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

The effect of Venalot, a combination of two benzo-pyrones, on canine experimental acute pancreatitis was examined. Activities of lymph and blood plasma enzymes, thoracic duct lymph flow, and morphological changes of the pancreas were compared with those of a control group of dogs. The drug was found to enhance the removal of amylase and trypsin via lymph from the gland and to decrease the elevation of plasma amylase and lactate dehydrogenase. When administered simultaneously with the induction of pancreatitis, benzo-pyrones were effective in the reduction of pancreatic edema and necroses.
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PMID:Lymph and blood enzymes and pathologic alterations in canine experimental pancreatitis after administration of benzo-pyrones. 44 82

Twenty-four dogs were divided into five groups. Under pentothal sodium anesthesia, those in the control group received no further manipulation; another group underwent laparotomy only; and dogs in the last three groups had induced pancreatitis, intestinal ischemia and duodenal perforation, respectively. An analysis was made of serum and peritoneal lavage fluid in the dog of each group at 30 minute intervals for four and one-half hours. Parameters which were significantly elevated in dogs with pancreatitis compared with other groups included fluid amylase, lactate dehydrogenase, proteolytic activity and intestinal alkaline phosphatase and serum amylase. We judge that these biochemical differences in the lavage fluid, when taken with the physical characteristics of the fluid and the clinical symptoms, can significantly aid the clinician in arriving at the diagnosis of acute pancreatitis.
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PMID:Use of peritoneal lavage in the diagnosis of experimental acute pancreatitis. 112 80

The redistribution of cathepsin B, a lysosomal enzyme, from the lysosomal pellet to the zymogen pellet in the subcellular fractionation, the colocalization of cathepsin B with digestive enzyme, and increased cellular, lysosomal, and mitochondrial fragility within acinar cells have been found during the early stages of caerulein-induced acute pancreatitis in rats. In the present study, the authors investigated the protective effects of prostaglandin E1 and E2, a combined therapy of these prostaglandins, and a new, synthetic, low molecular weight protease inhibitor, ONO3307, on the exocrine pancreas in this noninvasive model of experimental pancreatitis in vivo and in vitro. Prostaglandin E2, but not E1, prevented hyperamylasemia, congestion of amylase and trypsinogen in the acinar cells, redistribution of cathepsin B, and amylase and lactate dehydrogenase discharge from the dispersed acini. It also prevented cathepsin B leakage from the lysosomes and malate dehydrogenase leakage from the mitochondria in an almost dose-dependent manner, particularly at the dose of 100 micrograms/kg/hr continuous infusion. Furthermore, the combined therapy of prostaglandin E2 with ONO3307 strongly inhibited all the parameters tested in this study. This combination therapy seems to be the most effective against secretagogue-induced pancreatic injuries. These results indicate that cellular and subcellular organellar fragility seem to be closely involved in the pathogenesis of acute pancreatitis. Prostaglandin E2 seems to have important cytoprotective effects on the biologic membranes, such as a stabilizer of lysosomal or mitochondrial membranes. In addition, these findings also suggest the crucial roles of some unknown proteases in the etiology of acute pancreatitis, and indicate the clinical effectiveness of prostaglandins and this type of low molecular weight protease inhibitor for acute pancreatitis.
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PMID:Cytoprotective effects of prostaglandins and a new potent protease inhibitor in acute pancreatitis. 128 94

We analyzed the role of polymorphonuclear granulocytes (PMN)-elastase in predicting the prognosis of patients with acute pancreatitis in comparison with C-reactive protein (CRP), lactate dehydrogenase (LDH), and the two antiproteases alpha 1-antitrypsin (alpha 1-AT) and alpha 2-macroglobulin (alpha 2-M). Fifty-two patients with acute pancreatitis were subdivided according to morphological criteria into 29 patients with edematous pancreatitis and 23 patients with necrotizing pancreatitis. Within 5 days after the onset of acute pancreatitis, the accuracy rates for detecting necrotizing pancreatitis were 86%, 84%, 82%, 72%, and 69%, using cutoff levels of 120 mg/L for CRP, 120 micrograms/L for PMN-elastase, 270 U/L for LDH, 1.5 g/L for alpha 2-M, and 3.5 g/L for alpha 1-AT, respectively. The median peak value of PMN-elastase was reached on day 1 of acute pancreatitis in contrast to the median peak of CRP, which was at its highest between days 3 and 4. PMN-elastase represents a reliable indicator, comparable with CRP, for the staging of acute pancreatitis. The advantage of PMN-elastase over CRP appears to be its earlier increase and the greater dynamism of its serum course. Finally, the results suggest that CT scanning for the evaluation of the extent of intra- and extrapancreatic necrosis could be restricted to those patients with increased values of PMN-elastase and CRP.
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PMID:PMN-elastase in comparison with CRP, antiproteases, and LDH as indicators of necrosis in human acute pancreatitis. 171 69

A prospective study was carried out to evaluate the efficacy of somatostatin in the treatment of acute pancreatitis. Seventy one patients were randomised to control (h = 36), or to the somatostatin group (h = 35) who received somatostatin 100 micrograms/h after a 250 microgram bolus for the first two days. The following were compared in the two groups on admission and two days later: laboratory tests of prognostic significance, severity of pancreatitis, and also morbidity and mortality. Of the nine laboratory tests compared, the white blood cell count, lactate dehydrogenase, and urea concentrations were significantly lower in the somatostatin group two days after admission. Severity of pancreatitis after hospitalisation increased in fewer patients given somatostatin (NS). There was a trend toward fewer complications, especially local, in the somatostatin group. Mortality in both groups was low. Somatostatin appeared to reduce the local complications of acute pancreatitis. A larger trial is necessary to show its beneficial effect conclusively.
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PMID:Somatostatin in the treatment of acute pancreatitis: a prospective randomised controlled trial. 256 34

In an attempt to reduce the current morbidity and mortality from acute pancreatitis, a prospective randomized multicentre trial was begun in August 1982. Part of this study involved an attempt to develop a set of prognostic indices which would identify patients with severe pancreatitis on the day of admission to hospital. An analysis of a predetermined set of 10 indices (age, blood pressure, white cell count, blood urea, serum calcium, aspartate aminotransferase, lactate dehydrogenase, blood glucose, arterial blood pH and PO2) on admission to hospital, in 100 patients, is presented. The positive predictive value of these indices (excluding age) is 90%. These indices are readily available in most hospitals, and allow the early identification of the high risk patient with an accuracy equal to or better than that previously reported.
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PMID:Predictors of severity of attacks of acute pancreatitis. 346 82

During the past 3.5 years the authors have evaluated 191 patients, both retrospectively and prospectively, to establish factors which might help to identify those patients at higher risk of developing pancreatic abscesses. Those factors included etiology of pancreatitis, number of severity indices present, and specific indices present. Once an abscess developed, severity indices, etiology, and bacteriology were examined as factors in mortality. Six specific severity indices occurred more often (P less than 0.05) in patients developing abscesses. These indices were lactate dehydrogenase evaluation, leukocytosis, metabolic acidosis, hypoxemia, hypocalcemia, and fluid sequestration. In addition, seven of 18 abscess patients had six or more indices present as opposed to five of 161 pancreatitis patients. This was significant at P less than 0.05 level. The etiology of the pancreatitis was not a significant factor. Once an abscess developed, gram-negative infections were polymicrobial (8 of 9 patients) and were associated with a 56 per cent mortality. The gram-positive abscesses (6 patients) were all monomicrobial and none of these patients died. In addition, age greater than 55 years, serum glucose greater than 200 mg%, hematocrit decrease of 10 per cent, and fluid sequestration greater than 6 L were associated with a 50 per cent or greater mortality. The authors believe that patients presenting initially with six or more severity indices, especially the six mentioned above, are at significantly increased risk for developing a pancreatic abscess and those abscess patients with gram-negative abscesses, as well as having any of the four severity indices previously mentioned, have a much worse prognosis.
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PMID:Early diagnosis and outcome of pancreatic abscesses in pancreatitis. 380 Jan 61

Macroamylase is a circulating complex of immunoglobulin linked to normal amylase in most cases. Its physical properties are heterogeneous, but its large size impairs renal filtration. Macroamylasemia usually causes hyperamylasemia and an amylase clearance:creatinine clearance (C(AM):C(CR)) ratio of less than 1 percent. Macroamylasemia occurs in 2.5 percent of hyperamylasemic patients, and 1 percent of apparently healthy subjects with normal amylase levels. It often accompanies diseases of aberrant immunity or conditions in which pancreatitis must be ruled out. This disorder should be considered in a patient with asymptomatic hyperamylasemia because its detection can obviate a prolonged diagnostic workup. The condition requires no treatment and may be transient. Macroamylasemia is one of several immunoglobulin-complexed enzyme (ICE) disorders. MacroLDemia, an ICE disorder of lactate dehydrogenase (LD), shares features with macroamylasemia. These and other ICE disorders appear to represent nonspecific dysproteinemic responses to disease.
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PMID:Macroamylasemia and other immunoglobulin-complexed enzyme disorders. 616 78

The activity of elastase, elastase inhibitor and isozymes of lactate dehydrogenase (LDH) was studied in 11 dogs with experimental pancreatitis and 5 control dogs. All dogs with experimental pancreatitis died 6--14 hours after the induction of pancreatitis. Morbid anatomy studies proved severe pancreonecrosis. The results obtained show that after the induction of pancreatitis the elastase blood activity increased 3-fold as compared with the initial level, and remained unchanged up to the animals' death. At the same time the activity of elastase inhibitor fell, correlating with the rise in elastase activity. Also there was a disproportion between LDH 1 and LDH 2 which became more conspicuous to the 3d hour, and an increase in LDH 5 by the end of the experiment. A conclusion is made that dysfunction of the liver may be one of the causes of the decreased inhibitory activity of elastase in pancreonecrosis.
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PMID:[Elastase activity in experimental pancreatitis]. 690 51

Lazaroids, 21-aminosteroids without gluco- and mineralocorticoid activity, protect against oxidative injury in nervous system cells and may therefore also have a potential for treatment of pancreatitis, where oxidative stress contributes to cell injury. The present study evaluates the protective potential of the lazaroids U-78518F, U-74500A, and U-74389F against damage to isolated pancreatic acinar cells exposed to two models of oxidative stress: (a) a XOD/HX model, consisting of xanthine oxidase, hypoxanthine, and chelated FeCl3; and (b) an ADP/Fe model, consisting of FeSO4 and the reducing agent ADP. Both models caused time-dependent cell injury as assessed by uptake of trypan blue and release of lactate dehydrogenase. Short-term peak production of free radicals in the XOD/HX model--as monitored by the deoxyribose assay--was more injurious to cells than continuous radical generation at lower levels in the ADP/Fe model. In general, lazaroids at 1-10 microM reduced oxidative damage and deoxyribose oxidation in both models. The degree of reduction of cell damage and deoxyribose oxidation depended on the type and concentration of the lazaroid and the model used. Lazaroid concentrations < 0.1 microM were ineffective, and concentrations > 50 microM even accelerated cell injury, although lazaroids still served as scavengers at high concentrations. At least part of the noxious effects of high lazaroid concentrations is due to nonspecific membrane damage because these concentrations caused cell injury also in the absence of oxidative stress. The limited range of protective concentrations has to be observed in further in vivo studies. Interestingly, acinar cells in the absence of lazaroids also reduced radical-induced deoxyribose degradation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lazaroids protect isolated rat pancreatic acinar cells against damage induced by free radicals. 747 66


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