipase test thus seems to be useful for the diagnosis of acute pancreatitis, the differential diagnosis of extrapancreatic hyperamylasemia and the detection and monitoring of severe chronic pancreatitis.
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PMID:[Significance of immunoreactive lipase in the diagnosis of pancreatic diseases]. 241 82

Acute experimental pancreatitis was induced in male Wistar rats by retrograde injection of 0.4 ml 2% sodium taurocholate into the common choledochopancreatic duct. Prophylactic intraperitoneal injection of 20 mg glutaryl-trialanine-ethylamide, Glt-(Ala)3-NH-Et, 30 min. before induction of pancreatitis reduced the amount of fat necroses and the activity of amylase and lipase in ascites. Repeated intraperitoneal injection of this inhibitor decreased pancreatic hemorrhage. Simultaneous administration of 20 mg Glt-(Ala)3-NH-Et intraperitoneally, and 10 000 KIU of aprotinin intravenously was followed by the most extensive inhibitory effect. Prophylactic and repeated administration of both inhibitors also reduced the area of pancreatic hemorrhage. The same mode of administration of 20 mg undecenoyl-aspartyl-dialanyl-proline-ethylamide, UDE-Asp-(Ala)2-Pro-NH-Et, intraperitoneally and 20 000 KIU of aprotinin intramuscularly, resulted in selective inhibition of fat necroses in all localizations. Glt-(Ala)3-NH-Et and UDE-Asp-(Ala)2-Pro-NH-Et are considered effective inhibitors of various macroscopic and biochemical signs of acute pancreatitis in the rat during short-ferm experiments, if administered prophylactically or early after induction of the disease.
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PMID:Effect of new oligopeptide inhibitors of elastase on acute experimental pancreatitis in the rat. 241 98

Methyl alcohol intoxication has been reported to cause hyperamylasemia and pancreatitis. We describe a patient with severe, nonfatal methyl alcohol intoxication who had a rise in serum amylase activity with the level peaked on the second hospital day at tenfold the upper limit of normal. However, isoamylase analysis showed that this striking hyperamylasemia was due to salivary-type amylase. Furthermore, the serum lipase activity remained entirely normal during the peak amylase elevation. Thus, in cases of methyl alcohol intoxication, as in other clinical situations, hyperamylasemia, even when striking, should not be equated with pancreatitis. More specific laboratory tests for pancreatitis should be used before embarking on extensive investigations of the pancreas.
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PMID:Hyperamylasemia following methyl alcohol intoxication. Source and significance. 241 69


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