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

The article presents the case history of a 28 year-old male with alcohol-induced hypertension and extreme hypercholesterolemia (36 mmol/l) and hypertriglyceridemia (76 mmol/l). Blood pressure and blood lipids were completely normalized after a few months withdrawal from alcohol. Alcoholism is emphasized as a possible differential diagnosis for both hypertension and hyperlipemias. The upper referential value for alcoholic hyperlipemia should probably be adjusted in accordance with the values observed in the present case.
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PMID:[Alcohol-induced hyperlipemia. Hypertension and extreme hypercholesterolemia/hypertriglyceridemia in a patient with hidden alcohol abuse]. 291 78

The clinical recognition of dioxin-associated illness can be extremely difficult for the physician. After analyzing the relative sensitivity and specificity of reported manifestations of exposure to 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD), we suggest criteria for the diagnosis of dioxin toxicity. Exposure to higher doses of 2,3,7,8-TCDD may lead to the appearance of chloracne and the increased excretion of porphyrins and porphyria cutanea tarda. Liver function abnormalities, peripheral neuropathy, hyperlipidemia, and evidence of weakness and depression may occur following exposure; however, these findings are less specific since diseases such as diabetes or alcoholism could cause several of these problems. The long-term effects of exposure to low-dose TCDD are currently uncertain.
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PMID:The diagnosis of dioxin-associated illness. 296 9

Previous reports have described 5-20% prevalence of hyponatremia in extended care facilities, due largely to drugs or inappropriate antidiuretic hormone secretion. In our 400 bed VA extended care facility, 15 men with organic brain syndrome (Alzheimer's, multi-infarct dementia, anoxic encephalopathy or alcoholism) currently receive Isocal via gastrostomy as the sole source of nutrition. We noted intermittent hyponatremia in about half of these patients, and conducted a chart review to investigate the cause. Mean age was 68 yr (range 46-92); tube feeding duration was 3 mo.-3 yr; 266 Na concentrations were obtained from the charts. Simultaneous with these Na analyses, one of three diets prevailed: (A) mixed foods (3-6 g Na/day) orally before gastrostomy; (B) Isocal supplemented with NaCl to give 2 g Na/day; (C) unsupplemented Isocal providing 1 g Na/day. (B) and (C) had been randomly varied by rotating physicians. Serum Na was directly related to Na intake. On (A), Na was within normal range (135-145 mEq/l) in all men. One patient was hyponatremic during diet (B). During (C), eight patients were hyponatremic. Na was less than 135 mEq/l in 40% of all samples during diet (C) and less than 130 mEq/l in 14%. Changing from diet (A) or (B) to diet (C) caused nearly equivalent declines in Na and Cl; K and HCO-3 were unaffected. No hyponatremic patient took drugs known to cause hyponatremia, or had congestive heart failure, hypoalbuminemia, lipemia or fasting hyperglycemia. At the end of the study, four hyponatremic men were changed from (C) to (B); serum Na became normal in all four patients, without edema or hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyponatremia in tube-fed elderly men. 308 Apr 61

There is much evidence that altered lipid metabolism contributes to the development of coronary artery disease (CAD). It is generally accepted that there is a direct association between the extent of CAD and total plasma cholesterol, as well as an inverse association between the extent of CAD and plasma HDL-cholesterol. No general agreement exists about the atherogenetic potential of plasma triglycerides and of triglyceride-rich lipoproteins. Since lipoprotein lipase (LPL) is the key-enzyme in the catabolism of triglyceride-rich lipoproteins (chylomicrons and very low-density lipoproteins), we examine the relationship between triglyceride-rich lipoproteins and LPL in vitro and in vivo. The concentrations of the main lipoprotein density classes, namely very low-density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), low-density lipoproteins (LDL), high-density lipoproteins2 (HDL2) and HDL3, are measured by rate zonal ultracentrifugation. The preparation of VLDL, IDL, LDL, HDL2, and HDL3 is performed by sequential ultracentrifugation. The activity of LPL is measured radioenzymatically in a glycerol-based triolein emulsion. It can be demonstrated in vitro that VLDL, IDL, and HDL2 from normal plasma are able to increase LPL-activity in contrast to VLDL, IDL, and HDL2 from hyperlipemic plasma. This difference seems to be caused by an altered composition of apolipoproteins in hyperlipemic lipoproteins. An artificial acidosis in three healthy subjects shows in contrast to alkalotic and neutral blood-pH a significant decrease of LPL-activity. This result seems to be of some interest, since diseases associated with acidotic blood-pH, such as chronic renal disease, diabetes mellitus or chronic alcoholism, show secondary hyperlipemias caused by a deficit of LPL-activity. It can be shown in 15 male patients who produce a secondary type-V hyperlipemia during severe abuse of alcohol, that LPL-activity is decreased significantly as compared to 15 healthy controls. During sober phases, this alcohol-induced hyperlipemia and the impairment of LPL-activity disappears completely. In an other group of 8 male patients, who are not producing severe secondary hyperlipemia during approximately the identical alcohol intake, LPL-activity is also significantly decreased, but the activity of hepatic lipase is significantly increased. This increase of the activity of hepatic lipase seems to protect these patients from the development of secondary type-V hyperlipemia. In 89 male patients with angiographically assessed CAD a very strong inverse association between the activity of LPL and the extent of CAD is found.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Pathologic decrease in lipoprotein lipase activity in relation to the development of hyperlipemias and their significance for coronary heart disease]. 345 43

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

Between 1978 and 1985, we conducted a prospective study of 21 patients who survived several attacks of pancreatitis and were diagnosed as having primary hyperlipidemia. None of the patients suffered from chronic alcoholism, primary diabetes, or cholelithiasis or was receiving prolonged steroid therapy. Lowering of plasma lipid values toward normal was achieved in all patients following a program of combined dietary and drug (bezafibrate) therapy. Five patients had recurrent episodes of pancreatitis during the treatment program. These patients were diagnosed subsequently as suffering from bulimia and were all given cognitive behavioral therapy. One patient died following an attack of pancreatitis. An underlying eating disorder should be suspected in patients who relapse after treatment for pancreatitis and hyperlipidemia. Multidisciplinary treatment should be used in these patients to improve therapeutic efficacy and uncover behavioral patterns that have a direct impact on their life expectancy.
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PMID:Bulimia. An underlying behavioral disorder in hyperlipidemic pancreatitis: a prospective multidisciplinary approach. 382 58

Because of the high incidence for development of a secondary hyperlipemia during chronic alcohol intake, this study was performed to look for a possible reason, why some patients produce severe hyperlipemia and other ones not. 15 male patients with chronic alcoholism (group I) who produce under influence of alcohol a secondary type-V hyperlipoproteinemia (type-V HLP) were compared with 15 male controls. Additionally, 8 male patients with chronic alcoholism (group II) who were normolipemic under alcohol abuse, and 7 male patients (group II) who had also produced type-V HLP under chronic alcohol abuse, but were teetotal since at least 6 months, were investigated. In comparison with controls, patients of group I showed significantly (p less than 0.01) increased plasma concentrations of very low-density lipoproteins (VLDL) and significantly decreased plasma concentrations of low-density lipoproteins (LDL), high-density lipoproteins2 (HDL2) and HDL3 (all p less than 0.01). Furthermore, the activities of postheparin lipoprotein lipase (LPL) and hepatic lipase (HTGL) were significantly decreased (both p less than 0.01). In patients of group III, the plasma concentrations of lipoproteins did not differ significantly from controls, but the activity of LPL was also significantly impaired (p less than 0.01), whereas the activity of HTGL was distinctly (p less than 0.01) increased. No significant difference between patients of group II and controls could be demonstrated. It is concluded that severe alcohol intake strongly impairs LPL in patients with chronic alcoholism. The pronounced increase of HTGL in patients of group III seems to protect these individuals from producing severe hyperlipemia under the influence of alcohol.
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PMID:[Lipoproteins, post-heparin lipoprotein lipase and hepatic triglyceride lipase in patients with and without severe hyperlipemia caused by alcoholism]. 401 22

The effect of chronic alcohol intoxication on metabolic disturbances and fatty infiltration and degeneration was studied in genetically obese, hyperlipoproteinaemic, fa/fa Zucker rats. Sixteen obese Zucker (fa/fa) rats, sixteen lean Zucker rats (Fa/-) and sixteen Wistar rats, all male rats aged 7-8 weeks, were given either a control (C) diet (13% of energy from protein, 37% from fat, 50% from carbohydrate) or an ethanol (E) diet (13% of energy from protein, 37% from fat, 14% from carbohydrate, 36% from ethanol) for 4 weeks. The fa/fa rats given diet E consumed more energy than those given diet C, but after 4 weeks the weight gains and degrees of obesity were similar for both groups. With both diets, the developed hyperlipidaemia could be explained by the hyperinsulinaemia. Both hypertriglyceridaemia and hypercholesterolaemia were lower in fa/fa rats eating diet E than in those given diet C. Fatty infiltration of the liver, as assessed by hepatic triacyglycerol and cholesterol contents, was observed with both diets, but for fa/fa rats it was less extreme in those given diet E.
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PMID:Influence of chronic ethanol intake on obesity, liver steatosis and hyperlipidaemia in the Zucker fa/fa rat. 406 15

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

In order to study the effects of chronic alcoholism, 3 groups of patients were investigated and compared to 10 healthy controls. Group I consisted of 9 heavy drinkers, who exhibited type V hyperlipidemia (HLP) under alcohol intake. Group II consisted of 7 patients, who previously had type V HLP under the influence of alcohol. At the time of the investigation, however, they had ceased alcohol drinking for at least 6 months and were normolipidemic. Group III consisted of 7 heavy drinkers without hyperlipidemia. Compared to controls, group I had significantly decreased plasma concentrations of high density lipoproteins2 (HDL2) and HDL3 (both P less than 0.01); activities of post-heparin lipoprotein lipase (LPL) and hepatic lipase (HTGL) as well were excessively decreased (both P less than 0.01). In group III LPL was also decreased (P less than 0.01), but HTGL was distinctly (P less than 0.01) higher than in controls. No such differences could be demonstrated for the patients of group II. Acute alcohol withdrawal from a patient suffering from alcoholism with HLP led to a sharp increase of LPL with a simultaneous decrease of VLDL within 2 days and a more delayed increase of LDL, HDL2 and HTGL, all reaching normal values within 12 days after cessation of alcohol drinking. With respect to the apolipoprotein (apo) composition of HDL2, patients of group I and group III exhibited a significantly lower percentual content of apo C-I at the expense of a significantly higher content of apo A-II as compared to controls and patients of group II. In group I and II, the percentual content of apo D in HDL2 was significantly higher than in controls and in group III. It is concluded that severe alcohol intake strongly impairs LPL in patients with HLP. The pronounced increase of HTGL in some patients (group III) may protect these individuals from HLP. The increased content of apo D in HDL2 may be a possible primary trait for alcohol-inducible HLP.
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PMID:Post-heparin lipolytic activities and alterations of the chemical composition of high density lipoproteins in alcohol-induced type V hyperlipidemia. 649 35


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