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)

Alcohol promotes accumulation of fat in the liver mainly by substitution of ethanol for fatty acids as the major hepatic fuel. The degree of lipid accumulation depends on the supply of dietary fat. Progressive alteration of the mitochondria, which occurs during chronic alcohol consumption, decreases fatty acid oxidation by interfering with citric acid cycle activity. This block is partially compensated for by increased ketone body production, which results in ketonemia. Thus, mitochondrial damage perpetuates fatty acid accumulation even in the absence of ethanol oxidation. Alcohol facilitates esterification of the accumulated fatty acids to triglycerides, phospholipids, and cholesterol esters, all of which accumulate in the liver. The accumulated lipids are disposed of in part as serum lipoprotein, resulting in moderate hyperlipemia. In some individuals with pre-existing alterations of lipid metabolism, small ethanol dose may provoke marked hyperlipemia which responds to alcohol withdrawal. Inhibition of the catabolism of cholesterol to bile salt may contribute to the hepatic accumulation and hypercholesterolemia. The capacity of lipoprotein production and hyperlipemia development increases during chronic alcohol consumption, probably as a result of the concomitant hypertrophy of the endoplasmic reticulum and Golgi apparatus. However, this compensation is relatively inefficient in ridding the liver of fat. This inefficiency may be linked to alterations of hepatic microtubules induced by ethanol or its metabolites, which interfere with the export of protein from liver to serum, promoting hepatic accumulation of proteins as well as fat. As liver injury aggravates, hyperlipemia wanes and liver steatosis is exaggerated. Derangements of serum lipids similar to those found in other types of liver disease also become apparent. The changes in serum lipids may be a sensitive indicator of the progression of liver damage in the alcoholic.
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PMID:Effects of ethanol on lipid metabolism. 8 83

There are many changes in the plasma, lipids, and lipoproteins in patients with liver disease. They have proved difficult to study but our understanding of these changes has increased greatly during recent years. In obstructive jaundice hyperlipidaemia is a fairly constant finding and this appears to be due to the regurgitation of phospholipid from the obstructed biliary tree. The plasma lipids tend to fall with parenchymal liver disease. The composition of the lipoproteins depends on the activity of the plasma enzyme lecithin: cholesterol acyl transferase. When LCAT activity is high the individual lipoprotein fractions are normal. When it is reduced all of the lipoprotein fractions are affected but the pattern found with obstruction is quite different from that found with parenchymal disease. The changes in plasma lipoproteins appear to be associated with change in the lipid composition of cellular membranes and this may have important functional implications.
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PMID:Plasma lipids and lipoproteins in liver disease. 35 66

Benign symmetric lipomatosis (BSL) leads to characteristic multiple lipomas of the neck and submandibular region. BSL is easily diagnosed by its typical feature, "Madelung's neck". However, the early stages are often missed or lead to futile diagnostic endeavours. A report is presented on 7 men with BSL aged 36--65 years who were investigated with regard to alcohol consumption, clinical findings and liver histology. This is the first time that liver histology has been systematically worked up in patients with BSL. All admitted long standing ethanol intake (x = 111 ml/day) prior to the development of BSL. The growth of the lipomas was irregular and occurred over a period of months. There was no correlation with overweight or hyperlipidemia. However, liver biopsy revealed features consistent with alcoholic liver disease in all subjects. It is suggested that BSL is a symptom of alcoholic liver disease mainly affecting middle-aged men.
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PMID:[Benign symmetric lipomatosis: a symptom of alcoholic liver disease?]. 38 49

Individual serum bile acids were analysed by an improved gas liquid chromatography method in 12 patients with primary hyperlipidaemia. Total serum bile acid concentrations were raised in 10 subjects. Ursodeoxycholic acid was found in all 12 patients. It was present in significantly greater concentrations, accounted for a greater proportion of the total serum bile acids, and occurred more frequently than in patients with various forms of hepatobiliary disease. Patients with hyperlipidaemia had proportionately less deoxycholic acid than controls but more than patients with liver disease. There was proportionately less chenodeoxycholic acid in patients with hypercholesterolaemia, in whom the primary bile acid ratio was raised.
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PMID:Serum bile acids in patients with hyperlipidaemia. 62 19

Rats fed a diet containing a high percentage of butter, cholesterol, cholic acid and proply thiouracil (HFD) showed weight loss and developed hyperlipidemia, marked fatty infiltration of the liver, moderate elevation of SGPT, degenerative changes of the heart muscle, bradycardia, alterations of the QRS complex in the electrocardiogram, and initial hemoconcentration followed by moderate anemia. Treatment with adriamycin (18 X 1 mg/kg i.p.) resulted in significant augmentation of the cardiotoxic effects of this drug demonstrated by electrocardiographic measurements and myocardial histopathology. Adriamycin-induced atrophy of the lymphatic tissue was seen only in rats fed HFD and not in animals receiving ground chow. Adriamycin levels in the heart after single i.p. injection were higher in rats receiving HFD. This effect was present already after 10 days on HFD. At this time histopathological liver changes were present and SGPT was elevated. It is concluded that the increase in adriamycin toxicity is, at least in part, due to diminished excretion by the liver. These experimental findings are in accordance with clinical observations which have identified liver disease as one of the important risk factors for the development of adriamycin cardiomyopathy.
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PMID:Modification of adriamycin toxicity in rats fed a high fat diet. 86 Jun 72

Benign symmetric lipomatosis (BSL) leads to characteristic multiple lipomas of the neck and submandibullar region. Seven men with BSL, aged 36--65 years, were investigated with regard to alcohol consumption, clinical findings and liver histology. They admitted a long standing ethanol intake (x = 107 ml/day) prior to the development of BSL. The growth of the lipomas was irregular and occurred over a period of months. There was no correlation with overweight or hyperlipidemia. However, liver biopsy revealed features consistent with alcoholic liver disease in all subjects. It is concluded that BSL represents a symptom of alcoholic liver disease affecting middle aged men.
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PMID:[Benign symmetric lipomatosis--symptom of alcoholic liver disease]. 92 36

Chronic obstructive liver disease and secondary hyperlipidemia developed in an immunodeficient boy. Sequential addition of cholestyramine and phenobarbital to his medical regimen, following an initial response to bile drainage, resulted in the disappearance of xanthomas and pruritus, and the restoration of normal serum concentrations of lipids and bile acids. This improvement may result from shifting the bile acid pool from the peripheral blood compartment to the enterohepatic circulation.
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PMID:Immunodeficiency, xanthomas and obstructive liver disease. 96 2

In 1986, narrow plasma proton nuclear magnetic resonance (NMR) methyl and methylene line widths were reported to be associated with malignant disease, but more recent studies have not confirmed this relationship. The authors analyzed 106 plasma samples from healthy control subjects and patients with cirrhosis, hepatocellular carcinoma, metastatic liver tumors, other untreated cancers, and hyperlipidemia. NMR spectroscopy was performed using a proton NMR spectrometer operating at 399.65 MHz. A significant difference was found between the mean line widths of the plasma methyl resonances in control subjects and those in patients with cancer or hyperlipidemia. However, no significant difference was found between the mean plasma methylene line widths in control subjects and patients with cancer. Plasma samples from patients with liver disease or hyperlipidemia showed a characteristic methylene spectral pattern. The methylene pattern could be separated into three types: type A had a small peak on the right shoulder of the main peak; type B was a sharp single peak; and type C was a broad single peak. All control subjects had type A pattern; patients with liver disease had type C pattern; and patients who had hyperlipidemia had type B pattern, and hyperlipidemia may affect methyl and methylene line widths in NMR spectra. Because the methyl and methylene levels and their average line widths correlated inversely with triglyceride levels, considering the spectral patterns that indicate hyperlipidemia should decrease false-positive results and make the methyl line width useful for cancer screening.
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PMID:Use of proton nuclear magnetic resonance spectroscopy of plasma in screening for malignant disease. 132 78

Non-alcoholic steatohepatitis resembles alcoholic liver disease in hepatic morphology but appears to have a different natural history. We sought to assess the nature of non-alcoholic steatohepatitis by a prospective study of its clinical progression and the relationship of biochemical abnormalities to changes in serum lipids among 15 patients with this disorder. In addition, antipyrine clearance (Cl-AP), which reflects hepatic microsomal oxidative capacity, was measured serially. Although initial liver histology included micronodular cirrhosis in five cases and bridging fibrosis in another three, only one patient developed a hepatic complication during 1-10 years (median: 3.7) of follow up. This confirms the relatively benign nature of non-alcoholic steatohepatitis. Moreover, Cl-AP, which was below the normal range in 13 patients, did not change significantly during 10-40 months of follow up. However, compared with other chronic liver diseases, the reduced Cl-AP was disproportionately low relative to the uniformly normal serum albumin concentration and other indices of hepatic metabolic function. This is consistent with selective impairment of endoplasmic reticular drug oxidizing enzymes. Hyperlipidaemia was present in 11 patients. In three of these, diet-induced correction of serum triglyceride elevation was associated with reduction of hepatocellular damage as indicated by serum enzyme levels. A hypothesis that unites these and earlier findings is that release of cytokines may occur in non-alcoholic steatohepatitis and produce accumulation of free fatty acids in the liver, leading to focal necro-inflammatory lesions and the destruction or down-regulation of cytochrome P450.
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PMID:Non-alcoholic steatohepatitis: impaired antipyrine metabolism and hypertriglyceridaemia may be clues to its pathogenesis. 178 74

The ideal body weight (kg) of each individual can be calculated by the following formula: ideal body mass index x the height (m)2, since body mass index is expressed by the body weight in kilogram divided by the height squared in meters. We investigated an ideal body mass index with respect to morbidity in 4565 Japanese men and women aged 30-59 years. Ten medical problems served as indices of morbidity: lung disease, heart disease, upper gastrointestinal disease, hypertension, renal disease, liver disease, hyperlipidemia, hyperuricemia, diabetes mellitus and anemia. The value of body mass index associated with the lowest morbidity was 22.2 kg/m2 in men and 21.9 kg/m2 in women, according to the quadratic regression curves relating body mass index to morbidity. From these findings, we propose that the ideal body weight is 22 x height (m)2. Our recommendations apply to the age group studied, namely 30-59 years.
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PMID:Ideal body weight estimated from the body mass index with the lowest morbidity. 201 Feb 54


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