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[PMID]:28468836
[Au] Autor:Yoshikado T; Toshimoto K; Nakada T; Ikejiri K; Kusuhara H; Maeda K; Sugiyama Y
[Ad] Endereço:Sugiyama Laboratory, RIKEN Innovation Center, RIKEN, Kanagawa, Japan (T.Y., K.T., Y.S.); DMPK Research Laboratories Sohyaku, Innovative Research Division, Mitsubishi Tanabe Pharma, Saitama, Japan (T.N.); and Laboratory of Molecular Pharmacokinetics, Graduate School of Pharmaceutical Sciences, Univer
[Ti] Título:Comparison of Methods for Estimating Unbound Intracellular-to-Medium Concentration Ratios in Rat and Human Hepatocytes Using Statins.
[So] Source:Drug Metab Dispos;45(7):779-789, 2017 Jul.
[Is] ISSN:1521-009X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:It is essential to estimate concentrations of unbound drugs inside the hepatocytes to predict hepatic clearance, efficacy, and toxicity of the drugs. The present study was undertaken to compare predictability of the unbound hepatocyte-to-medium concentration ratios (K ) by two methods based on the steady-state cell-to-medium total concentration ratios at 37°C and on ice (K ) and based on their initial uptake rates (K ). Poorly metabolized statins were used as test drugs because of their concentrative uptake via organic anion-transporting polypeptides. K values of these statins provided less interexperimental variation than the K values, because only data at longer time are required for K K values for pitavastatin, rosuvastatin, and pravastatin were 1.2- to 5.1-fold K in rat hepatocytes; K values in human hepatocytes also tended to be larger than corresponding K To explain these discrepancies, theoretical values of K and K were compared with true K (K ), considering the inside-negative membrane potential and ionization of the drugs in hepatocytes and medium. Membrane potentials were approximately -30 mV in human hepatocytes at 37°C and almost abolished on ice. Theoretical equations considering the membrane potentials indicate that K values for the statins are 0.85- to 1.2-fold K , whereas K values are 2.2- to 3.1-fold K , depending on the ratio of the passive permeability of the ionized to nonionized forms. In conclusion, K values of anions are similar to K when the inside-negative membrane potential is considered. This suggests that K is preferable for estimating the concentration of unbound drugs inside the hepatocytes.
[Mh] Termos MeSH primário: Hepatócitos/metabolismo
Inibidores de Hidroximetilglutaril-CoA Redutases/metabolismo
[Mh] Termos MeSH secundário: Animais
Transporte Biológico/fisiologia
Seres Humanos
Fígado/metabolismo
Masculino
Potenciais da Membrana/fisiologia
Transportadores de Ânions Orgânicos/metabolismo
Permeabilidade
Pravastatina/metabolismo
Quinolinas/metabolismo
Ratos
Ratos Sprague-Dawley
Rosuvastatina Cálcica/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Organic Anion Transporters); 0 (Quinolines); 83MVU38M7Q (Rosuvastatin Calcium); KXO2KT9N0G (Pravastatin); M5681Q5F9P (pitavastatin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1124/dmd.116.074823


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[PMID]:29217137
[Au] Autor:Broniarek I; Jarmuszkiewicz W
[Ad] Endereço:Department of Bioenergetics, Institute of Molecular Biology and Biotechnology, Adam Mickiewicz University in Poznan, Poland.
[Ti] Título:Atorvastatin affects negatively respiratory function of isolated endothelial mitochondria.
[So] Source:Arch Biochem Biophys;637:64-72, 2018 01 01.
[Is] ISSN:1096-0384
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The purpose of this research was to elucidate the direct effects of two popular blood cholesterol-lowering drugs used to treat cardiovascular diseases, atorvastatin and pravastatin, on respiratory function, membrane potential, and reactive oxygen species formation in mitochondria isolated from human umbilical vein endothelial cells (EA.hy926 cell line). Hydrophilic pravastatin did not significantly affect endothelial mitochondria function. In contrast, hydrophobic calcium-containing atorvastatin induced a loss of outer mitochondrial membrane integrity, an increase in hydrogen peroxide formation, and reductions in maximal (phosphorylating or uncoupled) respiratory rate, membrane potential and oxidative phosphorylation efficiency. The atorvastatin-induced changes indicate an impairment of mitochondrial function at the level of ATP synthesis and at the level of the respiratory chain, likely at complex I and complex III. The atorvastatin action on endothelial mitochondria was highly dependent on calcium ions and led to a disturbance in mitochondrial calcium homeostasis. Uptake of calcium ions included in atorvastatin molecule induced mitochondrial uncoupling that enhanced the inhibition of the mitochondrial respiratory chain by atorvastatin. Our results indicate that hydrophobic calcium-containing atorvastatin, widely used as anti-atherosclerotic agent, has a direct negative action on isolated endothelial mitochondria.
[Mh] Termos MeSH primário: Atorvastatina Cálcica/toxicidade
Inibidores de Hidroximetilglutaril-CoA Redutases/toxicidade
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Respiração/efeitos dos fármacos
[Mh] Termos MeSH secundário: Cálcio/metabolismo
Transporte de Elétrons/efeitos dos fármacos
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Membranas Mitocondriais/efeitos dos fármacos
Membranas Mitocondriais/metabolismo
Fosforilação Oxidativa/efeitos dos fármacos
Consumo de Oxigênio/efeitos dos fármacos
Pravastatina/toxicidade
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Reactive Oxygen Species); 48A5M73Z4Q (Atorvastatin Calcium); KXO2KT9N0G (Pravastatin); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171209
[St] Status:MEDLINE


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[PMID]:28583351
[Au] Autor:Yasuda K; Sugimoto H; Hayashi K; Takita T; Yasukawa K; Ohta M; Kamakura M; Ikushiro S; Shiro Y; Sakaki T
[Ad] Endereço:Department of Pharmaceutical Engineering, Faculty of Engineering, Toyama Prefectural University, 5180 Kurokawa, Imizu, Toyama 939-0398, Japan; Department of Biotechnology, Faculty of Engineering, Toyama Prefectural University, 5180 Kurokawa, Imizu, Toyama 939-0398, Japan.
[Ti] Título:Protein engineering of CYP105s for their industrial uses.
[So] Source:Biochim Biophys Acta;1866(1):23-31, 2018 01.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Cytochrome P450 enzymes belonging to the CYP105 family are predominantly found in bacteria belonging to the phylum Actinobacteria and the order Actinomycetales. In this review, we focused on the protein engineering of P450s belonging to the CYP105 family for industrial use. Two Arg substitutions to Ala of CYP105A1 enhanced its vitamin D 25- and 1α-hydroxylation activities by 400 and 100-fold, respectively. The coupling efficiency between product formation and NADPH oxidation was largely improved by the R84A mutation. The quintuple mutant Q87W/T115A/H132L/R194W/G294D of CYP105AB3 showed a 20-fold higher activity than the wild-type enzyme. Amino acids at positions 87 and 191 were located at the substrate entrance channel, and that at position 294 was located close to the heme group. Semi-rational engineering of CYP105A3 selected the best performing mutant, T85F/T119S/V194N/N363Y, for producing pravastatin. The T119S and N363Y mutations synergistically had remarkable effects on the interaction between CYP105A3 and putidaredoxin. Although wild-type CYP105AS1 hydroxylated compactin to 6-epi-pravastatin, the quintuple mutant I95T/Q127R/A180V/L236I/A265N converted almost all compactin to pravastatin. Five amino acid substitutions by two rounds of mutagenesis almost completely changed the stereo-selectivity of CYP105AS1. These results strongly suggest that the protein engineering of CYP105 enzymes greatly increase their industrial utility. This article is part of a Special Issue entitled: Cytochrome P450 biodiversity and biotechnology, edited by Erika Plettner, Gianfranco Gilardi, Luet Wong, Vlada Urlacher, Jared Goldstone.
[Mh] Termos MeSH primário: Actinobacteria/genética
Substituição de Aminoácidos
Proteínas de Bactérias/química
Sistema Enzimático do Citocromo P-450/química
Mutação
Engenharia de Proteínas/métodos
[Mh] Termos MeSH secundário: Actinobacteria/enzimologia
Proteínas de Bactérias/genética
Proteínas de Bactérias/metabolismo
Colecalciferol/metabolismo
Sequência Conservada
Sistema Enzimático do Citocromo P-450/genética
Sistema Enzimático do Citocromo P-450/metabolismo
Ferredoxinas/metabolismo
Expressão Gênica
Hidroxilação
Isoenzimas
Lovastatina/análogos & derivados
Lovastatina/metabolismo
Simulação de Acoplamento Molecular
Pravastatina/biossíntese
Streptomyces/enzimologia
Streptomyces/genética
Especificidade por Substrato
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Ferredoxins); 0 (Isoenzymes); 1C6V77QF41 (Cholecalciferol); 1UQM1K0W9X (mevastatin); 57087-75-9 (putidaredoxin); 9035-51-2 (Cytochrome P-450 Enzyme System); 9LHU78OQFD (Lovastatin); EC 1.14.- (P450SU1 protein, Streptomyces griseolus); KXO2KT9N0G (Pravastatin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170607
[St] Status:MEDLINE


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[PMID]:29375110
[Au] Autor:Li H; Wang C; Sun J; Liu C; Li N; Chen J
[Ad] Endereço:Department of Pharmacology, Pharmaceutical College, Beihua University.
[Ti] Título:Pravastatin Decreases Infarct Size Induced by Coronary Artery Ischemia/Reperfusion with Elevated eNOS Expression in Rats.
[So] Source:Int Heart J;59(1):154-160, 2018.
[Is] ISSN:1349-3299
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Our previous study showed that pravastatin prevents ischemia and reperfusion-induced lethal ventricular fibrillation in rats. This study explored whether pravastatin decreases myocardial infarct size and this effect is associated with endothelial nitric oxide synthase (eNOS) expression in myocardium. Rats were treated with ischemia (30 minutes) and reperfusion (60 minutes) after chronic oral administration of pravastatin, fluvastatin, or vehicle once daily for 22 days. Electrocardiograms and blood pressure were continuously recorded, myocardial infarct size was measured by TTC-staining, and eNOS expression was measured by western blot. The results showed that pravastatin and fluvastatin significantly reduced myocardial infarct size. No statistical differences were found in the areas at risk among all groups. However, a significant reduction in infarct size was observed in three pravastatin groups and one fluvastatin group compared to control. Both pravastatin and fluvastatin significantly increased eNOS protein expression in ischemic and non-ischemic tissues compared to control. Our results suggest that pravastatin decreases cardiovascular mortality beyond its cholesterol-lowering effect. Pravastatin is more potent than fluvastatin in reducing infarct size. These effects may be associated with elevation of eNOS expression.
[Mh] Termos MeSH primário: Infarto do Miocárdio/tratamento farmacológico
Miocárdio/patologia
Óxido Nítrico Sintase Tipo III/biossíntese
Pravastatina/administração & dosagem
RNA/genética
Traumatismo por Reperfusão/complicações
[Mh] Termos MeSH secundário: Animais
Vasos Coronários
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Eletroforese em Gel de Poliacrilamida
Inibidores de Hidroximetilglutaril-CoA Redutases
Masculino
Infarto do Miocárdio/etiologia
Infarto do Miocárdio/metabolismo
Miocárdio/metabolismo
Ratos
Ratos Sprague-Dawley
Traumatismo por Reperfusão/diagnóstico
Traumatismo por Reperfusão/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 63231-63-0 (RNA); EC 1.14.13.39 (Nitric Oxide Synthase Type III); EC 1.14.13.39 (Nos3 protein, rat); KXO2KT9N0G (Pravastatin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180130
[St] Status:MEDLINE
[do] DOI:10.1536/ihj.16-607


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[PMID]:28465323
[Au] Autor:Walker ME; Souza PR; Colas RA; Dalli J
[Ad] Endereço:Lipid Mediator Unit, Centre for Biochemical Pharmacology, William Harvey Research Institute, Barts and the London School of Medicine, Queen Mary University of London, London, United Kingdom.
[Ti] Título:13-Series resolvins mediate the leukocyte-platelet actions of atorvastatin and pravastatin in inflammatory arthritis.
[So] Source:FASEB J;31(8):3636-3648, 2017 08.
[Is] ISSN:1530-6860
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Rheumatoid arthritis is an inflammatory condition characterized by overzealous inflammation that leads to joint damage and is associated with an increased incidence of cardiovascular disease. Statins are frontline therapeutics for patients with cardiovascular disease and exert beneficial actions in rheumatoid arthritis. The mechanism that mediates the beneficial actions of statins in rheumatoid arthritis remains of interest. In the present study, we found that the administration of 2 clinically relevant statins-atorvastatin (0.2 mg/kg) or pravastatin (0.2 mg/kg)-to mice during inflammatory arthritis up-regulated systemic and tissue amounts of a novel family of proresolving mediators, termed 13-series resolvins (RvTs), and significantly reduced joint disease. Of note, administration of simvastatin (0.2 mg/kg) did not significantly up-regulate RvTs or reduce joint inflammation. We also found that atorvastatin and pravastatin each reduced systemic leukocyte activation, including platelet-monocyte aggregates (∼25-60%). These statins decreased neutrophil trafficking to the joint as well as joint monocyte and macrophage numbers. Atorvastatin and pravastatin produced significant reductions (∼30-50%) in expression of CD11b and major histocompatibility complex class II on both monocytes and monocyte-derived macrophages in joints. Administration of an inhibitor to cyclooxygenase-2, the initiating enzyme in the RvT pathway, reversed the protective actions of these statins on both joint and systemic inflammation. Together, these findings provide evidence for the role of RvTs in mediating the protective actions of atorvastatin and pravastatin in reducing local and vascular inflammation, and suggest that RvTs may be useful in measuring the anti-inflammatory actions of statins.-Walker, M. E., Souza, P. R., Colas, R. A., Dalli, J. 13-Series resolvins mediate the leukocyte-platelet actions of atorvastatin and pravastatin in inflammatory arthritis.
[Mh] Termos MeSH primário: Anticolesterolemiantes/uso terapêutico
Artrite/tratamento farmacológico
Atorvastatina Cálcica/uso terapêutico
Ácidos Docosa-Hexaenoicos/metabolismo
Inflamação/tratamento farmacológico
Pravastatina/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Artrite/induzido quimicamente
Artrite/metabolismo
Inflamação/induzido quimicamente
Inflamação/metabolismo
Leucócitos/efeitos dos fármacos
Leucócitos/fisiologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anticholesteremic Agents); 25167-62-8 (Docosahexaenoic Acids); 48A5M73Z4Q (Atorvastatin Calcium); KXO2KT9N0G (Pravastatin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1096/fj.201700268


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[PMID]:29337671
[Au] Autor:Stolarczyk M; Apola A; Maslanka A; Kwiecien A; Opoka W
[Ad] Endereço:1Department of Inorganic and Analytical Chemistry Jagiellonian University Medical College, Faculty of Pharmacy 30-688 Kraków, Poland.
[Ti] Título:Spectrophotometric method for simultaneous determination of valsartan and substances from the group of statins in binary mixtures.
[So] Source:Acta Pharm;67(4):463-478, 2017 Dec 20.
[Is] ISSN:1846-9558
[Cp] País de publicação:Croatia
[La] Idioma:eng
[Ab] Resumo:Applicability of derivative spectrophotometry for the determination of valsartan in the presence of a substance from the group of statins was checked. The obtained results indicate that the proposed method may be effective by using appropriate derivatives: for valsartan and fluvastatin - D1, D2 and D3, for valsartan and pravastatin - D1 and D3, for valsartan and atorvastatin - D2 and D3. The method was characterized by high sensitivity and accuracy. Linearity was maintained in the following ranges: 9.28-32.48 mg mL-1 for valsartan, 8.16-28.56 mg mL-1 f or fluvastatin, 14.40-39.90 mg mL-1 for atorvastatin and 9.60-48.00 mg mL-1 for pravastatin. Determination coefficients were in the range of 0.989-0.999 depending on the analyte and the order of derivative. The precision of the method was high with RSD from 0.1 to 2.5 % and recovery of individual components was within the range of 100 ± 5 %. The developed method was successfully applied to the determination of valsartan combined with fluvastatin, atorvastatin and pravastatin in laboratory prepared mixtures and in pharmaceutical preparations.
[Mh] Termos MeSH primário: Inibidores de Hidroximetilglutaril-CoA Redutases/análise
Espectrofotometria/métodos
Valsartana/análise
[Mh] Termos MeSH secundário: Atorvastatina Cálcica/análise
Ácidos Graxos Monoinsaturados/análise
Indóis/análise
Pravastatina/análise
Reprodutibilidade dos Testes
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fatty Acids, Monounsaturated); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Indoles); 48A5M73Z4Q (Atorvastatin Calcium); 4L066368AS (fluvastatin); 80M03YXJ7I (Valsartan); KXO2KT9N0G (Pravastatin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180131
[Lr] Data última revisão:
180131
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE


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[PMID]:29197498
[Au] Autor:Raffoul-Orozco AK; Ávila-González AE; Rodríguez-Razón CM; García-Cobian TA; Pérez-Guerrero EE; García-Iglesias T; Rubio-Arellano ED
[Ad] Endereço:Institute of Experimental and Clinical Therapeutics, Department of Physiology, Health Sciences University Center, University of Guadalajara, Sierra Mojada st. 950. P.C. 44340, Guadalajara, Jal 01 33 1058 5200, Mexico.
[Ti] Título:Combination effect naringin and pravastatin in lipid profile and glucose in obese rats.
[So] Source:Life Sci;193:87-92, 2018 Jan 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: The purpose of this study was to compare the effect of naringin 100mg/kg in combination with pravastatin 10mg/kg by gavage for 6weeks compared with monotherapy over lipid profiles, glucose levels and weight in murine model of obesity. MAIN METHODS: The study design was planned with 5 groups of 6 male Wistar Albina rats: Group 1: control with balanced food and vehicle (C-); Group 2: control with Obesity and vehicle (C+); Group 3: Obesity+naringin (N); Group 4: Obesity+pravastatin (P); Group 5: Obesity+pravastatin+naringin (NP). Obesity was developed with a food model. KEY FINDINGS: The naringin groups showed a decrease in weight gain and low glucose values compared to the control group (weight NP:311.4 vs C+:348.6; glucose NP: 173.12 vs C+:235.56) (p<0.05); the group with naringin+pravastatin combination showed the total cholesterol (TC), LDL and triglycerides (TGs) to normal levels (TC NP:51.6 vs C+:83.4; LDL NP:9.32 vs C+:32.32; TGs NP:39.4 vs C+:89.4) (p<0.05); but was not statistically significant compared with monotherapy. SIGNIFICANCE: The combination of naringin and pravastatin did not appear to be better than monotherapy on lipids, but its use could generate euglycemic and antiobesogenic effects, in addition to diminishing the adverse hepatic effects of pravastatin in rats.
[Mh] Termos MeSH primário: Flavanonas/farmacologia
Metabolismo dos Lipídeos/efeitos dos fármacos
Pravastatina/farmacologia
[Mh] Termos MeSH secundário: Animais
Glicemia/metabolismo
HDL-Colesterol
Quimioterapia Combinada
Flavanonas/uso terapêutico
Glucose/metabolismo
Lipídeos/fisiologia
Masculino
Obesidade/tratamento farmacológico
Pravastatina/uso terapêutico
Ratos
Ratos Wistar
Triglicerídeos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Cholesterol, HDL); 0 (Flavanones); 0 (Lipids); 0 (Triglycerides); IY9XDZ35W2 (Glucose); KXO2KT9N0G (Pravastatin); N7TD9J649B (naringin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171204
[St] Status:MEDLINE


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[PMID]:29204620
[Au] Autor:Burns RB; Graham K; Sawhney MS; Reynolds EE
[Ad] Endereço:From Beth Israel Deaconess Medical Center, Boston, Massachusetts.
[Ti] Título:Should This Patient Receive Aspirin?: Grand Rounds Discussion From Beth Israel Deaconess Medical Center.
[So] Source:Ann Intern Med;167(11):786-793, 2017 Dec 05.
[Is] ISSN:1539-3704
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Aspirin exerts antiplatelet effects through irreversible inhibition of cyclooxygenase-1, whereas its anticancer effects may be due to inhibition of cyclooxygenase-2 and other pathways. In 2009, the U.S. Preventive Services Task Force endorsed aspirin for primary prevention of cardiovascular disease. However, aspirin's role in cancer prevention is still emerging, and no groups currently recommend its use for this purpose. To help physicians balance the benefits and harms of aspirin in primary disease prevention, the Task Force issued a guideline titled, "Aspirin Use for the Primary Prevention of Cardiovascular Disease and Colorectal Cancer" in 2016. In the evidence review conducted for the guideline, cardiovascular disease mortality and colorectal cancer mortality were significantly reduced among persons taking aspirin. However, there was no difference in nonfatal stroke, cardiovascular disease mortality, or all-cause mortality, nor in total cancer mortality, among those taking aspirin. Aspirin users were found to be at increased risk for major gastrointestinal bleeding. In this Beyond the Guidelines, the guideline is reviewed and 2 experts discuss how they would apply it to a 57-year-old man considering starting aspirin for primary prevention. Our experts review the data on which the guideline is based, discuss how they would balance the benefits and harms of aspirin therapy, and explain how they would incorporate shared decision making into clinical practice.
[Mh] Termos MeSH primário: Aspirina/uso terapêutico
Doenças Cardiovasculares/prevenção & controle
Inibidores da Agregação de Plaquetas/uso terapêutico
Prevenção Primária
[Mh] Termos MeSH secundário: Anticolesterolemiantes/uso terapêutico
Aspirina/administração & dosagem
Aspirina/efeitos adversos
Hemorragia Gastrointestinal/induzido quimicamente
Seres Humanos
Hipercolesterolemia/tratamento farmacológico
Masculino
Meia-Idade
Inibidores da Agregação de Plaquetas/administração & dosagem
Inibidores da Agregação de Plaquetas/efeitos adversos
Pravastatina/uso terapêutico
Medição de Risco
[Pt] Tipo de publicação:CASE REPORTS; CLINICAL CONFERENCE; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticholesteremic Agents); 0 (Platelet Aggregation Inhibitors); KXO2KT9N0G (Pravastatin); R16CO5Y76E (Aspirin)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171219
[Lr] Data última revisão:
171219
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE
[do] DOI:10.7326/M17-2162


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[PMID]:29049209
[Au] Autor:Otten LA; van der Ven K; Kühr M; Gembruch U; Merz WM
[Ad] Endereço:aDepartment of Obstetrics and Prenatal Medicine bDepartment of Gynecologic Endocrinology and Reproductive Medicine, University Bonn Medical School, Bonn, Germany.
[Ti] Título:Pravastatin for prevention of HELLP syndrome: A case report.
[So] Source:Medicine (Baltimore);96(42):e8229, 2017 Oct.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Pravastatin has emerged for prevention and treatment of preeclampsia; no reports are available on pravastatin and HELLP (hemolysis, elevated liver enzymes and low platelets) syndrome. PATIENT CONCERNS: The first pregnancy necessitated termination of pregnancy at gestational age (GA) 20+5 for HELLP. Intrauterine fetal death at GA 22+5 occurred in the second pregnancy, whilst on temporizing management of HELLP. DIAGNOSES: Severe, recurrent early-onset HELLP syndrome. INTERVENTIONS: In her fourth pregnancy, pravastatin was commenced at GA 13. OUTCOMES: The course of pregnancy was uncomplicated, and a healthy, appropriate for gestational age fetus was delivered at term. LESSONS: Pravastatin may be effective in prevention of HELLP. The hepatic uptake may be of particular advantage.
[Mh] Termos MeSH primário: Síndrome HELLP/prevenção & controle
Inibidores de Hidroximetilglutaril-CoA Redutases/administração & dosagem
Pravastatina/administração & dosagem
[Mh] Termos MeSH secundário: Adulto
Feminino
Idade Gestacional
Seres Humanos
Nascimento Vivo
Gravidez
Recidiva
Nascimento a Termo
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); KXO2KT9N0G (Pravastatin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171122
[Lr] Data última revisão:
171122
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171020
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008229


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[PMID]:28802576
[Au] Autor:Melendez QM; Wooten CJ; Lopez D
[Ad] Endereço:Department of Pharmaceutical Sciences, Biomanufacturing Research Institute and Technology Enterprise (BRITE), College of Arts and Sciences, North Carolina Central University, Durham, NC, 27707, USA.
[Ti] Título:Atorvastatin and lovastatin, but not pravastatin, increased cellular complex formation between PCSK9 and the LDL receptor in human hepatocyte-like C3A cells.
[So] Source:Biochem Biophys Res Commun;492(1):103-108, 2017 Oct 07.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Statins are the first-line treatment for hypercholesterolemic patients. Herein, the effects of three statins on complex formation between proprotein convertase subtilisin-kexin 9 (PCSK9) and the low density lipoprotein receptor (LDLR), a critical step for the PCSK9-dependent degradation of LDLR in the lysosome, were examined. Human hepatocyte-like C3A cells grown in control (containing 10% fetal bovine serum) or MITO+ (supplemented with BD™ MITO + serum extender) medium were also treated with atorvastatin (Atorv), lovastatin (Lov), or pravastatin (Prav) for 24 h. RNA and protein expression studies and determinations of PCSK9/LDLR complex formation were performed. As expected, the statins increased the expression of PCSK9 and LDLR independently of the medium employed. Interestingly, Atov and Lov caused increases in PCSK9/LDLR complex formation, whereas Prav decreased complex formation when compared to cells treated without drugs. These results may explain why Prav works better for statin intolerant patients than other statins such as Atorv and Lov.
[Mh] Termos MeSH primário: Atorvastatina Cálcica/farmacologia
Lovastatina/farmacologia
Pravastatina/farmacologia
Pró-Proteína Convertase 9/antagonistas & inibidores
Pró-Proteína Convertase 9/biossíntese
Receptores de LDL/antagonistas & inibidores
Receptores de LDL/biossíntese
[Mh] Termos MeSH secundário: Células Cultivadas
Seres Humanos
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, LDL); 48A5M73Z4Q (Atorvastatin Calcium); 9LHU78OQFD (Lovastatin); EC 3.4.21.- (PCSK9 protein, human); EC 3.4.21.- (Proprotein Convertase 9); KXO2KT9N0G (Pravastatin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170814
[St] Status:MEDLINE



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