Lopid is an effective medication which helps to fight with high levels of serum triglycerides. Lopid acts by reducing the production of triglycerides in the liver. It is fibrates.
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Also known as: Gemfibrozil.
Lopid target is to fight against high levels of serum triglycerides.
Lopid acts by reducing the production of triglycerides in the liver. It is fibrates.
Generic name of Lopid is Gemfibrozil.
Brand name of Lopid is Lopid.
Take Lopid tablets orally.
Take Lopid twice a day with water at the same time.
Do not crush or chew it.
If you want to achieve most effective results do not stop taking Lopid suddenly.
If you overdose Lopid and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Lopid overdosage: arthralgia, muscle pain, vomiting, abdominal cramps, diarrhea, nausea.
Store at room temperature between 20 and 25 degrees C (68 and 77 degrees F) away from moisture and heat. Protect from light and humidity. Throw away any unused medicine after the expiration date. Keep out of the reach of children.
The most common side effects associated with Lopid are:
Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.
Do not take Lopid if you are allergic to Lopid components.
Do not take Lopid if you're pregnant or you plan to have a baby, or you are a nursing mother.
Do not use potassium supplements or salt substitutes.
Be careful with Lopid if you are taking cholesterol-lowering medications (statins) such as atorvastatin (Lipitor), fluvastatin (Lescol), lovastatin (Mevacor), pravastatin (Pravachol), and simvastatin (Zocor); and repaglinide (Prandin), anticoagulants ('blood thinners') such as warfarin (Coumadin).
Be careful with Lopid if you suffer from or have a history of kidney, liver, gallbladder disease.
Do not stop taking Lopid suddenly.
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Condensed phase membrane introduction mass spectrometry (CP-MIMS) is an online analytical method that allows for the direct, trace level measurement of a wide range of analytes in complex samples. The technique employs a semi-permeable membrane that transfers analytes from a sample into a flowing acceptor solvent, which is directly infused to an atmospheric pressure ionization source, such as electrospray or atmospheric pressure chemical ionization. While CP-MIMS and variants of the technique have been in the literature for nearly a decade, much of the work has focused on instrument development. Few studies have thoroughly addressed quantitative methods related to detection limits, ionization suppression, or linear dynamic range. We examine ionization suppression in the direct rapid quantitation of analytes by CP-MIMS and introduce several analytical strategies to mitigate these effects, including the novel implementation of a continuously infused internal standard in the acceptor phase solvent, and modulation of acceptor phase flow rate. Several representative analytes were used to evaluate this approach with spiked, complex sample matrices, including primary wastewater effluent and artificial urine. Also reported are improved measured detection limits in the low part-per-trillion range, using a 'stopped-flow' acceptor mode.
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A series of gemfibrozil analogues with a thiourea moiety embedded in the side chain was prepared and evaluated as HDL-elevating agents. Derivatives 8b, 9b, 9c, and 9d were found to be approximately as effective as gemfibrozil (1) for HDL cholesterol elevation.
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NS-1, 4-[2-(4-isopropylbenzamido)ethoxy]benzoic acid, is a novel chemical compound which has been found to be a potent hypolipidemic agent in rhesus monkeys. Significant reductions in serum cholesterol and phospholipids were observed in normolipidemic monkeys following oral doses of 30-300 mg/kg/day. A dose of 300 mg/kg/day for 28 days lowered serum cholesterol and phospholipid levels by 49% and 41%, respectively. NS-1 was more potent than clofibrate, clinofibrate, simfibrate, bezafibrate, gemfibrozil, nicomol and probucol in hypolipidemic activity in the same model. Lipoprotein analysis showed that NS-1 reduced low density lipoprotein much more than high density lipoprotein. The results suggest that NS-1 may have hypolipidemic activity in hyperlipidemic patients.
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OATP1B1 and OATP1B3 are transporters that are expressed on the sinusoidal membrane of hepatocytes; they accept a number of therapeutic reagents as their substrates. In vitro and in vivo studies have shown that some drugs inhibit these transporters and cause clinically relevant drug-drug interactions (DDIs). Among these drugs, cyclosporin A markedly increases the plasma concentrations of OATP1B1 substrates. In such cases, the area under the plasma concentration-time curve and the maximum concentration of the affected drugs are increased to a similar degree. Even for OATP1B1 substrates that are metabolized in the liver, the hepatic uptake rate is a determinant of overall hepatic clearance, and the DDIs are partly caused by the inhibition of OATP1B1. Gemfibrozil displays DDIs with some OATP1B1 substrates, although their extent is small. Rifampicin and some HIV protease inhibitors are also OATP1B1 inhibitors. Rifampicin is also an inducer of metabolic enzymes, and although its single coadministration produces an increase in the plasma concentration of the affected drugs, multiple coadministrations may result in reductions in the plasma concentrations of OATP1B1 and CYP3A4 bisubstrates. As a large number of therapeutic reagents are substrates and/or inhibitors of OATP1B1 and OATP1B3, we should be aware of DDIs caused by the inhibition of these transporters.
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Gemfibrozil greatly increased the plasma concentration of parent pioglitazone and also inhibited the further metabolism of M-III and M-IV. Careful blood glucose monitoring and dosage adjustments are suggested during coadministration of pioglitazone and gemfibrozil.
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Antiretroviral agents, particularly protease inhibitors (PIs), may adversely affect lipid levels in patients with HIV infection. However, it is not known whether HIV-associated dyslipidemia is more difficult to treat.
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Plasminogen activator inhibitor type-1 (PAI-1), an established marker and mediator of cardiovascular risk, is produced extensively in adipose tissue. Fibrates are hypolipidemic peroxisome proliferator activated receptor-alpha (PPARalpha) agonists. Recent laboratory and clinical observations indicate that they are also anti-atherosclerotic. Mechanisms responsible, however, remain to be fully understood. The present study was designed to elucidate modulation of PAI-1 expression in adipose cells by fibrates as a potential mechanism. Expression of PPARalpha was verified by PCR, immunohistochemistry, and Western blotting. In cultured preadipocytes and adipocytes gemfibrozil and fenofibrate significantly reduced PAI-1 protein expression by up to 55 +/- 5% and 34 +/- 4% under basal conditions and up to 56 +/- 6% and 31 +/- 6% under conditions of stimulation of the cells with 40 pM transforming growth factor (TGF)beta, respectively. Quantification of mRNA showed that the gemfibrozil-induced effect was at least in part regulated at the transcriptional level. Incubations with non-fibrate PPARalpha agonists showed similar reductions in PAI-1 expression. The decrease in PAI-1 expression induced by gemfibrozil was inhibited by MK886, a PPARalpha inhibitor. Furthermore, preadipocytes isolated from PPARalpha-deficient mice produced significantly more PAI-1 than those from wild-type mice upon stimulation with TGFbeta. Finally, fenofibrate reduced PAI-1 expression both in plasma and adipose tissue of hyperlipidemic mice. Our data support the view that PPARalpha activation down-regulates PAI-expression in adipose cells that may contribute in part to the reduction in cardiovascular mortality seen with fibrates in clinical trials.
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Hypertriglyceridemic patients with non-insulin-dependent diabetes mellitus (NIDDM) have an increased risk of coronary heart disease (CHD) and acute pancreatitis. To examine the potential of hypolipidemic drugs for therapy of lipoprotein abnormalities in NIDDM, 10 patients maintaining marked (plasma triglycerides greater than 500 mg/dl) and 6 with moderate (plasma triglycerides 250-500 mg/dl) hypertriglyceridemia, despite good glycemic control, were studied in two phases. In the first phase, gemfibrozil alone (600 mg twice daily) was compared with a placebo, and in the second phase a combination of gemfibrozil and lovastatin (20 mg twice daily) was compared with gemfibrozil alone in a randomized, double-blind, placebo-controlled crossover study. In markedly hypertriglyceridemic patients, gemfibrozil reduced plasma triglycerides by 52% and very-low-density lipoprotein cholesterol (VLDL-chol) by 55% and increased high-density lipoprotein cholesterol by 23% compared with a placebo. However, low-density lipoprotein cholesterol (LDL-chol) levels increased (42%), and LDL apolipoprotein B (apoB) levels remained unchanged. Addition of lovastatin to gemfibrozil effectively reduced total cholesterol (25%), LDL-chol (30%), and LDL-apoB (19%). Lovastatin further reduced plasma triglycerides (11%) and VLDL-chol (27%). However, in moderately hypertriglyceridemic patients, gemfibrozil or the combination therapy did not seem to offer benefits over the previously reported study with lovastatin alone. Glycemic control was maintained throughout the study. In conclusion, the beneficial effects of the combination therapy on lipoprotein levels in markedly hypertriglyceridemic NIDDM patients could decrease the risk of development of both acute pancreatitis and CHD.
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Discuss the contribution of low-density lipoprotein subclass abnormalities to cardiovascular risk among individuals with low high-density lipoprotein cholesterol levels.
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Considerable amounts of pharmaceuticals are used in human and veterinary medicine, which are not efficiently removed during wastewater and slurries treatment and subsequently entering continuously into freshwater systems. The intrinsic biological activity of these non-regulated pollutants turns their presence in the aquatic environment into an ecological matter of concern. We present the first quantitative study relating the presence of pharmaceuticals and their predicted ecotoxicological effects with human population and livestock units. Four representative Iberian River basins (Spain) were studied: Llobregat, Ebro, Júcar and Guadalquivir. The levels of pharmaceuticals were determined in surface water and sediment samples collected from 77 locations along their stream networks. Predicted total toxic units to algae, Daphnia and fish were estimated for pharmaceuticals detected in surface waters. The use of chemometrics enabled the study of pharmaceuticals for: their spatial distribution along the rivers in two consecutive years; their potential ecotoxicological risk to aquatic organisms; and the relationships among their occurrence and predicted ecotoxicity with human population and animal farming pressure. The Llobregat and the Ebro River basins were characterized as the most polluted and at highest ecotoxicological risk, followed by Júcar and Guadalquivir. No significant acute risks of pharmaceuticals to aquatic organisms were observed. However potential chronic ecotoxicological effects on algae could be expected at two hot spots of pharmaceuticals pollution identified in the Llobregat and Ebro basins. Analgesics/antiinflammatories, antibiotics and diuretics were the most relevant therapeutic groups across the four river basins. Among them, hydrochlorothiazide and gemfibrozil, as well as azithromycin and ibuprofen were widely spread and concentrated pharmaceuticals in surface waters and sediments, respectively. Regarding their predicted ecotoxicity, sertraline, gemfibrozil and loratidine were identified as the more concerning compounds. Significantly positive relationships were found among levels of pharmaceuticals and toxic units and population density and livestock units in both surface water and sediment matrices.
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With the discontinuation of CC treatment and start of a specific lipid-lowering agent, the patient's lipid profile improved. After 3 months, CC therapy was restarted, and again severe hypertriglyceridemia developed, which resolved with the previous treatment strategies.
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Children have been tested and treated for hypercholesterolemia for more than 30 years. Although most treatment regimens have been limited to dietary intervention, statin use is increasing. Statins have been used in children since 1987, but published sources have only reported on small numbers of children with severe hypercholesterolemia. The available data indicates that statins can be useful and well tolerated. New data will be available in the next few years that will lead to the wider use of these drugs. Although statin drugs have proven to be safe in the adult population, physicians will be obliged to follow pediatric patients closely when these agents are widely used in the first few years. The use of highly effective safe drugs such as statins will allow for the assessment of the best time to initiate therapy in younger populations and what benefits may be found over the long term.
Ultracentrifugally isolated HDL subclasses; concentrations of apoA-I, apoA-II, LpA-I and LpA-I:A-II particles; post-heparin plasma lipoprotein lipase (LPL), hepatic lipase (HL) and plasma cholesteryl ester transfer protein (CETP) activities; phospholipid transfer protein (PLTP) and lecithine cholesteryl acyltransferase (LCAT) activities were measured in plasma from six patients from both groups.
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A case of elevated creatine phosphokinase (CPK) levels associated with linezolid therapy in a patient on chronic antihyperlipidemic therapy is presented.
A patient who was given tamoxifen as adjuvant treatment for breast cancer developed very severe hypertriglyceridaemia, hypercholesterolaemia and acute pancreatitis after being treated for 4 months. The hyperlipidaemia was corrected after cessation of the tamoxifen and the institution of gemfibrozil treatment. This patient appears to have type IV hyperlipidaemia. It is suggested that, in such patients, tamoxifen should be used with extreme caution because the weakly oestrogenic effect of this agent can cause severe and life threatening hyperlipidaemia.
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