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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Arteriosclerosis is caused by many factors. These pathogenic factors especially over-nutrition, nicotinabusus, deficiency of muscular exercise, muscular overstrain, emotional stress and concomitant basic diseases, especially arterial hypertension, diabetes mellitus and dyslipidemia are the most important points for preventive and therapeutical action. When possible the risk factors has to be eliminated, arterial hypertension, diabetes mellitus and dyslipidemia have to be treated orderly. In the pathogenesis of arteriosclerosis and atherosclerosis are known disturbances of the lipid metabolism, the blood coagulation and the metabolism of the arterial wall cells most important. Application of anticoagulants and lipid lowering medicaments did not come up to our expectations. Experiences with animal models and a double blind study (secondary prevention of myocardial infarction) have given good reason for recommending antirheumatic or as we like to say, mesenchyme suppressive drugs.
Aktuelle Gerontol 1978 Dec
PMID:[Prevention and therapy of arteriosclerosis (author's transl)]. 3 60

Insulin resistance is a frequently occurring abnormality. Although there can be insensitivity to any of insulin's actions, insulin resistance par excellence is a decreased insulin-mediated whole-body glucose disposal rate. A distinction is made between primary and secondary insulin resistance. Primary insulin resistance is of unknown origin, is only partially experimentally reproducible, and is essentially irreversible (spontaneously or by treatment). In addition, it is both pathway-specific (ie, glucose storage) and organ-specific (mostly skeletal muscle), and is compatible with a postreceptor defect in insulin action. Primary insulin resistance is found in a proportion (approximately 25%) of otherwise healthy people, in non-insulin-dependent diabetes mellitus, essential hypertension, and some forms of dyslipidemia. The idea of an insulin resistance syndrome derives from the striking pattern of overlap among these clinical conditions. Their tendency to cluster in the same individuals is evident from both cross-sectional and longitudinal observations. It is proposed that the insulin resistance syndrome is a large constellation of interrelated changes in metabolic, anthropometric, and hemodynamic variables centered around insulin resistance or hyperinsulinemia. There is a significant genetic component, a predisposing influence for non-insulin-dependent diabetes mellitus, hypertension, dyslipidemia, and possibly, a distinct atherogenic potential.
Curr Opin Nephrol Hypertens 1992 Dec
PMID:The insulin resistance syndrome. 134 29

The insulin resistance syndrome ("syndrome X") consists of hyperinsulinemia, glucose intolerance, dyslipidemia, and hypertension, although the inclusion of hypertension has been challenged. Insulin has biological effects that could produce a hyperdynamic circulation. We therefore postulated that an insulin-induced hyperdynamic circulation is an early feature of the insulin resistance syndrome and that this circulatory abnormality leads to later fixed hypertension. The San Antonio Heart Study cohort, a population-based cohort of 3,301 Mexican Americans and 1,857 non-Hispanic whites, was used to define individuals who were hyperdynamic (pulse pressure and heart rate in the upper quartile of their respective distributions), intermediate, and hypodynamic (pulse pressure and heart rate in the bottom quartile). The characteristics of the insulin resistance syndrome were then examined according to these three hemodynamic categories. We also examined the 8-year incidence of hypertension and of type II diabetes according to these hemodynamic categories. A hyperdynamic circulation was associated with statistically significant increases in body mass index (BMI) (p < 0.001), subscapular-to-triceps skinfold ratio (p = 0.042), triglyceride (p = 0.002), 2-hour glucose (p = 0.002), and fasting and 2-hour insulin (p = 0.019 and 0.006). When hemodynamic status was examined separately in lean (BMI < 27 kg/m2) and obese (BMI > or = 27 kg/m2) individuals, the above effects persisted, although they were somewhat attenuated. The odds ratio for the hyperdynamic state as a predictor of future hypertension was 1.66, although this was not statistically significant (p = 0.304). The odds ratio for predicting future type II diabetes was 3.97, which was statistically significant (p = 0.047).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Dec
PMID:Hyperdynamic circulation and the insulin resistance syndrome ("syndrome X"). 145 96

The evidence linking hypertriglyceridemia and coronary artery disease (CAD) is reviewed. A positive correlation between plasma triglyceride level and CAD incidence has been demonstrated in most prospective studies on univariate analysis. However, the significance is weakened on multivariate analysis, in particular when level of high-density lipoprotein (HDL) cholesterol is taken into account, perhaps because of the close metabolic interrelation between the triglyceride-rich lipoproteins and HDL particles. Recent analyses of clinical data have shown that the combination of elevations of low-density lipoprotein cholesterol and triglyceride and low levels of HDL cholesterol confers particularly high risk for CAD. The U.S. National Institutes of Health Consensus Development Conference on Triglyceride, High Density Lipoprotein, and Coronary Heart Disease in February 1992 made recommendations to integrate more fully HDL cholesterol and triglyceride levels into the assessment and treatment of dyslipidemia and CAD risk. Treatment of hypertriglyceridemia should focus on diet and weight control, exercise, and smoking cessation, as well as control of other major risk factors for CAD, notably hypercholesterolemia and hypertension.
Am J Cardiol 1992 Dec 14
PMID:Hypertriglyceridemia: risks and perspectives. 146 13

A detailed overview of the various forms of hyperlipidemia/dyslipidemia that constitute a major risk factor for coronary heart disease and a detailed discussion of the various types of cholesterol-lowering drugs are presented. The importance of identifying the type of dyslipidemia with respect to the choice of treatment is emphasized, as is the use of nonpharmacologic intervention, i.e., diet, exercise, and weight loss. The appropriate use and benefits of bile acid sequestrants, nicotinic acid, fibric acids, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, and probucol are individually discussed, whereas nonpharmacologic approaches used in conjunction with the drugs are recommended emphatically.
Am J Cardiol 1992 Dec 21
PMID:Cholesterol-lowering drugs as cardioprotective agents. 147 2

The effect of fish oil dietary supplementation on the dyslipidemia and coagulopathy of seven patients with nephrotic syndrome and hypoalbuminemia due to primary kidney disease was studied. Plasma lipids, platelet aggregation studies, simplate bleeding time, and fibrinogen levels were determined before and after 6 wk of treatment with fish oil (15 g/day of MaxEPA; 2.7 g of eicosapentenoic acid (EPA) and 1.8 g of docosahexenoic acid. Urea kinetics were determined from urine-urea concentration, urinary proteina, and urine volume. A 3-day dietary intake record was obtained from each patient before and after 6 wk of fish oil supplementation. There was no significant dietary change in protein, fat, or carbohydrate intake over the time period of the study. At study end, total triglycerides decreased from 2.98 +/- 1.31 to 2.18 +/- 1.14 mmol/L (P = 0.002), and very low-density lipoprotein-triglycerides decreased from 2.35 +/- 1.34 to 1.28 +/- 1.07 mmol/L (P = 0.01). Low-density lipoprotein (LDL) cholesterol increased from 5.18 +/- 1.74 to 7.35 +/- 2.83 mmol/L (P = 0.005). No significant changes occurred in bleeding time, platelet count, hematocrit, red blood cell flexibility, or whole blood viscosity. Platelet aggregation responses to collagen and arachidonic acid were consistently reduced after treatment, but there was no change in platelet response to ADP. The platelet membrane phospolipids showed a significantly increased incorporation of EPA after the fish oil diet (P = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)
J Am Soc Nephrol 1992 Dec
PMID:Omega-3 fatty acid supplementation in primary nephrotic syndrome: effects on plasma lipids and coagulopathy. 147 28

Hyperlipidemia is a prominent feature of the nephrotic syndrome. Lipoprotein abnormalities include increased very low and low density lipoprotein (VLDL and LDL) cholesterol and variable reductions in high density lipoprotein (HDL) cholesterol. We hypothesized that plasma cholesteryl ester transfer protein (CETP), which influences the distribution of cholesteryl esters among the lipoproteins, might contribute to lipoprotein abnormalities in nephrotic syndrome. Plasma CETP, apolipoprotein and lipoprotein concentrations were measured in 14 consecutive untreated and 7 treated nephrotic patients, 5 patients with primary hypertriglyceridemia, and 18 normolipidemic controls. Patients with nephrotic syndrome displayed increased plasma concentrations of apoB, VLDL, and LDL cholesterol. The VLDL was enriched with cholesteryl ester (CE), shown by a CE/triglyceride (TG) ratio approximately twice that in normolipidemic or hypertriglyceridemic controls (P < 0.001). Plasma CETP concentration was increased in patients with untreated nephrotic syndrome compared to controls (3.6 vs. 2.3 mg/l, P < 0.001), and was positively correlated with the CE concentration in VLDL (r = 0.69, P = 0.004) and with plasma apoB concentration (r = 0.68, P = 0.007). Treatment with corticosteroids resulted in normalization of plasma CETP and of the CE/TG ratio in VLDL. An inverse correlation between plasma CETP and HDL cholesterol was observed in hypertriglyceridemic nephrotic syndrome patients (r = -0.67, P = 0.03). The dyslipidemia of nephrotic syndrome includes increased levels of apoB-lipoproteins and VLDL that are unusually enriched in CE and likely to be atherogenic. Increased plasma CETP probably plays a significant role in the enrichment of VLDL with CE, and may also contribute to increased concentrations of apoB-lipoproteins and decreased HDL cholesterol in some patients.
J Lipid Res 1992 Dec
PMID:Increased concentration of plasma cholesteryl ester transfer protein in nephrotic syndrome: role in dyslipidemia. 147 91

Insulin resistance and consecutive hyperinsulinemia in individuals with the metabolic syndrome are associated with dyslipidemia. This latter is characterised by hypertriglyceridemia and a diminishment of high-density lipoprotein (HDL) cholesterol in the plasma. In severe forms of insulin resistance, low density lipoprotein (LDL) cholesterol may also be elevated. Hypertriglyceridemia is due to an increase in the rate of synthesis of very low density lipoproteins (VLDL) in the liver, and a reduction in their breakdown by the lipoprotein lipase in non-hepatic tissue. Changes in VLDL metabolism are associated with a reduction in HDL concentrations. In addition, direct effects of insulin on the lipid metabolism have been described. Changes in lipid metabolism due to insulin resistance and hyperinsulinemia may be of significance for the atherosclerosis risk in patients with the metabolic syndrome.
Fortschr Med 1992 Dec 10
PMID:[Dyslipoproteinemia and metabolic syndrome. Effects of insulin resistance and hyperinsulinemia on lipid metabolism]. 148 17

Ten patients have been studied for lipidic behaviour during hemodialysis using as anticoagulant heparin and prostacyclin. Hearing has been administered at infusion rate of 2000 U/h and prostacyclin in 5 ng/kg/min. Lipidic behaviour (before and after hemodialysis) has been studied for apolipoproteins A and B, total serum cholesterol and serum triglycerides, HDL-cholesterol, lipoprotein. Total serum cholesterol/HDL-cholesterol, apolipoproteins A/apolipoproteins B, apolipoproteins A/HDL-cholesterol ratios have been also studied. Our findings show that heparin produces acute changes in lipidic behaviour after hemodialysis and suggest that administrations may contribute to lipidic derangement of uremic dialytic patient while heparin free dialysis (prostacyclin infusion) doesn't show lipidic derangement after dialytic treatment. Prostacyclin infusion suggests that may be a useful anticoagulant and therapeutic drug especially in uremic dialytic subject with high atherosclerosis involvement, dyslipidemia and arterial hypertension.
Minerva Med 1992 Dec
PMID:[Lipid behavior during hemodialysis using heparin and prostacyclin]. 149 59

Non-insulin-dependent (type II) diabetes mellitus is an inherited metabolic disorder characterized by hyperglycemia with resistance to ketosis. The onset is usually after age 40 years. Patients are variably symptomatic and frequently obese, hyperlipidemic and hypertensive. Clinical, pathological and biochemical evidence suggests that the disease is caused by a combined defect of insulin secretion and insulin resistance. Goals in the treatment of hyperglycemia, dyslipidemia and hypertension should be appropriate to the patient's age, the status of diabetic complications and the safety of the regimen. Nonpharmacologic management includes meal planning to achieve a suitable weight, such that carbohydrates supply 50% to 60% of the daily energy intake, with limitation of saturated fats, cholesterol and salt when indicated, and physical activity appropriate to the patient's age and cardiovascular status. Follow-up should include regular visits with the physician, access to diabetes education, self-monitoring of the blood or urine glucose level and laboratory-based measurement of the plasma levels of glucose and glycated hemoglobin. If unacceptably high plasma glucose levels (e.g., 8 mmol/L or more before meals) persist the use of orally given hypoglycemic agents (a sulfonylurea agent or metformin or both) is indicated. Temporary insulin therapy may be needed during intercurrent illness, surgery or pregnancy. Long-term insulin therapy is recommended in patients with continuing symptoms or hyperglycemia despite treatment with diet modification and orally given hypoglycemic agents. The risk of pancreatitis may be reduced by treating severe hypertriglyceridemia (fasting serum level greater than 10 mmol/L) and atherosclerotic disease through dietary and, if necessary, pharmacologic management of dyslipidemia. Antihypertensive agents are available that have fewer adverse metabolic effects than thiazides and beta-adrenergic receptor blockers. New drugs are being developed that will enhance effective insulin secretion and action and inhibit the progress of complications.
CMAJ 1991 Dec 15
PMID:Non-insulin-dependent (type II) diabetes mellitus. 174 94


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