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)

Among the adverse effects attributed to antiretroviral therapy, one of the most striking is probably the appearance of the lipodystrophy syndrome and its associated metabolic derangements, given its potential long-term effect as a cardiovascular risk factor. Since not all patients who receive antiretroviral drugs experience these adverse effects, a host genetic predisposition has been postulated. However, currently available data on this issue is inconclusive and preliminary. It has been consistently demonstrated that polymorphisms in the genes that encode for apolipoproteins A5, C3 and E, for the cholesterol ester transporter proteins (CETP), and in the ATP binding cassette type A1 (ABCA1) influence the development of dyslipidemia in patients treated with antiretroviral drugs, particularly if the therapeutic regimen includes protease inhibitors. Data on the effect of polymorphisms in the sterol regulatory ester binding protein type 1 (SREBP1) are inconsistent. The effect of mitochondrial DNA mutations on the risk of lipodystrophy has been assessed, with inconclusive data. No polymorphisms in the lamin A gene have been detected. Investigations have assessed the effect of diverse polymorphisms in the genes that encode for several proinflammatory cytokines such as tumour necrosis factor alpha (TNF-alpha), interleukin-1-beta (IL-1beta) and interleukin-6 (IL-6). The results show inconsistent data in the case of TNF-alpha, no association in the case of IL-6, and preliminary positive associations in IL-1beta. In contrast, polymorphisms in the genes encoding for stromal derived factor 1 (SDF-1) and for monocyte chemoattractant protein 1 (MCP-1) have been shown to influence the development of subclinical atherosclerosis in HIV-1-infected patients treated with antiretroviral drugs.
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PMID:[Toxicogenetics of antiretroviral treatment (1): lipodystrophy, metabolic perturbations and atherosclerosis]. 1868 Jun 92

Dyslipidemia is an established cardiovascular risk factor in the general population. However, in patients suffering from chronic kidney disease (CKD) this relationship is less clear, and many studies show that low, rather than high, cholesterol levels predict mortality in this patient population. This review presents an overview of the major disorders of lipid metabolism in the course of CKD and their clinical implications. We also discuss the role of genetic determinants predisposing to dyslipidemia, as well as current therapeutic approaches. Finally, the mendelian randomization approach as a novel tool to elucidate the seemingly paradoxical association between hypercholesterolemia and mortality in CKD will be discussed.
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PMID:Lipid disorders in chronic kidney disease: reverse epidemiology and therapeutic approach. 1894 17

TREATMENT OF ARTERIAL HYPERTENSION - Blood pressure (BP) should be regularly measured in all patients with CKD (Strength of Recommendation C). - BP control and proteinuria reduction delay progression of CKD (Strength of Recommendation A) and reduce cardiovascular risk (Strength of Recommendation C). Thus, control of both factors should be the treatment objective. - The BP target in patients with CKD should be < 130/80 mmHg, and 125/75 mmHg if proteinuria is > 1 g/24 hours (Strength of Recommendation A). - Lifestyle changes should be made: low-sodium diet (less than 100 mEq/day of sodium or 2.4 g/day of salt); weight reduction if patient is overweight (body mass index 20-25 kg/m2); regular aerobic physical exercise and moderate alcohol intake for BP control and prevention of cardiovascular risk (Strength of Recommendation A). - The choice of the antihypertensive drug in patients with CKD depends on the etiology of CKD, cardiovascular risk, or presence of clinical or subclinical cardiovascular disease (Strength of Recommendation A). - Two or more antihypertensive drugs are usually required to control blood pressure in patients with CKD (Strength of Recommendation B), and will frequently include a diuretic, which in stages 4-5 should be a loop diuretic (Strength of Recommendation B). - Renin-angiotensin-aldosterone system (RAAS) inhibitors are first choice drugs in patients with diabetic nephropathy, patients with non-diabetic nephropathy with a protein/creatinine ratio higher than 200 mg/g, and patients with heart failure (Strength of Recommendation A). The combination of ACEIs and ARBs is indicated for reducing proteinuria that remains high despite treatment with a RAAS inhibitor, provided potassium levels do not exceed 5.5 mEq/L (Strength of Recommendation B). - When RAAS blockers are started or their dose is changed in patients with advanced CKD, kidney function and serum potassium levels should be monitored at least after 1-2 weeks. DIAGNOSIS AND TREATMENT OF DYSLIPIDEMIA - A complete evaluation of the lipid profile including total cholesterol, LDL-C, HDL-C, and triglycerides should be performed in any patient with CKD at baseline and at least annually (Strength of Recommendation B). - In patients with stage 4-5 CKD and LDL-C >or= 100 mg/dL, treatment to decrease levels to < 100 mg/dL should be considered because of their high CV risk. This reduction is recommended in secondary prevention and in primary prevention in diabetic patients. Lipid-lowering treatment is recommended in all other patients, although no evidence showing its benefits is available yet (Strength of Recommendation C). - In patients with stage 4-5 CKD and triglyceride levels >or= 500 mg/dL which are not corrected by treating the underlying cases, treatment with triglyceride-lowering drugs may be considered to reduce the risk of pancreatitis. However, treatment with fibrates should be used with caution, and these drugs should not be associated to statins due to the risk of rhabdomyolysis (Strength of Recommendation C). There is little experience on the efficacy and safety of omega-3 fatty acids for the treatment of hypertriglyceridemia in patients with grade 4-5 CRF, but they may be considered a possibly safer alternative to fibrates (Strength of Recommendation C). SMOKING - Smoking is a cardiovascular risk factor and a risk factor for progression of kidney disease in patients with CRF (Strength of Recommendation B). - Use of active measures to achieve smoking cessation is recommended in patients with CRF (Strength of Recommendation C). HOMOCYSTEINE - Hyperhomocysteinemia has been postulated as a cardiovascular risk factor in the general population and in kidney patients, but the available evidence is not consistent. - There is no evidence that vitamin therapy decreases cardiovascular risk in patients with CRF, and recommendation of routine vitamin measurement and start of vitamin therapy to reduce cardiovascular risk in these patients is therefore questionable (Strength of Recommendation B). LEFT VENTRICULAR HYPERTROPHY - Left ventricular hypertrophy (LVH) is a cardiovascular risk factor in patients with CRF (Strength of Recommendation B). - It is advisable to perform an echocardiogram at baseline and every 12-24 months and to consider treatments allowing for LVH regression (Strength of Recommendation C). The approach to LVH should be early and multifactorial because its reversibility is limited once established (Strength of Recommendation C). - RAAS blockade with ACEIs or ARBs partially reverts LVH in patients with CRF (Strength of Recommendation B). ANTI-PLATELET AGGREGATION - Because of the high cardiovascular risk in patients with CKD, anti-platelet aggregant therapy, especially low-dose aspirin, would be indicated in patients with type 2 diabetes as primary prevention, and in all patients with CKD as secondary prevention. There is however no evidence of the benefits of anti-platelet aggregant therapy in primary prevention in patients with CKD, particularly in stages 4-5; indication for treatment in this situation should therefore be individualised because of its greater risk of bleeding. - Adequate good blood pressure control should previously be achieved to minimise the risk of haemorrhagic stroke (Strength of Recommendation C).
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PMID:[Arterial hypertension and dyslipidemia in patients with chronic kidney disease (CKD). Anti-platelet aggregation. Goal oriented treatment]. 1901 37

Low levels of high-density lipoprotein cholesterol (HDL-C) represent a major cardiovascular risk factor, with a stronger relationship to coronary heart disease than that seen with elevated levels of low-density lipoprotein cholesterol (LDL-C). HDL-C has important antiatherogenic effects, including reverse cholesterol transport, inhibition of LDL-C oxidation, and antiplatelet and anti-inflammatory actions. Patients with low HDL-C are also at an amplified risk of coronary heart disease due to the common coexistence of other risk factors, including excess adiposity, metabolic syndrome, type 2 diabetes mellitus, hypertriglyceridemia, and the atherogenic dyslipidemia characterized by small dense LDL-C. First-line therapy of low HDL-C generally consists of nonpharmacologic measures such as improved fitness and weight loss. Current pharmaceutical options include statins, fibrates, and nicotinic acid. A host of novel approaches involving HDL-C and reverse cholesterol transport hold the promise of fundamentally changing the natural history of atherosclerosis, the most common and important chronic disease in humans.
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PMID:The importance of recognizing and treating low levels of high-density lipoprotein cholesterol: a new era in atherosclerosis management. 1912 82

The objective of this study was to verify the clustering of anthropometric and metabolic variables related to metabolic syndrome, by sex. Data were collected from 579 subjects aged 18-94 years living in two rural areas of Brazil. Factor analysis was performed using principal components analysis with varimax orthogonal rotation. The study reduced a complex set of cardiovascular risk factor into 3 independent factors, each reflecting a different aspect of metabolic syndrome. In both sexes, factor 1 related to obesity and dyslipidemia, factor 2 to obesity and blood pressure, and factor 3 to obesity and insulin resistance. The total variance explained for men and women was, respectively, 66.61% and 68.98%. The findings corroborate the hypothesis that at least 3 pathophysiological domains act in the clustering of cardiovascular risk factors related to metabolic syndrome in this population.
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PMID:[A multidimensional exploration of metabolic syndrome components]. 1948 92

Male hypogonadism now has a new spectrum of complications. They are mainly cardiometabolic in nature. Low serum testosterone levels are a risk factor for diabetes, metabolic syndrome, inflammation and dyslipidemia. These metabolic and inflammatory complications are not without consequences. Recent studies have shown low serum testosterone levels to be an independent risk factor of cardiovascular and all-cause mortality. It is time to welcome low serum testosterone levels as a cardiovascular risk factor.
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PMID:Welcoming low testosterone as a cardiovascular risk factor. 1953 27

Atherosclerotic cardiovascular disease is a leading cause of morbidity and premature mortality in Western countries and dyslipidemia is a recognized major cardiovascular risk factor. Evidences demonstrate that the atherosclerotic process begins early in childhood. Children showing dyslipidemia, as well as other cardiovascular risk factors, including hypertension, overweight/obesity and diabetes mellitus, are defined at high risk. To identify these children a selective screening between 2 to 10 years of age is necessary. This program must be performed to those children showing a familiarity for primary dyslipidemia and/or precocious cardiovascular events. These subjects need to undergo lipid biochemical analysis and assessment of other emergent risk factors (as ApoB, ApoA-I and their ratio). Given that total cholesterol and low-density lipoprotein cholesterol (LDL-C) concentrations vary by age and sex, the use of percentile values according to these parameters is now recommended. In these high-risk subjects the first step to lower LDL-C under the value of 130 mg/dL is represented by an appropriate physical activities and Step II diet. This entails further reduction of saturated fatty acid intake to less than 7% of daily calories and of cholesterol to less than 200 mg/day (since two years of age). When diet therapy is insufficient to lower LDL-C to the acceptable concentration, the use of non-pharmacologic agents (soluble fibers, plant stanols, sterols) is suggested. The third approach, for children showing persistent elevated LDL-C >95(th) percentile, is represented by drugs, that are allowed only in children older than eight years.
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PMID:Identification and management of dyslipidemic children. 1975 48

Dyslipidemia is a known cardiovascular risk factor in subjects without kidney disease. In patients with kidney disease, however, the relation of dyslipidemia to cardiovascular risk is confounded and the underlying pathomechanisms are complex. Statins have proven to be highly effective in patients with initial stages of chronic kidney disease (CKD). Definite evidence from prospective controlled trials in hemodialyzed (diabetic) patients and transplanted patients is not available. Although no significant impact on the primary composite endpoint was observed, significant effects on secondary endpoints were noted. In our opinion, in view of excessive cardiovascular risk statins should be administered in patients with advanced CKD as well.
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PMID:Dyslipidemia in chronic kidney disease: pathogenesis and intervention. 1977 89

The metabolic syndrome is a common and complex disorder combining obesity, dyslipidemia, hypertension and insulin resistance. It is associated with a high cardiovascular risk that can only partially be explained by its components. There is evidence that low-grade inflammation and high oxidative stress add to this risk. Oxidized LDL, a marker of lipoprotein-associated oxidative stress, is an emerging cardiovascular risk factor. In this review, we demonstrate that the metabolic syndrome exacerbates oxidized LDL in a feedback loop. We introduce molecular mechanisms underlying this loop. Finally, we demonstrate that weight loss and statin treatment lower metabolic syndrome factors associated with a reduction of oxidized LDL. The current data warrant further investigation into the role of lifestyle and therapeutic interventions that inhibit tissue-associated oxidation of LDL in the prevention of the metabolic syndrome.
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PMID:Oxidized LDL and the metabolic syndrome. 1980 39

The authors describe the case of a 55-year old patient, with dyslipidemia as single cardiovascular risk factor, who previously underwent chemo and radiotherapy for Hodgkin lymphoma (stage 2b). The patient developed early coronary atherosclerosis followed by aortic and mitral valve disease and initial constrictive pericarditis. The role of chemo and radiotherapy in the development of cardiovascular disease, in particular valvular and pericardial disease, is discussed.
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PMID:[Cardiotoxicity induced by chemo- and radiotherapy]. 2006 79


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