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

Lipemic serum from three patients with acute pancreatitis and type IV hyperlipemia was fractionated into very-low-density lipoproteins and clear serum. Amylase activity (determined by the Phadebas method) in the component fractions did not exceed that in the original lipemic serum. Addition of these fractions or VLDL and chylomicrons from asymptomatic patients with hyperlipemia to nonlipemic serum from patients with "routine acute pancreatitis" did not inhibit amylase activity or alter the electrophoretic mobility of amylase isoenzymes. Therefore the normal amylase activity often observed in hyperlipemic pancreatitis does not result from an inhibition of amylase activity by serum lipoproteins.
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PMID:Possible mechanisms of normal amylase activity in hyperlipemic pancreatitis. 20 33

This case focuses on the biochemical findings in acute pancreatitis and the role of the laboratory in the diagnosis and management of such patients. It also illustrates a major unappreciated problem in the use of amylase determinations in patients with acute pancreatitis: normal serum amylase activity in the presence of hyperlipemia.
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PMID:(Washington University case conference): acute pancreatitis, hyperlipemia, and normal amylase. 64 16

The procedure used with the Du Pont aca for alpha-amylase (1,4,-alpha-D-glucan glucanohydrolase, EC 3.2.1.1) was evaluated in our laboratory and compared with the Roche Diagnostics "Amylochrome" and Perkin-Elmer Coleman 91 amylase assays. The within-run coefficients of variation (CV) for samples of fresh normal sera were: aca 5.8% and 4.3% on two different lots of reagent, Amylochrome 7.4%, and Coleman 91 3.3%. In sera with abnormally high amylase activity, the respective CV's were: aca, 1.2% and 0.8%; Amylochrome, 2.0%; and Coleman 91, 2.8%. Day-to-day precision studies on fresh and lyophilized normal and abnormal sera gave CV's in the following ranges: aca, 1.8% to 6.7%; Amylochrome, 3.0% to 5.2%; and Coleman 91, 4.5% to 5.9%. Results by the aca procedure were linearly related to activity to about 10-fold the upper limit of normal amylase activity. For serum, correlations were: r = 0.977 for aca vs. Coleman 91 and r = 0.974 for aca vs. Amylochrome. For urine they were: r = 0.978 for aca vs. Coleman 91 and r = 0.975 for aca vs. Amylochrome. Mean recovery from 53 supplemented samples was 98%. Icterus, hemolysis, and lipemia did not interfere with method correlation of aca vs. Coleman 91 or Amylochrome.
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PMID:Evaluation of the Du Pont aca alpha-amylase procedure. 83 42

The operative discovery of acute pancreatitis associated with gross hyperlipidaemia but a normal or high elevated serum amylase concentration has been described. We report a case of acute pancreatitis in which serial dilutions of serum resulted in a 338% rise in the serum amylase concentrations. The importance of appreciating this effect of hyperlipidaemia on the serum level measurements in patients with acute pancreatitis is re-emphasised.
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PMID:A cause of misleading serum amylase concentrations in acute pancreatitis. 87 Sep 64

A patient is described with acute pancreatitis which was probably caused by furosemide. Administration of furosemide on two separate occasions was associated with increases in serum amylase concentrations and recurrence of abdominal pain. This case is of further interest because of the presence of hyperlipemia in the absence of an underlying lipid abnormality. Following recovery from pancreatitis, the lipoprotein pattern evolved from type V to type III, type IIA, and finally to normal.
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PMID:Acute pancreatitis secondary to furosemide with associated hyperlipidemia. 90 Jan 1

Twelve patients with prior episodes of alcoholic pancreatitis and hyperlipemia were admitted to a metabolic ward during a quiescent period. By lipid feeding (316 to 894 Gm. per day), significant hypertriglyceridemia (greater than 600 mg. per 100 ml.) was induced in 11 of the 12 patients. Seven of the 11 patients with hypertriglyceridemia developed abdominal pain similar to but not as severe as that experienced during prior attacks of pancreatitis. Four of the seven patients with abdominal pain developed serum amylase elevations, and, of the remaining three, one had a serum lipase elevation and one a urinary amylase elevation. Alcohol ingestion is known to increase serum triglyceride levels in many individuals. A prior study demonstrated that 41 percent of the patients presenting to our hospital with alcoholic pancreatitis had serum triglyceride elevations. The data from the present study suggest that increased serum triglycerides act as an important intermediary in the pathogenesis of acute pancreatitis in some alcoholic patients.
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PMID:A pathogenesis for alcoholic pancreatitis. 114 40

In 6 of 7 patients with acute pancreatitis and hyperlipemia, inhibition of serum amylase activity was detected by dilution of the serum before assaying for amylase and by correcting for tthe dilution factor. In 4 patients the inhibition phenomenon disappeared within the first few days of hospitalization as the elevated serum triglycerides fell. However, in 2 others there was no relation between triglyceride level and amylase inhibition. Removal of the excess serum lipids by ultracentrifugation did not eliminate the inhibition of amylase activity. Inhibition of amylase activity also occurred in the urine of these patients. No amylase inhibition was demonstrable in lipemic serum from patients without pancreatitis or in pancreatitis serum to which excess lipids were added. The data suggest the presence of a circulating inhibitor of amylase, distinct from the elevated serum lipids, in the serum and urine of patients with acute pancreatitis associated with hyperlipemia. The diagnosis of acute pancreatitis in the patient with abdominal pain and lactescent serum can be facilitated by correcting the serum amylase activity by dilution.
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PMID:Inhibition of serum and urine amylase activity in pancreatitis with hyperlipemia. 114 12

A total of 164 patients with alcoholism-induced osteonecrosis were seen over a 22-year period, from 1962 to 1984. Twenty-three percent of patients were female and 30.5% were black. The average duration of alcohol abuse was 9.5 years, ranging from 8 to 20 years. The presence of femoral head necrosis was diagnosed in patients aged 21-67 years; 28% of patients were under 40 years of age and 76% were under 50 years. Bilateral hip necrosis was present in 44.5% of patients and, within three years of the diagnosis of FHN, the presence of multifocal necrosis became evident in 23 cases at sites away from the hip (shoulders and knees). Hyperlipidemia was found in 38.4% of cases, involving both cholesterol and triglycerides. Serum amylase was elevated in 33 patients; liver dysfunction was present in 50; hepatomegaly was found in 32; and biopsy-confirmed cirrhosis was present in 22 cases. Hyperuricemia was found in 22 patients, some of whom had received steroids. Disabling hip pain was the first manifestation of disability related to alcohol abuse in 158 patients, most of whom required total hip joint replacement. This study supports the hypothesis that alcoholism-induced bone necrosis is caused by fat embolism linked to co-existent hyperlipidemia. The treatment of hyperlipidemia by dietary means or lipotropic medication and the cessation of alcohol abuse is advised. Multi-center studies employing such treatment should provide evidence of its effect on the evolution of necrosis as well as the incidence of bilateral hip femoral head necrosis and multifocal lesions.
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PMID:Alcoholism-induced bone necrosis. 151 11

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

We report here a case of diabetic ketoacidosis associated with hyperlipidemia and acute pancreatitis following alcohol abuse. A 23-year-old man was admitted to the hospital because of right upper abdominal and back pain developing into a state of unconsciousness and shock. He had been drinking 720 ml of whisky daily for 4 years. Laboratory data on admission revealed metabolic acidosis (pH 7.01, PaO2 84.6 mmHg, PaCO2 41.1 mmHg, HCO3- 16.3 mmol/l, BE-16.4 mmol/l), a high blood glucose level (640 mg/dl), strongly positive urinary ketone bodies, hypercholesteremia (913 mg/dl) and hypertriglyceridemia (8500 mg/dl). Furthermore, the levels of pancreatic enzyme including serum amylase (770 U/l) and elastase I (2721 ng/dl) were elevated. After successful treatment of the diabetic ketoacidosis with insulin and fluid supplementation, serum cholesterol, triglyceride and pancreatic enzyme levels decreased concomitantly with stabilization of the blood glucose level. From these findings, it is suggested that hyperlipidemia might have caused the acute pancreatitis which developed into diabetic ketoacidosis in this patient.
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PMID:[A case of non-insulin-dependent diabetes mellitus associated with diabetic ketoacidosis after the onset of hyperlipidemia and acute pancreatitis following alcohol abuse]. 193 46


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