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)

Magnesium deficiency can occur in congestive heart failure, after diuresis with furoxemide, ethacrynic acid and mercurials, and with digitalis intoxication, diabetic acidosis, acute and chronic alcoholism, delerium tremens, cirrhosis, malabsorption syndromes, protracted postoperative cases, open heart surgery, the diuretic phase of acute tubular necrosis, and with hypoparathyroidism, primary aldosteronism, juxta-glomerular hyperplasia and pancreatitis. Two cases of serious ventricular arrhythmias associated with magnesium depletion are described. Clinical manifestations are vague but center around neurologic symptoms such as weakness, tremors, stupor, coma, nausea, vomiting and anorexia. Serious cardiac arrhythmias also occur with magnesium depletion. Magnesium appears to be very useful in hypomagnesemic or digitalis-toxic tachyarrhythmias. Magnesium may also be valuable in normomagnesemic tachyarrhythmias. Ten to fifteen milliliters of a 20 percent magnesium sulfate solution, given intravenously over 1 minute, followed by a slow 4 to 6 hour infusion of 500 ml of 2 per cent magnesium sulfate in 5 per cent dextrose in water is recommended. Recurrence of arrhythmias is common and a second infusion of magnesium sulfate may be necessary. Hypermagnesemia occurs frequently in renal insufficiency, and magnesium therapy may then be contraindicated. Serum levels above 5.5 meq/liter should be avoided. Loss of deep tendon reflexes and a decrease in respiratory rate can be used as guides to magnesium therapy. A plea is made for frequent analysis of serum magnesium so that more knowledge can be gained regarding this important biologic element in cardiovascular disorders.
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PMID:Magnesium deficiency and cardiac disorders. 80 29

Total parenteral nutrition (TPN) is a relatively new innovation in patient care which allows us to replace and maintain essential nutrients in patients in whom oral or tube feedings are contraindicated or inadequate. Insertion of a catheter into a large central vein permits one to concentrate hypertonic dextrose calories in normal daily fluid requirements. In addition, TPN solutions contain synthetic amino acids or protein hydrolysates, macroelements, electrolytes, and vitamins. Indications for TPN include intestinal fistulas, severe short bowel syndrome, unresolving pancreatitis, advanced inflammatory bowel disease, delayed postoperative gastrointestinal function, developmental anomalies of the intestinal tract, protracted diarrhea of infancy, and hypermetabolic states. Complications encountered in patients receiving TPN are catheter-related mechanical problems, infections, and metabolic abnormalities. In select patients, who otherwise would require repeated hospitalizations for malnutrition, encouraging results have been achieved by the use of TPN in the home.
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PMID:Total parenteral nutrition. 81 25

A previously healthy 35-year-old woman was seen at 37 weeks' gestation with a 10-day history of fever, vomiting, diarrhea and malaise. Serum laboratory findings included elevation of serum bilirubin and AST, prolongation of serum prothrombin time and a positive monospot. A tentative diagnosis of acute fatty liver of pregnancy was made, and a healthy male infant was delivered by emergency cesarean section because of fetal distress. Over the subsequent 3 days, acute progressive oliguric renal failure, disseminated intravascular coagulation, hypoglycemia requiring intravenous dextrose infusion and pancreatitis developed; her mental status progressed to stage III encephalopathy. Quantitative computed tomography estimated the liver volume to be 770 cm3. The decision to proceed with orthotopic liver transplantation was made on the basis of progressive clinical deterioration despite aggressive support and because of her small liver size. After transplant, the patient's multisystem failure rapidly reversed. Histopathological examination of the native liver demonstrated predominantly zone 3 microvesicular steatosis with characteristic ultrastructural changes consistent with acute fatty liver of pregnancy. Southern blot analysis for Epstein-Barr virus DNA was negative. We conclude that orthotopic liver transplantation should be considered for the small group of patients with fulminant hepatic failure associated with acute fatty liver of pregnancy who manifest signs of irreversible liver failure despite delivery of the fetus and aggresive supportive care.
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PMID:Fulminant hepatic failure caused by acute fatty liver of pregnancy treated by orthotopic liver transplantation. 240 63

Effects of sustained ethanol intoxication and dietary fat content on pancreatic morphology were investigated in the rat model implanted with gastrostomy catheters, which permitted continuous intragastric infusion of ethanol plus liquid diet containing one of three levels of corn oil: 5% (low-fat), 25% (high-fat), and 35% (extra-high-fat) of total calories. After various durations of infusion ranging from 30 to 160 days, the pancreatic histology was examined. Mean blood alcohol levels achieved in the low, high, and extra-high fat diet groups were similarly high: 210 +/- 120, 224 +/- 122, and 289 +/- 110 mg/dl. The average weight gain of these ethanol-fed groups during the first 8 weeks of experiments was 15.4 +/- 1.9, 19.6 +/- 8.0, and 14.9 +/- 5.2 g/wk, respectively, and was not statistically different from that of pair-fed controls infused with isocaloric amount of dextrose and respective diet, nor from that of age-matched animals given the regular chow. None of control animals showed abnormal pancreatic morphologic features except occasional mild steatosis in those fed the extra-high-fat diet. With the low dietary intake of unsaturated fat, chronic ethanol intoxication produced only mild pancreatic pathology such as steatosis and interstitial edema. Administration of ethanol and the high-fat and extra-high-fat diets caused hypogranulation and apoptosis of acinar cells. Focal lesions of chronic pancreatitis were also observed in 20% or 30% of ethanol-fed animals given the high-fat or extra-high-fat diet. These lesions were characterized by fat necrosis, mononuclear cell infiltration, fibrosis, acinar atrophy, ductal dilatation, and intraductal mucious or proteinacious plugs. The incidence of focal acute pancreatitis was less (7-20%) but appeared increased with higher dietary fat content. Induction of either acute or chronic pancreatitis was not correlated with plasma levels of triglycerides or cholesterol. These results demonstrate potentiation by dietary unsaturated fat of ethanol-induced pancreatic injury. This model possesses many features analogous to those seen in alcoholic pancreatic injury in man. The hyperlipidemia does not appear to be an important pathogenetic factor for ethanol-induced pancreatitis produced in this model.
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PMID:Potentiation of ethanol-induced pancreatic injury by dietary fat. Induction of chronic pancreatitis by alcohol in rats. 335 54

Prostaglandin E1 (PGE1) was tested for cytoprotective activity against the development of experimental acute pancreatitis in the rat induced by the closed duodenal loop technique. Sham-operated, untreated and PGE1-treated pancreatic rats were investigated. All rats received an initial bolus of 3 ml 5% dextrose in normal saline (D5NS) via jugular catheter 30 min prior to surgery, and a continuous subcutaneous infusion of 35 ml D5NS over 24 h. Each treated rat received 10 micrograms/kg PGE1 in the initial bolus and a maintenance dosage of 10 micrograms/kg/h via the infusate. Serum amylase rose significantly in all pancreatic rats with no significant difference between treated and untreated. Pancreatic edema was more pronounced in PGE1-treated than in untreated rats. The ischemic and autolytic damage to acinar cells and vascular endothelial cells typical of untreated pancreatitis was delayed by PGE1. Mortality rates were unaffected by PGE1.
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PMID:Prostaglandin E1 treatment in experimental acute pancreatitis in the rat. 620 76

The aim of this study was to evaluate the adverse effects on the exocrine pancreas of ethanol and ethanol with congeners which coexist in alcoholic beverages most commonly consumed by the Portuguese population. Eighteen male Wistar rats were divided into three groups and submitted to a daily intraperitoneal injection of a hydroalcoholic solution of ethanol (SHAE) and a hydroalcoholic solution of ethanol, acetaldehyde, methanol and higher alcohols (SHAF); the third group served as a control and received an equivalent volume of an isocaloric solution of dextrose. All the animals were sacrificed at the end of the 9th week of the experiment. The following histological lesions were considered: acinar cell necrosis and steatosis, ductal dilatation, intraluminal plugs, parenchymal inflammation, fibrosis, peripancreatic fat necrosis and inflammation. Their severity was graded by means of a scoring system. The histopathologic changes which characterize pancreatitis (acinar cell necrosis, parenchymal inflammation, fibrosis and peripancreatic fat necrosis and inflammation) were found in the majority of animals of both study groups, but in none of the control group. The lesions tend to be more frequent and severe in the group treated with ethanol and its congeners (SHAF) than in the SHAE group; these differences are statistically significant when necrosis, ductal dilatation and overall severity of lesions are considered. The results of this study suggest that in the pancreas the toxicity of ethanol is enhanced by interaction with other components of alcoholic beverages.
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PMID:[The effect of combined toxicity on the development of alcoholic pancreatic lesions. A long-term experimental trial]. 748 40

17 patients with acute necrotic pancreatitis were proved by CT or operation. These patients were randomly assigned to fat-glucose-based group (n = 9) and glucose-based group (n = 8). Their PN regimen consisted of nonprotein calories (NPC) 35-40KJ (146-167KJ)/kg/d and nitrogen 0.19-0.29g/kg/d. NPC was supplied by either dextrose or dextrose and intralipid. The PN duration was 2 weeks. The following measurements were performed: triglyceride, chorestrol, HDL, LDL, Apo-A, Apo-B and free fatty acids. The results showed that there was no hypertriglyceridemia developed after fat emulsion was administered for two weeks. It confirmed that fat emulsion could be rapidly oxidigzed. In our group, the patients with hyperglycemia were 64% at the admission time, and hyperglycemia was difficult to control in early period (10 days). But hyperglycemia was easly to control when patients received fat emulsion. There was no harmful effect on liver function during 2 weeks of intralipid administration. The data showed no difference between the two groups on conventional measurements, lysosomal enzymes and blood gas analysis. Intralipid infusion did not make ANP deterioration. These results indicated long-term intravenous intralipid in patients with ANP was safe and useful.
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PMID:[Effect of intralipid on patients with acute necrotic pancreatitis: a prospective clinical study]. 758 87

Alcohol consumption i associated with pancreatitis, but the mechanism underlying this injury remains unclear. Alcohol consumption has recently been shown to increase the fragility of both rat pancreatic lysosomes and zymogen granules in vitro, which may predispose to autodigestion via the intracellular activation of digestive enzymes by lysosomal enzymes. Cerulein-induced pancreatitis is also associated with lysosomal fragility. To determine the effect of alcohol consumption on this form of pancreatic injury, the severity of pancreatitis was compared in three groups of rats following i.v. cerulein infusion: rats fed alcohol in a liquid diet, pair-fed dextrose controls, and chow-fed controls. The histological severity of pancreatitis induced by supramaximal cerulein infusion was not found to be increased by prior alcohol consumption. Since alcohol did not appear to increase the severity of pancreatic injury induced by cerulein, we sought to define biochemical parameters that might precede obvious injury. The subcellular distribution of cathepsin B activity and markers of lysosomal fragility were compared in the same groups of experimental animals. Cerulein infusion led to a marked redistribution of cathepsin B activity from the lysosomal to the zymogen-granule-enriched fractions.For animals killed in the fed state, a redistribution of cathepsin B activity toward the zymogen-granule-enriched fraction was also demonstrated in alcohol-fed animals compared to their pair-fed controls. However, chronic alcohol administration did not influence the effect of cerulein on subcellular cathepsin B distribution or lysosomal fragility. In this rat study, administration of alcohol did not increase the effects of supramaximal doses of cerulein on the pancreas.
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PMID:The effect of chronic alcohol administration on cerulein-induced pancreatitis. 759 67

An alpaca and a llama in late stages of gestation were evaluated for lethargy, anorexia, and recumbency. Both camelids had cloudy, white, turbid serum, elevated serum triglyceride (1564, 5658 mg/dL, respectively) and cholesterol (158, 297 mg/dL, respectively) concentrations, and ketonuria. Signs of fetal stress were evident ultrasonographically in the alpaca, and a live cria was delivered by Cesarean section performed under general anesthesia. The alpaca developed severe metabolic acidosis, hepatic lipidosis, and acute renal failure secondary to renal lipidosis and died 36 hours after admission despite medical therapy. Histopathology revealed renal and hepatic lipidosis and neutrophilic pancreatitis. The cria died 72 hours after birth. The llama responded to IV electrolyte, dextrose, and regular crystalline insulin therapy. The pregnancy was maintained, and the llama was discharged from the hospital 20 days after admission. Two months after discharge, the llama gave birth to a live, 5 kg cria. Findings of hypertriglyceridemia, hypercholesterolemia, elevated sorbitol dehydrogenase activity, metabolic acidosis, azotemia, and ketonuria occurred in these two camelids. Based on this report, camelids appear to be similar to both horses and cattle in their response to severe energy imbalances in late gestation.
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PMID:Hyperlipemia and ketonuria in an alpaca and a llama. 806 56

For evaluating abdominal hemodynamic changes and diagnosing mass lesion, recently color Doppler ultrasonography (CDUS) have been applied. However, there are limitations in visualizing Doppler signals in small vessels with low flow velocity. To overcome these shortcomings, several contrast agents that facilitate evaluation of abdominal hemodynamics have been developed. We underwent Contrast enhanced color Doppler ultrasonography (CECD) with a galactose-based contrast agent in three patients with pancreatic tumor. In the patient with tumor forming pancreatitis, only CECD visualized the color signal in and around the tumor. In the patient with duct cell cancer, CDUS and CECD visualized only the color signal of the splenic artery penetrating the tumor, whereas in the patient with islet cell tumor, CECD visualized numerous color signals in the tumor. CECD appears to be useful in diagnosing pancreatic tumor.
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PMID:[Differential diagnosis of pancreatic tumor by contrast enhanced color Doppler ultrasonography]. 957 28


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