Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two Swedish kindreds with hereditary pancreatitis are reported. The onset of symptoms was in early childhood. Otherwise the clinical course did not differ from the non-hereditary form. In no patients were found signs of alcohol-overconsumption, hyperparathyreoidism, hyperlipidemia or mucoviscoidosis. Three patients with intractable pain and frequent hospitalization were operated on with pancreatico-jejunostomy as described by Puestow-Gillesby, with excellent results. Although the observation periods are short (0.5, 2 and 4 years, respectively) it seems legitimate to recommend the operation also for the hereditary form of pancreatitis if intractable pain or frequent exacerbations are present.
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PMID:Hereditary pancreatitis-a report on two kindreds. 65 33

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

Pancreatitis occurring in late pregnancy and in the puerperium has been documented as an entity unrelated to cholelithiasis or hyperlipidemia. Canine pancreatic exocrine function has been studied during pregnancy and the puerperium. Pancreatic secretion was evaluated in eight pregnant female mongrel dogs prepared with Thomas duodenal and gastric fistulae, during pregnancy (corresponding to the third trimester in humans), during the puerperium, and several months after whelping. Basal secretion (volume and HCO3) was increased during pregnancy and the puerperium. The response to exogenous secretin (submaximal and maximal) was unchanged during pregnancy but decreased in the puerperium. Resting enzyme output was increased during pregnancy and the puerperium; the responses to cholecystokinin-pancreozymin during pregnancy were even more profoundly increased. Although the mechanism is speculative, these alterations in pancreatic function might contribute to the development of pancreatitis in pregnancy and the puerperium.
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PMID:Pancreatic exocrine secretion during and after pregnancy. 111 67

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

Case reports of 2 patients who developed pancreatitis and hyperlipidemia while using oral contraceptives are presented. The 1st patient had been taking Ovulen for 2 years when severe abdominal pain suddenly developed. Initially cholecystitis was diagnosed. Symptoms subsided within 1 week but recurred 2 months later, when the white blood count was increased to 16,400/cubic mm. Serum was grossly lipemic with a triglyceride level of 3500 mg% and serum cholesterol 560 mg%. 3 days later triglycerides had fallen to 400 mg% and cholesterol to 270 mg%. Cholecystography was normal. The pain had subsided. Symptoms have not recurred since stopping use of Ovulen. The 2nd patient was admitted with severe abdominal pain of 48 hours duration. Similar attacks of pain had occurred previously but had been of short duration. She had been taking Ovulen for 3 years. White blood count was increased to 18,000. Serum was grossly lipemic. Serum glyceride concentration was 7000 mg% and cholesterol 1200 mg%. Afer 3 days triglycerides were 500 mg% and cholesterol 475 mg%. Pancreatitis was diagnosed. Therapy was Ryles tube suction, atropine, intravenous saline, and a broad spectrum antibiotic. Symptoms subsided in 10 days. The hyperlipidemia is thought to have been a primary condition causing the pancreatitis. [Patients known to have such a condition should avoid use of oral contraceptives.
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PMID:Hyperlipidaemia and pancreatitis associated with oral contraceptive therapy. 118 40

It is discussed the case of a patient, a 45 year old female, who suffered two episodes of acute pancreatitis in one year. This patient is not an alcoholic but diabetic, atherosclerotic and with type IV hyperlipemia. It is presented some reports of the medical literature on the matter and some possible pathogenic mechanisms to explain the pancreatitis associated to hyperlipemia. In this particular case the authors do not consider the hyperlipemia secondary to a pancreatitis but a precipitating factor.
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PMID:[Recurrent pancreatitis and hyperlipemia. Clinical case and review of the literature]. 120 40

We have characterized the clinical and biochemical features of three siblings of a kindred with severe hypertriglyceridaemia due to apolipoprotein C-II (apo C-II) deficiency caused by the mutation described as apo C-IIHamburg. The clinical syndrome is characterized by recurrent pancreatitis in two of three affected individuals, with discrete hepatosplenomegaly in all three patients and cholelithiasis in one. Eruptive xanthomas and lipemia retinalis were absent. Plasma lipoproteins were characterized by fasting chylomicronaemia, reduced low density lipoproteins (LDL) and low high density lipoproteins (HDL). The marked hypertriglyceridaemia could be corrected promptly by infusion of normal plasma. Apolipoprotein C-II (apo C-II) levels in homozygotes were very low (0.01 mg dl-1), and mean apo C-II levels in heterozygotes were lower (2.08 +/- 0.11 mg dl-1) than in normal family members (3.38 +/- 0.75 mg dl-1). Lipoprotein lipase and hepatic triglyceride lipase activities in post-heparin plasma were normal. Zonal ultracentrifugation revealed a marked increase in triglyceride-rich lipoproteins and reduced LDL and HDL. LDL consisted of two fractions with higher hydrated density of the main fraction compared with normals with a trend to normalization on a fat-free diet. The molecular defect in the apo C-II Hamburg gene has been previously identified as a donor splice site mutation in the second intron. This leads to abnormal splicing of the apo C-II Hamburg mRNA and apo C-II deficiency in plasma. The mutation causes the loss of an HphI restriction enzyme site present in the normal apo C-II gene.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Apolipoprotein C-II deficiency syndrome due to apo C-IIHamburg: clinical and biochemical features and HphI restriction enzyme polymorphism. 134 86

Isotretinoin, a retinoid derivative, is in wide use as a treatment for severe acne and other dermatologic conditions. Its effects on serum lipids, most notably the induction of hypertriglyceridemia, have been well documented. We present a case of a young woman with a previous history of gestational hyperlipidemia who developed hypertriglyceridemia and pancreatitis after initiation of isotretinoin therapy. A history of gestational hyperlipidemia may serve as a marker to help identify patients who are at increased risk for developing severe hypertriglyceridemia while receiving isotretinoin. Her case emphasizes the need to consider the possibility of pancreatitis in patients who develop abdominal pain while receiving this drug.
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PMID:Marked hyperlipidemia and pancreatitis associated with isotretinoin therapy. 144 57

From 1981 to 1990, 14 of 70 patients hospitalized at our institution for severe acute pancreatitis were selected to undergo percutaneous drainage of pancreatic abscess, under computed tomographic (CT) scan guidance. Pancreatic abscess was defined, on contrast-enhanced CT scan, as an infected fluid collection without pancreatic necrosis. There were nine men and five women, ranging in age from 28 to 46 years. The main cause of pancreatitis was alcohol abuse (eight patients). Other causes were gallstones (two patients), hyperlipidemia (two patients), postoperative (one patient) and one unknown. Ranson criteria were available in ten patients and ranged from three to six. Percutaneous drainage was performed as the primary treatment in 13 patients and for removal of a residual collection postoperatively in one patient. In two critically ill patients, percutaneous drainage was performed as a temporizing measure. In 12 patients with well-limited hypodense collections, percutaneous drainage was expected to result in the definitive cure of the abscess. Pigtail drains (No. 14F), were inserted using local anesthesia and CT scan guidance. Two patients had two drains and 12 patients had only one drain. Two patients were definitively cured by percutaneous drainage and all other patients were operated upon for removal of infected necrosis. In this study, the lack of accuracy of contrast-enhanced CT scan in the diagnosis of peripancreatic necrosis is highlighted and that percutaneous drainage has a better efficiency in the treatment of residual collections postoperatively than as a primary treatment of infected fluid collections is illustrated.
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PMID:Failure of percutaneous drainage of pancreatic abscesses complicating severe acute pancreatitis. 173 73


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