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[PMID]:29381696
[Au] Autor:Copeland LA; Swendsen CS; Sears DM; MacCarthy AA; McNeal CJ
[Ad] Endereço:VA Central Western Massachusetts Healthcare System, Leeds, Massachusetts, United States of America.
[Ti] Título:Association between triglyceride levels and cardiovascular disease in patients with acute pancreatitis.
[So] Source:PLoS One;13(1):e0179998, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Conventional wisdom supports prescribing "fibrates before statins", that is, prioritizing treatment of hypertriglyceridemia (hTG) to prevent pancreatitis ahead of low-density lipoprotein cholesterol to prevent coronary heart disease. The relationship between hTG and acute pancreatitis, however, may not support this approach to clinical management. This study analyzed administrative data from the Veterans Health Administration for evidence of (1) temporal association between assessed triglycerides level and days to acute pancreatitis admission; (2) association between hTG and outcomes in the year after hospitalization for acute pancreatitis; (3) relative rates of prescription of fibrates vs statins in patients with acute pancreatitis; (4) association of prescription of fibrates alone versus fibrates with statins or statins alone with rates of adverse outcomes after hospitalization for acute pancreatitis. Only modest association was found between above-normal or extremely high triglycerides and time until acute pancreatitis. CHD/MI/stroke occurred in 23% in the year following AP, supporting cardiovascular risk management. Fibrates were prescribed less often than statins, defying conventional wisdom, but the high rates of cardiovascular events in the year following AP support a clinical focus on reducing cardiovascular risk factors.
[Mh] Termos MeSH primário: Doenças Cardiovasculares/sangue
Hipertrigliceridemia/sangue
Pancreatite/complicações
Triglicerídeos/sangue
[Mh] Termos MeSH secundário: Doença Aguda
Idoso
Doenças Cardiovasculares/complicações
Feminino
Ácidos Fíbricos/uso terapêutico
Seres Humanos
Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico
Hipertrigliceridemia/complicações
Masculino
Meia-Idade
Análise Multivariada
Pancreatite/tratamento farmacológico
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fibric Acids); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Triglycerides)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180131
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179998


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[PMID]:29176657
[Au] Autor:Agrawal S; Zaritsky JJ; Fornoni A; Smoyer WE
[Ad] Endereço:Center for Clinical and Translational Research, The Research Institute at Nationwide Children's Hospital, and Department of Pediatrics, The Ohio State University, 700 Children's Drive, W303, Columbus, Ohio 43205, USA.
[Ti] Título:Dyslipidaemia in nephrotic syndrome: mechanisms and treatment.
[So] Source:Nat Rev Nephrol;14(1):57-70, 2018 Jan.
[Is] ISSN:1759-507X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Nephrotic syndrome is a highly prevalent disease that is associated with high morbidity despite notable advances in its treatment. Many of the complications of nephrotic syndrome, including the increased risk of atherosclerosis and thromboembolism, can be linked to dysregulated lipid metabolism and dyslipidaemia. These abnormalities include elevated plasma levels of cholesterol, triglycerides and the apolipoprotein B-containing lipoproteins VLDL and IDL; decreased lipoprotein lipase activity in the endothelium, muscle and adipose tissues; decreased hepatic lipase activity; and increased levels of the enzyme PCSK9. In addition, there is an increase in the plasma levels of immature HDL particles and reduced cholesterol efflux. Studies from the past few years have markedly improved our understanding of the molecular pathogenesis of nephrotic syndrome-associated dyslipidaemia, and also heightened our awareness of the associated exacerbated risks of cardiovascular complications, progressive kidney disease and thromboembolism. Despite the absence of clear guidelines regarding treatment, various strategies are being increasingly utilized, including statins, bile acid sequestrants, fibrates, nicotinic acid and ezetimibe, as well as lipid apheresis, which seem to also induce partial or complete clinical remission of nephrotic syndrome in a substantial percentage of patients. Future potential treatments will likely also include inhibition of PCSK9 using recently-developed anti-PCSK9 monoclonal antibodies and small inhibitory RNAs, as well as targeting newly identified molecular regulators of lipid metabolism that are dysregulated in nephrotic syndrome.
[Mh] Termos MeSH primário: Anticolesterolemiantes/uso terapêutico
Dislipidemias/tratamento farmacológico
Ácidos Fíbricos/uso terapêutico
Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico
Síndrome Nefrótica/metabolismo
[Mh] Termos MeSH secundário: Colesterol/metabolismo
HDL-Colesterol/metabolismo
VLDL-Colesterol/metabolismo
Dislipidemias/complicações
Dislipidemias/metabolismo
Ezetimiba/uso terapêutico
Seres Humanos
Hipolipemiantes/uso terapêutico
Lipase/metabolismo
Lipase Lipoproteica/metabolismo
Lipoproteínas/metabolismo
Síndrome Nefrótica/complicações
Niacina/uso terapêutico
Pró-Proteína Convertase 9/metabolismo
Triglicerídeos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anticholesteremic Agents); 0 (Cholesterol, HDL); 0 (Cholesterol, VLDL); 0 (Fibric Acids); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Hypolipidemic Agents); 0 (Lipoproteins); 0 (Triglycerides); 0 (lipoprotein cholesterol); 2679MF687A (Niacin); 97C5T2UQ7J (Cholesterol); EC 3.1.1.3 (Lipase); EC 3.1.1.3 (hepatic lipase, human); EC 3.1.1.34 (Lipoprotein Lipase); EC 3.4.21.- (PCSK9 protein, human); EC 3.4.21.- (Proprotein Convertase 9); EOR26LQQ24 (Ezetimibe)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180117
[Lr] Data última revisão:
180117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1038/nrneph.2017.155


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[PMID]:28667876
[Au] Autor:Niu H; Wang W; Li J; Lei Y; Zhao Y; Yang W; Zhao C; Lin B; Song S; Wang S
[Ad] Endereço:Key Laboratory of Structure-Based Drugs Design & Discovery of Ministry of Education, School of Pharmaceutical Engineering, Shenyang Pharmaceutical University, 103 Culture Road, Shenhe District, Shenyang 110016, People's Republic of China; Center for Drug Evaluation, China Food and Drug Administr
[Ti] Título:A novel structural class of coumarin-chalcone fibrates as PPARα/γ agonists with potent antioxidant activities: Design, synthesis, biological evaluation and molecular docking studies.
[So] Source:Eur J Med Chem;138:212-220, 2017 Sep 29.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:A series of structurally interesting coumarin-chalcone fibrates were synthesized and evaluated for their PPARα/γ agonist activities and antioxidant activities. Among these compounds, compounds 5a, 5d, and 7a were identified as potent PPARα and γ dual agonists, and their PPARα agonist activities were found to be more potent than that of Fenofibrate. Furthermore, the results of antioxidant investigations revealed that compounds 5d and 6a-6d had greater potency than Trolox with IC values ranging from 9.40 µM to 18.63 µM. The structure-activity relationship revealed that the electron-withdrawing nitro group substituted at the C6' position of the benzopyran moiety increased the PPARα and γ agonist efficacy. Moreover, the presence of a double bond on the benzopyran moiety was essential for PPARα and γ agonist efficacy. The agonist activity of PPARα exhibited by compound 5d was examined by molecular docking studies. Taken together, the results we obtained showed that compound 5d had the potential to be a lead compound for further research.
[Mh] Termos MeSH primário: Antioxidantes/farmacologia
Chalconas/farmacologia
Cumarínicos/farmacologia
Ácidos Fíbricos/farmacologia
PPAR alfa/agonistas
PPAR gama/agonistas
[Mh] Termos MeSH secundário: Antioxidantes/síntese química
Antioxidantes/química
Chalconas/química
Cumarínicos/química
Relação Dose-Resposta a Droga
Desenho de Drogas
Ácidos Fíbricos/síntese química
Ácidos Fíbricos/química
Seres Humanos
Simulação de Acoplamento Molecular
Estrutura Molecular
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Chalcones); 0 (Coumarins); 0 (Fibric Acids); 0 (PPAR alpha); 0 (PPAR gamma)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170702
[St] Status:MEDLINE


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[PMID]:28391898
[Au] Autor:Nobecourt E; Cariou B; Lambert G; Krempf M
[Ad] Endereço:Department of Endocrinology, Metabolic diseases and Nutrition, l'institut du thorax, CHU de Nantes, Nantes, France; CRNH, Human Nutrition Research Center, CHU, Nantes, France; INRA, UMR 1280, Physiologie des Adaptations Nutritionnelles, CHU Hôtel-Dieu, Nantes, France. Electronic address: estelle.nob
[Ti] Título:Severe decrease in high-density lipoprotein cholesterol with the combination of fibrates and ezetimibe: A case series.
[So] Source:J Clin Lipidol;11(1):289-293, 2017 Jan - Feb.
[Is] ISSN:1933-2874
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A sudden and severe drug-induced decrease in plasma high-density lipoprotein cholesterol (HDL-C) is a rare condition. We report 2 patients with familial hypercholesterolemia treated with statins and fibrates and 2 others with mixed dyslipidemia treated with fibrates, who presented with a sudden and severe decrease in HDL-C (from -44% to -95%, compared with baseline). Three of the patients were treated with fibrates and had a sudden decrease in HDL-C after the adjunction of ezetimibe. HDL-C returned to normal levels after discontinuation of the offending therapies. In 2 of these patients, the reintroduction of ezetimibe with no fibrates did not affect HDL-C. In conclusion, we report a new profile of patients who are at risk for a sudden drop of HDL-C related to treatment with a combination of fibrates and ezetimibe. Although a sudden drop of HDL-C is a rare event, we recommend to carefully monitor plasma HDL-C in patients submitted to both drugs.
[Mh] Termos MeSH primário: HDL-Colesterol/sangue
Ezetimiba/farmacologia
Ácidos Fíbricos/farmacologia
[Mh] Termos MeSH secundário: Interações Medicamentosas
Ezetimiba/uso terapêutico
Ácidos Fíbricos/uso terapêutico
Seres Humanos
Hiperlipoproteinemia Tipo II/sangue
Hiperlipoproteinemia Tipo II/tratamento farmacológico
Masculino
Meia-Idade
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cholesterol, HDL); 0 (Fibric Acids); EOR26LQQ24 (Ezetimibe)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170411
[St] Status:MEDLINE


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[PMID]:28343425
[Au] Autor:Ferri N; Corsini A; Sirtori C; Ruscica M
[Ad] Endereço:a Dipartimento di Scienze del Farmaco , Università degli Studi di Padova , Padua , Italy.
[Ti] Título:PPAR-α agonists are still on the rise: an update on clinical and experimental findings.
[So] Source:Expert Opin Investig Drugs;26(5):593-602, 2017 May.
[Is] ISSN:1744-7658
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Non-fasting plasma triglyceride (TG) and remnant cholesterol levels, cholesterol content of triglyceride-rich lipoproteins, have been suggested to be an additional cause of cardiovascular diseases; thus, pharmacological TG-lowering with fibrates, activators of PPAR-alpha system, has been linked to risk reduction. Areas covered: This manuscript reviews available evidence on clinical trials involving highly selective PPAR-α agonists (i.e., pemafibrate) and drugs used in the pre-clinical and experimental setting (e.g., WY14,643). Original publications in English were selected, as well as Abstracts of international meetings' presentations. Clinical trials were identified using the clinicaltrial.gov database and the EU Clinical Trials Register (clinicaltrialsregister.eu). Expert opinion: In addition to the aim of improving lipid profile with fibrates, the interest in new PPAR-α activators stems from the need to overcome some of the clinical problems encountered with dose-dependent adverse events; a rise of plasma creatinine, gallstone formation, drug-drug interactions (i.e. gemfibrozil), and myopathy. New PPAR-α agonists improved TG and HDL-C levels as well as other parameters related to TG metabolism (remnant cholesterol and apoB), without raising liver enzymes. Although the use of fibrates is rated 'second choice' by many clinicians, new PPAR-α agonists may offer a more accessible route to the management of hypertriglyceridemia, a frequent clinical condition.
[Mh] Termos MeSH primário: Doenças Cardiovasculares/prevenção & controle
Hipolipemiantes/farmacologia
PPAR alfa/agonistas
[Mh] Termos MeSH secundário: Animais
Doenças Cardiovasculares/etiologia
Desenho de Drogas
Dislipidemias/complicações
Dislipidemias/tratamento farmacológico
Ácidos Fíbricos/farmacologia
Ácidos Fíbricos/uso terapêutico
Seres Humanos
Hipolipemiantes/uso terapêutico
Lipídeos/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Fibric Acids); 0 (Hypolipidemic Agents); 0 (Lipids); 0 (PPAR alpha)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170605
[Lr] Data última revisão:
170605
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170328
[St] Status:MEDLINE
[do] DOI:10.1080/13543784.2017.1312339


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[PMID]:28153024
[Au] Autor:Sahebkar A; Simental-Mendía LE; Watts GF; Serban MC; Banach M; Lipid and Blood Pressure Meta-analysis Collaboration (LBPMC) Group
[Ad] Endereço:Biotechnology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. sahebkara@mums.ac.ir.
[Ti] Título:Comparison of the effects of fibrates versus statins on plasma lipoprotein(a) concentrations: a systematic review and meta-analysis of head-to-head randomized controlled trials.
[So] Source:BMC Med;15(1):22, 2017 Feb 03.
[Is] ISSN:1741-7015
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Raised plasma lipoprotein(a) (Lp(a)) concentration is an independent and causal risk factor for atherosclerotic cardiovascular disease. Several types of pharmacological approaches are under evaluation for their potential to reduce plasma Lp(a) levels. There is suggestive evidence that statins and fibrates, two frequently employed lipid-lowering drugs, can lower plasma Lp(a). The present study aims to compare the efficacy of fibrates and statins in reducing plasma concentrations of Lp(a) using a meta-analysis of randomized head-to-head trials. METHODS: Medline and Scopus databases were searched to identify randomized head-to-head comparative trials investigating the efficacy of fibrates versus statins in reducing plasma Lp(a) levels. Meta-analysis was performed using a random-effects model, with inverse variance weighted mean differences (WMDs) and 95% confidence intervals (CIs) as summary statistics. The impact of putative confounders on the estimated effect size was explored using random effects meta-regression. RESULTS: Sixteen head-to-head comparative trials with a total of 1388 subjects met the eligibility criteria and were selected for this meta-analysis. Meta-analysis revealed a significantly greater effect of fibrates versus statins in reducing plasma Lp(a) concentrations (WMD, -2.70 mg/dL; 95% CI, -4.56 to -0.84; P = 0.004). Combination therapy with fibrates and statins had a significantly greater effect compared with statin monotherapy (WMD, -1.60 mg/dL; 95% CI, -2.93 to -0.26; P = 0.019) but not fibrate monotherapy (WMD, -1.76 mg/dL; 95% CI, -5.44 to +1.92; P = 0.349) in reducing plasma Lp(a) concentrations. The impact of fibrates versus statins in reducing plasma Lp(a) concentrations was not found to be significantly associated with treatment duration (P = 0.788). CONCLUSIONS: Fibrates have a significantly greater effect in reducing plasma Lp(a) concentrations than statins. Addition of fibrates to statins can enhance the Lp(a)-lowering effect of statins.
[Mh] Termos MeSH primário: Ácidos Fíbricos/administração & dosagem
Inibidores de Hidroximetilglutaril-CoA Redutases/administração & dosagem
Lipoproteína(a)/sangue
[Mh] Termos MeSH secundário: Aterosclerose/sangue
Feminino
Ácidos Fíbricos/farmacologia
Seres Humanos
Inibidores de Hidroximetilglutaril-CoA Redutases/farmacologia
Ensaios Clínicos Controlados Aleatórios como Assunto
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Fibric Acids); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Lipoprotein(a))
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170524
[Lr] Data última revisão:
170524
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170204
[St] Status:MEDLINE
[do] DOI:10.1186/s12916-017-0787-7


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[PMID]:28077274
[Au] Autor:Kersten S; Stienstra R
[Ad] Endereço:Nutrition, Metabolism and Genomics Group, Division of Human Nutrition, Wageningen University, The Netherlands. Electronic address: sander.kersten@wur.nl.
[Ti] Título:The role and regulation of the peroxisome proliferator activated receptor alpha in human liver.
[So] Source:Biochimie;136:75-84, 2017 May.
[Is] ISSN:1638-6183
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:The peroxisome proliferator-activated receptor α (PPARα) is a ligand-activated transcription factor that is abundantly expressed in liver. PPARα is activated by fatty acids and various other lipid species, as well as by a class of chemicals referred to as peroxisome proliferators. Studies in mice have shown that PPARα serves as the master regulator of hepatic lipid metabolism during fasting. In addition, PPARα suppresses inflammation and the acute phase response. Comparatively little is known about PPARα in human liver. Here, an overview is provided of the role and regulation of PPARα in human liver. The main outcomes are: 1) the level of PPARA mRNA expression in human and mouse liver is similar. 2) Expression of PPARA in human liver is reduced in patients with non-alcoholic steatohepatitis or infected with the hepatitis C virus. 3) PPARα in human liver is able to effectively induce the expression of numerous genes involved in numerous lipid metabolic pathways, including microsomal, peroxisomal and mitochondrial fatty acid oxidation, fatty acid binding and activation, fatty acid elongation and desaturation, synthesis and breakdown of triglycerides and lipid droplets, lipoprotein metabolism, gluconeogenesis, bile acid metabolism, and various other metabolic pathways and genes. 4) PPARα activation in human liver causes the down-regulation of a large number of genes involved in various immunity-related pathways. 5) Peroxisome proliferators do not promote tumour formation in human liver as opposed to mouse liver because of structural and functional differences between human and mouse PPARα. 6) In addition to helping to correct dyslipidemia, PPARα agonists may hold promise as a therapy for patients with cholestatic liver diseases, non-alcoholic fatty liver disease, and/or type 2 diabetes.
[Mh] Termos MeSH primário: Fígado/fisiopatologia
PPAR alfa/fisiologia
[Mh] Termos MeSH secundário: Animais
Ácidos Fíbricos/uso terapêutico
Regulação da Expressão Gênica
Seres Humanos
Ligantes
Metabolismo dos Lipídeos
Fígado/efeitos dos fármacos
Fígado/metabolismo
Camundongos
Modelos Biológicos
Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico
Hepatopatia Gordurosa não Alcoólica/metabolismo
PPAR alfa/efeitos dos fármacos
PPAR alfa/genética
PPAR alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Fibric Acids); 0 (Ligands); 0 (PPAR alpha)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170524
[Lr] Data última revisão:
170524
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170113
[St] Status:MEDLINE


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[PMID]:27956003
[Au] Autor:Ballantyne CM; Shah S; Kher U; Hunter JA; Gill GG; Cressman MD; Ashraf TB; Johnson-Levonas AO; Mitchel YB
[Ad] Endereço:Section of Cardiovascular Research, Department of Medicine, Baylor College of Medicine, Houston, Texas. Electronic address: cmb@bcm.edu.
[Ti] Título:Lipid-Modifying Efficacy and Tolerability of Anacetrapib Added to Ongoing Statin Therapy in Patients with Hypercholesterolemia or Low High-Density Lipoprotein Cholesterol.
[So] Source:Am J Cardiol;119(3):388-396, 2017 Feb 01.
[Is] ISSN:1879-1913
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:To assess the effects of anacetrapib added to statin ± other lipid-modifying therapies in patients with hypercholesterolemia and not at their low-density lipoprotein cholesterol (LDL-C) goal (as per National Cholesterol Education Program Adult Treatment Panel III [NCEP ATP III] guidelines) and in those with low high-density lipoprotein cholesterol (HDL-C). Patients on a stable dose of moderate/high-intensity statin ± other lipid-modifying therapies with LDL-C ≥70, ≥100, ≥130, or ≥160 mg/dl for very high, high, moderate, and low coronary heart disease risk, respectively, or at LDL-C goal with HDL-C ≤40 mg/dl, were randomized 1:1:1, stratified by background therapy use, to anacetrapib 100 mg (n = 153), anacetrapib 25 mg (n = 152), or placebo (n = 154) for 24 weeks, followed by a 12-week off-drug reversal phase. The primary end points were percent change from baseline in LDL-C (beta-quantification method) and HDL-C, as well as the safety profile of anacetrapib. Both doses of anacetrapib reduced LDL-C, non-HDL-C, apolipoprotein (Apo) B, and lipoprotein a and increased HDL-C and Apo AI versus placebo (p <0.001 for all). There were no meaningful differences between the anacetrapib 25 mg, 100 mg, and placebo groups in the proportions of discontinuations due to drug-related adverse events (0.7%, 1.3% vs 1.3%) or in abnormalities in liver enzymes (0%, 0% vs 0.7%), creatine kinase elevations overall (0%, 0.7% vs 0%) or with muscle symptoms (none seen), blood pressure, electrolytes, or adjudicated cardiovascular events (0.7%, 0.7% vs 1.3%). In conclusion, treatment with anacetrapib resulted in substantial reductions in LDL-C and increases in HDL-C and was generally well tolerated.
[Mh] Termos MeSH primário: Anticolesterolemiantes/uso terapêutico
Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico
Hipercolesterolemia/tratamento farmacológico
Oxazolidinonas/uso terapêutico
[Mh] Termos MeSH secundário: Idoso
Proteínas de Transferência de Ésteres de Colesterol/antagonistas & inibidores
HDL-Colesterol/sangue
LDL-Colesterol/sangue
Método Duplo-Cego
Quimioterapia Combinada
Dislipidemias/sangue
Dislipidemias/tratamento farmacológico
Ezetimiba/uso terapêutico
Feminino
Ácidos Fíbricos/uso terapêutico
Seres Humanos
Hipercolesterolemia/sangue
Masculino
Meia-Idade
Niacina/uso terapêutico
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Anticholesteremic Agents); 0 (Cholesterol Ester Transfer Proteins); 0 (Cholesterol, HDL); 0 (Cholesterol, LDL); 0 (Fibric Acids); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Oxazolidinones); 2679MF687A (Niacin); EOR26LQQ24 (Ezetimibe); P7T269PR6S (anacetrapib)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170524
[Lr] Data última revisão:
170524
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161214
[St] Status:MEDLINE


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[PMID]:27890243
[Au] Autor:Nichols GA; Reynolds K; Olufade T; Kimes TM; O'Keeffe-Rosetti M; Sapp DS; Anzalone D; Fortmann SP
[Ad] Endereço:Kaiser Permanente Center for Health Research, Science Programs Department, Portland, Oregon. Electronic address: greg.nichols@kpchr.org.
[Ti] Título:Effect of Combination Cholesterol-Lowering Therapy and Triglyceride-Lowering Therapy on Medical Costs in Patients With Type 2 Diabetes Mellitus.
[So] Source:Am J Cardiol;119(3):410-415, 2017 Feb 01.
[Is] ISSN:1879-1913
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:High triglyceride (TG) levels among patients with type 2 diabetes mellitus (DM) are associated with higher medical costs. We analyzed the economic impact of TG-lowering therapies and whether the association between medical costs and therapy differed according to TG reduction. We conducted an observational cohort study of 184,932 patients with diabetes mellitus who had a TG measurement between January 2012 and June 2013 and a second TG measurement 3 to 15 months later. We identified 4 therapy groups (statin monotherapy, TG-specific monotherapy, statin/TG-specific combination therapy, or no therapy) and stratified those groups by percent change in TG (increased ≥5%, change of ≤4.9%, decreased 5% to 29%, decreased ≥30%). We compared change in medical costs between the year before and after therapy, adjusted for demographic and clinical characteristics. Of the 184,932 total patients, 143,549 (77.6%) received statin monotherapy, 900 (0.5%) received TG-specific monotherapy, 1,956 (1.1%) received statin and TG-specific combination therapy, and 38,527 (20.8%) received no prescription lipid agents. After covariate adjustment, statin/TG-specific agent recipients had a mean 1-year total cost reduction of $1,110. The greatest cost reduction was seen among statin/TG-specific combination therapy patients who reduced TG levels by ≥30% (-$2,859). Statin monotherapy patients who reduced TG by ≥30% also had a large reduction in adjusted costs (-$1,079). In conclusion, we found a substantial economic benefit to treating diabetic patients with statin/TG-specific combination lipid therapy compared with monotherapy of either type or no lipid pharmacotherapy. A TG reduction of ≥30% produced a particularly large reduction in 1-year medical costs.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/complicações
Custos de Cuidados de Saúde
Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico
Hipercolesterolemia/tratamento farmacológico
Hipertrigliceridemia/tratamento farmacológico
Hipolipemiantes/uso terapêutico
[Mh] Termos MeSH secundário: Idoso
HDL-Colesterol/sangue
LDL-Colesterol/sangue
Estudos de Coortes
Análise Custo-Benefício
Diabetes Mellitus Tipo 2/economia
Quimioterapia Combinada
Ácidos Graxos Ômega-3/uso terapêutico
Feminino
Ácidos Fíbricos/uso terapêutico
Seres Humanos
Hipercolesterolemia/complicações
Hipercolesterolemia/economia
Hipertrigliceridemia/complicações
Hipertrigliceridemia/economia
Masculino
Meia-Idade
Niacina/uso terapêutico
Estudos Retrospectivos
Triglicerídeos/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Cholesterol, HDL); 0 (Cholesterol, LDL); 0 (Fatty Acids, Omega-3); 0 (Fibric Acids); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Hypolipidemic Agents); 0 (Triglycerides); 2679MF687A (Niacin)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170524
[Lr] Data última revisão:
170524
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161129
[St] Status:MEDLINE


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[PMID]:27819772
[Au] Autor:Handelsman Y; Shapiro MD
[Ti] Título:TRIGLYCERIDES, ATHEROSCLEROSIS, AND CARDIOVASCULAR OUTCOME STUDIES: FOCUS ON OMEGA-3 FATTY ACIDS.
[So] Source:Endocr Pract;23(1):100-112, 2017 Jan.
[Is] ISSN:1530-891X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To provide an overview of the roles of triglycerides and triglyceride-lowering agents in atherosclerosis in the context of cardiovascular outcomes studies. METHODS: We reviewed the published literature as well as ClinicalTrials.gov entries for ongoing studies. RESULTS: Despite improved atherosclerotic cardiovascular disease (ASCVD) outcomes with statin therapy, residual risk remains. Epidemiologic data and recent genetic insights provide compelling evidence that triglycerides are in the causal pathway for the development of atherosclerosis, thereby renewing interest in targeting triglycerides to improve ASCVD outcomes. Fibrates, niacin, and omega-3 fatty acids (OM3FAs) are three classes of triglyceride-lowering drugs. Outcome studies with triglyceride-lowering agents have been inconsistent. With regard to OM3FAs, the JELIS study showed that eicosapentaenoic acid (EPA) significantly reduced major coronary events in statin-treated hypercholesterolemic patients. Regarding other agents, extended-release niacin and fenofibrate are no longer recommended as statin add-on therapy (by some guidelines, though not all) because of the lack of convincing evidence from outcome studies. Notably, subgroup analyses from the outcome studies have generated the hypothesis that triglyceride lowering may provide benefit in statin-treated patients with persistent hypertriglyceridemia. Two ongoing OM3FA outcome studies (REDUCE-IT and STRENGTH) are testing this hypothesis in high-risk, statin-treated patients with triglyceride levels of 200 to 500 mg/dL. CONCLUSION: There is consistent evidence that triglycerides are in the causal pathway of atherosclerosis but inconsistent evidence from cardiovascular outcomes studies as to whether triglyceride-lowering agents reduce cardiovascular risk. Ongoing outcomes studies will determine the role of triglyceride lowering in statin-treated patients with high-dose prescription OM3FAs in terms of improved ASCVD outcomes. ABBREVIATIONS: AACE = American Association of Clinical Endocrinologists ACCORD = Action to Control Cardiovascular Risk in Diabetes AIM-HIGH = Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides: Impact on Global Health Outcomes apo = apolipoprotein ASCEND = A Study of Cardiovascular Events in Diabetes ASCVD = atherosclerotic cardiovascular disease BIP = Bezafibrate Infarction Prevention CHD = coronary heart disease CI = confidence interval CV = cardiovascular CVD = cardiovascular disease DHA = docosahexaenoic acid DO-IT = Diet and Omega-3 Intervention Trial EPA = eicosapentaenoic acid FIELD = Fenofibrate Intervention and Event Lowering in Diabetes GISSI-HF = GISSI-Heart Failure HDL-C = high-density-lipoprotein cholesterol HPS2-THRIVE = Heart Protection Study 2-Treatment of HDL to Reduce the Incidence of Vascular Events HR = hazard ratio JELIS = Japan Eicosapentaenoic Acid Lipid Intervention Study LDL = low-density lipoprotein LDL-C = low-density-lipoprotein cholesterol MI = myocardial infarction OM3FAs = omega-3 fatty acids VITAL = Vitamin D and Omega-3 Trial.
[Mh] Termos MeSH primário: Aterosclerose/prevenção & controle
Ácidos Graxos Ômega-3/uso terapêutico
Hipertrigliceridemia/tratamento farmacológico
Hipolipemiantes/uso terapêutico
[Mh] Termos MeSH secundário: Aterosclerose/metabolismo
Doenças Cardiovasculares/metabolismo
Doenças Cardiovasculares/prevenção & controle
Fenofibrato/uso terapêutico
Ácidos Fíbricos/uso terapêutico
Seres Humanos
Hipertrigliceridemia/metabolismo
Niacina/uso terapêutico
Triglicerídeos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Fatty Acids, Omega-3); 0 (Fibric Acids); 0 (Hypolipidemic Agents); 0 (Triglycerides); 2679MF687A (Niacin); U202363UOS (Fenofibrate)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170622
[Lr] Data última revisão:
170622
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161108
[St] Status:MEDLINE
[do] DOI:10.4158/EP161445.RA



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