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)

Differences on measures of metabolic syndrome X and coronary heart disease (CHD) risk, as well as potential pathophysiological mediators, inflammation, and oxidative stress, were examined as a function of HIV serostatus and highly active antiretroviral therapy (HAART) regimen with and without protease inhibitors (PIs). Data from 164 men and women, aged 18 to 55 yr, were used to compare 82 HIV+ subjects who were free of hepatitis C virus and were on a stable HAART regimen for >/=6 mo, with 82 seronegative subjects matched on age, sex, body mass index, and ethnicity. For the HIV+ subjects, after controlling for diabetes status and HIV disease progression, PI exposure was associated with greater oxidative stress, triglyceridemia, and lipidemia than it was for non-PI-exposed HIV+ subjects, and the risk of a future myocardial infarction was up to 56% greater in PI-exposed than in non-PI-exposed subjects and 129% greater than in controls. Although it is likely that the greatest proportion of CHD risk in the HIV+ subjects may be accounted for by pathological conditions linked to HIV infection in interaction with mediating processes such as inflammation, central obesity, and dyslipidemia, which was greater than in controls, it appears that PI medications may exacerbate oxidative stress and hypertriglyceridemia to enhance this risk.
Cardiovasc Toxicol 2004
PMID:HIV, metabolic syndrome X, inflammation, oxidative stress, and coronary heart disease risk : role of protease inhibitor exposure. 1547 Feb 77

Insulin resistance syndrome, also referred to as the metabolic syndrome, affects 1 in 3 to 4 adults older than 20 years. This syndrome consists of a clustering of metabolic abnormalities that put people at risk for type 2 diabetes and cardiovascular disease. These clinical abnormalities include dyslipidemia, specifically elevated triglycerides and low high-density lipoprotein cholesterol, elevated glucose, and hypertension. The incidence of this morbid syndrome is expected to continue to grow both in the United States and worldwide, and thus is of tremendous interest to nurses seeking to measure their impact on patient outcomes. The key lifestyle interventions essential to treating this syndrome are weight loss and physical activity. The purpose of this article is to (1) describe the insulin resistance syndrome and discuss the current focuses for inquiry in major outcome areas (eg, mortality, morbidity, costs); (2) describe the status of specific lifestyle interventions (weight loss, diet, and exercise); (3) identify outcomes that nurses could measure to assess their impact on patient care; and (4) identify areas for future nursing research.
J Cardiovasc Nurs
PMID:Insulin resistance syndrome. 1549 94

Cardiac transplantation is a highly effective therapy for selected patients with end-stage cardiac disease. The management of the patient after heart transplant involves three main strategies: optimization of immunosuppressive therapy, prevention of complications resulting from the transplant or the immunosuppressive agents, and treatment of those complications when they arise. For most patients, optimal current immunosuppression in the first year after transplantation consists of combination therapy with a calcineurin inhibitor (eg, cyclosporine or tacrolimus), corticosteroids, and an antimetabolite agent (eg, azathioprine or mycophenolate mofetil). Ideally, the corticosteroid is weaned and discontinued 1 to 2 years following transplantation and the patient is managed chronically with a two-drug immunosuppressive regimen. The major complications that occur following cardiac transplantation include infection, hypertension, diabetes, dyslipidemia, osteoporosis, graft coronary disease, renal insufficiency, and malignancy. Preventive efforts focused on infection, osteoporosis, renal insufficiency, and malignancy include minimization of immunosuppression. Once established, treatment of any of the above conditions generally relies on standard pharmacologic therapies; however, an understanding of potential drug interactions is critical. In addition, although standard nonpharmacologic therapies may be used to treat several of these conditions, one must be cognizant of special issues related to the post-transplant state.
Curr Treat Options Cardiovasc Med 2004 Dec
PMID:Management of the Patient After Heart Transplant. 1549 63

3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) and peroxisome proliferator-activated receptor alpha activators (fibrates) are the backbone of pharmacologic hypercholesterolemia and dyslipidemia treatment. Many of their clinical effects, however, are still enigmatic. This article describes how a side road of the mevalonate pathway, characterized in recent years, can rationalize a major fraction of these unexplained observations. This side road is the enzymatic isopentenylation of selenocysteine-tRNA([Ser]Sec) (Sec-tRNA), the singular tRNA to decode the unusual amino acid selenocysteine. The functionally indispensable isopentenylation of Sec-tRNA requires a unique intermediate from the mevalonate pathway, isopentenyl pyrophosphate, which concomitantly constitutes the central building block for cholesterol biosynthesis, and whose formation is suppressed by statins and fibrates. The resultant inhibition of Sec-tRNA isopentenylation profoundly decreases selenoprotein expression. This effect might seamlessly explain the immunosuppressive, redox, endothelial, sympatholytic, and thyroidal effects of statins and fibrates as well as their common side effects and drug interactions.
Trends Cardiovasc Med 2004 Oct
PMID:Selenoproteins, cholesterol-lowering drugs, and the consequences: revisiting of the mevalonate pathway. 1554 79

Although less clinical intervention studies have been performed with fibrates than with statins, there are evidences indicating that fibrates may reduce risk of cardiovascular events. The potential clinical benefit of the fenofibrate will be specified by the ongoing Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study, which rationale, methods and aims have been just published. Controlled clinical trials show similar or even greater cardiovascular benefits from statins-based therapy in patient subgroups with diabetes compared with overall study populations. Therefore, statins are the drug of first choice for aggressive lipid lowering actions and reducing risk of coronary artery disease in these patients. However, current therapeutic use of statins as monotherapy is still leaving many patients with mixed atherogenic dyslipidemia at high risk for coronary events. A combination statin/fibrate therapy may be often necessary to control all lipid abnormalities in patients with metabolic syndrome and diabetes adequately, since fibrates provide additional important benefits, particularly on triglyceride and HDL-cholesterol levels. Thus, this combined therapy concentrates on all the components of the mixed dyslipidemia that often occurs in persons with diabetes or metabolic syndrome, and may be expected to reduce cardiovascular morbidity and mortality. Safety concerns about some fibrates such as gemfibrozil may lead to exaggerate precautions regarding fibrate administration and therefore diminish the use of the seagents. However, other fibrates, such as bezafibrate and fenofibrate appear to be safer and better tolerated. We believe that a proper co-administration of statins and fibrates, selected on basis of their safety, could be more effective in achieving a comprehensive lipid control as compared with monotherapy.
Cardiovasc Diabetol 2004 Dec 01
PMID:Which is the best lipid-modifying strategy in metabolic syndrome and diabetes: fibrates, statins or both? 1557 99

The pharmacologic regulation of lipid metabolism in patients with dyslipidemia is unequivocally associated with significant reductions in risk for cardiovascular morbidity and mortality. A number of therapeutic drug classes have been developed in an effort to ever more precisely and intensively modulate lipid metabolism. Statins, fibrates, ezetimibe, and niacin exert their effects via different mechanisms and afford physicians the opportunity to beneficially impact multiple pathways in patients. When used alone or in combination, these drugs decrease risk for the development and progression of atherosclerotic disease. There are strong clinical trial data to support of the use of lipid-lowering therapies in the settings of both primary and secondary prevention. This article (1) discusses the mechanisms of action of antilipidemic medications, (2) reviews dosing regimens and the pharmacokinetic differences among drugs of the same class, (3) assesses risk for drug interactions, and (4) reviews the clinical trial evidence used to support the use of particular antilipidemic medications in specific physiologic settings. The incidence of dyslipidemia is rising worldwide. This trend portends an ever-growing need for the aggressive and judicious use of different antilipidemic medication(s) in patients at risk for all forms of atherosclerotic vascular disease.
Prog Cardiovasc Dis
PMID:Comparative effects of lipid-lowering therapies. 1558 50

Because atherosclerosis has been proven to be an inflammatory disease, it became obvious that the proper treatment of dyslipidemic patients should not only correct lipid parameters but also inhibit the inflammatory state. One of the crucial proinflammatory and procoagulant cytokines participating in the pathogenesis of atherosclerosis is interleukin-1beta (IL-1beta). Therefore, the aim of the study was to asses the effect of statin and fibrate therapy (for dyslipidemia IIa and IIb, respectively) on IL-1beta gene expression and monocyte release evaluated in each patient. Additionally, the effect of hypolipidemic therapy on fibrinolysis was evaluated. The study was carried out in 37 patients: 12 with biochemically confirmed type IIa dyslipidemia (treated with atorvastatin), 12 with type IIb dyslipidemia (treated with fenofibrate), and 13 age- and sex-matched normolipidemic persons (control). IL-1beta concentrations in cultured monocytes and PAI-1 (Plasminogen Activator Inhibitor) plasma levels were measured using the ELISA method. To evaluate the expression of IL-1beta gene in monocytes, a semiquantitive RT-PCR procedure was performed. The results were normalized with the expression of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as a housekeeping gene. Although IL-1beta monocyte release was markedly elevated in patients with atherogenic dyslipidemias, IL-1beta gene expression was only slightly and nonsignificantly higher in the studied groups versus control. We have observed significant reduction of IL-1beta mRNA expression after 30-day treatment with the examined drugs (atorvastatin, 2.10 +/- 0.50 versus 1.05 +/- 0.15; P < 0.001, fenofibrate; 2.27 +/- 0.48 versus 1.23 +/- 0.27; P < 0.01). There was no significant difference between statin and fibrate effect on IL-1beta mRNA expression. Similarly, we have noticed significant reduction of IL-1beta release by cultured monocytes after 30-day statin therapy (133.0 +/- 5.7 pg/mL versus 77.0 +/- 3.6 pg/mL; P < 0.01) and fibrate therapy (143.9 +/- 6.5 pg/mL versus 86.2 +/- 5.9 pg/mL; P < 0.01). Besides this antiinflammatory effect, we have observed a 30% reduction of PAI-1 plasma levels in both treated groups. In conclusion, effective 1-month hypolipidemic therapy with atorvastatin or fenofibrate diminished plasma levels of proinflammatory and procoagulatory state markers.
J Cardiovasc Pharmacol 2005 Feb
PMID:Hypolipidemic drugs affect monocyte IL-1beta gene expression and release in patients with IIa and IIb dyslipidemia. 1565 65

The aim of this editorial was to discuss evidence indicating a role for low-grade inflammation as a pathogenetic event of the metabolic syndrome. The metabolic syndrome has emerged as an important cluster of risk factors for atherosclerotic disease. Common features are central (abdominal) obesity, insulin resistance, hypertension, and dyslipidemia, namely high triglycerides and low high-density lipoprotein cholesterol. According to the clinical criteria developed by ATP III, it has been estimated that 1 out of 4 adults living in the United States merits the diagnosis. The presence of the metabolic syndrome is highly prognostic of future cardiovascular events. Chronic inflammation may represent a triggering factor in the origin of the metabolic syndrome: stimuli such as overnutrition, physical inactivity, and ageing would result in cytokine hypersecretion and eventually lead to insulin resistance and diabetes in genetically or metabolically predisposed individuals. Alternatively, resistance to the anti-inflammatory actions of insulin would result in enhanced circulating levels of proinflammatory cytokines resulting in persistent low-grade inflammation. A generally enhanced adipose tissue derived cytokine expression may be another plausible mechanism for the inflammation/metabolic syndrome relationship. The role of adipose tissue as an endocrine organ capable of secreting a number of adipose tissue-specific or enriched hormones, known as adipokines, is gaining appreciation. Although the precise role of adipokines in the metabolic syndrome is still debated, an imbalance between increased inflammatory stimuli and decreased anti-inflammatory mechanisms may be an intriguing working hypothesis. The proinflammatory state that accompanies the metabolic syndrome associates with both insulin resistance and endothelial dysfunction, providing a connection between inflammation and metabolic processes which is highly deleterious for vascular functions.
Nutr Metab Cardiovasc Dis 2004 Oct
PMID:The metabolic syndrome and inflammation: association or causation? 1567 55

Cardiovascular disease is the leading cause of mortality among people with diabetes mellitus, accounting for 70% of all deaths. As the prevalence of diabetes increases significantly worldwide, greater attention must be focused on preventing cardiovascular events in this group. One contributor to this increased event rate is the characteristic pattern of dyslipidemia in diabetic patients, consisting of elevated serum triglyceride levels, decreased high-density lipoprotein levels, and an increased proportion of small, dense, low-density lipoproteins. Several pharmacologic agents have been used to treat this dyslipidemia including HMG-CoA reductase inhibitors, fibric acid derivatives, niacin (nicotinic acid), thiazolidinediones, and fish oils, as well as other non-pharmacologic measures. Currently, the most extensive data for a reduction in cardiovascular events in patients with diabetes exist for HMG-CoA reductase inhibitors. The results of these trials indicate that HMG-CoA reductase inhibitor therapy should be considered for all patients with diabetes at sufficient risk for cardiovascular events, regardless of serum low-density lipoprotein-cholesterol level. Several ongoing trials of various pharmacologic agents should help clarify the role of these agents alone and in combination with HMG-CoA reductase inhibitors in the management of diabetic dyslipidemia.
Am J Cardiovasc Drugs 2005
PMID:Management of diabetic dyslipidemia: need for reappraisal of the goals. 1572 39

The aim of this study was to compare the effect of 30-day treatment with atorvastatin and fenofibrate on monocyte release and plasma levels of monocyte chemoattractant protein-1 (MCP-1). We studied 52 atherosclerotic patients with primary mixed dyslipidemia and 16 age-, sex-, and weight-matched control subjects with asymptomatic atherosclerosis. Dyslipidemic patients enrolled into the study were randomly divided into three groups, simultaneously treated with atorvastatin (20 mg/d, n = 18), fenofibrate (267 mg/d, n = 16), or placebo (n = 18). Plasma lipid-profile and content of MCP-1, and monocyte release of this chemokine were measured at baseline and after 30 days of therapy. Compared with the control subjects, dyslipidemic patients exhibited the increased plasma levels and monocyte MCP-1 release. Atorvastatin and fenofibrate not only improved lipid profile but also decreased monocyte secretion of this chemokine. Moreover, hypolipemic agents slightly reduced its plasma levels. MCP-1-lowering effect of atorvastatin and fenofibrate did not correlate with the lipid-lowering potential of these agents. Our results suggest that atorvastatin and fenofibrate produce their antiinflammatory effect partially via inhibiting monocyte release of MCP-1. The treatment-induced reduction in its secretion may contribute to the clinical effectiveness of statins and fibrates in the therapy for atherosclerosis and other chronic fibroproliferative diseases.
J Cardiovasc Pharmacol 2005 Apr
PMID:Effect of monthly atorvastatin and fenofibrate treatment on monocyte chemoattractant protein-1 release in patients with primary mixed dyslipidemia. 1577 19


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