Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

The benefits of blood pressure lowering, lipid lowering, and glycemic control on morbidity and mortality have been established in major long-term clinical trials. The most extensive information is available for diuretics or beta-blockers in hypertension, hepatic hydroxymethyl glutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) in dyslipidemia, and insulin or sulfonylureas in diabetes. Other drug classes provide similar improvements in blood pressure, lipid profile, and glycemic control, and thereby might be expected to provide comparable long-term benefits. As a result, national guidelines advocate treating patients aggressively in order to achieve control of blood pressure low-density lipoprotein (LDL) cholesterol, and blood glucose. The risks associated with drug treatment are generally class-specific. Among antidiabetic agents, sulfonylureas and insulin are associated with risk for severe hypoglycemia, metformin with risk for lactic acidosis, and troglitazone with risk for idiosyncratic hepatocellular injury. Similarly, widely used antihypertensive and lipid-lowering agents are associated with risk for serious complications, such as angioedema with angiotensin-converting enzyme inhibitors, possible increased risk for myocardial infarction and cancer with calcium antagonists, and myositis and liver dysfunction with statins. Physicians must take an aggressive approach to patient management in order to achieve a level of disease control that optimally reduces risk for morbidity and mortality. Serious adverse events may occur rarely with most drug classes; these events can be minimized by appropriately monitoring or selecting patients for treatment.
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PMID:Safety of drugs commonly used to treat hypertension, dyslipidemia, and type 2 diabetes (the metabolic syndrome): part 1. 1146 7

Cerivastatin is a synthetic and enantiomerically pure 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor. It has been recognized for its high pharmacologic potency, uncomplicated pharmacokinetic profile, and low drug-interaction potential. The efficacy of cerivastatin has been demonstrated in a number of clinical trials involving patients with primary hypercholesterolemia and mixed dyslipidemia. Cerivastatin was found to have dose-dependent reduction in total cholesterol and low-density lipoprotein (LDL) cholesterol. At the 0.4 mg daily dose, cerivastatin was found to lower LDL cholesterol by approximately 35% (mean reductions of 33-39%). The triglyceride-lowering effect of cerivastatin is also dose dependent; however, there is a much stronger association between baseline triglyceride levels and the triglyceride-lowering effect of cerivastatin. A dosage of 0.4 mg daily has been shown to reduce triglycerides by a mean of 28% in patients with baseline triglyceride levels of > 300 mg/dL. At the time of its initial approval by the US Food and Drug Administration (FDA) in 1997, cerivastatin was available only in 0.2 mg and 0.3 mg strengths. The recent FDA approval of the 0.4-mg strength dose has made cerivastatin a more competitive drug in lipid-lowering efficacy among the HMG-CoA reductase inhibitors.
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PMID:Cerivastatin. 1172 45

Clinical data and experimental studies have established the important role of abnormal lipid metabolism in the causation of atherosclerosis and enthroned the hydroxymethylglutaryl coenzyme reductase inhibitors (statins) as a mainstay in management of patients with coronary heart disease. However, emerging experimental data underline the role of vascular renin-angiotensin systems in mediating the early stages of vascular endothelial dysfunction and inflammation as prerequisites for unleashing the cascade of cellular and molecular events that lead to the deposition of foam cells and their eventual progression to the atherosclerotic plaque. We discuss here the biological effects of statins and angiotensin II in the evolution of atherogenesis, underscoring possible links between statins and angiotensin receptor blockers. From the assessment of the commonality of effects resulting from the nonlipidic actions of statins and angiotensin II on the process of atherogenesis, we develop the argument that dyslipidemia may influence the ability to control blood pressure in hypertensive subjects and hypothesize that the combined use of statins and blockers of the renin-angiotensin system may have an additive effect in the management of hypertensive subjects.
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PMID:The hypertension-lipid connection: insights into the relation between angiotensin II and cholesterol in atherogenesis. 1181 37

Diabetic dyslipidemia is featured by hypertriglyceridemia, low high-density lipoprotein (HDL) cholesterol levels, and elevated low-density lipoprotein (LDL) cholesterol commonly in the form of small, dense LDL particles. First-line treatment, fibrates versus statins or both, of dyslipidemia in diabetic patients has been the focus of debate. We investigated the potential hypolipidemic effects of atorvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor with good triglyceride lowering properties, in patients with combined dyslipidemia and evidence of impaired fasting glucose or type 2 diabetes. Twenty patients were recruited for the study, and after a 60-day wash out period, baseline measurements of lipoprotein parameters, LDL particle diameter, and apolipoprotein B (apoB) degradation fragments were obtained. The group was then randomized, in a double-blinded manner, into 2 subgroups. Group A received atorvastatin (80 mg) and group B received placebo daily for 60 days. After the first treatment period, all patients were reanalyzed for the above parameters. The treatment regime then crossed over for the second treatment period in which group A received placebo and group B received atorvastatin (80 mg) daily for 60 days. All parameters were remeasured at the end of the study. Treatment with atorvastatin resulted in a statistically significant reduction in total cholesterol (41%), LDL cholesterol (55%), triglycerides (TG) (32%), and apoB (40%). Mean LDL particle diameter significantly increased from 25.29 +/- 0.24 nm (small, dense LDL subclass) to 26.51 < 0.18 nm (intermediate LDL subclass) after treatment with atorvastatin (n = 20, P <.005). At baseline, LDL particles were predominantly found in the small, dense subclass; atorvastatin treatment resulted in a shift in the profile to the larger and more buoyant LDL subclass. Atorvastatin treatment did not produce consistent changes in the appearance of apoB degradation fragments in plasma. Our results suggest that atorvastatin beneficially alters the atherogenic lipid profile in these patients and significantly decreases the density of LDL particles produced resulting in a shift from small, dense LDL to more buoyant and less atherogenic particles.
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PMID:Atorvastatin treatment beneficially alters the lipoprotein profile and increases low-density lipoprotein particle diameter in patients with combined dyslipidemia and impaired fasting glucose/type 2 diabetes. 1188 70

Diabetes mellitus is increasing throughout the world. Cardiovascular disease (CVD) accounts for up to 80% of excess mortality in this high-risk population. Patients with diabetes have the same CVD risk factors as those people without diabetes. However, these risk factors are much more powerful in diabetic patients. CVD risk is especially high for diabetic women, and premenopausal diabetic women lose all the protection normally afforded to them by female sex hormones. Controlled clinical trials have clearly demonstrated that rigorous treatment of blood pressure, dyslipidemia and platelet hyperaggrebility strikingly reduces CVD risk in diabetic patients. Strategies directed at interrupting the renin-angiotensin system (both tissue and systemic systems) and the use of 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase inhibitors have proven to be especially beneficial for this high-risk population.
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PMID:Vascular complications in diabetes and their prevention. 1195 92

Dyslipidemia increases the risk of cardiovascular events among individuals with renal disease, and there is a growing body of evidence that it hastens the progression of renal disease itself. Children with nephrotic syndrome or renal transplants have easily recognized hyperlipidemia. Among those with chronic renal insufficiency or end-stage renal disease, detection of dyslipidemia requires more careful analysis and knowledge of normal pediatric ranges. Disordered lipoprotein metabolism results from complex interactions among many factors, including the primary disease process, use of medications such as corticosteroids, the presence of malnutrition or obesity, and diet. The systematic treatment of dyslipidemia in children with chronic renal disease is controversial because conclusive data regarding the risks and benefits are lacking. Hepatic 3-methylglutaryl coenzyme A reductase inhibitors (statins), fibrates, plant stanols, bile acid-binding resins, and dietary manipulation are options for individualized treatment. Prospective investigations are required to guide clinical management.
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PMID:Dyslipidemia in pediatric renal disease: epidemiology, pathophysiology, and management. 1198 Dec 90

Type IIB hyperlipidemia is associated with premature vascular disease, an atherogenic lipoprotein phenotype characterised by elevated levels of triglyceride-rich VLDL and small dense LDL, together with subnormal levels of HDL. The dose-dependent and independent effects of a potent HMGCoA reductase inhibitor, Atorvastatin, at daily doses of 10 and 40 mg, were evaluated on triglyceride-rich lipoprotein subclasses (VLDL-1, VLDL-2 and IDL), on the major LDL subclasses (light LDL, LDL-1+LDL-2, D: 1.019-1.029 g/ml; intermediate LDL, LDL-3, D: 1.029-1.039 g/ml and small dense LDL, LDL-4+LDL+5, D: 1.039-1.063 g/ml), on CETP-mediated cholesteryl ester transfer from HDL to apoB-containing lipoproteins, on phospholipid transfer protein activity and on plasma-mediated cellular cholesterol efflux in patients (n=10) displaying type IIB hyperlipidemia. Plasma concentrations of triglyceride-rich lipoprotein subclasses (TRL: VLDL-1, Sf 60-400; VLDL-2, Sf 20-60 and IDL, Sf 12-20) and of LDL (D: 1.019-1.063 g/ml) were markedly diminished after 6 weeks of statin treatment at 10 mg per day (-31 and -36%, respectively; P<0.002) and by 42 and 51%, respectively at the 40 mg per day dose. Increasing doses of atorvastatin progressively normalised both the quantitative and qualitative features of the LDL subclass profile, in which dense LDL predominated at baseline. Indeed, dense LDL levels were reduced by up to 57% at the 40-mg dose, leading to a shift in the peak of the density profile towards larger, buoyant LDL particles typical of normolipidemic subjects. In addition, marked reduction in numbers of apoB100-containing particle acceptors led to a 30% decrease (P<0.02) in CETP-mediated CE transfer from HDL. Finally, a significant dose-dependent statin-mediated elevation (+15% at 10 mg; P=0.0003 and +35% at 40 mg; P<0.0001 compared to baseline) in the capacity of plasma from type IIB subjects to mediate free cholesterol efflux from Fu5AH hepatoma cells was observed. Moreover, atorvastatin (40 mg per day) significantly increased plasma apoAI levels (+24%; P<0.05), thereby suggesting that this statin enhances production of apoAI and with it, formation of nascent pre-beta HDL particles. Plasma PLTP activity was not affected by either dose of atorvastatin. We conclude that increasing the dose of atorvastatin leads to dose-dependent, preferential and progressive reduction in particle numbers of atherogenic VLDL-2, IDL and dense LDL, and concomitantly, to enhanced cellular cholesterol efflux in type IIB dyslipidemia, thereby diminishing the atherosclerotic burden in subjects characterised by high cardiovascular risk.
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PMID:Dose-dependent action of atorvastatin in type IIB hyperlipidemia: preferential and progressive reduction of atherogenic apoB-containing lipoprotein subclasses (VLDL-2, IDL, small dense LDL) and stimulation of cellular cholesterol efflux. 1205 75

Patients with type 2 diabetes are known to have abnormalities in their remnant metabolism and low density lipoprotein (LDL) subfraction pattern, with a preponderance of small dense LDL. The effects of pitavastatin, a newly synthesized 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor, on lipoprotein profiles in patients with type 2 diabetes were determined. Thirty-three patients were treated with pitavastatin with a daily dose of 2 mg for 8 weeks. After treatment, triglyceride, total and LDL cholesterol were significantly reduced by 28.7 +/- 36.7%, 25.2 +/- 14.3% and 36.1 +/- 14.3%, respectively. Remnant-like particle cholesterol (RLP-C), an independent risk factor for CAD which is known to be elevated in diabetic patients, was also significantly reduced (-30.9 +/- 30.5%) by the treatment and this decrease correlated well with the decrease in triglyceride level. The proportion of small dense LDL, which is known for its atherogenisity, decreased from 29.9 +/- 26.2% to 19.7 +/- 22.7% and the mean LDL particle size significantly increased from 26.36 +/- 1.13 nm to 27.10 +/- 1.36 nm. Pitavastatin, which is known to improve triglyceride levels and cholesterol levels, also improves RLP-C level and LDL subfraction profiles, and this in turn may reduce the cardiovascular risk in patients with type 2 diabetes and dyslipidemia.
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PMID:HMG-CoA reductase inhibitor decreases small dense low-density lipoprotein and remnant-like particle cholesterol in patients with type-2 diabetes. 1223 1

Patients with combined dyslipidemia are at greatly increased coronary heart disease (CHD) risk. The threat of rhabdomyolysis with dual pharmacologic treatment (hepatic hydroxymethyl glutaryl coenzyme A [HMG-CoA] reductase inhibitors plus fibric acid derivatives) has tended to limit therapy in patients with combined dyslipidemia to a choice of one or the other drug. Judgment of the potential benefits of either agent has rarely taken into account their effect on the postprandial accumulation of highly atherogenic, triglyceride (TG)-rich, remnant lipoprotein particles (RLPs). Because this information could be of substantial clinical relevance, we addressed this question in patients with type 2 diabetes and combined dyslipidemia by comparing the effects of gemfibrozil versus HMG-CoA reductase inhibitors (statins) on both fasting and postprandial lipid and lipoprotein concentrations. For this purpose, 22 patients with type 2 diabetes and combined dyslipidemia were randomized to treatment with either a statin or gemfibrozil for 3 months. Glycemic control was similar in both groups at baseline and did not change in response to treatment. Baseline lipid and lipoprotein concentrations were also similar in the 2 treatment groups, but the responses to therapy were quite different. Statin-treated patients had a statistically significant decrease in low-density lipoprotein (LDL) cholesterol concentration (156 mg/dL to 96 mg/dL, P <.001), whereas there was no change in patients treated with gemfibrozil. In contrast, there was a statistically significant decrease (P <.05) in plasma TG concentrations (116 mg/dL) in gemfibrozil-treated individuals, without any change in subjects treated with statins. However, the decrease in total integrated postprandial plasma RLP response measured hourly from 8 AM to 4 PM was not different in patients treated with either gemfibrozil (-43%) or statins (-34%). These results indicate that statin treatment, in addition to its beneficial effect on hypercholesterolemia, was as effective as gemfibrozil in reducing postprandial accumulation of triglyceride-rich, atherogenic RLPs in patients with type 2 diabetes and combined dyslipidemia. As such, the clinical utility of statin monotherapy in the treatment of combined dyslipidemia may have been underestimated.
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PMID:Comparison in patients with type 2 diabetes of fibric acid versus hepatic hydroxymethyl glutaryl-coenzyme a reductase inhibitor treatment of combined dyslipidemia. 1237 Aug 58

Peritoneally dialyzed subjects (CAPD) are prone to dyslipidemia and have a high risk of cardiovascular death. Statins (hydroxy-methylglutaryloCoA reductase inhibitors) show beneficial effects on serum lipids and hemostasis in kidney diseases. The purpose of this study was to assess platelet functions, some hemostatic parameters-extrinsic coagulation pathway-total, truncated, free TFPI (tissue factor pathway inhibitor), TF (tissue factor), TFPI/Xa and TF/VIIa complexes, as well as a marker of endothelial cell injury--von Willebrand factor--vWF and serum lipids in 10 hyperlipidemic CAPD patients treated with simvastatin (Zocor, MSD, at a dose of 10 mg at bedtime) for 3 months. Cholesterol and LDL fell significantly as early as after 1 month and remained lowered during further months of the therapy. No significant changes in von Willebrand factor, free TFPI, TF, TFPI/Xa and TF/VIIa complexes were found during therapy with simvastatin. Truncated TFPI decreased significantly as early as after 1 month and total TFPI decreased after 3 months of the therapy with simvastatin. Simvastatin is an effective hypolipemic agent. It seems that simvastatin have no or only little effect on endothelial function and extrinsic coagulation pathway in peritoneally dialyzed patients.
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PMID:[Simvastatin and extrinsic coagulation pathway in peritoneally dialyzed patients]. 1237 84


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