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

Patients with diabetes mellitus have a much higher rate of cardiovascular disease (CVD) than the general population, and, in addition to glycaemia and hypertension, dyslipidemia has emerged as an important modifiable cardiovascular risk factor in these patients. In most patients with type 2 diabetes, the major features of dyslipidemia are increased triglyceride levels, decreased high-density lipoprotein cholesterol (HDL-C) levels, and changes in the composition and level of low-density lipoprotein cholesterol (LDL-C). Clinical trials evaluating both primary and secondary prevention of CVD demonstrate that lipid-lowering therapy results in a substantial reduction of cardiovascular risk in patients with type 2 diabetes. Low-density lipoprotein cholesterol is the first priority for treatment, with a statin in adequate dosage as the first choice for pharmacological therapy. The first statin trial conducted solely in patients with type 2 diabetes and no prior CVD demonstrated a 37% reduction in cardiovascular events in patients randomized to atorvastatin 10 mg compared with placebo. Additional trials that further address the benefits of lipid-lowering therapy in patients with diabetes are near completion, or are underway, and should provide important information about further attenuating risk in patients with diabetes.
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PMID:Reducing cardiovascular risk in diabetes: beyond glycemic and blood pressure control. 1628 73

Type 2 diabetes is an important cardiovascular risk factor. A significant component of the risk associated with type 2 diabetes is thought to be because of its characteristic lipid "triad" profile of raised small dense low-density lipoprotein levels, lowered high-density lipoprotein, and elevated triglycerides (TGs). Trials of statins and fibrates have included substantial numbers of patients with diabetes and indicate that lipid lowering reduces cardiovascular event rates in these patients. However, statins alone do not always address all the lipid abnormalities of diabetes. Fibrates, which have low affinity for peroxisome proliferator-activated receptor alpha (PPARalpha), improve most aspects of the atherogenic dyslipidemia of diabetes. Chronic elevations of free fatty acids (FFA) induce insulin resistance and contribute to the lipid triad of diabetes. Therefore, reducing their levels is likely to ameliorate insulin resistance and improve the lipid triad of diabetes. PPARs are intimately involved in the regulation of FFA: PPARalpha modulation increases FFA catabolism and PPARgamma agonism (eg, by thiazolidinediones) increases TG lipolysis, FFA transport, conversion of FFA to TGs, and safe storage of FFA. Integrating potent PPARalpha and PPARgamma activity may deliver greater improvement of the diabetic dyslipidemic profile and its attendant risks than selective PPAR activation.
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PMID:Type 2 diabetes, dyslipidemia, and vascular risk: rationale and evidence for correcting the lipid imbalance. 1629 Sep 51

Gout is an increasingly common medical problem. The traditional risk factors of male sex and high red meat or alcohol consumption have been joined by a wave of newer risk factors, such as increased longevity, the metabolic syndrome (hypertension, diabetes, dyslipidemia, truncal obesity, increased cardiovascular disease risk), use of diuretics, low-dose aspirin, or cyclosporine, and end-stage renal disease. Atypical presentations of gout in the elderly can mimic osteoarthritis and rheumatoid arthritis. There is a resurgence of interest in hyperuricemia as an independent and potentially modifiable cardiovascular risk factor. The pharmacologic management of gout in general practice suffers from a number of quality-control issues. This article reviews these and other new epidemiologic data on this ancient disease.
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PMID:Epidemiology of hyperuricemia and gout. 1630 Apr 57

Patients with type 2 diabetes mellitus are at high risk for cardiovascular events and heart failure. The major serious complication of this disorder is large vessel atherosclerosis leading to myocardial infarction and stroke. Aggressive target setting for modifiable cardiovascular risk factors such as dyslipidemia, hypertension, and a procoagulant state, and judicious choice of efficacious therapies have been shown to produce significant reductions in cardiovascular events. The effectiveness of percutaneous coronary intervention (PCI) in diabetes is discussed, and the factors that may influence outcomes are explored. A major unresolved question is the potential role of tight glucose control for reducing macrovascular complications in patients with diabetes. With the increased attention being given to cardiovascular risk factor reduction, the opportunity exists to substantially decrease the largest causes of mortality in diabetic patients. This article reviews the current and emerging therapeutic strategies for these purposes from the cardiologists' point of view.
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PMID:[Type 2 diabetes mellitus and cardiovascular diseases: evaluation, treatment and prevention strategies]. 1650 21

We have previously demonstrated abnormalities in insulin secretion in adolescents with type 2 diabetes mellitus (DM2) in response to the mixed meal test and to glucagon. In order to further assess beta-cell function in DM2, we measured insulin and C-peptide responses to oral glucose in adolescents with DM2 in comparison to non-diabetic obese and lean adolescents. We studied 20 patients with DM2, 25 obese adolescents with matching body mass index (BMI) (33.8 +/- 1.4 vs 34.3 +/- 1.0 kg/m2), and 12 non-obese control adolescents (BMI 22.6 +/- 0.6 kg/m2). Mean age, sex and sexual maturation did not differ between the three groups. All adolescents with DM2 had negative islet cell antibodies (ICA); five patients were on diet and 15 on insulin treatment. Fasting lipid profiles were determined in all participants. Plasma glucose and serum C-peptide and insulin levels were measured at 0, 30, 60, 90, and 120 min after an oral glucose load. The C-peptide increment (deltaCP) was calculated as peak minus fasting C-peptide. Area under the curve (AUC) was estimated using the trapezoid method. Insulin resistance was estimated using the HOMA model (HOMA-IR). The first phase of insulin secretion (PH1) was computed using a previously published formula. Serum triglyceride levels were significantly higher in the patients with DM2 compared to the non-obese controls (1.4 +/- 0.1 vs 0.9 +/- 0.1 mmol/l; p = 0.02). Plasma glucose AUC was greater in the patients with DM2 compared to the obese and non-obese control groups (1,660 +/- 130 vs 717 +/- 17 vs 647 +/- 14 mmol/l x min; p < 0.0001). ACP was lower in adolescents with DM2 than in obese and non-obese adolescents (761 +/- 132 vs 1,721 +/- 165 vs 1,225 +/- 165 pmol/l; p < 0.001). Insulin AUC was lower in the patients with DM2 compared to obese controls (888 +/- 206 vs 1,606 +/- 166 pmol/l x h; p = 0.009), but comparable to that of the non-obese controls (888 +/- 206 vs 852 +/- 222 pmol/l x h; p = 0.9). Insulin AUC was also higher in the obese than in the non-obese group (p = 0.05). PH1 was significantly higher in the obese group compared to the patients with DM2 as well as to the non-obese controls (2,614 +/- 2,47.9 vs 929.6 +/- 403.5 vs 1,946 +/- 300.6 pmol/l, respectively; p = 0.001). PH1 was also higher in the non-obese controls than in the patients with DM2 (p = 0.05). HOMA-IR was three-fold higher in the patients with DM2 than in the BMI-matched obese group, and five-fold higher than in the lean controls (14.3 +/- 1.2 vs 5.4 +/- 0.8 vs 2.9 +/- 0.4; p = 0.0002). Adolescents with DM2 have dyslipidemia, a significant cardiovascular risk factor. Decreased beta-cell function is characteristic of adolescents with DM2 in the presence of severe insulin resistance.
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PMID:Type 2 diabetes mellitus in African-American adolescents: impaired beta-cell function in the face of severe insulin resistance. 1656 86

Cardiovascular disease is the leading cause of morbidity and mortality in both genders. Although premenopausal women display a lower prevalence in cardiovascular diseases compared with age-matched men, they lose this ''female advantage'' following menopause. There are significant gender differences in a wide spectrum of cardiovascular incidence, ranging from delayed disease onset to higher prevalence of comorbid diseases for females. Several factors have been suggested to contribute to such difference in cardiovascular incidence including sex hormones, gender-specific intrinsic organ function, difference in body size and cardiovascular risk factor profiles (e.g., use of tobacco and alcohol, hypertension, diabetes mellitus, dyslipidemia, obesity, sedentary lifestyle and atherogenic diet). A gender difference also exists for diabetes and diabetic complications. Heart diseases exhibits a 2-fold and a 5-fold increase in men and women with diabetes, respectively. Although female hearts are usually more tolerable to stress insults than their male counterparts, female sex hormone such as estrogen interacts with diabetic risk factors to precipitate cardiomyopathy. This review aims at recaping our knowledge on gender difference in diabetic heart disease with an emphasis on disease pathogenesis. Deficits and obstacles to optimal risk factor management in diabetic women are also discussed in an effort to improve the overall cardiovascular health of diabetic women.
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PMID:Cardiac health and diabetes mellitus in women: problems and prospects. 1673 4

Atherosclerosis and cardiovascular disease (CVD) are the main causes of death in the Western world, for both men and women. The onset and development of diseases of the cardiovascular and cerebrovascular system are strongly dependent on multiple risk factors that promote pathologic conditions like atherosclerosis, hypertension and thrombosis. Besides genetic factors also environmental influences such as diet composition are known to be closely related to CVD. In this context obesity has been postulated as an independent cardiovascular risk factor. Data from the Framingham Heart Study have consistently shown that increasing degrees of obesity are accompanied by greater rates of CVD. At present, obesity affects 10-35% of the European and US population and increases steadily. As obesity is a serious health problem which promotes metabolic abnormalities (insulin resistance, hyperinsulinemia and dyslipidemia) and dramatically increases the risk for CVD, this review will focus on the epidemiologic and genetic background of obesity. Furthermore, the molecular mechanisms involved in obesity development and their contribution to CVD will be discussed.
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PMID:Molecular basis of obesity and the risk for cardiovascular disease. 1677 May 55

In recent years, increasing evidence has been provided that even minor renal dysfunction is a powerful cardiovascular risk factor that induces typical cardiovascular alterations and thus predisposes to coronary heart disease as well as to noncoronary cardiovascular problems. This first had been noted in patients with diabetes but now has been confirmed amply in patients without diabetes as well. Numerous heterogeneous abnormalities have been described in patients with early renal dysfunction (e.g., microalbuminuria, reduced estimated GFR). One final common pathway seems to be endothelial cell dysfunction. The link between albuminuria and generalized endothelial cell dysfunction (as indicated by diminished flow-mediated vasodilation, markers of endothelial cell dysfunction, sloughed off endothelial cells, and high transcapillary albumin escape rate) is unclear. In patients with early renal dysfunction, a long list of classical and nonclassical cardiovascular risk factors have been identified: Elevated asymmetric dimethyl-l-arginine concentrations, markers of microinflammation, oxidative stress, features of metabolic syndrome, abnormal adipokine concentrations, dyslipidemia, inappropriate activation of the renin-angiotensin system, and sympathetic overactivity. The mechanisms that link dysfunction of the kidney and the cardiovascular system are being sought. The most interesting unifying concept, however, is deranged fetal programming linking nephron underdosing to the increased cardiovascular risk.
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PMID:Cross-talk between the kidney and the cardiovascular system. 1682 29

Metabolic syndrome is a complex disorder and an emerging clinical challenge. It is considered a "multiplex" cardiovascular risk factor, in that each component of the cluster of abnormalities is a risk factor in its own right. Introduced as Syndrome X by Reaven in 1988 and also termed insulin resistance syndrome, metabolic syndrome is recognized clinically by the findings of abdominal obesity, elevated triglycerides, atherogenic dyslipidemia - i.e. low levels of high-density lipoprotein cholesterol (HDL-C), elevated blood pressure, high blood glucose and/or insulin resistance. The goal of our research was to investigate intensity of "complete metabolic syndrome"- (abdominal obesity, dyslipidemia, elevated blood pressure, high blood glucose and/or insulin resistance) in patients with different degrees of obesity. In our study 570 patients have been involved. The patients were divided into 3 groups: I group--123 patients with first degree of obesity (body mass index - BMI - 30-34,9 kg/m2), II group--189 patients with II degree of obesity (BMI - 35-39,9 kg/m2), III group--258 patients with III degree of obesity (BMI >40 kg/m2). Results of carried out investigations have shown that the complete picture of metabolic syndrome was present in 132 (23,16%) patients and should note, that according to the increasing of obesity degrees also increases the intensity of metabolic syndrome.
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PMID:[Intensity of metabolic syndrome in patients with different degrees of obesity]. 1690 22

In non-diabetic patients with (primary) kidney diseases a syndrome of insulin resistance can be diagnosed even before the onset of impaired renal function and uremia. It is presenting with hyperinsulinemia, glucose intolerance, hyperglycemia and dyslipidemia. As a result, patients with kidney diseases own the same metabolic cardiovascular risk factors as patient with the classic metabolic syndrome. Thus, this renal insulin resistance syndrome may not only contribute to the excessive cardiovascular risk of patients with kidney diseases, but may also help to explain why even a minor impairment of renal function is a significant and independent cardiovascular risk factor in the general population.
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PMID:Insulin resistance and renal disease. 1692 43


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