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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The efficacy and safety of hydroxymethylglutaric coenzyme A reductase inhibitor (statins) in the treatment of hyperlipidemia were evaluated in 12 infants and children with steroid-resistant nephrotic syndrome followed prospectively for 1 to 5 years. All patients experienced a hypolipidemic response with a marked reduction in their total cholesterol (40%), low-density lipoprotein cholesterol (44%), and triglyceride levels (33%), but no appreciable change in high-density lipoprotein cholesterol. Statin therapy was well tolerated without clinical or laboratory adverse effects. In spite of a significant hypolipidemic response to statin therapy there were no changes observed in the degree of proteinuria, hypoalbuminemia, or in the rate of progression to chronic renal failure. Long-term controlled studies with statin therapy are needed to further document or negate their renoprotective role in refractory nephrotic syndrome.
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PMID:Management of hyperlipidemia in children with refractory nephrotic syndrome: the effect of statin therapy. 906 27

The successful use of statins in major coronary prevention trials has resulted in an explosive widening of their use. In most instances, statin therapy will result in adequate and sustained lowering of lipids. Comparing equal-weight doses, simvastatin is twice as effective as pravastatin and lovastatin in LDL-cholesterol lowering, and all three are more effective than fluvastatin according to recent comparative studies. Statin monotherapy is not always effective in severe hypercholesterolemia or in mixed (combined) hyperlipidemia with marked triglyceride elevations. All statins accepted for therapeutic use can be combined with resin or fibrate. Myopathy resulting from statin-fibrate combinations is less frequent than had been thought on the basis of early reports, and these combinations can be used in long-term therapy of mixed hyperlipidemia.
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PMID:Statins: within-group comparisons, statin escape and combination therapy. 911 43

The natural statins should be used as first line agents in the prevention of stroke. The effects of the synthetic statins on the prevention of coronary events and stroke have not been reported at this time. The National Stroke Association's Stroke Prevention Advisory Board has prepared a consensus statement on risk reducing intervention. The Board identified hypertension, MI, atrial fibrillation, hyperlipidemia and asymptomatic carotid artery stenosis (60% to 99% occlusion) as proven stroke risk factors. The Board's recommendations for the prevention of a first stroke are: 1. Hypertension should be treated with lifestyle, pharmacologic and multidisciplinary management strategies. 2. Aspirin post MI and warfarin (international normalized ratio, 2 to 3) for patients with atrial fibrillation, left ventricular thrombus or significant left ventricular dysfunction. Statin agents should be used post MI. 3. Atrial fibrillation patients age 75 or older should be treated with warfarin. Younger patients 65 to 75 with atrial fibrillation and risk factors should be treated with warfarin [corrected]. Younger patients 65 to 75 with atrial fibrillation without risk factors should be treated with warfarin or aspirin [corrected]. 4. Patients with hyperlipidemia and coronary artery disease should be on statin agents. 5. Carotid endarterectomy is recommended for asymptomatic carotid stenosis (60% to 99%) when surgical morbidity and mortality are less than 3%. 6. Adherence to a low-fat diet, smoking avoidance, mild alcohol use, and physical activity should follow published guidelines.
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PMID:Stroke risk, cholesterol and statins. 1055 83

Statin-fibrate combinations are commonly used to treat hyperlipidemia. These drugs have been previously reported to cause rhabdomyolysis with acute renal failure. Whether different statin-fibrate combinations have different risks for rhabdomyolysis is not known. We report a patient who developed rhabdomyolysis with acute renal failure promptly after switching from the combination of pravastatin and fenofibrate to simvastatin and gemfibrozil.
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PMID:Rhabdomyolysis and acute renal failure after changing statin-fibrate combinations. 1117 85

Statin treatment is widely used in both primary and secondary prevention of diseases in which hyperlipidaemia is a major risk factor, for example, ischaemic heart disease. The development of ulcerative colitis as an adverse reaction to simvastatin is reported, which, despite withdrawal of the drug, proved fatal. The adverse reaction profile of the statins is reviewed, which suggests that this is a class effect and not one limited to simvastatin.
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PMID:Ulcerative colitis after statin treatment. 1215 72

Recent studies suggest that the mevalonate pathway plays an important role in skeletal metabolism. HMG CoA reductase inhibitors ("statins"), which inhibit a key enzyme in the mevalonate pathway, are widely used for the treatment of hyperlipidemia. In vitro and animal studies demonstrate that statins stimulate the production of BMP-2, a potent regulator of osteoblast differentiation and activity, suggesting that statins may have an anabolic effect on bone. Statin use in most, but not all observational studies is associated with a reduced risk of fracture, particularly hip fracture, even after adjustment for the confounding effects of age, weight and other medication use. This beneficial effect has not been observed in clinical trials designed to assess cardiovascular endpoints. The effects of statins on bone mass and bone turnover are controversial, but increased bone mass and reduced bone turnover have been observed in controlled studies. Further studies of the skeletal effects of statins are needed, particularly their effects on surrogate markers such as bone mass, bone turnover, and microarchitecture, to determine the optimal formulation, dosing and route of administration. Clinical trials with fracture endpoints are needed before statins can be recommended as therapeutic agents for osteoporosis.
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PMID:HMG CoA reductase inhibitors and the skeleton: a comprehensive review. 1273 72

Statins and fibrates are well-established treatments for hyperlipidaemias and the prevention of vascular events. However, fibrate + statin therapy has been restricted following early reports of rhabdomyolysis that mainly involved gemfibrozil, originally with bovastatin, and recently, with cerivastatin. Despite this limitation, several reports describing combination therapy have been published. This review considers these studies and the relevant indications and contraindications. Statin + fibrate therapy should be considered if monotherapy or adding other drugs (e.g. cholesterol absorption inhibitors, omega-3 fatty acids ornicotinic acid) did not achieve lipid targets or is impractical. Combination therapy should be hospital-based and reserved for high-risk patients with a mixed hyperlipidaemia characterised by low density lipoprotein cholesterol (LDL) >2.6 mmol/l(100 mg/dl, high density lipoprotein cholesterol (HDL) <1.0 mmol/l (40 mg/dl) and/or triglycerides> 5.6 mmol/l (500 mg/dl. These three 'goals' are individually mentioned in guidelines. Patients should have normal renal, liver and thyroid function tests and should not be receiving therapy with cyclosporine, protease inhibitors or drugs metabolised through cytochrome P450 (especially 3A4). Combination therapy is probably best conducted using drugs with short plasma half-lives; fibrates should be prescribed in the morning and statins at night to minimise peak dose interactions. Both drug classes should be progressively titated from low doses. Regular (3-monthly) monitoring of liver function and creatine kinase is required. In conclusion, fibrate + statin therapy remains an option in high-risk patents. However, long-term studies involving safety monitoring and vascular endpoints are required to demonstrate the efficacy of this regimen.
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PMID:Statin-fibrate combination: therapy for hyperlipidemia: a review. 1281 27

Statin therapy (3-hydroxy-3methylglutaryl coenzyme A reductase inhibitor) is beneficial for primary prevention of cardiovascular events in patients younger than age 65 years with hyperlipidemia, yet there is uncertainty about using these agents for primary prevention in octogenarians. We present the case that can be made for not treating octogenarians with statins for the primary prevention of cardiovascular disease. This case is built on three points: 1) cholesterol levels are not associated with cardiovascular disease events in octogenarians without overt coronary artery disease; 2) no randomized, controlled trials have assessed the role of statins in reducing events in octogenarians without coronary artery disease; and 3) statins may increase risks of myositis, rhabdomyolysis, and cancer in the elderly. In view of gaps in the current evidence and the resulting clinical uncertainty, it is unclear whether the balance of risk and benefit favors treatment for the primary prevention of coronary artery disease in octogenarians. The use of statins in this age group should be based on patient preference.
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PMID:Are statins indicated for the primary prevention of CAD in octogenarians? antagonist viewpoint. 1461 Mar 84

Statins are central to the government's National Service Framework (NSF) for coronary heart disease (CHD). NHS spending on statins is currently about pounds sterling 500 million per annum and rising at an annual rate of 30%. Although generally considered to be a cost-effective treatment for hyperlipidaemia and cardiovascular disease, given the high and rising expenditure on statins in the UK, there is a pressing need to ensure that the choice between available statins reflects cost-effectiveness considerations. A decision model was developed to establish the cost-effectiveness of treating new hypercholesterolaemic patients to UK and European target levels of blood total cholesterol (TC) and low density lipoprotein-cholesterol (LDL-C), using rosuvastatin, atorvastatin, simvastatin, pravastatin or fluvastatin. The model was used to estimate the proportion of patients reaching target and the associated costs over a one-year period from the perspective of the NHS. The effectiveness of the alternative statins were modelled using data from the Statin Therapies for Elevated Lipid Levels compared Across doses to Rosuvastatin (STELLAR) trial. Monte Carlo simulation was used to reflect uncertainty in the parameter estimates applied in the model. Rosuvastatin is demonstrated to dominate (i.e. lower costs and a higher number of patients treated to target) atorvastatin, simvastatin and pravastatin. Compared with fluvastatin, the incremental cost per additional patient to target (PTT) for rosuvastatin was pounds sterling 24 using LDL-C and pounds sterling 83 using TC. The probability that rosuvastatin is cost-effective exceeds 95%, provided the NHS is prepared to pay at least pounds sterling 35 per PTT to achieve target LDL-C cholesterol levels (pounds sterling 160 for TC). The analysis demonstrates rosuvastatin is more cost-effective than the other statins in achieving UK and European cholesterol targets.
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PMID:The cost-effectiveness of a new statin (rosuvastatin) in the UK NHS. 1468 71

Hypertension and hyperlipidaemia are major risk factors for the development of atherosclerosis. Calcium channel blockers (CCBs) have been used for decades and have established antihypertensive effects. Statins have been extensively used because of their potent lipid lowering properties. Amongst other factors, inflammation and oxidation are involved in enhanced progression of atherosclerosis and new lesion development. Therefore, research has been initiated focusing on the antioxidant and anti-inflammatory properties of CCBs and statins, beyond their primary effect, in order to evaluate the possible additive effects of combined treatment of CCBs with statins as antiatherosclerotic therapy. Clinical studies (e.g., the International Nifedipine Trial on Antiatherosclerotic Therapy [INTACT]) have demonstrated that the antiatherosclerotic action of CCBs is limited to the attenuation of the first stage of atherosclerogenesis (fatty streak formation or new lesion growth). The lesions that pre-existed at the start of CCB therapy did not demonstrate progression or regression on angiography. However, because the mechanisms of action of lipid-lowering drugs and CCBs, and their role in preventing the progression of atherosclerosis differ, it is conceivable to conclude that these two classes may have an additive or synergic effect, not only on new lesion formation but also on inhibiting the progression of established coronary atherosclerosis. Indeed, this combined effect of lipid-lowering therapy and CCBs on human coronary atherosclerosis has been reported in the Regression Growth Evaluation Statin Study (REGRESS) trial. This beneficial effect of combining CCBs with statins has now been replicated in transgenic atherosclerotic mice, where the combination of amlodipine and atorvastatin produced an additional 60% reduction of atherosclerosis compared with that observed with the statin alone. Serum markers of atherosclerosis and vascular integrity also improved most in the combination group. Synergistic effects of the combination of atorvastatin and amlodipine on acute nitric oxide release/endothelial function, and additive effects of the combination of amlodipine and atorvastatin in the improvement of arterial compliance in hypertensive hyperlipidaemic patients has been demonstrated. Collectively, these studies support the clinical antiatherosclerotic advantages of combination of CCBs and statins and in particular, of atorvastatin with amlodipine beyond their established antihyperlipidaemic and antihypertensive modes of action.
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PMID:Amlodipine and atorvastatin in atherosclerosis: a review of the potential of combination therapy. 1499 41


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