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Query: UMLS:C0020473 (hyperlipidemia)
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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

Acute recurrent pancreatitis in the absence of alcoholism and gallstones is a frustrating illness for both the patient and the physician. Over a 10 year period, 33 patients were operated on and found to have a duct of Wirsung entering the duodenum through the fibers of the sphincter of Oddi. Recurrent pancreatitis of sufficient intensity to require hospitalization had occurred an average of 4.2 times per patient, and each had experienced numerous episodes of abdominal pain of lesser severity. At least two attacks of pancreatitis that required hospitalization had occurred in all patients. All known causes of pancreatitis, including alcoholism, gallstones, hypercalcemia, hyperlipidemia, drug reactions, and pancreas divisum were excluded. Endoscopic retrograde cholangiopancreatography showed no ductal abnormalities. Twenty-eight of the patients had previously undergone cholecystectomy 8 months to 20 years before operation. A sphinteroplasty of the common bile duct and duct of Wirsung resulted in elimination of attacks of pancreatitis in all except two patients. Follow-up has been more than 5 years in 16 patients, more than 4 years in 10 patients, and more than 1 year in 5 patients. There have been no deaths. It appears that the entrance of the duct of Wirsung into the duodenum through a separate orifice through the fibers of the sphincter of Oddi causes recurrent acute pancreatitis. It seems likely that the problem is one of intermittent pancreatic duct obstruction. Normal pancreatic duct caliber is attributed to the intermittent nature of the obstruction. Enlargement of the orifice of the duct of Wirsung and division of the sphincter of Oddi relieved attacks of recurrent pancreatitis.
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PMID:Misplaced pancreatic duct orifice as a cause of recurrent acute pancreatitis. 381 90

Mild to moderate hypertriglyceridemia is not associated with specific signs or symptoms in either IDDM or NIDDM. However, symptoms of the "chylomicronemia syndrome," including abdominal pain and acute pancreatitis, can occur when poorly controlled diabetes is present in a patient with a familial form of hyperlipidemia. The low-carbohydrate, high-fat diet that was commonly recommended for diabetics during past years may have contributed to the elevated plasma LDL levels in some individuals. Such "diabetic diets" may also have played a role in the predisposition of diabetics toward atherosclerotic complications.
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PMID:Hyperlipidemia: forestalling complications in older diabetics. 388 43

The case of a 28-year-old man with alcohol-induced bouts of recurrent acute pancreatitis after a partial ileal bypass performed for hyperlipidaemia is presented. Serial computed tomography proved valuable for assessing the resolution of the pancreatic mass. Peripheral parenteral hyperalimentation for 6 weeks had a beneficial effect on the course of the pancreatitis and proved to be useful for nutritional support.
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PMID:Recurrent pancreatitis after partial ileal bypass for hyperlipidaemia. A case report. 393 Dec 62

No single pathophysiologic factor has been identified as the cause of recurrent acute pancreatitis. A systematic search should be undertaken in every patient to identify one of a myriad of factors that have been shown to play a part in causing this distressing illness. The abuse of alcohol remains the likeliest cause, and further research may reveal an inborn error of metabolism that jeopardizes some people. Biliary tract disease, gallstones, choledochal cyst, papillary stenosis, and duodenal diverticula show a clear relationship. Metabolic disorders such as hypercalcemia, hyperlipidemia, and hyperparathyroidism remain suspect. Systemic illnesses such as systemic lupus erythematosus and cystic fibrosis must be considered. Development anomalies such as pancreas divisum may precipitate acute pancreatitis through aberrant anatomic structures. Cancer must always be disproved. Not yet firmly established but worthy of thorough investigation are uncommon causes, such as the ingestion of certain drugs or combinations of drugs and trauma, either recent or past. Pancreatitis remains frightening for those with the disease and puzzling and frustrating for the medical people who treat it. A careful history and investigation in accordance with a systematic diagnostic plan that includes many disparate factors will lead to identification of the cause in the majority of patients.
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PMID:Pathophysiologic factors in recurrent acute pancreatitis. 393 40

Six patients had apparent hyponatremia associated with hyperlipidemia and acute pancreatitis. To our knowledge, only one such patient with acute pancreatitis has previously been described, although the association of hyperlipidemia with "pseudohyponatremia" had been well documented. One of the above patients, whose condition was hemodynamically unstable on admission, developed dangerous symptoms of hyperosmolarity and cerebral dysfunction following aggressive resuscitation with hypertonic saline solution. The pseudohyponatremia results from displacement of water in the serum by the lipids, with sodium existing only in the aqueous phase. This volume displacement results in errors of sodium measurement when the latter is determined by flame photometry or indirect potentiometry, but not when determined by ultracentrifugation and direct potentiometry.
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PMID:Pseudohyponatremia in acute hyperlipemic pancreatitis. A potential pitfall in therapy. 402 58

The correspondents describe a case of acute pancreatitis 2 months after starting oral contraceptives in a 32-year-old obese, virilized woman whose familial hyperlipidemia was discovered during hospitalization. She was hospitalized for violent abdominal pain twice; on the second admission laparotomy permitted a diagnosis of typical hemorrhagic acute pancreatitis. When tested a few weeks later, her blood lipids varied from 14-54 gm per 1, triglycerides from 5-32 gm per 1, cholesterol 3-6 gm per 1, pre-beta-lipoprotein peak fell between 50 and 68%, and chylomicrons were absent. Since hyperlipidemia is not known to be assoicated with pancreatitis, the crisis was probably due to oral contraceptives.
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PMID:[Letter: Acute pancreatitis and hyperlipemia under oral contraceptives]. 484 28

Eleven patients with acute pancreatitis who received a lipid-based system of total parenteral nutrition were studied. The safety and efficacy of the intravenous feedings were assessed by comparing the clinical course and serum amylase and urinary diastase levels before treatment and during total parenteral nutrition. Lipid profiles were determined in four of the patients, and nutritional indices including nitrogen balance data were obtained in three patients. No exacerbations of pancreatitis were attributable to the intravenous feedings and the manifestations of the disease resolved or improved in eight patients. Nutritional indices stabilized or improved during total parenteral nutrition, and positive nitrogen balance was achieved in each of the three patients in whom it was measured. Significant hyperlipemia was not observed before or during the lipid infusions. The lipid-based system of parenteral nutrition was well tolerated and effective in this series of patients with pancreatitis.
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PMID:The safety and efficacy of a lipid-based system of parenteral nutrition in acute pancreatitis. 617 87

The known relationship of hyperlipidemia and pancreatitis raises the question whether intravenous fat emulsion is detrimental in acute pancreatitis. Pancreatitis was induced in 52 male Sprague-Dawley rats followed by placement of a jugular catheter which was anchored to the back with a Teflon button. The animals were placed NPO in metabolic cages and continuously infused, initially with normal saline. The 37 animals surviving 24 hr were randomly assigned to group I (mean iv intake: glucose 222 kcal/kg/day; amino acids 13.1 g/kg/day) or group II (glucose 191 kcal/kg/day; intravenous fat emulsion 10% 47 kcal/kg/day; amino acids 12.9 g/kg/day). Nine animals were eliminated from the study because of mechanical problems leaving 14 in each group for analysis. Per cent survival on days 3, 5, and 7 was 64, 50 and 36 in group I, and 50, 36 and 36 in group II. Mean urinary amylase excretion was 244 +/- 185 units/day in group I and 262 +/- 127 units/day in group II. There was no significant difference in survival or urine amylase excretion nor in pancreatic histology or gross appearance of the animals between the two groups. In this model of acute pancreatitis, intravenous fat emulsion was not detrimental as measured by survival, urinary amylase excretion, and pancreatic histology.
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PMID:Effect of intravenous fat emulsion on experimental acute pancreatitis. 619 Oct 54

We report an alcoholic patient with acute relapsing pancreatitis in whom the intravenous infusion of a fat emulsion precipitated a bout of acute pancreatitis. The various relationships between pancreatitis, alcoholism, and hyperlipemia are not clear, and guidelines for the use of intravenous fat emulsions in patients with pancreatitis should take into account their complex interrelationship.
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PMID:Pancreatitis induced by intravenous infusion of a fat emulsion in an alcoholic patient. 619 52


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