Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Familial combined hyperlipidemia (FCHL) is a frequent cause of premature coronary artery disease. Affected family members are characterized by different combinations of elevated cholesterol and/or triglyceride levels. A reduction in lipoprotein lipase (LPL) activity has been observed in a subgroup of FCHL patients. Recently, we have demonstrated an increased frequency of mutations in the LPL gene in Dutch FCHL patients compared to normolipidemic controls. In the present study, we have applied a pedigree-based maximum likelihood method to study the effect of LPL mutations on the phenotypic expression of FCHL in families. In 40 FCHL probandi, three different previously reported mutations in the LPL gene were identified resulting in amino acid changes, D9N, N291S, and S447X. The D9N mutation in exon 2 appeared to be in strong linkage disequilibrium with a T-->G substitution at position -93 in the promoter region of the LPL gene. We present data that the -93T-->G/D9N haplotype is associated with significantly higher levels of LDL and VLDL cholesterol, and VLDL triglycerides. Interestingly, the effect was only observed in male carriers. In line with our previous observations, these results further sustain that the LPL gene is a susceptibility gene for dyslipidemia which explains part of the variability in the phenotype observed among FCHL family members.
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PMID:Gender-related association between the -93T-->G/D9N haplotype of the lipoprotein lipase gene and elevated lipid levels in familial combined hyperlipidemia. 967 74

A direct, continuous, and independent association between blood pressure values and incidence of coronary artery disease has been well documented. However, the evidence that the reduction of blood pressure alone is not able to completely reverse the increase in the risk of coronary artery disease associated with essential hypertension suggests that the link between hypertension and coronary artery disease is a complex process including other factors beside the increase in blood pressure values. In this regard, the main determinant of coronary artery disease in hypertensive patients seems to be the development of left ventricular hypertrophy (LVH). In fact, hypertensive patients who died from sudden cardiac death showed a lesser degree of coronary atherosclerosis compared with normotensives, but a higher incidence of LVH. Several mechanisms can account for the increased coronary risk with LVH, including (1) an increase in left ventricular (LV) mass, which by itself requires more oxygen for tissue perfusion; (2) impairment of coronary flow reserve; (3) perivascular fibrosis, which then impairs oxygen supply to the myocardium; and (4) deterioration of LV diastolic function, which hampers myocardial perfusion. Recently, a study reported an impairment of endothelial function and abnormal control of the sympathetic tone in hypertensive patients, which may contribute to the risk of coronary artery disease. In particular, the impaired endothelial function resulting in a prevalence of vasoconstrictive, thrombogenic, and proliferative factors may account for the enhanced ischemic susceptibility of these patients. Furthermore, the cardiac adrenergic system plays an important role in regulating myocardial blood flow. On one hand, hypertensive patients show an exaggerated sympathetic response to physiologic stimuli, whereas on the other hand, the beta-adrenergic receptor-mediated vasodilating component of the sympathetic response is blunted in hypertension. Finally, excess body weight, dyslipidemia, glucose intolerance, and hyperinsulinemia, which are frequently interrelated, represent independent predictors of both coronary artery disease and hypertension.
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PMID:Systemic hypertension and coronary artery disease: the link. 971 15

The large ethnic differences in prevalence of coronary artery disease between China and Europe may relate to both genetic and environmental differences. To assess possible genetic factors we have therefore studied the frequencies of disease-related variants of genes involved in lipid transport in 69 hypertriglyceridemic Chinese subjects and 74 healthy Chinese controls. The loci studied include lipoprotein lipase (Asp9Asn, Asn291Ser, Ser447Ter, and Thr361Thr); apolipoprotein A1 (restriction sites at MspI, XmnI, and PstI); and apolipoprotein (apo) CIII (G3175C). All these variants have been shown in previous literature publications to relate to either dyslipidemia and/or premature coronary heart disease in Caucasians. Two disease-related genetic variants in Europeans (Asp9Asn and Asn291Ser) were not found in the Chinese sample. The apo CIII G3175C variant was found more frequently in the upper tertile distributions for apolipoprotein CIII, apolipoprotein E, and plasma triglyceride/HDL ratios (P < 0.05). The rare allele of the apo AI MspI restriction site polymorphic variant was also found more frequently in the upper tertiles for apo CIII, apo E, and plasma triglyceride/HDL ratios (P < 0.04). Eleven of the most lipaemic Chinese subjects (with fasting plasma triglycerides >700 mg/dl) were analyzed for DNA sequence variation. One novel mutation was observed C1338A (which is a silent mutation at Thr361) and two others that are also found in European subjects (Ala261Thr and Ser447Ter). We conclude that genetic differences between Chinese and Europeans may have an effect on the prevalence of coronary artery risk factors involved in lipid transport, and further extended study is warranted.
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PMID:Common genetic variants of lipoprotein lipase and apolipoproteins AI-CIII that relate to coronary artery disease: a study in Chinese and European subjects. 971 26

In recent years, a substantial body of evidence has emerged to support the use of lipid-lowering therapy in the prevention of coronary artery disease, and many physician groups have endorsed the management of dyslipidemia in at-risk patients. An important consideration in such endorsements has been the issue of the safety of lipid intervention; many early primary- and secondary-prevention studies reported either no reduction in all-cause mortality rates or an increase in non-coronary artery disease mortality rates in treated patients. These observations raised serious concerns about the safety of such therapy. However, 2 landmark studies, the Scandinavian Simvastatin Survival Study (4S) and the West of Scotland Coronary Prevention Study (WOSCOPS), have contributed greatly to alleviating these concerns. In this article, a review of the epidemiologic evidence supporting the use of lipid modification will be presented, including important trials and meta-analyses, and the cost-effectiveness of lipid-modifying treatment will be discussed.
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PMID:Assessing the benefits of lipid-lowering therapy. 976 41

Little doubt remains about the value of lipid-lowering therapy since publication of the results of large, randomized, controlled trials that show decreased total, as well as coronary, mortality with the use of statins for primary and secondary prevention of coronary artery disease. All of the available statins are effective and safe, but they vary greatly in terms of cost-effectiveness. Fluvastatin has been determined to be a cost-effective therapeutic agent in the large proportion of the population with mild-to-moderate dyslipidemia who fit treatment guidelines of the National Cholesterol Education Program (NCEP). Atorvastatin and simvastatin are cost-effective for the relatively smaller number of patients who require greater reductions in cholesterol.
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PMID:Economic implications of lipid-lowering trials: current considerations in selecting a statin. 976 45

HMG reductase inhibitors have significant desirable effects on patients with dyslipidemia. Multiple factors are involved in these desirable effects. Other factors that might play a role in the risk of coronary artery disease are fibrinogen concentration, homocysteine, Lp (a), small dense LDL, insulin resistance, and infection with chlamydia. High-dose reductase inhibitors may be indicated in select patients. The ideal end point may be 150 mg/dL for adults.
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PMID:Present status of HMG reductase inhibitors in treatment of dyslipidemia. 978 44

Diuretics and beta-blockers have a strong tendency to affect serum lipids adversely, whereas the peripherally acting alpha-blocking agents consistently result in beneficial effects. Most of the other antihypertensive agents (calcium channel blockers, ACE inhibitors, angiotensin II receptor antagonists, and drugs that act centrally) are lipid neutral. The effect of steroid hormones varies with the drug, dose, and route of administration. In general, androgens lower HDL-C and have a variable effect on LDL-C. The effects of progestins vary greatly depending on their androgenicity, and estrogens are beneficial except when hypertriglyceridemia occurs with oral estrogens. Glucocorticoids raise HDL-C and may also increase triglycerides and LDL-C. Retinoids increase triglycerides and LDL-C and also reduce HDL-C. Interferons can cause hypertriglyceridemia. Following organ transplantation, a dyslipidemia often ensues. This is caused in part by the medications used to prevent rejection (glucocorticoids, cyclosporine, and FK-506) and requires close attention and, in some patients, drug therapy to prevent coronary artery disease.
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PMID:Drugs causing dyslipoproteinemia. 978 60

The increased risk of coronary artery disease in subjects with diabetes mellitus can be partially explained by the lipoprotein abnormalities associated with diabetes mellitus. Hypertriglyceridemia and low levels of high-density lipoprotein are the most common lipid abnormalities. In type 1 diabetes mellitus, these abnormalities can usually be reversed with glycemic control. In contrast, in type 2 diabetes mellitus, although lipid values improve, abnormalities commonly persist even after optimal glycemic control has been achieved. Screening for dyslipidemia is recommended in subjects with diabetes mellitus. A goal of low-density lipoprotein cholesterol of less than 130 mg/dL and triglycerides lower than 200 mg/dL should be sought. Several secondary prevention trials, which included subjects with diabetes, have demonstrated the effectiveness of lowering low-density lipoprotein cholesterol in preventing death from coronary artery disease. The benefit of lowering triglycerides is less clear. Initial approaches to lowering the levels of lipids in subjects with diabetes mellitus should include glycemic control, diet, weight loss, and exercise. When goals are not met, the most common drugs used are hydroxymethylglutaryl coenzyme A reductase inhibitors or fibrates.
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PMID:Hyperlipidemia and diabetes mellitus. 978 48

Hypertension is a very important cardiovascular risk factor and directly leads to major atherosclerotic cardiovascular diseases, including coronary artery disease, stroke cardiac failure and peripheral artery disease. Hypertension tends to cluster with other atherogenic risk factors like dyslipidemia, insulin resistance, obesity and others. The association between hypertension and dyslipidemia is very frequent and the risk is more than additive and its possible pathogenesis may be of a common mechanism. Insulin resistance is the main cause of both risk factors. Endothelium dysfunction is present in arterial hypertension and dyslipidemia and the pathogenesis of atherosclerosis. The treatment of hypertensive patients must be individualized to accommodate both the concomitant dyslipidemia and other atherogenic factors.
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PMID:[Hypertension and dyslipidemia]. 988 66

Postprandial lipemia is an inherent feature of diabetic dyslipidemia and highly prevalent in diabetic patients even with normal fasting triglyceride concentrations. Postprandial lipemia is characterized by long residence time of chylomicron and VLDL remnants in the circulation. Insulin resistance causes increased flux of free fatty acids, and thus enhanced VLDL apolipoprotein B (apo B) synthesis in the liver. Together with chylomicron and VLDL remnant competition for the common removal mechanisms the increased substrate input results in exaggerated and prolonged postprandial lipemia. Studies using both apo B-48 and retinyl esters as a marker for intestinally derived particles have shown that increased postprandial lipemia does not predict the presence or absence of coronary artery disease between non-insulin-dependent diabetes mellitus (NIDDM) subjects. Recent data have shown that postprandial triglyceride-rich remnants are atherogenic, and postprandial hypertriglyceridemia contributes to the metabolic disturbances transforming LDL and HDL subclasses into more atherogenic direction in diabetic subjects.
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PMID:Postprandial lipid metabolism in diabetes. 988 43


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