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)

A clinical and laboratory examination of abnormalities not attributable to atherosclerosis has been performed on 188 male and 126 female adult subjects with hyperlipidaemia. The sample was recruited from 20000 subjects screened at a health control centre who had an initial serum cholesterol and/or triglyceride (TG) concentration above 350 mg/100 ml and 3.50 mmol/l. All were subjectively healthy and had no history of atherosclerotic disease. Known cases of secondary hyperlipidaemia were excluded. Lipoprotein (LP) analysis with preparative ultracentrifugation and electrophoresis was made on all subjects including control group with "nonelevated" serum lipids. Typing of hyperlipoproteinaemia (HLP) was performed according to the modified system of Fredrickson et al. Compared to controls, subjects who had elevated very low density ?LP (VLDL) (types II B, III, IV and V) were more obsese, while subjectI B and women with type IV HLP than in the control groups. Arcus corneae was seen in 29% of control groups. Arcus corneae was seen in 29% of controls and in higher frequencies in types II A and II B. A positive correlation existed between the frequency of arcus corneae and the mean low density LP cholesterol in the different types. Multiple tendon xanthomata (n equals 11) were found exclusively in type II A HLP, palmar xanthomata (n equals 3) only in the presence of floating beta-LP and eruptive xanthomata in one male with type V HLP. The mean ESR was increased in all types of HLP. The mean S-GPT and uric acid concentrations were higher in type IV HLP in both sexes than in the control groups. In men with type IV HLP S-GPT was positively correlated to tvldl tg. the uric acid level was correlated to both the VLDL TG concentration and body weight independently. Of the male subjects with HLP 1/3-1/2 had a diabetic or borderline i.v. glucose tolerance.
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PMID:Studies in asymptomatic primary hyperlipidaemia II. Clinical findings. 16 37

Ten episodes of massive transaminase increase with hepatic necrosis were observed in 7 patients after infusion of megluminioglycamide (Biligram). The patients were 3 men and 4 women aged 49 to 65 years with biliary tract disease (n = 1), recurrent pancreatitis (n = 1), hyperlipidaemia and minimal toxic liver damage (n = 1), pyelonephritis (n = 1), , arteriitis (n = 1), and pseudo-LE (n = 1). In 6 patients there was an increase of the alkaline phosphatase without icterus before the investigation and a slight increase of transaminases in 3 patients. After infusion of 100 ml of Biligram in 5 patients and of 200 ml in 2 patients there was an abrupt increase of GPT (98-2202 U/l) with a lesser increase of GOT. The alkaline phosphatase activity remained unchanged. Three patients showed symptoms such as upper abdominal pain, fever erythema, or conjunctivitis. Histologically all patients showed centrolobular necroses. Transaminases should be checked 2 days after intravenous cholangiograms. In patients with a definite increase reexposure should be avoided.
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PMID:[Hepatic necroses after infusion cholangiography (author's transl)]. 63 57

To develop the prophylactics and the curatives for atherosclerosis, thyroxine derivative, CG-635, was assayed for its physiological activities in experimental atherosclerosis in rabbits fed with cholesterol. It was found that CG-635 possessed serum TC/TP value lowering activity (total cholesterol/total phospholipid) in normal and cholesterol fed rabbits for 3 weeks, and prevented the elevation of the value of cholesterol fed rabbits by daily injection for 7 weeks. CG-635 also depressed the hyperlipemia induced by cholesterol feeding, and its inhibitory effect was shown to be more marked on the increase of cholesterol than triglyceride, phospholipid and free fatty acid in serum. CG-635 did not, however, influence GOT, GPT and G-6-Pase activities in serum with increased cholesterol intake. From the histological findings it was proved that this compound prevented to a high degree the occurrence of atherosclerosis and fatty liver of cholesterol fed rabbits. Furthermore, it was recognized that thyroid hormone and the thyroid simulating hormone-like activities of CG-635 were much weaker than thyroxine, except for the action in the lipid metabolism.
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PMID:[Effect of d,l-alpha-methyl-3, 5, 3, 5-tetraiodothyronine ethylester hydrochloride (CG-635) on experimental hypercholesterolemia and atherosclerosis in rabbits (author's transl)]. 117 Oct 31

Hyperlipidemia may be one of the risk factors in the development of atherosclerotic disease in renal transplant recipients. In the present study, 24 kidney recipients with hyperlipidemia were treated with an HMG-CoA reductase inhibitor, pravastatin (10 mg/day). All recipients had been treated with cyclosporine (CsA), azathioprine (Az), and prednisolone (Pred). The mean total cholesterol (T-chol) level decreased from 323 +/- 7.4 to 261 +/- 7.9 mg/dl at one month after starting treatment (P less than 0.01) and this level did not change during treatment for further 6 months. The mean LDL cholesterol level was also decreased from 205.9 +/- 11.2 to 118.7 +/- 8.1 mg/dl at 3 months after starting treatment (P less than 0.01). On the other hand, pravastatin did not affect the levels of HDL-cholesterol and triglycerides. Pravastatin did not show any effects on the white blood cell, monocyte, and lymphocyte counts, or the hemoglobin concentration (NS). One patient displayed a slight elevation of aspartate aminotransferase and alanine aminotransferase levels, but this was not sufficient to cease treatment. Pravastatin did not adversely affect the renal function or creatinine phosphokinase (CPK) levels. Two recipients developed nausea and vomiting and their treatment was stopped. Pravastatin appears to be a safe and efficacious method of treating hyperlipidemia in renal transplant recipients.
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PMID:The effects of pravastatin on hyperlipidemia in renal transplant recipients. 173 92

The medical records of 18 dogs that had hepatic disease and received phenobarbital as an anticonvulsant for 5 to 82 months were reviewed. Clinical signs included sedation and ataxia in all dogs, 5 dogs were also anorectic, 2 had coagulopathy, 3 were icteric, and 5 had ascites. Serum biochemical analysis revealed serum albumin concentration less than or equal to 2.2. g/dl in 12 dogs, serum alkaline phosphatase activity greater than or equal to 169 U/L in 18 dogs, serum alanine transaminase activity greater than or equal to 57 U/L in 15 dogs, and total bilirubin concentration greater than or equal to 1 mg/dl (in the absence of lipemia) in 7 dogs. Serum phenobarbital concentration was greater than or equal to 40 micrograms/ml in 12 of 17 dogs. Sulfobromophthalein excretion was prolonged in 8 of 10 dogs. Preprandial serum bile acid concentrations were high in 8 of 10 dogs, and 2-hour postprandial serum bile acid concentrations were high in 9 of 10 dogs. Two of 4 dogs tested had resting plasma ammonia concentrations greater than 200 mg/dl. An ammonia tolerance test was performed on 2 other dogs; both had ammonia concentration greater than or equal to 200 mg/dl in the plasma 30 minutes after receiving 100 mg of ammonium chloride/kg of body weight, PO. Nine dogs died, 1 was euthanatized, and necropsies were performed on these 10 dogs. Biopsies and necropsies of 6 dogs revealed chronic hepatic fibrosis with nodular regeneration (cirrhosis). One dog had hepatocellular carcinoma and mild cirrhosis. In 1 dog, after phenobarbital had been withheld, necropsy revealed complete recovery of the previously observed lesions.
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PMID:Hepatotoxicity of phenobarbital in dogs: 18 cases (1985-1989). 174 13

Hypolipidemic effects of gamma-oryzanol (OZ) and cycloartenol ferulic acid ester (CAF) on the hyperlipidemia induced by ingestion of a high cholesterol diet (HCD) in male Sprague-Dawley rats were investigated. The test drugs were given orally and intravenously, daily for 12 days with the HCD feeding. The oral administration with OZ and CAF at 100 mg/kg daily for 6 or 12 days did not apparently prevent the hyperlipidemia induced by HCD-feeding. The intravenous administrations with OZ and CAF at 10 mg/kg for 6 days significantly inhibited the increases in serum total cholesterol (TC), phospholipid (PL) and free cholesterol by HCD. OZ and CAF did not inhibit the decreases of TC in high density lipoprotein (HDL-TC) and HDL-PL by HCD. The increases of atherogenic index [( TC-HDL-TC]/[HDL-TC] and [PL-HDL-PL]/[HDL-PL]) with the HCD feeding were reduced by the intravenous administrations of OZ and CAF. Triglyceride, nonesterified fatty acid, lactate dehydrogenase and transaminase (GOT and GPT) markedly decreased below the control level by the intravenous administrations of OZ and CAF for 12 days. These results suggest that the intravenous administrations of OZ and CAF may have accelerated the excretion of lipids in the blood.
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PMID:Effects of gamma-oryzanol and cycloartenol ferulic acid ester on cholesterol diet induced hyperlipidemia in rats. 344 23

The effect of nicardipine on experimental hyperlipemia induced by a 1% cholesterol diet in spontaneously hypertensive rats (SHR) was investigated by the change of hemodynamics and the determination of lipid contents of the serum, liver, heart and aorta. Nicardipine increased liver weight and liver weight per body weight ratio, and it decreased heart and kidney weight significantly. Nicardipine inhibited the increase in blood pressure with cholesterol and normal diets. Nicardipine decreased heart rate in SHR fed the normal diet, and it inhibited the increase in heart rate in SHR fed the cholesterol diet. Serum lipid levels significantly increased with the cholesterol diet. Nicardipine significantly increased cholesterol in high density lipoprotein (HDL-C) and phospholipid in HDL (HDL-PL) with cholesterol and normal diets, and it decreased triglyceride and improved the atherogenic index "(total cholesterol-HDL-C)/HDL-C" with the normal diet. Serum GOT and GPT significantly increased with the cholesterol diet. Nicardipine significantly enhanced an increase in GOT and GPT levels with the cholesterol diet. Nicardipine increased phospholipid content in the liver, triglyceride in the heart, and it decreased total cholesterol in the aorta. A morphologic study showed a fatty liver in SHR fed the cholesterol diet, but nicardipine had no effect on the morphological changes in the liver, heart and aorta. These results suggest that nicardipine may prevent atherosclerotic degeneration by the inhibition of hypertension, increase in serum HDL and decrease in total cholesterol in the aorta.
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PMID:[Effect of nicardipine on cholesterol-fed S.H.R]. 405 35

Adriamycin, an anticancer drug, caused dramatic increases in the serum lipid levels of rats fed a high-cholesterol diet. Male Lewis inbred rats were fed a basal or 1.5% cholesterol diet containing 0.5% cholic acid for 8 weeks. The rats were injected with adriamycin in doses of 1.5 mg/kg body weight, twice a week, and 6.0 mg/kg body weight, every other week. The serum lipid peroxide level gradually rose in adriamycin-treated rats, reaching a four-fold level at the end of the experiment. Cholesterol feeding, however, had a lowering effect on the lipid peroxide level. Adriamycin treatment or cholesterol feeding moderately elevated serum lipid levels, but their combination exerted a synergistic effect. In rats injected with a large dose of adriamycin and fed a high-cholesterol diet, the serum cholesterol, triglyceride and phospholipid levels strikingly increased by approx. 2000, 1500 and 1300 mg/100 ml, respectively. However, the ester ratio of cholesterol remained almost constant. Furthermore, serum GOT, GPT and ALP activities were only slightly different from the control values. Adriamycin treatment produced severe hypoalbuminemia. Ascites was also observed in rats given a large dose of adriamycin. The present findings indicate that the hyperlipidemia we observed may basically result from adriamycin-induced nephrosis and can be markedly enhanced when rats are fed a high-cholesterol diet. In spite of remarkably high levels of serum lipids and lipid peroxides, the aortic cholesterol level increased only slightly.
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PMID:Hyperlipidemic effects of adriamycin in rats. 409 81

The effect of a four-week experiment on ten fa/fa Zucker rats (aged seven weeks at the beginning) fed on a lipid-rich diet (HL: 31 per cent w/w lipids, 45.6 per cent starch) was compared to that of a control diet (C: 10 per cent lipids, 66 per cent starch) on control Fa/- rats using a special pair-feeding apparatus that made it possible to obtain an identical intake rhythm. Energy level of the intake was significantly higher for the HL diet than for the C diet. At the end of the experiment, fa/fa rats remained obese and hyperlipemic, and still showed liver steatosis. With equal energy levels ingested, the obesity of fa/fa rats was comparable for both diets; hypertriglyceridemia and hypercholesterolemia were identical for both diets. When compared to the C diet, the HL diet modified neither their obesity nor their hyperlipemia. Obese rat liver on the HL diet showed lower levels for triacylglycerols, cholesterol, GGT, ALT, LDH and aldolase activities, while hepatic glycerol kinase and AST activities were higher than and comparable to, respectively, the C diet. Thus the HL diet led to a decreased liver steatosis for fa/fa rats as compared to the C diet.
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PMID:Influence of diet composition on obesity, hyperlipemia and liver steatosis in Zucker fa/fa rats pair-fed with Zucker Fa/- rats. 637 17

The chemical measurements on our Technicon SMAC of lipemic sera before and after clearing lipemia by ultracentrifugation showed that uric acid, creatinine, carbon dioxide, calcium, phosphorus, potassium, and alkaline phosphatase were not affected significantly by lipemia, whereas sodium, urea, glucose, chloride and total protein showed small but significant increases with averages of less than 1.9 percent. Albumin showed a significant decrease of 1.2 percent. In contrast, the results for the enzymes, alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) showed striking differences between pre- and post-centrifuged sera in a number of specimens. With lactate dehydrogenase, thirty-two of fifty specimens registered an increase in activity while with the aminotransferases, thirty-five and forty-one out of fifty specimens showed a decrease in aspartate aminotransferase and alanine aminotransferase activities, respectively. Although much of the lipemic interference can be explained by the volume displacement of serum by lipids or by interference by lipemia with colorimetry, the anomalous effects observed with the enzymes indicate the possibility of other, as yet, undetermined factor(s).
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PMID:The effect of hyperlipidemia on Technicon SMAC measurements. 712 23


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