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

We have previously demonstrated a direct relationship between the activity of the arachidonic acid cascade in vivo and the extent of cellular damage following several types of experimental injury. Since phospholipase activity has been shown to regulate arachidonic acid availability, we tested the ability of circulating phospholipase A2 (PLA2) of pancreatic origin to stimulate prostanoid production or induce cellular injury in the isolated, perfused rabbit liver. Experimental conditions were similar to those present during pancreatitis or early splanchnic artery occlusion shock. The administration of PLA2 at a rate of 100 U/min for 10 min resulted in enhanced rates of thromboxane B2 and 6-ketoprostaglandin F1 alpha release between 1 and 5 min into the infusion period. No changes in hepatic perfusion pressure, vascular resistance, wet tissue weight, or release of lactic dehydrogenase or acid phosphatase into the effluent were observed in either vehicle or PLA2-treated livers. This indicates that cellular injury was not a factor in the prostanoid release. These data suggest that circulating PLA2 can directly stimulate de novo prostanoid synthesis in noninjured tissues. Thus, enhanced plasma prostanoid concentrations in intact animals during periods or regional cellular injury may be due in part to circulating PLA2 released from damaged tissues.
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PMID:Phospholipase A2 stimulated release of prostanoids from the isolated, perfused rabbit liver: implications in regional cellular injury. 733 80

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

During August 1989-August 1994 at the referral-based obstetric practice of MacKay Memorial Hospital in Taipei, Taiwan, obstetricians saw 8 pregnant women with acute pancreatitis. All but 1 patient had gallstones and/or hyperlipidemia. None had ever been diagnosed with pancreatitis or gallstones in the past. None suffered from alcoholism. One woman was lost to follow-up at 33 weeks gestation. No pregnant woman died. Magnesium sulfate and nifedipine controlled preterm labor in 2 patients. Two women underwent cesarean section (fetal distress and elective). Pancreatitis struck all but 1 during the 3rd trimester of pregnancy. One woman presented at 23 weeks gestation with loss of consciousness, abnormally low volume of circulating plasma in the body, upper gastrointestinal bleeding, and a dead fetus. She also had diabetes mellitus which had gone untreated for 2 years. After spontaneous delivery of the dead fetus, she developed metabolic encephalopathy, sepsis, respiratory distress, and acute renal failure. She completely recovered and left the hospital 62 days after arriving. Physicians instituted conservative treatment for pancreatitis and a fat-restricted diet for hyperlipidemia. Labor was induced in 3 women after determining fetal lung maturity. Pancreatitis symptoms diminished after delivery. At 2 weeks postpartum, they underwent cholecystectomy. In fact, all but 3 women underwent cholecystectomy. Five patients had a fever greater than 38 degrees Celsius upon admission. Three patients were jaundiced. All 8 patients experienced nausea and/or vomiting and abdominal pain. Six women had low serum calcium levels. Only 1 had a serum lactic dehydrogenase level above 350 IU/L. Primiparous women were just as likely to develop pancreatitis during pregnancy as multiparous women. These findings suggest that early diagnosis and prompt treatment of acute pancreatitis are essential to a favorable outcome.
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PMID:Acute pancreatitis in pregnancy. 766 Jul 65

The main purpose of this study was to investigate the influence of early total parenteral nutrition on acute sodium-taurocholate-induced pancreatitis in rats. Total parenteral nutrition did not change the survival rate, serum amylase, calcium or liver transaminase level on the degree of pancreatic damage, but reduced serum acid phosphatase and lactate dehydrogenase levels. Hyperglycemia occurred during the use of total parenteral nutrition. Total parenteral nutrition is not harmful in the course of acute experimental pancreatitis, and could be used with few side effects.
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PMID:The influence of early total parenteral nutrition on experimental pancreatitis in rats. 768 45

A retrospective study was undertaken of 14 patients (eleven men, three women; mean age 52 [33-68] years in whom haemolysis had occurred during chronic haemodialysis (n = 12) or haemofiltration (n = 2). The haemolysis was of mechanical cause in eight patients, by an osmotic mechanism in one, and of unknown cause in five. Cardinal symptoms were nausea in 14 patients, abdominal pain in nine, vomiting in eight and raised blood pressure in ten. The plasma was discoloured in all patients and there was also an increase in free haemoglobin (110-2400 mg/dl) and (or) lactate dehydrogenase (311-7403 U/l). In all of eleven patients in whom it was measured the activity of serum amylase and (or) lipase was more than doubled (to 73-2400 U/l and 473-16,740 U/l, respectively). All patients were treated symptomatically, three had a blood exchange, two others plasma separation. Eight patients recovered within a few days, but necrotizing pancreatitis developed in six, three of whom died while two had permanent sequelae. This series shows that dialysis-induced acute haemolysis can cause life-threatening pancreatitis. Narrowings within the extracorporeal circuit, not always recognized in current dialysis equipment, are the most frequent cause of the mechanical haemolysis.
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PMID:[Acute hemolysis with subsequent life-threatening pancreatitis in hemodialysis. A complication which is not preventable with current dialysis equipment]. 792 17

The effects of prostaglandin E2 on the fragility of cellular and subcellular organelles in caerulein-induced acute pancreatitis were investigated in rats. PGE2 at doses of 50 and 100 micrograms/kg/hr infused for 2 hours before and during caerulein (5 micrograms/kg/hr for 3.5 hours) infusion significantly prevented the increased discharge of both amylase and lactate dehydrogenase from dispersed acini, and the leakage of cathepsin B from lysosomes and of malate dehydrogenase from mitochondria in the subcellular fraction in vitro. These results suggest that PGE2 has a cytoprotective effect against caerulein-induced pancreatitis by stabilizing cell and lysosomal and mitochondrial membranes.
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PMID:Effect of prostaglandin E2 on cellular, lysosomal and mitochondrial fragility in caerulein-induced pancreatitis in rats. 827 Feb 35

The main purpose of this study was to investigate the influence of thyroid releasing hormone on acute sodium-taurocholate-induced pancreatitis in rats. Thyroid-releasing hormone did not change the survival rate, serum amylase, glucose calcium, liver transaminases levels or the degree of pancreatic damage, but reduced lactate dehydrogenase. Our findings suggest that the use of thyroid-releasing hormone has no beneficial effect on the course of acute experimental pancreatitis.
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PMID:Influence of thyrotropin-releasing hormone on experimental pancreatitis in rats. 852 75

Ten hemolytic reactions occurred in our outpatient hemodialysis unit over a 12-month period (December 1989 to December 1990). Eight patients were hospitalized and one died. All patients developed severe abdominal or back pain an average of 2.5 hours into a 4-hour hemodialysis session using a bleach/formaldehyde reprocessed hollow-fiber cupraphan dialyzer (average reuse, three times) with blood flow rates of 375 mL/min. All had visible hemolysis in a spun hematocrit, seven had a significant decrease in hematocrit, and six developed pancreatitis. Hemolysis was further confirmed by a decrease in haptoglobin in all patients and an increase in lactic dehydrogenase in all but the last case. Investigation of each episode failed to find an abnormality in dialysate temperature or tonicity; dialysate or water levels of copper, zinc, nitrates, chloramine, or formaldehyde; or blood pump or venous alarm. Hemolytic reactions continued despite changing to 15-gauge needles, removing bleach from the reuse procedure, or stopping reuse. During the eighth episode, a kink was noted in the arterial blood line. Two subsequent hemolytic reactions occurred, and in each kinks were found in the arterial blood line, either in the excess tubing between the blood pump and drip chamber or in the predialyzer. No further hemolytic reactions occurred after changing to a new arterial blood line without redundant tubing and securing all lines. Hemolytic reactions occurring during hemodialysis have many etiologies, including mechanical trauma, which we report may result from kinking of dialyzer lines. With new blood lines on the market, attention to this aspect of dialysis is mandatory.
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PMID:Hemolytic reactions mechanically induced by kinked hemodialysis lines. 865 3

The lowering of activity of succinate dehydrogenase (SDH), alpha-glycerophosphate dehydrogenase (alpha GPDH), glucose-6-phosphate dehydrogenase (G-6-PDH), the raising of activity of lactate dehydrogenase (LDH) was noted in neutrophil granulocytes in an acute experimental pancreatitis. The prophylaxis of SDH, alpha GPDH, G-6-PDH activity lowering and LDH activity raising was promoted by trental and thiotriazoline injection.
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PMID:[Effects of trental and thiotriazoline on neutrophil dehydrogenase activity in acute experimental pancreatitis]. 967 Jul 35

Early assessment of severity in acute pancreatitis (AP) has a major impact on further treatment. Previous studies have shown that human pancreas-specific protein (hPASP)/procarboxypeptidase B (PCPB) is a new diagnostic and prognostic marker in AP. In the present study we focused on the prognostic properties of this parameter and analyzed the clinical value of hPASP in discriminating edematous from necrotizing AP. The results were compared to those for C-reactive protein (CRP) and lactate dehydrogenase (LDH). A total of 70 patients was enrolled in this prospective study. Based on contrast-enhanced computed tomography or intraoperative results, 39 patients (27 male, 12 female; median age, 42 years; median Ranson score, 6) suffered from necrotizing pancreatitis (NP) and 31 patients (12 male, 19 female; median age, 57; median Ranson score, 1.5) from acute interstitial-edematous pancreatitis (AIP). Serum concentrations of hPASP/PCPB, CRP, and LDH were measured at 24-h intervals over 14 days after admission by a radioimmunoassay (upper normal value, 60 ng/ ml), a lasernephelometric assay (upper normal value, 4 mg/L), and an enzymekinetic method (upper normal value, 240 U/L), respectively. During the overall observation period concentrations of hPASP/PCPB, CRP, and LDH were significantly higher in patients with NP compared to those with AIP. Based on receiver operating characteristics, the best cutoff levels for predicting NP were >200 ng/ml for hPASP/PCPB, >140 mg/L for CRP, and >290 U/L for LDH. Discrimination between AIP and NP was best on day 3 for both hPASP/PCPB (sensitivity, 91%; specificity, 64%; accuracy, 79%) and CRP (sensitivity, 83%; specificity, 84%; accuracy, 83%) and on day 5 of AP for LDH (sensitivity, 88%; specificity, 100%; accuracy, 91%). The overall accuracy in differentiating AIP from NP within the first 4 days after onset of symptoms was 74% for hPASP/PCPB, 75% for CRP, and 76% for LDH. None of the parameters correlated with the extent of necrosis or the etiology of AP. hPASP/PCPB provides good discrimination between AIP and NP at an early stage of the disease, with results comparable to those for CRP and LDH. Although hPASP/PCPB is both disease specific and predictive for necrosis, the clinical use of this test in its present form is limited due to drawbacks in terms of test performance and cost factors.
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PMID:The clinical value of human pancreas-specific protein procarboxypeptidase B as an indicator of necrosis in acute pancreatitis: comparison to CRP and LDH. 970 Sep 43


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