Drugs online research references
Eur J Clin Invest. 2000 Oct;30(10):843-52.
Effect of gemfibrozil on peripheral atherosclerosis and platelet activation in a pig model of hyperlipidemia.
Royo T, Alfon J, Berrozpe M, Badimon L.
Cardiovascular Research Centre, IIBB/CSIC-Hospital de la Santa Creu i, Sant Pau-UAB, Spain.
BACKGROUND: Gemfibrozil has been shown to have beneficial effects in the primary and secondary prevention of atherosclerosis. However, a platelet pro-activating effect induced by the drug has been reported. MATERIAL AND METHODS: We analysed the effect of hyperlipidemia and its treatment with gemfibrozil on platelet-fibrinogen binding and the development of early fibrinogen-rich vascular lesions in a porcine model of atherosclerosis. Polyclonal antibodies were raised against purified pig fibrinogen and intact platelets. Two groups of animals were fed a cholesterol/saturated fat-enriched diet for 50 days; one group was treated with gemfibrozil and the other with placebo. RESULTS: The hyperlipidemic diet induced a significant increase in total cholesterol; this was prevented by gemfibrozil (P<0.05). The increase in platelet-fibrinogen binding induced by hypercholesterolemia was mildly reduced in the gemfibrozil treated animals. Histological analysis of aortic vascular wall (abdominal aorta at the iliac bifurcation) from hyperlipidemic animals showed early lesions with fibrinogen infiltration; the lesions were reduced in the fibrate-treated animals. CONCLUSIONS: Gemfibrozil delayed the development of peripheral atherosclerotic plaque, normalised the impaired lipid profile induced by the hyperlipidemic diet and did not show a functionally detectable platelet pro-activating effect able to increase platelet-fibrinogen binding.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11029597&dopt=Abstract
Manag Care Interface. 2000 Mar;13(3):52-8.
Predicting risk reduction of coronary disease in patients who are glucose intolerant: a comparison of treatment with fenofibrate and other lipid-modifying agents.
Haffner SM, Ashraf T.
University of Texas Health Science Center at San Antonio, USA.
A clinical outcomes model was developed to estimate the ability of fibrates and statins to reduce the relative and absolute risk of developing coronary heart disease (CHD) in patients with diabetes. A database was constructed, drawing on results from 83 applicable published studies. Risk factor outcomes reported by the model were chosen according to those found to be statistically significant in the data set parameters from the Framingham Heart Study. In the analysis, fenofibrate was compared with gemfibrozil (an earlier fibrate) and six 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase-inhibitor or "statin" agents. Among the agents studied, only fenofibrate was found to significantly affect all six cardiovascular disease risk factors used in this analysis. For men with diabetes, the estimated absolute risk of developing CHD after five years of treatment was lowered equally and most effectively by fenofibrate, simvastatin, and atorvastatin, from 10% to 6%. For women with diabetes, fenofibrate and simvastatin reduced absolute risk from 9% to 6% over five years of treatment, while atorvastatin reduced risk from 9% to 6%. An accompanying cost comparison analysis found that reducing absolute risk of CHD in these patients would result in significant reductions in the medical expense of treating cardiac events, and that significant differences in the amount saved were driven by treatment choice. Fenofibrate, simvastatin, and atorvastatin produced the greatest long-term savings.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11066277&dopt=Abstract
J Lipid Res. 1985 Aug;26(8):940-9.
Apolipoprotein changes associated with the plasma lipid-regulating activity of gemfibrozil in cholesterol-fed rats.
Krause BR, Newton RS.
Gemfibrozil (Lopid) is a new plasma lipid-regulating drug that decreases very low and low density lipoprotein (VLD/LDL) and increases high density lipoprotein (HDL) concentrations in man. The present experiments tested the effects of gemfibrozil on plasma lipoproteins and apolipoproteins in rats fed high fat/high cholesterol diets. Compared to chow-fed rats, cholesterol feeding for 2 weeks (20% olive oil/2% cholesterol) produced the expected increases in VLDL and intermediate density lipoprotein (IDL) while lowering plasma HDL. This was documented by using three methods of lipoprotein isolation: sequential ultracentrifugation, density gradient ultracentrifugation, and agarose gel filtration. Gemfibrozil gavaged at 50 mg/kg per day for 2 weeks during cholesterol feeding prevented these changes such that lipoprotein patterns were similar to those in chow-fed animals. Whole plasma apoE and apoA-I concentrations were decreased and apoB increased due to cholesterol feeding as determined by electroimmunoassay, but again gemfibrozil treatment prevented these diet-induced alterations. Gradient polyacrylamide gel electrophoresis patterns of the total d less than 1.21 g/ml lipoprotein fractions reflected the changes in apolipoprotein concentrations and further demonstrated a greater increase of apoBl compared to apoBh in cholesterol-fed rats. Gemfibrozil lowered the concentration of both apoB variants and prevented the shift of apoE from HDL to lower density lipoproteins. Changes in the distribution of apoE were confirmed using agarose gel column chromatography followed by electroimmunoassay. These methods also revealed a shift of apoA-IV from HDL to the d greater than 1.21 g/ml, lipoprotein-free fraction with gemfibrozil treatment when blood was taken from fasted or postabsorptive animals. Since it was also noted that in chow-fed rats more apoA-IV was present in the d greater than 1.21 g/ml fraction in the postabsorptive or fed state compared to fasted animals, it could be postulated that the shift of apoA-IV into this fraction in gemfibrozil-treated rats is related to an accelerated clearance of chylomicrons. It is concluded that gemfibrozil largely prevents the accumulation of abnormal lipoproteins in this model of dyslipoproteinemia, and that apoE may play a critical role in this normalization process.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3862732&dopt=Abstract
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