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

A clinical and metabolic study of 61 patients with myoocardial infarct before the age of 40 yr showed a high frequency of familial involvement, particularly in subjects with type IIA and IIB hyperbetalipoproteinaemia. Excess weight and arterial hypertension were rare, while premonitory angina was absent in 59%. Four subjects were diabetic. Oral glucose tolerance was normal in 14 and of diabetic type in 26 of 40 patients examined; the insulin response pointed to insulin-resistance. Dyslipidaemia was noted in 45%, including type IIA and IIB hyperbetalipoproteinaemia in 27%. Distribution of the frequency of infarct in function of cholesterolaemia classes gave a bimodal curve indicative of distinct normo- and hypercholesterolaemic groups within the series. Reduced glucose tolerance was more frequent in patients with low blood cholesterol. This suggests that reduced tolerance and high blood cholesterol are independent risk factors in coronary disease. No relation between the clinical and metabolic data could be ascertained.
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PMID:[Clinical and metabolic aspects of juvenile myocardial infarct]. 99 98

Insulin resistance and hyperinsulinemia is now recognized in non-insulin-dependent diabetes, essential hypertension, obesity, atherosclerotic heart disease, dyslipidemia, heart failure, and in heavy smokers. Several mechanisms have been proposed to explain hyperinsulinemia, insulin resistance and its relationship to hypertension; reduced sodium excretion, activation of the sympathetic nervous system, increased activity of the sodium/hydrogen pump, and stimulation of cellular growth. Some of the nonpharmacological methods to control hyperinsulinemia are of benefit in the management of hypertension, most notably weight loss, exercise program, and reduced salt intake. High-fiber and reduced-protein diets also reduce hyperinsulinemia. Thiazide diuretics can result in insulin resistance, and insulin secretion may be inhibited, possibly associated with concomitant hypokalemia. beta-Blockers result in some reduction of glucose tolerance and mask some of the features of hypoglycemia. Angiotensin-converting enzyme (ACE) inhibitors and alpha-receptor blockers do not effect insulin resistance; probably the same is true for calcium antagonists. Although the effect on risk factors should not be discounted, it is the effect of treatment on hard end points, cerebrovascular accidents, myocardial infarction, or death that is most important. Evidence in hypertension is at present restricted to diuretics and beta-blocking drugs.
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PMID:Hypertension and insulin resistance. 128 47

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.
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PMID:The insulin resistance syndrome. 134 29

It is clearly recognized that patients with NIDDM have an increased risk for CHD. Recent data indicate that persons with glucose concentrations in the nondiabetic range also may be at higher risk for CHD. These associations may not represent cause and effect, however. Emerging data suggest that hyperglycemia and CHD may both arise from hyperinsulinemia/insulin resistance. In support of this hypothesis are studies showing that NIDDM and CHD have many risk factors in common, including age, elevated blood pressure, dyslipidemia, adiposity, and a central pattern of fat distribution. Moreover, these risk factors are frequent concomitants of hyperinsulinemia, itself a risk factor for CHD and perhaps for NIDDM. Although the duration of NIDDM has been infrequently related to risk of CHD, the authors hypothesize that duration of hyperinsulinemia/insulin resistance would be a more sensitive marker for risk of CHD. The relation of IDDM to CHD is a different situation. The etiological process leading to IDDM, namely the destruction of beta-cells in genetically predisposed persons, is not related to cardiovascular risk. However, IDDM patients still have an excess of CVD, the risk factors for which may vary according to the location of the diseases (e.g., LEAD vs. CHD). There is a strong relationship between proteinuria and CVD, which has led to a general theory of vascular complications in IDDM based on defective heparan sulfate metabolism (Steno hypothesis). Recent evidence challenges parts of this hypothesis, and the possibility is raised that a higher case-fatality rate in a subgroup of patients with both renal and CVD explains part of the renal connection, as does the general worsening of CVD risk factors.
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PMID:Diabetes mellitus and macrovascular complications. An epidemiological perspective. 139 12

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)
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PMID:Hyperdynamic circulation and the insulin resistance syndrome ("syndrome X"). 145 96

Hypertension, dyslipidemia, insulin resistance, and hyperinsulinemia--acknowledged risk factors for coronary artery disease--are all more common in persons with non-insulin-dependent diabetes than in nondiabetic persons. The interrelationships of these risk factors are becoming increasingly recognized. This article discusses the dyslipidemias commonly seen in type II diabetes and describes their relationship to glucose metabolism.
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PMID:Lipid metabolism in type II diabetes. 149 73

The risk for cardiovascular complications is already substantially increased in persons with borderline elevation of arterial pressure (141-159/90-94 mmHg and transiently below). It increases progressively with higher grades of hypertension. The main aim of treatment is thus a significant improvement in survival for the patient. Persons with raised blood pressure (BP) have often additional cardiovascular risk factors such as deranged carbohydrate metabolism, dyslipidemia, left ventricular hypertrophy, smoking and others. Treatment of hypertensive patients should thus not only normalize BP but should at the same time reduce associated risk factors or at least not increase them. Conventional antihypertensive treatment based on thiazides in high doses or beta-blocking agents led to marked reduction of strokes and heart failure, but did not satisfactorily reduce coronary heart disease or sudden cardiac death. It has been suspected that other cardiac risk factors are insufficiently influenced or eventually even deteriorated by conventional therapy, thus counteracting partly a beneficial effect of lowered BP. Beta-blockers however have at least a secondary preventive effect after myocardial infarction. Newer antihypertensive drugs such as ACE-inhibitors, calcium antagonists and alpha 1-blockers reduce left ventricular hypertrophy and are at least neutral with regard to metabolism of lipids and carbohydrates. The non-thiazide diuretic indapamide and the serotonin (S2-) blocker ketanserin likewise are neutral with regard to glucose and lipid metabolism. The efficacy of these new drugs regarding long term survival is as yet undetermined. Persisting borderline or established hypertension should as a rule always be approached with basic non-pharmacologic measures: loss of overweight, reduction of alcohol intake, exercise, avoidance of high salt foods, abstention from smoking and withdrawal of BP-raising drugs. If antihypertensive medication is indicated, potential first line drugs are ACE-inhibitors, calcium antagonists, beta-blockers, thiazides at low dose, indapamide, ketanserin, the alpha 1-blocker prazosin and others; initially as monotherapy, if needed in combinations of 2 or 3. Older patients or those will with additional disturbances such as diabetes, hypercholesterolemia, nephropathy, heart failure, ischemic heart disease, arrhythmias, claudication, asthma and others need problem-adjusted modifications of treatment.
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PMID:[Antihypertensive therapy in the nineties]. 153 54

The effect of metformin treatment was studied in 13 patients with noninsulin-dependent diabetes mellitus (NIDDM), whose fasting plasma glucose concentration was greater than 10 mmol/L with maximal sulfonylurea doses. Patients were studied before and 3 months after receiving 2.5 g/day metformin. The fasting plasma glucose concentration (12.4 +/- 0.8 vs. 8.8 +/- 0.7 mmol/L), mean hourly postprandial plasma glucose concentration from 0800-1600 h (14.0 +/- 1 vs. 9.4 +/- 0.9 mmol/L), and glycosylated hemoglobin level (12.3 +/- 0.6% vs. 9.0 +/- 0.6%) were all significantly (P less than 0.005-0.001) lower after the administration of metformin. The improvement in glycemic control was associated with a 24% increase (P less than 0.05) in insulin-stimulated glucose uptake during glucose clamp studies and a 16% decrease in basal hepatic glucose production (P less than 0.05). Mean hourly concentrations of plasma insulin (411 +/- 73 vs. 364 +/- 73 pmol/L) and FFA concentrations (440 +/- 31 vs. 390 +/- 40 mumol/L) were also lower after 3 months of metformin treatment. However, neither insulin binding nor insulin internalization by isolated monocytes changed in response to metformin. Finally, plasma triglyceride, very low density lipoprotein triglyceride, and very low density lipoprotein cholesterol were significantly decreased (P less than 0.01-0.001), and high density lipoprotein cholesterol was significantly increased (P less than 0.001) after metformin treatment. Thus, the addition of metformin to sulfonylurea-treated patients with NIDDM not in good glycemic control significantly lowered fasting and postprandial plasma glucose concentrations, presumably due to the combination of enhanced glucose uptake and decreased hepatic glucose production. Since the dyslipidemia present in these patients also improved, the results suggest that metformin may be of significant clinical utility in patients with NIDDM not well controlled with sulfonylurea compounds.
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PMID:Combined metformin-sulfonylurea treatment of patients with noninsulin-dependent diabetes in fair to poor glycemic control. 156 49

Non-insulin-dependent diabetes (NIDDM) has long been recognized as being associated with a cluster of disorders including obesity, hypertension, dyslipidemia, and atherosclerotic heart disease. It was only recently, however, that Reaven, DeFronzo, and Ferrannini with techniques to quantitate insulin resistance suggested that this represents a common factor in this group of disorders and that hyperinsulinemia resulting from insulin resistance could be the cause of the hypertension, dyslipidemia, and atherosclerosis. The names syndrome X or the insulin-resistance syndrome have been used to identify this pathological entity, and considerable investigations have been done and are in progress to establish whether or not these coexisting disorders represent an as yet unexplained association of cardiovascular risk factors or if, indeed, insulin resistance and hyperinsulinism represent the primary cause for most of the other disorders. To paraphrase a philosophical comment, if syndrome X did not exist, we probably would have had to invent it. In addition to the intellectual satisfaction of being able to "lump" these diverse ills under a single etiology, the main value of grouping these disorders as a syndrome is to continually remind physicians that the therapeutic goals are not only to correct hyperglycemia in NIDDM but also to manage the elevated blood pressure and dyslipidemia that cause cerebrovascular and cardiac morbidity as well as mortality in these patients. Having a syndrome X reduces the fragmentation of medical care among subspecialties and decreases the likelihood of prescribing drugs that correct hypertension but raise lipids or drugs that lower lipids but raise blood glucose. Finally, it encourages the selection of drugs that reduce hyperglycemia without increasing insulin secretion and to the development of new drugs for this purpose. Unfortunately, the concept of insulin resistance with hyperinsulinism being a cause of the other associated disorders is still unproved but continues to be open to experimental investigation. The remainder of this article reviewed the use of sulfonylureas in the management of NIDDM, discussed new molecular and cellular mechanisms by which they promote insulin secretion, and reviewed the controversy as to whether an extrapancreatic action contributes to their glucose-lowering effects in NIDDM. A closing section listed some other oral drugs that can lower blood glucose without stimulating the pancreatic beta cell. Their insulin-sparing hypoglycemic effect makes them potentially useful in NIDDM therapy, particularly if the fundamental premise of syndrome X is substantiated, which implicates hyperinsulinemia as contributing to the morbidity and mortality from atherosclerotic vascular disease.
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PMID:Type II diabetes and syndrome X. Pathogenesis and glycemic management. 161 69

Accelerated atherosclerosis is a major complication of long-term diabetes mellitus, and this is partly due to associated abnormalities of lipoprotein metabolism. Hypertriglyceridemia is usually due to poorly controlled diabetes and responds to improved glucose control. Hypercholesterolemia is usually not related to poor diabetic control and should be treated with a cholesterol lowering diet and drugs according to the National Cholesterol Education Program guidelines. Low HDL-C is common in NIDDM and does not fully return to normal with improved diabetic control. Dyslipidemia in diabetics should be aggressively identified and treated to decrease cardiovascular risk.
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PMID:Management of hyperlipidemia in diabetes mellitus. 161 72


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