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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of chronic pancreatitis in an 8-year-old boy with glycogen storage disease type 1a (GSD 1a) is presented. This patient had a history of hyperlipidaemia unresponsive to dietary therapy, e.g., a carbohydrate-rich diet, uncooked cornstarch, and nocturnal intragastric tube feedings. He had recently suffered bouts of abdominal pain and diarrhoea. Serum amylase and trypsin were elevated, abdominal CT revealed the presence of a pseudocyst of the pancreas. The presence of chronic pancreatitis was confirmed by endoscopic retrograde cholangiopancreatography and an infected pseudocyst was removed at laparotomy.
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PMID:Chronic pancreatitis in a child with glycogen storage disease type 1. 768 58

Acute pancreatitis is a disease characterized by abdominal pain, low-grade fever, abdominal tenderness and rigidity, and moderate elevation of the white blood cell count. A widely used revised classification of pancreatitis is that proposed in 1984 at Marseille. It only distinguishes between acute and chronic pancreatitis. In 61 cases were 40 men and 21 women. The mean age in the total series was 52.5 years. The etiology of the acute condition was alcoholism in 32.8% and biliary tract disease in 23%. In 9.8% the acute pancreatitis is associated with alimentary tract diseases (adipositas, hyperlipidemia). The severity of acute pancreatitis is pathological anatomy determined by three stages. In pathogenesis the process of digestion is caused by activated pancreatic enzyme with acinar cell injury. The acinar cell is normally protected from the action of its own enzymes by elaborate intracellular compartmentation of enzymes. Acute pancreatitis is triggered by pancreatic phospholipase A leading to necrosis of lipolytically active fat cells with release of membrane-toxic fatty acids with following destruction of adjacent tissue. Fat necrosis initiates an acute inflammatory reaction with immigration of granulocytes and liberation of kinins, which activate pancreatic enzyme. Pancreatic enzymes are similar to lysosomal enzymes with regard to substrate specificity. Activation will be also triggered by lysosomal enzymes of necrotic acinar cells.
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PMID:[Acute pancreatitis--etiology, pathological anatomy and pathogenesis]. 226 Mar 61

In a Chinese family with hereditary pancreatitis, two members are proven to have chronic pancreatitis. The propositus, a 31-year-old man, had epigastric pain since the age of 18. Multiple calcifications in the region of the pancreas were seen on plain film of the abdomen, ultrasonography, computed tomography, and endoscopic retrograde pancreatography. Pancreatolithotomy and side-to-side pancreatojejunostomy gave symptomatic improvement. His 60-year-old mother also had pancreatic calcifications in addition to diabetes. Known causes of secondary pancreatitis, such as hyperlipidemia, hyperparathyroidism, and amino aciduria, were ruled out in both patients.
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PMID:Hereditary pancreatitis in a Chinese family. 230 90

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

A rare case of pregnancy and successful transvaginal delivery in secondary diabetes due to chronic pancreatitis is reported. At the age of 16 the patient was diagnosed as having chronic pancreatitis probably caused by hyperlipemia. Three years later diabetes and calcification of the pancreas was found. Blood glucose was well controlled using both self-monitoring of blood glucose and multiple subcutaneous insulin injection just before she became pregnant at age 23. The dose of insulin was slightly increased and no acute exacerbation of pancreatitis occurred during pregnancy, partly due to an appropriate low fat diet with digestive enzyme preparations.
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PMID:Juvenile-onset pancreatic diabetes to whom a healthy infant was born. 760 97

"Hyperlipidemic crisis" is a term used to describe episodic abdominal pain in patients with hyperlipidemia. The morphologic correlates of this phenomenon have not been investigated and the etiology of the disorder is uncertain. We report a unique histologic finding in the pancreas of a 34-year-old woman with a 17-year history of episodic abdominal pain, sometimes accompanied by hyperamylasemia. At the age of 18 years, grossly elevated cholesterol and triglyceride levels were documented and type V hyperlipidemia was diagnosed. At the age of 34 years, subtotal pancreatectomy was performed for intractable abdominal pain. Histologic examination identified an increased number of enlarged pancreatic nerves that were infiltrated by foamy macrophages and encircled by fibrous tissue; endoneurial infiltration with macrophages occasionally split nerves into individual fascicles. Otherwise, the pancreas had only minimal fibrosis, nesidioblastosis, mucinous metaplasia of some pancreatic ducts, and scattered small collections of chronic inflammatory cells, subtle features suggesting very mild chronic pancreatitis. We propose that this novel xanthomatous neuropathy mimicked pancreatitis and was one of the underlying pathophysiologic mechanisms of abdominal pain in this patient. Further studies are necessary to document the prevalence of this new entity in patients with hyperlipidemia and to correlate its occurrence with "hyperlipidemic crisis" in those individuals.
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PMID:Pancreatic xanthomatous neuropathy associated with hyperlipidemia: a cause of abdominal pain mimicking chronic pancreatitis. 811 25

We conducted a retrospective study of patients younger than 20 years of age who had a diagnosis of chronic pancreatitis and underwent assessment at the Mayo Clinic between 1960 and 1990. Those with a known etiologic factor for the pancreatitis (such as a virus, trauma, alcohol, or hyperlipidemia) were excluded from the study. We compared the clinical course of the 42 patients who had hereditary pancreatitis (HP)--defined as at least two family members affected by the condition--with that of the 28 patients who had idiopathic pancreatitis (IP). The mean age at initial assessment was 7 years for those with HP and 12 years for those with IP. All patients in both groups had abdominal pain. Vomiting was more frequent in patients with HP than in those with IP; otherwise the initial symptoms were similar in both groups. Patients with HP, however, had more complications, including pseudocysts (seven patients), steatorrhea (four), ascites (three), portal hypertension (two), and diabetes (one), than did patients with IP (one each had diabetes, steatorrhea, and a pseudocyst). Complications or pain necessitated surgical intervention in 23 of 42 patients with HP versus 4 of 28 patients with IP. Overall in comparison with IP, HP seems to be a more severe variant of chronic pancreatitis, inasmuch as it is associated with more frequent complications and need for surgical intervention.
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PMID:Long-term follow-up of young patients with chronic hereditary or idiopathic pancreatitis. 847 8

Chronic pancreatitis (CP), a disease described only in 1946 by Comfort and colleagues is currently a global disease. Chronic alcoholism, albeit is the most frequent etiologic factor for the disease in most of the affluent nations, a form of CP of undetermined etiology, tropical calculous pancreatitis (nutritional pancreatitis, Afro-Asian pancreatitis, or tropical calculous pancreatopathy) has been recognized to be prevalent in many developing nations. Hereditary pancreatitis inherited as an autosomal dominant disease is reported from all parts of the world. A landmark is the recent discovery of a gene that transmits the disease. Nearly 10% of cases of CP are truly "idiopathic" with no identifiable cause. Recent studies indicate that the idiopathic variety of CP has two subsets--a juvenile form and a senile or late onset form, with distinct clinical features. It is extremely rare to see CP secondary to hyperlipidemia or hypercalcemia. These etiologic associations appear to be overemphasized. Epidemiological studies indicate that alcoholism is growing in incidence all over the world along with an increase in all alcohol-associated disorders such as cirrhosis of the liver or pancreatitis. A genetic predisposition to alcoholic pancreatitis is suspected based on population studies, but not proven. The influence of cigarette smoking in enhancing alcohol-induced injury to the pancreas underscores the health hazard associated with alcoholism and cigarette smoking--two habits that often coexist in many individuals. The recent finding that all forms of CP are premalignant further emphasizes the need to enforce preventive measures. The hope is that CP is a preventable disease. The despair is that alcoholism is increasing and spreads across geographic and religious boundaries.
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PMID:Chronic pancreatitis: a historical and clinical sketch of the pancreas and pancreatitis. 953 Nov 14

Chronic pancreatitis is a rare disease in children and is usually secondary to underlying diseases such as hereditary pancreatitis, cystic fibrosis, hyperlipidemia, prolonged malnutrition, gallstones or anomalies of the biliary-pancreatic duct system. Hereditary pancreatitis is a common cause of chronic pancreatitis in children but is often unrecognized until months or years later. We report here a family with hereditary pancreatitis in which four members are affected.
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PMID:Hereditary pancreatitis: report of a family from Turkey. 989 1


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