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)

Recent reports of risk factors for and survival of patients with diabetic retinopathy do not include exudative maculopathy as a separate entity. We therefore studied a group of hypertensive Type II diabetic subjects with exudative maculopathy (n = 26) compared to a carefully matched hypertensive diabetic comparison group without retinopathy (n = 26) over seven years. Diabetic maculopathy patients had higher mean diastolic blood pressure (101.6 +/- 14 versus 94.8 +/- 10 mmHg, p less than 0.05), serum cholesterol (6.65 +/- 2.2 versus 5.9 +/- 1.31 mmol/l), HDL2 subfraction levels (0.46 +/- 0.23 versus 0.32 +/- 0.18 mmol/l) and a higher prevalence of hyperlipidaemia (54% versus 35%) compared to the comparison group. After seven years, the maculopathy group showed a strikingly higher prevalence of renal failure and nephrotic syndrome (42% versus 8%, p less than 0.05) and of macroproteinuria (58% versus 15%, p less than 0.01) compared to the comparison group. Mortality and cardiovascular disease event rate was 12% and 38% in the maculopathy and 15% and 31% respectively in the comparison group. We conclude that although mortality is not significantly higher in diabetics with exudative maculopathy, proteinuria, renal failure and nephrotic syndrome may be associated features on long term follow-up. Hypertension and hypercholesterolaemia may also be risk factors in the development of diabetic maculopathy.
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PMID:Long-term follow-up of and underlying medical conditions in patients with diabetic exudative maculopathy. 180 Jan 69

Increased cholesterol levels above 200 mg/dl, LDL levels above 130 mg/dl and total cholesterol/HDL ratio above 4.5 in males and above 5.0 in females are recognized as indicators of increased risk of atherosclerosis. Risk associated to increased triglyceride levels (above 200 mg/dl) must be judged in relation to associated factors such as family history of coronary heart disease, presence of remnants (type III hyperlipidemia), presence of Lp(a), increased levels of Apo B, reduced levels of HDL2 or Apo A1. VLDL and chylomicron remnants and Lp(a) have an atherogenic power in vitro 2 to 4 times that of LDL. There is a correlation between hypertriglyceridemia and reduced HDL2 and Apo A1 levels. Hypertriglyceridemia is frequently associated to other risk factors like diabetes, obesity, hyperinsulinism, and high blood pressure. Finally, VLDL may elevate levels of plasma plasminogen inhibitor. Thus, hypertriglyceridemia should be investigated when, evaluating risk of atherosclerosis.
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PMID:[Cholesterol and triglycerides in atherosclerosis: epidemiologic and physiopathologic considerations]. 184

Previous studies have indicated an inverse relation between circulating high density lipoprotein (HDL) concentrations and the rate of chylomicron clearance. Because chronic exercise has been shown to augment chylomicron clearance, we measured HDL cholesterol concentrations and plasma triglyceride and retinyl palmitate responses to high- (140 g) and low- (50 g) fat meals in endurance-trained men. Plasma HDL cholesterol concentrations in these men ranged from 36 to 105 mg/dl. Intraindividual variation in the cholesterol concentration of the HDLs occurred primarily in HDL2. The magnitude of postprandial lipemia induced by both the high- and the low-fat meals was uniformly low compared with values reported previously for sedentary men and was not correlated with HDL cholesterol concentrations. Postprandial retinyl palmitate concentrations, which reflect chylomicron remnant metabolism, also showed no correlation with HDL cholesterol concentrations. These data indicate that the degree of postprandial lipemia is not the primary determinant of HDL cholesterol concentrations in endurance-trained men. Accordingly, the wide range of HDL cholesterol concentrations measured in these men must be attributable to other factors.
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PMID:Dissociation between postprandial lipemia and high density lipoprotein cholesterol concentrations in endurance-trained men. 206 37

Hepatic diseases differ from most other causes of secondary dyslipidaemia in that the circulating lipoproteins are not only present in abnormal amounts but they frequently also have abnormal composition, electrophoretic mobility and appearance. Pre-beta and alpha bands can be absent on electrophoresis in all types of liver disease although material in the VLDL and HDL ranges can be isolated in the ultracentrifuge. Cholestatic liver disease has been the most extensively studied and the hyperlipidaemia can be extreme with marked elevations of free cholesterol and phospholipids. This results largely from the presence of LP-X, an abnormal LDL, with a vesicular structure that appears in rouleaux formation under the electron microscope. It is virtually specific for cholestasis and familial LCAT deficiency. The LDL, however, is heterogeneous and may also contain a large triglyceride-rich particle (LP-Y) as well as more normal-looking particles, which are none the less depleted in cholesteryl esters and rich in triglycerides. Indeed, when patients with cholestasis are hypertriglyceridaemic the excess triglyceride is to be found predominantly in these two LDL fractions rather than in VLDL. HDL in cholestasis may contain disc-like particles, similar to those newly secreted by the liver and intestine, as well as more normal-looking spherical particles. In extrahepatic obstruction concentrations of HDL and its major apolipoproteins, apoAI and apoAII, are frequently reduced, although a subfraction rich in apoE is often found. In all but the latest stages of chronic intrahepatic cholestasis due to primary biliary cirrhosis, however, HDL, especially HDL2, concentrations are increased, probably due to the presence of a circulating inhibitor of HL. Many of these lipoprotein changes found in cholestasis resemble those of familial LCAT deficiency, although the hyperlipidaemia is not usually so severe in the latter condition. Indeed, in patients with cholestasis but well-preserved LCAT activity many of the characteristic lipoprotein changes, such as LP-X, LP-Y and discoidal HDL, may not be seen. In acute hepatocellular disease, such as alcoholic or viral hepatitis, it is not unusual for the patient to go through a cholestatic phase and many of the same lipoprotein changes may be seen. In cirrhosis without cholestasis the patients are not usually significantly hyperlipidaemic and in advanced cases cholesterol and apoB levels may be reduced. Although LCAT activity and the proportion of plasma cholesterol esterified may also be markedly reduced, LP-X is not usually seen, possibly because the flux of free cholesterol and phospholipid (lecithin), the LCAT substrates, is relatively low. Discoidal HDLs are often present.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Dyslipoproteinaemia of liver disease. 208 7

Accelerated coronary atherosclerosis is a major risk limiting long-term survival after heart transplantation and is commonly associated with dyslipoproteinemia even in subjects who were not dyslipoproteinemic before intervention. The purpose of this study was to analyse the abnormalities in the lipid profiles of 2 different groups of heart-transplanted males: 18 subjects with underlying ischemic heart disease (IHD) and 19 subjects with non-obstructive cardiomyopathy of unknown aetiology (CM). Both groups were compared to 33 healthy males. All patients were under immunosuppressive therapy including prednisone, cyclosporin A and azathioprine. A moderate hyperlipidemia was found in all transplant recipients, associated with high HDL-cholesterol concentrations in the CM group (1.80 +/- 0.37 vs. 1.29 +/- 0.23 mmol/l) and normal HDL-cholesterol levels in the IHD group (1.40 +/- 0.23 mmol/l). HDL subfractionation showed a marked increase in HDL2-cholesterol (CM: 1.12 +/- 0.32; IHD: 0.69 +/- 0.28; control: 0.40 +/- 0.17 mmol/l) while HDL3-cholesterol was significantly lower than in the control group. Analysis of HDL particle sizes showed in all transplant subjects an increase of an intermediate size particle HDL2a (diameter 9.0 +/- 0.10 nm) which is a minor form in control subjects. In the CM group, both the common HDL2b (10.2 +/- 0.13 nm) and HDL2a were abundant in 13 of 17 patients. The pattern was more heterogeneous in the IHD group but witnessed to a high frequency of HDL2a particles either alone (5/14) or associated with larger HDL2b (4/14) or with small HDL3 (4/14).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum lipid abnormalities in heart transplant recipients: predominance of HDL2-like particles in the HDL pattern. 232 20

In this research, 68 patients suffering from hyperlipemia were divided into observation group taking Tiao-Zhi-Tang (TZT) and control group taking inositol and Mai Tong at random and matched-pair, and the serum levels of HDL-c, HDL2-c, LDL-c, Apo A-I and Apo B were measured respectively by the methods of polyethylene glycol precipitation separation and single radial immunodiffusion. The results showed that there were significant difference in the levels of lipoprotein, apolipoprotein between the patient groups and the healthy group before taking medicines. After taking medicines for four weeks, the serum levels of total cholesterol, triglyceride (TG), LDL-c and Apo B were lowered and the serum levels of HDL-c, HDL2-c and Apo A-I were elevated in the observation group. The serum level of TG was lowered and the serum levels of HDL2-c, Apo A-I were elevated in the control group. The effects of TZT, with the serum levels of LDL-c and Apo B being lowered and the serum level of HDL-c being elevated, were more beneficial than inositol and Mai Tong. These results suggested that TZT had a good effect on regulating the lipoprotein metabolism.
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PMID:[Effects of tiao-zhi-tang on lipoprotein and apolipoprotein in hyperlipemic patients]. 235 Aug 32

To better characterize the severity and course of hyperlipidemia in diabetic ketosis and ketoacidosis, we measured plasma triglyceride and cholesterol concentrations in 50 episodes in 46 adults hospitalized on a municipal hospital medical service. Moderate hypertriglyceridemia was common: 32 patients (64%) had triglyceride levels above the 95th percentile (adjusted for age and sex), and 18 patients (36%) had cholesterol levels above the 95th percentile. Severe hypertriglyceridemia (levels above 5.65 mmol/L) was found in 14 patients (28%). Plasma high-density lipoprotein (HDL) cholesterol and the HDL2 and HDL3 subclasses were measured in 22 episodes. The initial HDL cholesterol levels were usually subnormal in the patients who had not received insulin previously and normal in those who had. Treatment of the ketoacidosis was usually associated with a rapid decrease in plasma lipid levels. At late follow-up (between 1 1/2 and 14 1/2 months), only 2 of the 14 patients with initial plasma triglyceride levels above 5.65 mmol/L still had such high concentrations.
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PMID:Plasma triglycerides and cholesterol in diabetic ketosis. 250 5

Prevention of vascular disease and acute pancreatitis is the goal of hyperlipidemia treatment. The risk of coronary heart disease (CHD) increases with increasing plasma cholesterol levels because low-density lipoprotein (LDL), the major carrier of cholesterol in the plasma, is atherogenic. High-density lipoprotein (HDL), especially the HDL2 subfraction, protects against CHD. Hypertriglyceridemia, although not an independent risk factor for CHD, is generally accompanied by low HDL cholesterol (HDLch), which may predispose to CHD. Reducing plasma LDL and raising HDL levels are thus goals in preventing CHD. Serum LDL levels may be lowered by reducing saturated fat and cholesterol intake; weight loss may decrease LDL but is more effective in lowering plasma triglycerides and raising HDLch. The percent of total calories from polyunsaturated, monounsaturated, and saturated fats should be less than 10%, up to 10-15%, and less than 10%, respectively. High cholesterol intake increases the flux of cholesterol, which may be harmful to arterial walls, but beyond a certain point does not increase plasma cholesterol levels. Some diets change the composition rather than the level of LDL and apoproteins. Weight reduction and maintenance are the most effective dietary measures to lower plasma triglycerides; omega-3 fatty acids (fish oils) have shown promise in reducing triglyceride but not cholesterol levels. Substitution of starch for sugar lowered triglyceride levels toward normal in hypertriglyceridemia patients. Fasting triglyceride levels rise in all individuals fed high-carbohydrate diets, but the high levels persist in hypertriglyceridemia patients. Weight loss, cessation of cigarette smoking, increased physical activity, good control of diabetes, and moderate alcohol use all raise HDLch levels. Vitamin E deficiency causes neurological sequelae in children with severe malabsorption problems due to abetalipoproteinemia or cholestatic liver disease.
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PMID:Nutritional management of plasma lipid disorders. 255 90

The study comprised 128 patients with chronic lymphocytic leukemia (CLL) aged 65.7 +/- 8 years, 59 women and 69 men. Among the patients studied 70 were treated and 58 yet not underwent therapy. The Rai classification of patients with CLL has been used. The control group consisted of 68 subjects aged 56.8 +/- 14 years, 35 women and 33 men, showing no diseases affecting the blood lipid disturbances. The following determinations have been performed in the blood serum: apo B, CH, TG, PL, and CH or PL in the isolated HDL fraction; LDL-CH ratio has also been calculated. In patients with CLL the total CH concentration has been noted which advanced parallel to the disease progress. It resulted first of all from the decrease in LDL-CH (p less than 0.05). Similar alterations have been noted so far as apo B is concerned. It has been demonstrated that the decrease in HDL-CH (p less than 0.05) is also dependent on the disease stage. The simultaneously increasing index HDL-PL/HDL-CH indicate on changes within the HDL2 and HDL3 subfractions suggesting a deficiency of the HDL2 subfraction. The total lipemia and the lipoprotein fraction alterations observed make the diagnostic value of the atherosclerotic threat in patients with CLL doubtful with the use of that parameters.
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PMID:[Disorders of lipid and lipoprotein metabolism in patients with chronic lymphocytic leukemia. I. Preliminary evaluation of lipemia and HDL fractions in various stages of the disease]. 259 88

The family at risk has at least one member who has (1) hyperlipidemia; (2) low HDL2-cholesterol; (3) essential hypertension; (4) a family history of premature CHD; or (5) actively smokes. The predictive value of CHD risk factors in adults is well documented and quantified. Familial aggregation, genetic studies, and tracking of blood pressure provide evidence that children born to families with a high prevalence of hypertension or who as adolescents track in the upper part of the blood pressure distribution are themselves at risk for hypertension. Similarly, familial aggregation, tracking, and autopsy studies provide evidence for the relationship of serum lipids to the subsequent development of coronary atherosclerosis. Smoking by parents adversely affects the hearts and lungs of children. In addition, the child with a parent who smokes is more likely to become an active smoker. Preventive strategies are now available to the pediatrician to reduce the risk of premature CHD.
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PMID:The management of the family at high risk for coronary heart disease. 265 86


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