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[PMID]:28382723
[Au] Autor:De Marco V; Noronha KSM; Casado TC; Nakandakare ER; Florio JC; Santos EZ; Gilor C
[Ad] Endereço:University of Santo Amaro, São Paulo, Brazil.
[Ti] Título:Therapy of Canine Hyperlipidemia with Bezafibrate.
[So] Source:J Vet Intern Med;31(3):717-722, 2017 May.
[Is] ISSN:1939-1676
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Bezafibrate (BZF) is effective in the treatment of hypertriglyceridemia in human patients, but there are no data on its use in dogs. OBJECTIVE: To assess the safety of BZF in hyperlipidemic dogs and its efficacy in decreasing serum triglyceride (TG) and cholesterol (CHO) concentrations. ANIMALS: Forty-six dogs, 26 females and 20 males, mean (±SD) age of 9 (±3) years, with TG ≥150 mg/dL (33 dogs also were hypercholesterolemic [>300 mg/dL]). METHODS: Prospective, uncontrolled clinical trial. Dogs were treated with bezafibrate once daily, using 200 mg tablets at a dosage of 4-10 mg/kg (depending on body weight). Serum TG and CHO concentrations and alanine aminotransferase (ALT) and creatine kinase (CK) activity before and after 30 days of treatment were compared. RESULTS: Sixteen dogs (34.8%) had primary hyperlipidemia, and 30 dogs (65.2%) had secondary hyperlipidemia (including spontaneous hyperadrenocorticism [41.3%, n = 19/46], chronic treatment with glucocorticoids [10.8%, n = 5/46], and hypothyroidism [15.2%, n = 7/46]). After 30 days, serum TG concentration normalized (<150 mg/dL) in 42 dogs (91.3%) and CHO concentration normalized (<270 mg/dL) in 22 of 33 dogs (66.7%). There was no difference in baseline TG concentration between the primary and secondary hyperlipidemia subgroups, but the decrease in TG concentration after treatment was greater in the primary hyperlipidemia subgroup. No adverse effects were observed, but ALT activity decreased significantly after 30 days of treatment. CONCLUSIONS AND CLINICAL IMPORTANCE: Over 30 days, BZF was safe and effective in treatment of primary and secondary hyperlipidemia in dogs.
[Mh] Termos MeSH primário: Bezafibrato/uso terapêutico
Doenças do Cão/tratamento farmacológico
Hiperlipidemias/veterinária
Hipolipemiantes/uso terapêutico
[Mh] Termos MeSH secundário: Administração Oral
Animais
Bezafibrato/administração & dosagem
Doenças do Cão/sangue
Cães
Feminino
Hiperlipidemias/tratamento farmacológico
Hipolipemiantes/administração & dosagem
Masculino
Estudos Prospectivos
Resultado do Tratamento
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hypolipidemic Agents); Y9449Q51XH (Bezafibrate)
[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:170407
[St] Status:MEDLINE
[do] DOI:10.1111/jvim.14701


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[PMID]:28118709
[Au] Autor:Sui Q; Gebhardt W; Schröder HF; Zhao W; Lu S; Yu G
[Ad] Endereço:State Environmental Protection Key Laboratory of Environmental Risk Assessment and Control on Chemical Process, School of Resources and Environmental Engineering, East China University of Science and Technology , 200237, Shanghai, China.
[Ti] Título:Identification of New Oxidation Products of Bezafibrate for Better Understanding of Its Toxicity Evolution and Oxidation Mechanisms during Ozonation.
[So] Source:Environ Sci Technol;51(4):2262-2270, 2017 Feb 21.
[Is] ISSN:1520-5851
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bezafibrate (BF), a frequently detected pharmaceutical in the aquatic environment, could be effectively removed by ozonation. However, the toxicity of treated water increased, suggesting the generation of toxic oxidation products (OPs). In this study, eight OPs of BF ozonation were identified using a LTQ Orbitrap hybrid mass spectrometer coupled with HPLC, and six of them have not been previously reported during BF ozonation. Based on the abundant fragments and high assurance of accurate molar mass, structure elucidation was comprehensively performed and discussed. Hydroxylation, loss of methyl propionic acid group, and Crigée mechanism were observed as the oxidation mechanisms of BF ozonation. The toxicity of identified OPs calculated by quantitative structure activity relationship indicated that three OPs were probably more toxic than the precursor compound BF. This result together with the evolution of identified OPs in the treated solutions, indicated that two OPs, namely N-(3,4-dihydroxyphenethyl)-4-chlorobenzamide and N-(2,4-dihydroxyphenethyl)-4-chlorobenzamide, were the potential toxicity-causing OPs during BF ozonation. To the best of our knowledge, this is the first attempt to identify toxicity-causing OPs during the BF ozonation.
[Mh] Termos MeSH primário: Bezafibrato
Purificação da Água
[Mh] Termos MeSH secundário: Oxirredução
Ozônio/química
Poluentes Químicos da Água/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Water Pollutants, Chemical); 66H7ZZK23N (Ozone); Y9449Q51XH (Bezafibrate)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170609
[Lr] Data última revisão:
170609
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170126
[St] Status:MEDLINE
[do] DOI:10.1021/acs.est.6b03548


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[PMID]:27886564
[Au] Autor:Weinstein G; Lutski M; Goldbourt U; Tanne D
[Ad] Endereço:School of Public Health, Faculty of Social Welfare and Health Sciences, University of Haifa, Haifa, Israel. Electronic address: galitwai@bu.edu.
[Ti] Título:C-reactive protein is related to future cognitive impairment and decline in elderly individuals with cardiovascular disease.
[So] Source:Arch Gerontol Geriatr;69:31-37, 2017 Mar - Apr.
[Is] ISSN:1872-6976
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: To explore the association of C-reactive protein (CRP) plasma levels with subsequent cognitive performance and decline among elderly individuals with pre-existing cardiovascular disease (CVD), and to assess the role of cerebrovascular indices in this relationship. METHODS: CRP levels were measured in a subgroup of individuals with chronic CVD, who previously participated in a secondary prevention trial. Cognitive performance was evaluated 14.7±1.9 and 19.9±1.0years after entry to the trial. A validated set of computerized cognitive tests was used (Neurotrax Computerized Cognitive Battery) to assess performance globally and in memory, executive function, visuospatial and attention domains. Linear regression and mixed models were used to assess the relationship of CRP plasma levels with cognitive scores and decline, respectively. In addition, we tested whether cerebrovascular reactivity, carotid intima media thickness and presence of carotid plaques modify these associations. RESULTS: Among 536 participants (mean age at the first cognitive evaluation 72.6±6.4years; 95% males), CRP at the top tertile vs. the rest was associated with subsequent poorer performance overall (ß=-2.2±1.0; p=0.031) and on tests of executive function and attention (ß=-2.3±1.1; p=0.043 and ß=-2.0±1.4; p=0.047, respectively). Moreover, CRP levels were positively related to a greater decline in executive functions (ß=-2.4±1.1; p=0.03). These associations were independent of potential confounders and were not modified by cerebrovascular indices. CONCLUSION: Our findings suggest that systemic chronic inflammation, potentially associated with underlying atherosclerosis, is related to cognitive impairment and decline two decades later, in elderly individuals with pre-existing CVD.
[Mh] Termos MeSH primário: Atenção/fisiologia
Proteína C-Reativa/metabolismo
Doenças Cardiovasculares/sangue
Cognição/fisiologia
Disfunção Cognitiva/sangue
[Mh] Termos MeSH secundário: Idoso
Bezafibrato/administração & dosagem
Biomarcadores/sangue
Doenças Cardiovasculares/complicações
Doenças Cardiovasculares/prevenção & controle
Espessura Intima-Media Carotídea
Disfunção Cognitiva/complicações
Disfunção Cognitiva/diagnóstico
Relação Dose-Resposta a Droga
Feminino
Seres Humanos
Hipolipemiantes/administração & dosagem
Inflamação/sangue
Inflamação/complicações
Israel/epidemiologia
Masculino
Meia-Idade
Prevalência
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Biomarkers); 0 (Hypolipidemic Agents); 9007-41-4 (C-Reactive Protein); Y9449Q51XH (Bezafibrate)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170705
[Lr] Data última revisão:
170705
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161126
[St] Status:MEDLINE


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[PMID]:27591119
[Au] Autor:Yamada K; Kobayashi H; Bo R; Purevsuren J; Mushimoto Y; Takahashi T; Hasegawa Y; Taketani T; Fukuda S; Yamaguchi S
[Ad] Endereço:Department of Pediatrics, Shimane University, Faculty of Medicine, Izumo, Shimane, Japan. Electronic address: k-yamada@med.shimane-u.ac.jp.
[Ti] Título:Efficacy of bezafibrate on fibroblasts of glutaric acidemia type II patients evaluated using an in vitro probe acylcarnitine assay.
[So] Source:Brain Dev;39(1):48-57, 2017 Jan.
[Is] ISSN:1872-7131
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: We evaluated the effects of bezafibrate (BEZ) on ß-oxidation in fibroblasts obtained from patients with glutaric acidemia type II (GA2) of various clinical severities using an in vitro probe (IVP) assay. METHODS: Cultured fibroblasts from 12 patients with GA2, including cases of the neonatal-onset type both with and without congenital anomalies (the prenatal- and neonatal-onset forms, respectively), the infantile-onset, and the myopathic forms, were studied. The IVP assay was performed by measuring acylcarnitines (ACs) in the cell culture medium of fibroblasts incubated with palmitic acid for 96h in the presence of 0-800µM BEZ using tandem mass spectrometry. RESULTS: The IVP assay showed that 100µM BEZ markedly reduced the level of palmitoylcarnitine (C16) in the neonatal-onset, infantile-onset, and myopathic forms of GA2, either increasing or maintaining a high level of acetylcarnitine (C2), which serves as an index of energy production via ß-oxidation. In the prenatal-onset form, although a small reduction of C16 was also observed in the presence of 100µM BEZ, the level of C2 remained low. At concentrations higher than 100µM, BEZ further decreased the level of ACs including C16, but a concentration over 400µM decreased the level of C2 in most cases. DISCUSSION: BEZ at 100µM was effective for all GA2 phenotypes except for the prenatal-onset form, as a reduction of C16 without deterioration of C2 is considered to indicate improvement of ß-oxidation. The effects of higher doses BEZ could not be estimated by the IVP assay but might be small or nonexistent.
[Mh] Termos MeSH primário: Bezafibrato/farmacologia
Carnitina/análogos & derivados
Fibroblastos/efeitos dos fármacos
Reguladores do Metabolismo de Lipídeos/farmacologia
Deficiência Múltipla de Acil Coenzima A Desidrogenase/tratamento farmacológico
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idade de Início
Carnitina/metabolismo
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Relação Dose-Resposta a Droga
Avaliação Pré-Clínica de Medicamentos
Ativadores de Enzimas/farmacologia
Feminino
Fibroblastos/metabolismo
Seres Humanos
Lactente
Recém-Nascido
Masculino
Deficiência Múltipla de Acil Coenzima A Desidrogenase/metabolismo
Palmitoilcarnitina/metabolismo
Receptores Ativados por Proliferador de Peroxissomo/agonistas
Pele/citologia
Pele/efeitos dos fármacos
Pele/metabolismo
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Enzyme Activators); 0 (Lipid Regulating Agents); 0 (Peroxisome Proliferator-Activated Receptors); 0 (acylcarnitine); 1935-18-8 (Palmitoylcarnitine); S7UI8SM58A (Carnitine); Y9449Q51XH (Bezafibrate)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170214
[Lr] Data última revisão:
170214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160904
[St] Status:MEDLINE


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[PMID]:27849333
[Au] Autor:Jakob T; Nordmann AJ; Schandelmaier S; Ferreira-González I; Briel M
[Ad] Endereço:Basel Institute for Clinical Epidemiology and Biostatistics, University Hospital Basel, Basel, Switzerland.
[Ti] Título:Fibrates for primary prevention of cardiovascular disease events.
[So] Source:Cochrane Database Syst Rev;11:CD009753, 2016 11 16.
[Is] ISSN:1469-493X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Fibrates are effective for modifying atherogenic dyslipidaemia, and particularly for lowering serum triglycerides. However, evidence that fibrates reduce mortality and morbidity associated with cardiovascular disease (CVD), or overall mortality and morbidity, in the primary prevention of CVD is lacking. OBJECTIVES: This Cochrane Review and meta-analysis aimed to evaluate the clinical benefits and harms of fibrates versus placebo or usual care or fibrates plus other lipid-modifying drugs versus other lipid-modifying drugs alone for the primary prevention of cardiovascular disease (CVD) morbidity and mortality. SEARCH METHODS: We searched the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE (Ovid), Embase (Ovid), CINAHL (EBSCO), and Web of Science (all from inception to 19 May 2016). We searched four clinical trial registers (last searched on 3 August 2016) with the help of an experienced professional librarian. We searched the databases to identify randomised controlled trials (RCTs) evaluating the clinical effects of fibrate therapy in the primary prevention of CVD events. We did not impose any language restrictions. SELECTION CRITERIA: We aimed to include all RCTs comparing the effects of fibrate monotherapy versus placebo or usual care, or fibrates plus other lipid-modifying drugs versus other lipid-modifying drugs alone. Included studies had a follow-up of at least six months for the primary prevention of CVD events. We excluded trials with clofibrate, because it was withdrawn from the market in 2002. DATA COLLECTION AND ANALYSIS: Two review authors independently screened titles and abstracts for potential study inclusion. Two review authors independently retrieved the full-text papers and extracted data. Disagreements were resolved by consensus. We calculated risk ratios (RRs) and accompanying 95% confidence intervals (CIs) for aggregate data on primary and secondary outcomes. We tested for heterogeneity with the Cochrane Q-test and used the I statistic to measure inconsistency of treatment effects across studies. Using the GRADE approach, we assessed the quality of the evidence and used the GRADE profiler software (GRADEpro GDT) to import data from Review Manager 5 to create 'Summary of findings' tables. MAIN RESULTS: We identified six eligible trials including 16,135 individuals. The mean age of trial populations varied across trials; between 47.3 and 62.3 years. Four trials included individuals with diabetes mellitus type 2 only. The mean treatment duration and follow-up of participants across trials was 4.8 years. We judged the risks of selection and performance bias to be low; risks of detection bias, attrition bias, and reporting bias were unclear. Reporting of adverse effects by included trials was very limited; that is why we used discontinuation of therapy due to adverse effects as a proxy for adverse effects. Patients treated with fibrates had a reduced risk for the combined primary outcome of CVD death, non-fatal myocardial infarction, or non-fatal stroke compared to patients on placebo (risk ratio (RR) 0.84, 95% confidence interval (CI) 0.74 to 0.96; participants = 16,135; studies = 6; moderate-quality of evidence). For secondary outcomes we found RRs for fibrate therapy compared with placebo of 0.79 for combined coronary heart disease death or non-fatal myocardial infarction (95% CI 0.68 to 0.92; participants = 16,135; studies = 6; moderate-quality of evidence); 1.01 for overall mortality (95% CI 0.81 to 1.26; participants = 8471; studies = 5; low-quality of evidence); 1.01 for non-CVD mortality (95% CI 0.76 to 1.35; participants = 8471; studies = 5; low-quality of evidence); and 1.38 for discontinuation of therapy due to adverse effects (95% CI 0.71 to 2.68; participants = 4805; studies = 3; I = 74%; very low-quality of evidence). Data on quality of life were not available from any trial. Trials that evaluated fibrates in the background of statins (2 studies) showed no benefits in preventing cardiovascular events. AUTHORS' CONCLUSIONS: Moderate-quality evidence suggests that fibrates lower the risk for cardiovascular and coronary events in primary prevention, but the absolute treatment effects in the primary prevention setting are modest (absolute risk reductions < 1%). There is low-quality evidence that fibrates have no effect on overall or non-CVD mortality. Very low-quality evidence suggests that fibrates are not associated with increased risk for adverse effects.
[Mh] Termos MeSH primário: Doenças Cardiovasculares/prevenção & controle
Hipolipemiantes/uso terapêutico
Prevenção Primária
[Mh] Termos MeSH secundário: Atorvastatina Cálcica/uso terapêutico
Bezafibrato/uso terapêutico
Doenças Cardiovasculares/mortalidade
Ácido Clofíbrico/análogos & derivados
Ácido Clofíbrico/uso terapêutico
Fenofibrato/uso terapêutico
Genfibrozila/uso terapêutico
Seres Humanos
Hipolipemiantes/efeitos adversos
Meia-Idade
Infarto do Miocárdio/epidemiologia
Infarto do Miocárdio/mortalidade
Prevenção Primária/normas
Sinvastatina/uso terapêutico
Acidente Vascular Cerebral/epidemiologia
Acidente Vascular Cerebral/mortalidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Hypolipidemic Agents); 23TF67G79M (etofibrate); 48A5M73Z4Q (Atorvastatin Calcium); 53PF01Q249 (Clofibric Acid); AGG2FN16EV (Simvastatin); Q8X02027X3 (Gemfibrozil); U202363UOS (Fenofibrate); Y9449Q51XH (Bezafibrate)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161117
[St] Status:MEDLINE


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[PMID]:27793156
[Au] Autor:Younis A; Younis A; Tzur B; Peled Y; Shlomo N; Goldenberg I; Fisman EZ; Tenenbaum A; Klempfner R
[Ad] Endereço:The Leviev Heart Center, Sheba Medical Center, Tel Hashomer, Sheba Road 2, 52620, Ramat Gan, Israel. or.younis@gmail.com.
[Ti] Título:Metabolic syndrome is independently associated with increased 20-year mortality in patients with stable coronary artery disease.
[So] Source:Cardiovasc Diabetol;15(1):149, 2016 Oct 28.
[Is] ISSN:1475-2840
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Data regarding long-term association of metabolic syndrome (MetS) with adverse outcomes are conflicting. We aim to determine the independent association of MetS (based on its different definitions) with 20 year all-cause mortality among patients with stable coronary artery disease (CAD). METHODS: Our study comprised 15,524 patients who were enrolled in the Bezafibrate Infarction Prevention registry between February 1, 1990, and October 31, 1992, and subsequently followed-up for the long-term mortality through December 31, 2014. MetS was defined according to two definitions: The International Diabetes Federation (IDF); and the National Cholesterol Education Program-Third Adult Treatment Panel (NCEP). RESULTS: According to the IDF criteria 2122 (14%) patients had MetS, whereas according to the NCEP definition 7446 (48%) patients had MetS. Kaplan-Meier survival analysis showed that all-cause mortality was significantly higher among patients with MetS defined by both the IDF (67 vs. 61%; log rank-p < 0.001) as well as NCEP (67 vs. 54%; log rank-p < 0.001) criteria. Multivariate adjusted mortality risk was 17% greater [Hazard Ratio (HR) 1.17; 95% Confidence Interval (CI) 1.07-1.28] in patients with MetS according to IDF and 21% (HR 1.21; 95% CI 1.13-1.29) using the NCEP definition. Subgroup analysis demonstrated that long-term increased mortality risk associated with MetS was consistent among most clinical subgroups excepted patients with renal failure (p value for interaction < 0.05). CONCLUSIONS: Metabolic syndrome is independently associated with an increased 20-year all-cause mortality risk among patients with stable CAD. This association was consistent when either the IDF or NCEP definitions were used. Trial registration retrospective registered.
[Mh] Termos MeSH primário: Doença da Artéria Coronariana/mortalidade
Síndrome Metabólica/mortalidade
[Mh] Termos MeSH secundário: Fatores Etários
Idoso
Bezafibrato/uso terapêutico
Distribuição de Qui-Quadrado
Doença da Artéria Coronariana/diagnóstico
Feminino
Seres Humanos
Hipolipemiantes/uso terapêutico
Estimativa de Kaplan-Meier
Masculino
Síndrome Metabólica/diagnóstico
Síndrome Metabólica/tratamento farmacológico
Meia-Idade
Análise Multivariada
Prognóstico
Modelos de Riscos Proporcionais
Ensaios Clínicos Controlados Aleatórios como Assunto
Sistema de Registros
Insuficiência Renal/mortalidade
Estudos Retrospectivos
Medição de Risco
Fatores de Risco
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hypolipidemic Agents); Y9449Q51XH (Bezafibrate)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161030
[St] Status:MEDLINE


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[PMID]:27678447
[Au] Autor:Thériault S; Don-Wauchope A; Chong M; Lali R; Morrison KM; Paré G
[Ad] Endereço:Department of Pathology and Molecular Medicine, McMaster University, Hamilton, ON, Canada.
[Ti] Título:Frameshift mutation in the APOA5 gene causing hypertriglyceridemia in a Pakistani family: Management and considerations for cardiovascular risk.
[So] Source:J Clin Lipidol;10(5):1272-7, 2016 Sep-Oct.
[Is] ISSN:1933-2874
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We report a novel homozygous apolipoprotein A5 (APOA5) frameshift mutation (c.G425del-C, p.Arg143AlafsTer57) identified in a 12-year-old boy of Pakistani origin with severe hypertriglyceridemia (up to 35 mmol/L) and type V hyperlipoproteinemia. The patient did not respond to fibrate therapy, but his condition improved under a very low fat diet, although compliance was suboptimal. Heterozygous status was detected in both parents (consanguineous union) and one sibling, all showing moderate hypertriglyceridemia (between 5 and 10 mmol/L). There was a significant family history of premature cardiovascular disease. The index case was also diagnosed with a coronary artery anomaly. Considering the recently reported association of rare mutations in APOA5 with the risk of early myocardial infarction, we discuss the implications of these findings for the young man and his family.
[Mh] Termos MeSH primário: Apolipoproteína A-V/genética
Grupo com Ancestrais do Continente Asiático/genética
Hipertrigliceridemia/diagnóstico
[Mh] Termos MeSH secundário: Bezafibrato/uso terapêutico
Criança
Análise Mutacional de DNA
Mutação da Fase de Leitura
Seres Humanos
Hipertrigliceridemia/tratamento farmacológico
Hipertrigliceridemia/genética
Masculino
Paquistão
Linhagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APOA5 protein, human); 0 (Apolipoprotein A-V); Y9449Q51XH (Bezafibrate)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160929
[St] Status:MEDLINE


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[PMID]:27629963
[Au] Autor:Shima A; Yasuno T; Yamada K; Yamaguchi M; Kohno R; Yamaguchi S; Kido H; Fukuda H
[Ad] Endereço:Department of Neurology, Saiseikai Noe Hospital, Japan.
[Ti] Título:First Japanese Case of Carnitine Palmitoyltransferase II Deficiency with the Homozygous Point Mutation S113L.
[So] Source:Intern Med;55(18):2659-61, 2016.
[Is] ISSN:1349-7235
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Carnitine palmitoyltransferase II (CPT II) deficiency is a rare inherited disorder related to recurrent episodes of rhabdomyolysis. The adult myopathic form of CPT II deficiency is relatively benign and difficult to diagnose. The point mutation S113L in CPT2 is very common in Caucasian patients, whereas F383Y is the most common mutation among Japanese patients. We herein present a case of CPT II deficiency in a Japanese patient homozygous for the missense mutation S113L. The patient showed a decreased frequency of rhabdomyolysis recurrence after the administration of a diet containing medium-chain triglyceride oil and supplementation with carnitine and bezafibrate.
[Mh] Termos MeSH primário: Bezafibrato/uso terapêutico
Carnitina O-Palmitoiltransferase/deficiência
Carnitina/uso terapêutico
Suplementos Nutricionais
Erros Inatos do Metabolismo Lipídico/dietoterapia
Erros Inatos do Metabolismo/dietoterapia
Rabdomiólise/diagnóstico
[Mh] Termos MeSH secundário: Grupo com Ancestrais do Continente Asiático
Bezafibrato/sangue
Carnitina/sangue
Carnitina O-Palmitoiltransferase/sangue
Carnitina O-Palmitoiltransferase/genética
Homozigoto
Seres Humanos
Erros Inatos do Metabolismo Lipídico/sangue
Erros Inatos do Metabolismo Lipídico/genética
Masculino
Erros Inatos do Metabolismo/sangue
Erros Inatos do Metabolismo/genética
Meia-Idade
Mutação Puntual
Rabdomiólise/dietoterapia
Rabdomiólise/genética
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.3.1.21 (Carnitine O-Palmitoyltransferase); S7UI8SM58A (Carnitine); Y9449Q51XH (Bezafibrate)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170519
[Lr] Data última revisão:
170519
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160916
[St] Status:MEDLINE
[do] DOI:10.2169/internalmedicine.55.6288


  9 / 1134 MEDLINE  
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[PMID]:27511723
[Au] Autor:Sakamoto T; Morishita A; Nomura T; Tani J; Miyoshi H; Yoneyama H; Iwama H; Himoto T; Masaki T
[Ad] Endereço:Department of Gastroenterology and Neurology, Kagawa University Faculty of Medicine, Miki­cho, Kagawa 761­0793, Japan.
[Ti] Título:Identification of microRNA profiles associated with refractory primary biliary cirrhosis.
[So] Source:Mol Med Rep;14(4):3350-6, 2016 Oct.
[Is] ISSN:1791-3004
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:MicroRNAs (miRNAs) are small, endogenous, non-coding RNAs that control the target gene translation by RNA interference; miRNAs are associated with cellular processes, including proliferation, differentiation, apoptosis, and cell survival. Primary biliary cirrhosis (PBC) is a chronic cholestatic liver disease of unknown etiology. One third of patients with PBC demonstrate suboptimal responses, which result in worse outcomes. It has been previously reported that miRNAs are involved in drug resistance, however, the association between miRNA expression levels and refractory PBC remains to be fully elucidated. In the present study, among the 20 patients with PBC treated with ursodeoxycholic acid or bezafibrate, 15 patients were classed as treatment­effective, and 5 were classed as being treatment­resistant. Using the miRNA array technique, miRNA profiles were identified for each group. A total of 35 miRNAs were significantly upregulated, and 23 were significantly downregulated in the treatment­resistant group compared with the treatment­effective group. In order to examine the association between the highly altered miRNAs and clinical features of the two groups, numerous parameters were analyzed. Elevated levels of direct bilirubin, aspartate transaminase (AST), and alanine transaminase (ALT) were identified to be associated with miRNA­122 upregulation. AST, ALT, and γ guanosine triphosphate were additionally associated with miRNA­378f upregulation. However, the reduction of miRNA­4311 was associated with reduced levels of AST and ALT. miRNA­4714­3p was also negatively correlated with total bilirubin and lactate dehydrogenase. Therefore, identifying the miRNA profile was demonstrated to be a useful approach in the characterization of PBC development. It is suggested that highly altered miRNAs may be potential biomarkers for use in the development of treatment of patients with refractory PBC.
[Mh] Termos MeSH primário: Cirrose Hepática Biliar/genética
MicroRNAs/genética
Transcriptoma
[Mh] Termos MeSH secundário: Adulto
Idoso
Anti-Inflamatórios/uso terapêutico
Bezafibrato/uso terapêutico
Colagogos e Coleréticos/uso terapêutico
Resistência a Medicamentos
Feminino
Regulação da Expressão Gênica
Seres Humanos
Hipolipemiantes/uso terapêutico
Cirrose Hepática Biliar/sangue
Cirrose Hepática Biliar/tratamento farmacológico
Masculino
MicroRNAs/sangue
Meia-Idade
Prednisolona/uso terapêutico
Ácido Ursodesoxicólico/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Cholagogues and Choleretics); 0 (Hypolipidemic Agents); 0 (MicroRNAs); 724L30Y2QR (Ursodeoxycholic Acid); 9PHQ9Y1OLM (Prednisolone); Y9449Q51XH (Bezafibrate)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170410
[Lr] Data última revisão:
170410
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160812
[St] Status:MEDLINE
[do] DOI:10.3892/mmr.2016.5606


  10 / 1134 MEDLINE  
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[PMID]:27284107
[Au] Autor:Franko A; Huypens P; Neschen S; Irmler M; Rozman J; Rathkolb B; Neff F; Prehn C; Dubois G; Baumann M; Massinger R; Gradinger D; Przemeck GK; Repp B; Aichler M; Feuchtinger A; Schommers P; Stöhr O; Sanchez-Lasheras C; Adamski J; Peter A; Prokisch H; Beckers J; Walch AK; Fuchs H; Wolf E; Schubert M; Wiesner RJ; Hrabe de Angelis M
[Ad] Endereço:Institute of Experimental Genetics, Helmholtz Zentrum München, Neuherberg, Germany Division of Endocrinology, Diabetology, Angiology, Nephrology and Clinical Chemistry, Department of Internal Medicine, University Hospital Tübingen, Tübingen, Germany German Center for Diabetes Research (DZD e.V.), Ne
[Ti] Título:Bezafibrate Improves Insulin Sensitivity and Metabolic Flexibility in STZ-Induced Diabetic Mice.
[So] Source:Diabetes;65(9):2540-52, 2016 Sep.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bezafibrate (BEZ), a pan activator of peroxisome proliferator-activated receptors (PPARs), has been generally used to treat hyperlipidemia for decades. Clinical trials with type 2 diabetes patients indicated that BEZ also has beneficial effects on glucose metabolism, although the underlying mechanisms of these effects remain elusive. Even less is known about a potential role for BEZ in treating type 1 diabetes. Here we show that BEZ markedly improves hyperglycemia and glucose and insulin tolerance in mice with streptozotocin (STZ)-induced diabetes, an insulin-deficient mouse model of type 1 diabetes. BEZ treatment of STZ mice significantly suppressed the hepatic expression of genes that are annotated in inflammatory processes, whereas the expression of PPAR and insulin target gene transcripts was increased. Furthermore, BEZ-treated mice also exhibited improved metabolic flexibility as well as an enhanced mitochondrial mass and function in the liver. Finally, we show that the number of pancreatic islets and the area of insulin-positive cells tended to be higher in BEZ-treated mice. Our data suggest that BEZ may improve impaired glucose metabolism by augmenting hepatic mitochondrial performance, suppressing hepatic inflammatory pathways, and improving insulin sensitivity and metabolic flexibility. Thus, BEZ treatment might also be useful for patients with impaired glucose tolerance or diabetes.
[Mh] Termos MeSH primário: Bezafibrato/uso terapêutico
Diabetes Mellitus Experimental/tratamento farmacológico
Resistência à Insulina/fisiologia
[Mh] Termos MeSH secundário: Animais
Glicemia/efeitos dos fármacos
Células Cultivadas
Diabetes Mellitus Experimental/metabolismo
Diabetes Mellitus Experimental/fisiopatologia
Teste de Tolerância a Glucose
Seres Humanos
Hiperglicemia/tratamento farmacológico
Hiperglicemia/metabolismo
Hiperglicemia/fisiopatologia
Hipoglicemiantes/uso terapêutico
Hipolipemiantes/uso terapêutico
Fígado/efeitos dos fármacos
Fígado/metabolismo
Masculino
Metabolômica
Camundongos
Camundongos Endogâmicos C57BL
Mitocôndrias Hepáticas/efeitos dos fármacos
Mitocôndrias Hepáticas/metabolismo
Análise de Sequência com Séries de Oligonucleotídeos
Consumo de Oxigênio/efeitos dos fármacos
Receptores Ativados por Proliferador de Peroxissomo/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Hypoglycemic Agents); 0 (Hypolipidemic Agents); 0 (Peroxisome Proliferator-Activated Receptors); Y9449Q51XH (Bezafibrate)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170605
[Lr] Data última revisão:
170605
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160611
[St] Status:MEDLINE
[do] DOI:10.2337/db15-1670



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