Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifty nine cases with hyperlipidemia were divided randomly into two groups. In group I, each patient took simvastatin 10-40mg/day (mean 17.9mg/day). In group 2, each patient took gemfibrozil 1200mg/day. After treatment with simvastatin, in comparing with baseline values, serum level of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) triglyceride (TG), apolipoprotein B (ApoB), and TC/HDL-C (high-density lipoprotein cholesterol) reduced by 34.6% (P < 0.001), 45.4% (P < 0.001), 22.1% (P < 0.01), 21.1% (P < 0.001), and 39.4% (P < 0.001) respectively, and HDL-C, apolipoprotein A-I(Apo A-I) and Apo A-I/Apo B elevated by 14.2%, 21.9% and 64.5% respectively. For lowering TC, LDL-C, Apo B and elevating Apo A-I/Apo B, Simvastatin was better than gemfibrozil (P < 0.01-0.001). However, for lowering TG, gemfibrozil was better than simvastatin (P < 0.001). As for increasing HDL-C and Apo A-I, no significant differences were found between the two groups. No significant side effects were found in all patients but one who developed hypersensitive eruption after gemfibrozil taken, and he was excluded from the trial.
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PMID:[Clinical evaluation of simvastatin in the treatment of hyperlipidemia]. 819 33

Familial hypercholesterolemia (FHC) in swine, which resembles human familial combined hyperlipidemia, is a complex lipid and lipoprotein disorder associated with the development of severe coronary lesions similar to those occurring in advanced human coronary disease. The disorder is characterized by elevated plasma total cholesterol (TC), triglycerides (TG), LDL-cholesterol (LDL-C), apolipoproteins (apo) B, C-III, and E, and by decreased levels of HDL-cholesterol (HDL-C), apoA-I, and lecithin:cholesterol acyltransferase (LCAT) activity. A dose-response study with simvastatin, a specific inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, was conducted in four treatment groups of FHC animals, exhibiting TC > or = 250 mg/dL. The animals were fed 0, 80, 200, or 400 mg simvastatin daily for 3 weeks. The measured serum parameters included the levels of TC, VLDL-C, LDL-C, HDL-C, TG, lathosterol, apoA-I, B, C-III, and E, as well as LCAT activity. Simvastatin at 200 mg/d significantly decreased the levels of TC (-25%), LDL-C (-27%), lathosterol (-40%), apoB (-22%), apoC-III (-37%), and apoE (-24%) and modestly decreased the levels of HDL-C (-12%) and apoA-I (-11%) (percent relative to the average pretreatment and posttreatment baseline values) but did not affect the levels of TG, VLDL-C, the lathosterol/TC ratio, or LCAT activity. The levels of TC, LDL-C, apoB, and E were also lowered by simvastatin at 80 or 400 mg/d, but to a lesser extent than at 200 mg/d, while the other parameters were not influenced at these doses. The simvastatin-induced decreases of LDL-C, HDL-C, and apoA-I, B, C-III, and E were significantly correlated among each other. These results show that the trend of responses in TC, LDL-C, apoB, apoC-III, and apoE to simvastatin in the FHC swine is similar to that observed in humans, although the drugs is less potent and efficacious in swine, while the results are different from those in humans with regard to the remaining parameters.
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PMID:Effects of simvastatin on plasma lipids and apolipoproteins in familial hypercholesterolemic swine. 854 14

In children with steroid-resistant nephrotic syndrome (SRNS) hyperlipidaemia may in the long term be associated with progressive renal insufficiency and increased risk of coronary heart disease. We have assessed the efficacy and tolerability of diet prior to and in combination with a hydroxymethylglutaryl CoA reductase inhibitor, simvastatin, in seven children with SRNS with a mean age of 8 years (range 1.8-16.3 years). Dietary advice to maintain adequate energy and protein intakes with reduced saturated fat and cholesterol intake had little impact on lipid levels pre treatment (mean reduction in cholesterol 1 mmol/l, triglyceride 1.1 mmol/l) but was maintained throughout the study duration. The mean cholesterol and triglyceride concentrations pre treatment were 12.1 +/- 2 (SEM) mmol/l and 8 +/- 2.1 (SEM) mmol/l, respectively. On a median simvastatin dose of 10 mg/day (range 5-40 mg) there was a 41% reduction in cholesterol to 6.6 +/- 0.77 (SEM) mmol/l and a 44% reduction in triglyceride to 3.9 +/- 1.38 (SEM) mmol/l at 6 months which was sustained at 12 months in five patients. The drug was well tolerated with no clinical side effects being noted. Over 6 months the mean plasma albumin concentrations increased from 18.2 +/- 1.26 (SEM) g/l to 23 +/- 2.51 (SEM) g/l, accounted for by three patients (1 complete remission, 1 partial remission, 1 end-stage renal failure). Plasma creatinine concentrations remained stable in five patients with two having progressive chronic renal failure. Growth parameters for both weight and height were maintained. Simvastatin has a beneficial effect on abnormal lipid levels in SRNS but the effectiveness of long-term therapy needs to be evaluated.
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PMID:Hyperlipidaemia, diet and simvastatin therapy in steroid-resistant nephrotic syndrome of childhood. 870 4

A wide consensus has been reached concerning the importance of lipid-lowering drug therapy in patients with dyslipidaemia with overt coronary heart disease. This consensus is also likely to be reflected in the more active treatment of other high-risk patient groups. The statin family of drugs has been tested in a large secondary prevention study, the Scandinavian Simvastatin Survival Study, and in angiographic trials. Their role in the treatment of hypercholesterolaemia and mixed hyperlipidaemia is increasing, whereas fibrates are increasingly limited to hypertriglyceridaemia.
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PMID:Selection of appropriate type and intensity of lipid-lowering therapy. 875 Feb 48

The objective of this study was to compare the lifetime cost-effectiveness of HMG-CoA reductase inhibitors and fibrates for the treatment of hyperlipidemia. Estimates of lipid modification achieved due to drug therapy were based on published head-to-head comparisons of specific HMG-CoA reductase inhibitors and fibrates in randomized, double-blind studies. We used a validated coronary heart disease (CHD) prevention computer model to estimate the costs and benefits of lifelong lipid modification. The patients were middle-aged men and women who were free of CHD, with either primary type IIa or IIb hyperlipidemia. The intervention used were specific HMG-CoA reductase inhibitors and fibrates at several dosages, which reduced total cholesterol 11-34% and increased high-density lipoprotein cholesterol 1-29%. The main outcome measure was the cost per year of life saved after discounting benefits and costs by 5% annually. The lifetime cost effectiveness of HMG-CoA reductase inhibitors (fluvastatin, lovastatin, pravastatin, simvastatin) and fibrates (bezafibrate, fenofibrate, gemfibrozil) for the treatment of primary hyperlipidemia varied according to patient population, the effectiveness of each drug in modifying lipid levels, and the price of each drug. The estimates of cost per year of life saved for HMG-CoA reductase inhibitors range from $19,886 to $73,632, and $16,955 to $59,488 for fibrates according to gender and type of primary hyperlipidemia. Fluvastatin 20 mg/day was significantly more cost effective than gemfibrozil 1200 mg/day for male patients with type IIa hyperlipidemia. Simvastatin 17.3 mg/day or 20 mg/day yielded similar cost-effectiveness ratios compared with fibrates among type II hyperlipidemic patients. However, micronized fenofibrate was more cost effective than simvastatin 20 mg/day among type IIb patients. The cost effectiveness of lipid therapy varies widely and can be maximized by selecting specific drugs for specific lipid abnormalities.
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PMID:A head-to-head comparison of the cost effectiveness of HMG-CoA reductase inhibitors and fibrates in different types of primary hyperlipidemia. 911 Jan 23

No monotherapy is able to tackle effectively all atherogenic features of familial combined hyperlipidemia: high low-density lipoprotein (LDL) cholesterol, triglycerides (TG), and plasma fibrinogen, as well as low high-density lipoprotein (HDL) cholesterol. The present study investigated the safety and efficacy of combined pravastotin or simvastatin with gemfibrozil or ciprofibrate treatment on total cholesterol, LDL, TG, plasma fibrinogen, and apoproteins B and A-I in patients with refractory familial combined hyperlipidemia, with or without coronary artery disease. From the initial 420 patients included in the study, 389 (294 men and 95 women, mean age 51 years [range 30 to 65]) completed the study. These patients were followed for a mean period of 29 months (1 year [n = 107], 2 years [n = 102], 3 years [n = 95], and 4 years [n = 85]). Patients given a hypolipidemic diet were randomly assigned to pravastatin + gemfibrozil (n = 135, 20 and 1,200 mg/day, respectively), simvastatin + gemfibrozil (n = 130, 20 and 1,200 mg), or simvastotin + ciprofibrate (n = 124, 20 and 100 mg). Lipid parameters, apoproteins B and A-I, and plasma fibrinogen were assessed every 3 months. Physical and laboratory investigations for adverse effects were performed every month for the first 3 months and every 3 months thereafter. No patient exhibited myopathy or rhabdomyolysis. Five patients (1.3%) were withdrawn from the study because of high transaminases (more than threefold the upper normal limit). Five nonfatal coronary artery disease events were recorded. All 3 combination treatments were more effective in normalizing lipid profile than any monotherapy in the past. Simvastatin + ciprofibrate was more effective than pravastatin + gemfibrozil in reducing LDL, TG, and plasma fibrinogen levels. Simvastatin + gemfibrozil increased HDL levels more than the other 2. The apoprotein B decrease was analogous to the LDL reduction by all combinations, whereas apoprotein A-I was increased more with simvastatin + gemfibrozil. The data suggest that the statin-fibrate combinations used in the study are safe and have a favorable effect on all major coronary artery disease risk factors in patients with refractory familial combined hyperlipidemia with or without coronary artery disease. Early detection of the rare drug-induced reversible hepatotoxicity calls for close monitoring of patients.
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PMID:Safety and efficacy of long-term statin-fibrate combinations in patients with refractory familial combined hyperlipidemia. 929 90

Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase are very common and effective treatments for hyperlipidemia. Epidermal cholesterol synthesis has been shown to be essential for maintaining the cutaneous barrier function. We present two patients who experienced cheilitis after beginning treatment of hyperlipidemia with simvastatin (Zocor). The rash resolved after discontinuation of medication and subsequent treatment with topical moisturizers and topical corticosteroids. We suspect that skin barrier dysfunction may occur in the mucosa from inhibitors of HMG-CoA reductase in a manner analogous to the epidermis.
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PMID:Cheilitis due to treatment with simvastatin. 979 10

Although hyperlipidemia is a known risk factor for coronary artery disease, lipid-lowering agents were not used widely until recently because evidence was lacking that they could prolong life. In 1987, a large clinical trial, the Scandinavian Simvastatin Survival Study (4S), was designed to test whether such therapy could decrease all-cause mortality in patients with documented coronary artery disease. The prospective, randomized, multicenter trial included 4,444 patients who had had angina pectoris or myocardial infarction (MI), serum total cholesterol of 213-310 mg/dL, and serum triglycerides < or =221 mg/dL. Patients received either simvastatin 20-40 mg/day or placebo and were followed for a median of 5.4 years. Therapy decreased total cholesterol an average of 25%; low-density lipoprotein (LDL) cholesterol, 35%; and triglyceride levels, 10%. Therapy increased high-density lipoprotein (HDL) cholesterol levels 8%. Although noncardiac death rates were similar among the groups, the relative risk of mortality (from any cause) was decreased 30%, and the relative risk of coronary mortality was decreased 42% in the simvastatin arm. The mortality risk reductions were profound in patients > or =60 years of age. Treatment also significantly decreased the relative risk of coronary events and the need for bypass surgery or coronary angioplasty. Patients with diabetes also benefited significantly from simvastatin therapy. The reductions in relative risk of major coronary events were achieved irrespective of such baseline risk factors as hypertension and smoking and such medication factors as aspirin, beta-blocker, and calcium-antagonist use. Simvastatin therapy has been shown to be cost-effective, decreasing per-patient hospitalization costs by 31% or $3,872 in 1995 dollars.
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PMID:Coronary artery disease: the Scandinavian Simvastatin Survival Study experience. 986 Mar 76

Much debate on the benefits and risks of cholesterol lowering to prevent coronary heart disease has focused on excess non-CHD mortality rates reported in some trials. Because of the wide variation in design of cholesterol-lowering trials and because the non-CHD mortality rate was not a controlled endpoint of statistical power in most published studies, it has been difficult to determine whether any excess mortality was due to certain therapies, to other mechanisms, or to chance. As a result, some investigators have performed retrospective analyses of pooled trial data in order to augment statistical power. Some investigators have hypothesized that the human brain is dependent on a constant supply of cholesterol from the circulation and that cholesterol loss in neuronal membranes, with the possible consequences of behavioral disorders and increased risk of accident and violent death. Indeed Weidner and Griffin suggest that low cholesterol is a marker for poor underlying health; physical illnesses are likely to cause depression and other negative emotional states, which are often accompanied by suppressed appetite and weight loss causing reduction in cholesterol levels. Such mental states may also increase the risk of non-CHD death, for example suicide. Rossouw reviews the evidence concerning non-CHD mortality in cholesterol-lowering trials and reports metaanalyses carried out for all trials combined. The findings indicated a significant (15%) increase in non-CHD mortality in all trials combined. However, this was not related to cholesterol lowering itself, because there was no increased risk in trials with > 10% cholesterol reduction, whereas there was a significant (22%) increase in trials with lesser degrees of cholesterol lowering. The publication of a large secondary prevention trial (4S) employing Simvastatin for cholesterol lowering supports the idea that cholesterol reduction itself does not have adverse effects on non-CHD mortality. The overview of all published trials demonstrates their effectiveness in reducing cholesterol and provides clear evidence of benefits on stroke and total mortality. A 10% reduction in cholesterol yielded about a 20% decrease in CHD mortality, which would be expected to result in about a 6% reduction in total mortality. Endothelium-dependent relaxations are reduced in hyperlipidemia and atherosclerosis. Exogenous L-arginine improves or restores the reduced endothelium-dependent relaxations. Moreover inflammation is associates with the initiation and progression of atherosclerosis. The fact of the matter is the Cardiovascular drugs already in clinical use or in development are able to interfere with certain aspects of endothelial function and may be useful in protecting the vessels and, hence, in preventing the development of cardiovascular disease.
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PMID:[All mortality by cause of death. The challenge of coronary prevention]. 1005 Jan 41

Xuezhikang is a new blood-lipid-regulating medicine. The components of Xuezhikang include HMG-CoA reductase inhibitor (lovastatin), unsaturated fatty acids and many kinds of amino acids. A comparative study on the effects of Xuezhikang and Simvastatin (Zocor) was carried out. One hundred and eight patients with primary hyperlipidemia were randomly divided into two groups. Group 1 consisted of 53 patients, each taking 4 Xuezhikang capsules/day (1.2 g/day) for 8 weeks and group 2 included 55 cases, each taking Zocor 10 mg/day for 8 weeks. At the end of 8 weeks, the lipid levels were compared with those of the baseline in each group. In group 1 serum levels of total cholesterol (TC), low density lipoprotein cholesterol (LDL-C) and triglycerides (TG) were decreased by 23.0%, 28.0% and 28.1% (P < 0.001) respectively and in group 2 they were reduced by 23.3%, 29.5% and 29.5% (P < 0.001) respectively. Serum level of high density lipoprotein (HDL-C) was increased by 5.0% (P > 0.05) with Xuezhikang and 14.3% (P < 0.01) with Zocor, but no significant differences were found between the two groups in TC, LDL-C, TG and HDL-C. The side effects of Xuezhikang were less than those of Zocor. It is suggested that Xuezhikang made in China is a safe, effective and tolerable lipid modulator.
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PMID:[Effect of xuezhikang on the treatment of primary hyperlipidemia]. 1043 58


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