Gemfibrozil In Patients Research Articles

Use of Statins and Gemfibrozil in Patients with Type 2 Diabetes Mellitus and Cardiovascular Risk Factors Attending Adult Day Health Care Centers: An Opportunity for Pharmacists Research and Reports

Identify the extent of statin use for primary prevention of macrovascular complications, the extent of statin or gemfibrozil use for the secondary prevention of cardiovascular morbidity and mortality, and the statin doses used in patients with type 2 diabetes and other cardiovascular risk factors. Retrospective chart review. Three adult day health care centers in Brooklyn and Queens, New York. Patients with a diagnosis of type 2 diabetes and either a history of coronary artery disease or at least one other significant cardiovascular risk factor as defined by the American College of Physicians guidelines (i.e., age greater than 55 years, hypertension, left-ventricular hypertrophy, previous cerebrovascular disease, or peripheral arterial disease). Percentage of patients prescribed a statin for primary prevention of macrovascular complications of type 2 diabetes, percentage of patients prescribed a statin or gemfibrozil for secondary prevention of cardiovascular mortality and morbidity, and the percentage of patients on at least moderate doses of statins. Ninety-three patients were evaluated-51 in the primary-prevention group and 42 in the secondary-prevention group. In the primary-prevention group, 33 (64.7%) patients were prescribed a statin, while in the secondary-prevention group, 26 (61.9%) patients were on statins, a nonsignificant difference (P = 0.8308). No patients were prescribed gemfibrozil. Of all patients prescribed statins, 63.2% were at least on moderate doses. This study demonstrates suboptimal treatment with statins in patients with type 2 diabetes and cardiovascular risk factors.

W01-P-015 Gemfibrozil in patients with acute coronary syndrome does not exhibit favourable rapid pleiotropic effects

W01-P-015 Gemfibrozil in patients with acute coronary syndrome does not exhibit favourable rapid pleiotropic effects

Atherosclerotic Risk Factors in Patients with Ischemic Cerebrovascular Disease.

Aggressive treatment of atherosclerotic risk factors can substantially reduce stroke risk in patients with a history of stroke or transient ischemic attack. Data from several recent large clinical trials provide convincing evidence of benefit for a number of specific therapies directed at this population. The authors recommend treatment with ramipril alone or perindopril plus indapamide regardless of blood pressure, provided there is no contraindication. For patients already taking a different angiotensin- converting enzyme (ACE) inhibitor, the authors do not routinely switch agents. The authors recommend use of simvastatin 40 mg per day in patients with a total cholesterol level of 135 mg/dL or greater, provided no contraindication exists. The authors also recommend consideration of gemfibrozil in patients with isolated low high- density lipoprotein levels. In patients with diabetes mellitus, tight glycemic control has not been shown to reduce macrovascular complications such as stroke, but does reduce microvascular complications. However, diabetics should receive especially aggressive treatment of other vascular risk factors. There is no role for post-menopausal hormone replacement therapy in prevention of stroke. Weight loss for overweight patients, regular exercise, and a diet rich in fruits, vegetables, cereals, and fish, as well as low in fat and cholesterol, should be a standard recommendation for this group of patients. Treatment with folic acid, B(6), and B(12) for patients with elevated homocysteine appears rational, though this is unproven. However, there is no benefit to vitamin E, vitamin C, or beta-carotene supplementation. Smokers should stop. For every 43 smokers who quit, one stroke is prevented. Moderate consumption of alcohol (one to two drinks a day) may be beneficial, but heavy alcohol use (more than five drinks a day) increases stroke risk.

Stroke prevention: management of modifiable vascular risk factors.

Stroke prevention is a crucial issue because (i) stroke is a frequent and severe disorder, and (ii) acute stroke therapies that are effective at the individual level have only a little impact in term of public health. Stroke prevention consists of the combination of 3 strategies: an optimal management of vascular risk factors, associated when appropriate with antithrombotic therapies, carotid surgery, or both. Primary prevention trials have shown that reducing blood pressure in hypertensive subjects reduces their vascular risk, including stroke. The association of perindopril plus indapamide reduces the vascular risk in patients who have had a stroke or TIA during the last 5 years, irrespective of their baseline blood pressure. Lowering serum cholesterol with statins or gemfibrozil in patients with hypercholesterolemia or coronary heart disease (CHD), reduces the risk of stroke. However, no trial of cholesterol-lowering therapy has been completed in stroke patients. A strict control of high cholesterol levels should be encouraged, because of benefits in terms of CHD. Statins should be prescribed for stroke patients with CHD, or increased cholesterol levels. Cigarette smoking is associated with an increased risk of stroke and should be avoided. Careful control of all risk factors, especially arterial hypertension in type 1 and type 2 diabetics is recommended, together with a strict glycemic control to reduce systemic microvascular complications. Estrogens prescribed in hormone replacement or oral contraceptive therapies are not recommended after an ischemic stroke. It is also recommended to reduce alcohol consumption and obesity, and to increase physical activity in patients at risk for first-ever or recurrent stroke. An optimal management of risk factors for stroke is crucial to reduce the risks of first-ever stroke, recurrent stroke, any vascular event after stroke and vascular death. One of the major public health issues for the coming years will be to focus more on risk factor recognition and management.

Efficacy of Concentrated n-3 Fatty Acids in Hypertriglyceridaemia

To compare the effects of concentrated n-3 fatty acids (Omacor™) and gemfibrozil in patients with severe hypertriglyceridaemia. The primary objective was to measure the change in serum triglyceride (TG), and the secondary objectives were to study the changes in total cholesterol (TC), high density lipoprotein cholesterol (HDL-C), very low density lipoprotein cholesterol (VLDL-C), apolipoproteins and free fatty acids. 89 patients with severe hypertriglyceridaemia (defined as plasma TG >4.5 mmol/L) were randomised to receive in a double-blind fashion either Omacor™, a capsule containing the n-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) at a dosage of 4 g/day, or gemfibrozil 1200 mg/day for 12 weeks. The baseline characteristics of the two randomised groups were similar. Compared with baseline, n-3 fatty acids and gemfibrozil reduced mean TG levels by 28.9 and 51.2%, respectively (p = 0.007). TC was decreased 10.2% with n-3 fatty acids, and 13.0% with gemfibrozil (p = 0.51), and VLDL-C was reduced 11.8 and 19.4% (p = 0.49) with n-3 fatty acids and gemfibrozil, respectively. HDL-C was increased by both compounds; n-3 fatty acids elevated HDL-C by only 1.2%, whereas it was elevated 27.9% by gemfibrozil (p = 0.012). Our study indicated that both n-3 fatty acids and gemfibrozil markedly decreased TG levels in patients with severe hypertriglyceridaemia. Gemfibrozil, however, decreased TG levels and increased HDL-C significantly more than n-3 fatty acids.

Micronised fenofibrate or gemfibrozil in patients with combined hyperlipidaemia: A double-blind randomised multicentre trial

Micronised fenofibrate or gemfibrozil in patients with combined hyperlipidaemia: A double-blind randomised multicentre trial

Lack of interaction of apolipoprotein E phenotype with the lipoprotein response to lovastatin or gemfibrozil in patients with primary hypercholesterolemia

The magnitude of serum lipid changes in response to hypolipidemic drugs varies considerably between individuals. These differences may be due to interactions between genetic and environmental factors that effect drug bioavailability or the capacity of the lipid-regulating enzyme and receptor targets to be affected. The apolipoprotein E (apoE) gene locus has been examined in this regard, but reports are conflicting on the effect of its variability on the response to hypolipidemic drugs. We investigated the effect of apoE polymorphism on the serum lipid response to the hepatic hydroxymethyl glutaryl coenzyme A (HMG CoA) reductase inhibitor lovastatin and the fibric acid derivative gemfibrozil. Lipoprotein changes were assessed after 12 weeks of therapy in 106 patients with primary hypercholesterolemia and combined hyperlipidemia treated with lovastastin and in 63 given gemfibrozil therapy. No significant effect of the apoE phenotypes E3/2, E3/3, or E4/3 on the heterogeneity of lipid responses to either drug was found.

Effect of a high dose of gemfibrozil in patients with hypertriglyceridemia and decreased high-density lipoprotein cholesterol

After 8 weeks of dietary stabilization, 25 hypertriglyceridemic (plasma triglyceride [TG] >250 mg/dL) patients with below-average high-density lipoprotein (HDL) cholesterol levels were randomized to receive gemfibrozil for 12 weeks in dosages of 600 mg twice daily or 600 mg in the morning and 1200 mg at night. Of the 25 patients who completed the study, 13 received the recommended dose of 1200 mg/d and 12 received 1800 mg/d. Patients receiving 1800 mg/d had significantly reduced plasma total cholesterol (TC) levels compared with the 1200-mg/d group (19% vs 12%, P = 0.05). No significant differences in the changes in TG, HDL cholesterol, apolipoprotein B, apolipoprotein A-I (apo A-I), lipoprotein (a) (Lp[a]), or lipoprotein A-I particles (LpA-I) were found between the two treatment groups. Among all patients, gemfibrozil treatment significantly reduced plasma TC and TG levels and raised HDL cholesterol. Gemfibrozil also decreased plasma LpA-I and coenzyme Q concentrations. High-dose (1800 mg/d) gemfibrozil treatment offers little advantage over the recommended dose (1200 mg/d) in the treatment of patients with hypertriglyceridemia and low HDL cholesterol.

Long-term combined treatment with pravastatin and gemfibrozil in patients with severe refractory familial combined hyperlipidemia

Long-term combined treatment with pravastatin and gemfibrozil in patients with severe refractory familial combined hyperlipidemia

Comparative efficacy and safety study of pravastatin and gemfibrozil in patients with primary hypercholesterolemia

Comparative efficacy and safety study of pravastatin and gemfibrozil in patients with primary hypercholesterolemia

Comparison of lipid-lowering effects of low-dose fluvastatin and conventional-dose gemfibrozil in patients with primary hypercholesterolemia

A total of 123 patients with primary hypercholesterolemia were randomized on a 2:1 ratio to receive either fluvastatin at 20 mg once daily at night (n = 82) or gemfibrozil at 600 mg twice daily (n = 41) in a double-blind, double-dummy comparison of the effects on plasma lipid parameters and tolerability over 8 weeks. All patients had either low-density lipoprotein cholesterol (LDL-C) concentrations ≥160 mg/dL (4.1 mmol/L) in association with definite coronary artery disease (CAD) or ≥2 risk factors, or LDL-C ⪰190 mg/dL 4.9 mmol/L) with no CAD and <2 risk factors. All had triglyceride (TG) levels ⪯350 mg/dL (4.0 mmol/L). After 8 weeks of treatment, fluvastatin produced significant reductions from baseline of 17.4% (P <0.001) in LDL-C, 13.2% (p <0.001) in total cholesterol (TC), 13.8% (p <0.001) in very low-density lipoprotein cholesterol (VLDL-C), and 6.4% (NS) in TG. High-density lipoprotein cholesterol (HDL-C) was increased by 5.6% (p <0.001), and the ratio of LDL-C:HDL-C (Friedewald) was decreased by 21.2% (p <0.001). Gemfibrozil reduced LDL-C by 15.8%, TC by 13.4%, VLDL-C by 32.2%, LDL-C:HDL-C by 24.8%, and TG by 34.2%, and increased HDL-C by 13.9% (all changes were statistically significant, p <0.001) compared with baseline. Gemfibrozil produced significantly greater changes in VLDL-C (p <0.01), HDL-C (p <0.001), and TG (p <0.001), but not in LDL-C: HDL-C, compared with fluvastatin Both drugs significantly reduced apolipoprotein (apo) B and lipoparticles (Lp) E:B, and increased apo A-I but had divergent effects on LpA-I (increased with fluvastatin and reduced with gemfibrozil; p <0.05). At the end of the study, 43.8% of fluvastatin patients and 45% of gemfibrozil patients achieved a reduction of >20% in LDL-C levels. Normalization of LDL-C levels was achieved (according to European Athesrosclerosis Society guidelines) by 13.4% of fluvastatin- and 14.6% of gemfibrozil-treated patients. Both drugs were well tolerated; adverse events occurred in 36.6% of fluvastatin recipients compared with 58.5% of patients taking gemfibrozil. No clinically notable elevations of aspartate or alanine aminotransferases, alkaline phosphatase, or creatine phosphokinase occurred. No patients developed new or worsening lens opacities associated with a reduction in optically corrected visual acuity. The most commonly reported adverse events were headache and gastrointestinal upset. There were no serious drug-related adverse events.

Combined Treatment with Pravastatin and Gemfibrozil in Patients with Refractory Familial Combined Hyperlipidaemia

This study was carried out to assess the efficacy and safety of combined therapy with pravastatin and gemfibrozil in patients with severe refractory familial combined hyperlipidaemia.

Once-daily, extended-release gemfibrozil in patients with dyslipidemia

This randomized, parallel-group, multicenter clinical trial compared a newly developed, once-daily, extended-release formulation of gemfibrozil (Lopid SR®) and gemfibrozil twice daily (Lopid®) in terms of lipid-regulating effects and toxicity. Patients were men and women with elevations of low-density lipoprotein cholesterol and low levels of high-density lipoprotein cholesterol. The trial consisted of a 1-week screening period, an 8-week diet baseline period (Step One Diet), and a 24-week double-blind treatment period (extended-release gemfibrozil 1,200 mg once daily vs gemfibrozil 600 mg twice daily). At the end of the trial, the 2 treatment groups showed comparable improvements in all primary lipid factors: mean percent changes in triglyceride, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol were −32, +10 and −10% for extended release (n = 325) and −36, +11 and −10% for twice daily (n = 330). The 90% confidence interval for the relative difference between the treatment means fell within the equivalence bounds of ±35% for all 3 factors, demonstrating equivalence of efficacy. Adverse events were reported at low rates and were similarly distributed in frequency and intensity between treatment groups; they were preponderantly mild or moderate, and gastrointestinal effects were the most frequent. The once-daily formulation of gemfibrozil may afford better control of dyslipidemia through improved compliance by patients who have this asymptomatic disease.

Long Term Treatment with Pravastatin, Simvastatin and Gemfibrozil in Patients with Primary Hypercholesterolaemia: A Controlled Study

Patients with primary hypercholesterolaemia (30 with familial hypercholesterolaemia and 17 with polygenic hypercholesterolaemia), were randomly treated with either simvastatin or pravastatin 40 mg/day or gemfibrozil 1200 mg/day for up to 18 months. Efficacy and safety parameters were measured every 3 months. To date, out of the initial 47 subjects who entered the study, 38 have been treated for 12 months and 34 for 18 months. Both simvastatin and pravastatin lowered total and low density lipoprotein (LDL) cholesterol (by about 30%). This effect was already maximal by the third month of therapy and the decrease was maintained for up to 18 months. The effect of gemfibrozil on these lipid parameters was slower (maximum lowering effect at the sixth month) and less marked during the first 6 months of therapy. However, after the sixth month the differences between the 3 drugs were no longer statistically significant, possibly because of large interindividual variability in the response to treatment. All 3 treatment groups had similar reductions in apolipoprotein- (Apo) A1 and Apo-B levels. High density lipoprotein (HDL) cholesterol levels were increased significantly during treatment with gemfibrozil, but not during therapy with either of the statins. However, intergroup analysis did not reveal consistent differences in HDL-cholesterol during treatment. Gemfibrozil markedly decreased triglyceride levels, and this effect was maintained throughout the study. Neither simvastatin nor pravastatin affected triglyceride levels. The statins therefore did not show different influences on any lipid parameter studied. All 3 drugs were well tolerated. Simvastatin was, however, associated with significant increases in GGT and CPK activities at the 6-month evaluation. In conclusion, there were no significant differences between simvastatin, pravastatin or gemfibrozil in long term effects on total, LDL- and HDL-cholesterol levels in patients with primary hypercholesterolaemia, although this finding may have been due to large interindividual variations in the response to therapy. It would therefore appear that gemfibrozil is an effective lipid-lowering agent which is suitable for long term treatment.

High-density lipoprotein cholesterol and coronary artery disease: Survey of the evidence

The epidemiologic evidence linking high-density lipoprotein (HDL) levels with coronary artery disease (CAD) is persuasive. Case-control studies have shown CAD patients to have lower HDL levels than control subjects. Several large-scale, observational epidemiologic studies in the United States and abroad have shown a strong independent inverse relation between HDL and CAD. Women have a lower incidence of CAD than men of the same age; this has been attributed to their higher HDL levels. Postmenopausal women taking estrogen replacement therapy have higher HDL and lower low-density lipoprotein (LDL) levels, and a much lower incidence of CAD. Statistical analysis suggests that much of this is attributable to HDL levels. In several clinical trials, reduced levels of total or LDL cholesterol have been accompanied by increased HDL levels. Cox proportional hazards analysis suggests that the increment in HDL levels made an independent contribution to the reduction in CAD risk. In several angiographic studies, the increase in HDL may have contributed to the decreased progression, increased stabilization and possible regression of coronary lesions. Despite this range of impressive evidence, a number of unresolved issues have prevented the emergence of a consensus regarding the prevention of CAD by increasing HDL levels. Between-population comparisons of HDL and CAD do not match the within-population relations. Animal research on the relation between HDL, atherogenesis and CAD has been relatively scanty. Although much evidence suggests that reverse cholesterol transport partially explains the protective effect of HDL, there are still doubts as to its role. Problems with measurement of HDL have inhibited widespread recommendations for its use in prevention programs. Our ability to increase low HDL levels by hygienic means is uncertain, and there is insufficient information regarding the use of drugs for such a purpose. The recent report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults, while not advocating universal screening for HDL, did assign a risk-factor status to a low HDL level, and recommended HDL measurement in a large proportion of persons classified initially on the basis of total cholesterol levels. The results of the Helsinki Heart Study support the use of gemfibrozil in patients with high-risk LDL levels who also have borderline hypertriglyceridemia and low HDL levels.