Drugs online research references
Circulation. 1992 May;85(5):1888-93.
Direct effects of gemfibrozil on the fibrinolytic system. Diminution of synthesis of plasminogen activator inhibitor type 1.
Fujii S, Sobel BE.
Cardiovascular Division, Washington University School of Medicine, St. Louis, MO 63110.
BACKGROUND. Platelet-associated epidermal growth factor (EGF) and transforming growth factor-beta (TGF-beta) can augment synthesis of plasminogen activator inhibitor type 1 (PAI-1). Accordingly, exacerbation of atherogenesis may accompany release of platelet-associated growth factors (or mitogens) occurring in association with occult, repetitive thrombosis and thrombolysis. In the Helsinki primary prevention trial, gemfibrozil decreased coronary events but did so essentially only in initially hypertriglyceridemic subjects. Such subjects are known to exhibit high concentrations of PAI-1 in plasma. METHODS AND RESULTS. To determine whether pharmacological concentrations of gemfibrozil directly affect PAI-1 synthesis, we characterized its effects on a human hepatoma cell line (Hep G2) in vitro. Gemfibrozil decreased basal PAI-1 secretion by 43% and attenuated the augmentation of PAI-1 synthesis over 24 hours induced by EGF and TGF-beta by 37% and 39% without altering overall protein synthesis. Furthermore, it blocked the EGF and TGF-beta-induced increases in PAI-1 mRNA over 6 hours by 65% and 60%. Increases in plasma PAI activity induced by infusion of purified growth factors or by autologous platelet lysates in rabbits were inhibited by gemfibrozil by more than 50%. CONCLUSIONS. Beneficial effects of gemfibrozil in reducing coronary events in hypertriglyceridemic patients may depend, in part, on potentiation of fibrinolysis by direct diminution of synthesis of endogenous PAI-1.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1572044&dopt=Abstract
Int Angiol. 1988 Jul-Sep;7(3):270-7.
Changes induced by gemfibrozil on lipidic, coagulative and fibrinolytic pattern in patients with type IV hyperlipoproteinemia.
Avellone G, Di Garbo V, Panno AV, Cordova R, Lepore R, Strano A.
Institute of Clinical Medicine, University of Palermo, Italy.
A short term open study (90 days) was carried out with Gemfibrozil in patients (n = 10) suffering from type IV hyperlipoproteinemia. For the whole observation period (120 days) the patients followed a standard diet. Every 30 days the following parameters were checked: total cholesterol, serum triglycerides, HDL-C and its fractions (HDL2-C and HDL3-C), apolipoprotein A1 and B, glucose, fibrinogen, plasminogen, euglobulin lysis time, antithrombin III, alpha-2-antiplasmin and PTT. The administration of the drug caused a reduction of serum triglycerides by 39.5%, an increase of HDL-C by 16.2% together with a significant increase of cholesterol bound to HDL2 (+27.6%). A significant increase was also noticed for the mean levels of apolipoprotein A1 (+19.8%), confirming thus the antidislipidemic effect of the drug. Significant reductions were also found in the mean levels of fibrinogen and alpha-2-antiplasmin together with a return to normality of mean values of antithrombin III and of the euglobulin lysis time. The effect on the lipid, haemocoagulative and fibrinolytic parameters shows that the administration of Gemfibrozil causes favourable changes both on the hyperlipoproteinemic pattern and on the thrombophilic state present in these patients.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3198979&dopt=Abstract
Coron Artery Dis. 1995 Mar;6(3):251-6.
Long-term effect of gemfibrozil on coronary heart disease risk profile of patients with primary combined hyperlipidaemia.
Athyros VG, Papageorgiou AA, Avramidis MJ, Kontopoulos AG.
Department of Cardiology, Aristotelian University, Ippocration Hospital, Thessaloniki, Greece.
BACKGROUND: The purpose of the present study was to assess the effect of gemfibrozil on 12 independent coronary heart disease risk factors in patients with primary combined hyperlipidaemia. METHODS: One hundred and five patients (62 men and 43 women), aged 53.2 +/- 4.8 years, were studied. The 10-year probability of myocardial infarction for the patients was calculated using the TYPMI (Ten-Year Probability for Myocardial Infarction) computer program, which is constructed to co-evaluate 12 independent coronary artery disease risk factors. All patients followed a lipid-lowering diet and placebo for 3 months. At month 0, the patients received 1200 mg gemfibrozil daily, divided into two equal doses, for a period of 12 months. At months -3, 0, 1, 3, 6, and 12, total cholesterol, high-density lipoprotein (HDL) cholesterol, triglycerides [only if the low-density lipoprotein (LDL) cholesterol to high-density lipoprotein cholesterol ratio was above 5], systolic blood pressure, plasma glucose, left ventricular mass index, and plasma fibrinogen were measured. Smoking habits, sex, age, physical activity and family history of coronary heart disease were also evaluated. The mean 10-year probability of myocardial infarction of all 105 patients at month 0 was 27.8%. This was significantly higher than the anticipated probability (10.4%, P < 0.001), resulting from an age- and sex-matched group of general population. RESULTS: During the third month of treatment, the following changes were recorded: total cholesterol -17%, LDL cholesterol -18%, very-low-density lipoprotein (VLDL) cholesterol -45%, HDL cholesterol 20%, triglycerides -43%, apoprotein B -12%, apoprotein A-I 9% and plasma fibrinogen -21%. The estimated risk for myocardial infarction was reduced to 13.5% (delta m = -51%). All changes were significant and sustained until the twelfth treatment month. None of the patients were withdrawn from the study because of adverse effects of the treatment. CONCLUSION: Gemfibrozil reduces the estimated risk for myocardial infarction in patients with primary combined hyperlipidaemia at a level no different from the one of the general population. This beneficial effect of gemfibrozil, which was expressed by the third month and was evident for some time afterwards, was attributed to a significant reduction of triglyceride and fibrinogen levels, an increase of HDL cholesterol concentrations and a moderate decrease of total cholesterol and LDL cholesterol levels.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7788039&dopt=Abstract
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