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Antimicrobial stewardship interventions targeting penicillin allergy and carbapenem utilization were fully implemented January 1, 2014. Multivariate logistic regression was used to examine impact of penicillin allergy and antimicrobial stewardship interventions on empirical carbapenem use. Kaplan‐Meier analysis was used to evaluate time to carbapenem deescalation in patients with penicillin allergy before and after interventions.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Results\u003C\u002Fjats:title>\u003Cjats:p>Patients with penicillin allergy (n=140) were more likely to receive empirical carbapenem therapy for community‐onset gram‐negative \u003Cjats:styled-content style=\"fixed-case\">BSI\u003C\u002Fjats:styled-content> compared to those without penicillin allergy (n=140) (27% vs 12%, p=0.002). After adjustments in the multivariate model, penicillin allergy (odds ratio [\u003Cjats:styled-content style=\"fixed-case\">OR\u003C\u002Fjats:styled-content>] 3.98, 95% confidence interval [\u003Cjats:styled-content style=\"fixed-case\">CI\u003C\u002Fjats:styled-content>] 1.98–8.45) and prior β‐lactam use (\u003Cjats:styled-content style=\"fixed-case\">OR\u003C\u002Fjats:styled-content> 2.72, 95% \u003Cjats:styled-content style=\"fixed-case\">CI\u003C\u002Fjats:styled-content> 1.07–6.64) were independently associated with empirical carbapenem use, whereas antimicrobial stewardship interventions were associated with decline in carbapenem utilization (\u003Cjats:styled-content style=\"fixed-case\">OR\u003C\u002Fjats:styled-content> 0.41, 95% \u003Cjats:styled-content style=\"fixed-case\">CI\u003C\u002Fjats:styled-content> 0.16–0.94). Among patients with penicillin allergy who were prescribed empirical carbapenems, median time to carbapenem deescalation was significantly shorter in the postintervention versus preintervention period (2.0 vs 4.2 days, p=0.004).\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Conclusion\u003C\u002Fjats:title>\u003Cjats:p>Penicillin allergy was a significant contributor to carbapenem use in community‐onset gram‐negative \u003Cjats:styled-content style=\"fixed-case\">BSI\u003C\u002Fjats:styled-content>. This was subject to modification by antimicrobial stewardship interventions, which successfully reduced overall carbapenem use and duration of carbapenem therapy in patients with penicillin allergy.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>",{"EN":103},"Impact of Penicillin Allergy on Empirical Carbapenem Use in Gram‐Negative Bloodstream Infections: An Antimicrobial Stewardship Opportunity",{"VOID":105},"29105102",{"VOID":107},"10.1002\u002Fphar.2054","PUBLICATION","VERIFIED","Auto Verify",[112],"EN","https:\u002F\u002Faccpjournals.onlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fphar.2054",[115,143,162,180,206],{"id":116,"sortIndex":24,"researcher":23,"roles":117,"affiliations":118,"properties":136,"displayName":140,"givenName":23,"familyName":23},"a8e97dcf-2744-4974-a57d-2e65d09358d4",[],[119,127],{"id":120,"sortIndex":24,"affiliation":121,"properties":23},"1074aa3a-4db2-46e5-9c0a-fe5f41b195c5",{"id":120,"createTime":23,"updateTime":23,"relativeEntities":122,"slug":23,"properties":123,"entityType":23,"verifyStatus":23,"verifyTime":23,"verifyNote":23,"languages":23,"translateLanguages":23,"viewCount":23,"url":23,"parentIds":126,"statistic":23},[],{"title":124},{"EN":125},"Department of Medicine Palmetto Health USC Medical Group Columbia South Carolina",[],{"id":128,"sortIndex":129,"affiliation":130,"properties":23},"6635da62-0698-4c1d-b6ac-597afef2658a",1,{"id":128,"createTime":23,"updateTime":23,"relativeEntities":131,"slug":23,"properties":132,"entityType":23,"verifyStatus":23,"verifyTime":23,"verifyNote":23,"languages":23,"translateLanguages":23,"viewCount":23,"url":23,"parentIds":135,"statistic":23},[],{"title":133},{"VI":134},"University of South Carolina School of Medicine, Columbia, South Carolina",[],{"orcid":137,"title":139,"openalex":141},{"VOID":138},"https:\u002F\u002Forcid.org\u002F0000-0001-6501-492X",{"EN":140},"Majdi N. 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Presented at the ASM Microbe 2016; Boston MA June 16–20 2016(Abstract: Friday 437).",{},{"id":23,"text":345,"url":23,"identifiers":346},"10.1111\u002F1469-0691.12085",{"doi":345},{"id":23,"text":348,"url":23,"identifiers":349},"10.1111\u002F1469-0691.12607",{"doi":348},{"id":23,"text":351,"url":23,"identifiers":352},"10.1345\u002Faph.1L486",{"doi":351},{"id":23,"text":354,"url":23,"identifiers":355},"10.1592\u002Fphco.31.5.469",{"doi":354},{"id":23,"text":357,"url":23,"identifiers":358},"Dash CH, 1975, Penicillin allergy and the cephalosporins, J Antimicrob Chemother, 1, 107, 10.1093\u002Fjac\u002F1.suppl_3.107",{"doi":359},"10.1093\u002Fjac\u002F1.suppl_3.107",{"id":23,"text":361,"url":23,"identifiers":362},"10.1093\u002Finfdis\u002F137.Supplement.S74",{"doi":361},{"id":23,"text":364,"url":23,"identifiers":365},"Bookstaver PB, 2017, Cumulative effect of an antimicrobial stewardship and rapid diagnostic testing bundle on early streamlining of antimicrobial therapy in gram‐negative bloodstream infections, Antimicrob Agents Chemother, 61, e00189‐17, 10.1128\u002FAAC.00189-17",{"doi":366},"10.1128\u002FAAC.00189-17",{"id":23,"text":368,"url":23,"identifiers":369},"10.1128\u002FAAC.03935-14",{"doi":368},{"id":23,"text":371,"url":23,"identifiers":372},"Battle SE, 2017, Association between inappropriate empirical antimicrobial therapy and hospital length of stay in gram‐negative bloodstream infections: stratification by prognosis, J Antimicrob Chemother, 72, 299, 10.1093\u002Fjac\u002Fdkw402",{"doi":373},"10.1093\u002Fjac\u002Fdkw402",{"id":23,"text":375,"url":23,"identifiers":376},"10.2146\u002Fajhp100272",{"doi":375},{"id":23,"text":378,"url":23,"identifiers":379},"TuckerK LashkovaL FlemmingT et al.Impact of antimicrobial stewardship initiatives on carbapenem utilization and antimicrobial resistance. Presented at the 55th ICAAC annual meeting San Diego CA September 17‐21 2015(Abstract: 2243).",{},false,{"id":382,"createTime":383,"updateTime":384,"relativeEntities":385,"slug":386,"properties":387,"entityType":108,"verifyStatus":109,"verifyTime":383,"verifyNote":110,"languages":404,"translateLanguages":405,"viewCount":24,"primaryUrl":407,"fullTextUrl":23,"authors":408,"publicationType":230,"publisherRelationship":462,"citationCount":507,"citationInfo":508,"publishDate":515,"publishYear":278,"citationAnalyzeStatus":22,"lastCitationAnalyze":23,"indexDatabases":516,"openAccess":23,"references":517,"isForceReanalyzing":380},"ea6844de-ef99-44ed-8c08-107e16f1620f","2024-11-25T07:47:03.718+00:00","2025-01-26T12:48:33.022+00:00",[],"Association-between-Development-of-Dementia-and-Use-of-Benzodiazepines-A-Systematic-Review-and-Meta-Analysis",{"mag":388,"keywords":390,"openalex":392,"abstract":394,"title":397,"pm":400,"doi":402},{"VOID":389},"2886515255",{"VI":391},"",{"VOID":393},"W2886515255",{"VI":395,"EN":396},"\u003Cjats:sec>\u003Cjats:title>Mục tiêu nghiên cứu\u003C\u002Fjats:title>\u003Cjats:p>Việc sử dụng benzodiazepines và sự phát triển của bệnh sa sút trí tuệ là một vấn đề gây tranh cãi, với các nghiên cứu chỉ ra rằng benzodiazepines có thể là một yếu tố bảo vệ hoặc một yếu tố nguy cơ cho bệnh sa sút trí tuệ, hoặc không có mối liên hệ nào giữa hai yếu tố này. Mục tiêu của chúng tôi là xác định xem liệu có một mối liên hệ như vậy hay không.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Thiết kế\u003C\u002Fjats:title>\u003Cjats:p>Tổng quan hệ thống và phân tích tổng hợp 12 nghiên cứu đoàn hệ tiềm năng và hồi cứu cũng như các nghiên cứu trường hợp-đối chứng.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Tham gia\u003C\u002Fjats:title>\u003Cjats:p>Tổng cộng có 981.133 (trong tổng quan hệ thống) và 980.860 (trong phân tích tổng hợp) người trưởng thành hoặc người cao tuổi.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Đo lường và Kết quả chính\u003C\u002Fjats:title>\u003Cjats:p>Một tìm kiếm trong các cơ sở dữ liệu PubMed, \u003Cjats:styled-content style=\"fixed-case\">LILACS\u003C\u002Fjats:styled-content>, và Cochrane Central Register of Controlled Trials, cũng như tìm kiếm thủ công danh sách tài liệu tham khảo của các ấn phẩm và tài liệu tổng quan được bao gồm, đã được thực hiện. Chúng tôi đã bao gồm các nghiên cứu báo cáo tỷ lệ mắc bệnh sa sút trí tuệ và ở những người đã từng sử dụng benzodiazepines. Dữ liệu đã được phân tích bằng cách sử dụng mô hình ngẫu nhiên trong phần mềm R. Chất lượng của chứng cứ được đánh giá bằng hệ thống xếp hạng độ tin cậy Grading of Recommendations Assessment, Development and Evaluation (\u003Cjats:styled-content style=\"fixed-case\">GRADE\u003C\u002Fjats:styled-content>). Kết quả của phân tích tổng hợp chính gợi ý rằng benzodiazepines có thể là một yếu tố nguy cơ đối với sự phát triển của bệnh sa sút trí tuệ (tỷ lệ odds 1.38, khoảng tin cậy 95% 1.07–1.77; \u003Cjats:italic>I\u003C\u002Fjats:italic>\u003Cjats:sup>2\u003C\u002Fjats:sup> = 98%; khoảng tin cậy dự đoán 95% 0.58–3.25; độ chắc chắn rất thấp).\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Kết luận\u003C\u002Fjats:title>\u003Cjats:p>Kết quả của chúng tôi cho thấy có một mối liên hệ giữa việc sử dụng benzodiazepines và sự phát triển của bệnh sa sút trí tuệ. Tuy nhiên, chứng cứ hiện tại không đủ sức mạnh để suy luận sự khác biệt giữa các tác động của bệnh Alzheimer và các dạng sa sút trí tuệ mạch máu, giữa benzodiazepines tác dụng ngắn và tác dụng dài, và các mức độ phơi nhiễm khác nhau (thời gian và liều lượng). Các nghiên cứu đoàn hệ tiềm năng dài hạn trong tương lai là cần thiết, với việc điều chỉnh thích hợp cho các biến nhiễu, các chiến lược nhằm giảm thiểu nguyên nhân đảo ngược, báo cáo các nhóm phụ nhằm tăng cường tính đồng nhất của các phát hiện, sức mạnh thống kê đủ để xác định các tác động lớn, và phân tích liều lượng hàng ngày xác định cho độ dốc đáp ứng liều.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>","\u003Cjats:sec>\u003Cjats:title>Study Objective\u003C\u002Fjats:title>\u003Cjats:p>The use of benzodiazepines and the development of dementia is controversial, with studies indicating that benzodiazepines could be either a protective factor or a risk factor for dementia, or no association may exist between the two. Our objective was to identify whether such an association exists.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Design\u003C\u002Fjats:title>\u003Cjats:p>Systematic review and meta‐analysis of 12 prospective and retrospective cohort studies and case‐control studies.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Participants\u003C\u002Fjats:title>\u003Cjats:p>A total of 981,133 (in the systematic review) and 980,860 (in the meta‐analysis) adults or elderly individuals.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Measurements and Main Results\u003C\u002Fjats:title>\u003Cjats:p>A search of the PubMed, \u003Cjats:styled-content style=\"fixed-case\">LILACS\u003C\u002Fjats:styled-content>, and Cochrane Central Register of Controlled Trials databases, as well as a manual search of the reference lists of the included publications and reviews, was performed. We included studies that reported the incidence of dementia and in ever users of benzodiazepines. Data were analyzed by using a random effects model in R software. Quality of the evidence was assessed with the Grading of Recommendations Assessment, Development and Evaluation (\u003Cjats:styled-content style=\"fixed-case\">GRADE\u003C\u002Fjats:styled-content>) certainty ratings system. The results of the main meta‐analysis suggest that benzodiazepines can be a risk factor for developing dementia (odds ratio 1.38, 95% confidence interval 1.07–1.77; \u003Cjats:italic>I\u003C\u002Fjats:italic>\u003Cjats:sup>2\u003C\u002Fjats:sup> = 98%; 95% prediction interval 0.58–3.25; very low certainty).\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Conclusion\u003C\u002Fjats:title>\u003Cjats:p>Our results suggest an association between the use of benzodiazepines and the development of dementia. However, the current evidence lacks the power to infer differences between the effects of Alzheimer's disease and vascular dementias, long‐acting and short‐acting benzodiazepines, and various exposure loads (duration and dose). Future long‐term prospective cohort studies are necessary, with adequate adjustments for confounding variables, strategies to minimize reverse causality, reporting of subgroups aimed at greater homogeneity of findings, adequate statistical power to identify high‐magnitude effects, and defined daily dose analyses for dose‐response gradient.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>",{"EN":398,"VI":399},"Association between Development of Dementia and Use of Benzodiazepines: A Systematic Review and Meta‐Analysis","Mối liên hệ giữa sự phát triển của bệnh sa sút trí tuệ và việc sử dụng benzodiazepines: Một nghiên cứu tổng quan hệ thống và phân tích tổng hợp",{"VOID":401},"30098211",{"VOID":403},"10.1002\u002Fphar.2170",[112],[406],"VI","https:\u002F\u002Faccpjournals.onlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fphar.2170",[409,428,445],{"id":410,"sortIndex":24,"researcher":23,"roles":411,"affiliations":412,"properties":421,"displayName":425,"givenName":23,"familyName":23},"82fd7339-1366-4b15-a7c1-7929dc8f3689",[],[413],{"id":414,"sortIndex":24,"affiliation":415,"properties":23},"4533be99-8a78-4302-95ce-5f3a2791fc73",{"id":414,"createTime":23,"updateTime":23,"relativeEntities":416,"slug":23,"properties":417,"entityType":23,"verifyStatus":23,"verifyTime":23,"verifyNote":23,"languages":23,"translateLanguages":23,"viewCount":23,"url":23,"parentIds":420,"statistic":23},[],{"title":418},{"EN":419},"Pharmacy, Federal University of Paraná 632, Av. 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Nói chung, phụ nữ thường báo cáo triệu chứng bệnh lý với tỷ lệ cao hơn, thường xuyên thăm khám bác sĩ hơn, và sử dụng nhiều dịch vụ chăm sóc sức khỏe khác hơn so với nam giới. Mặc dù lý do cho những khác biệt này giữa hai giới chưa được làm sáng tỏ hoàn toàn, nhưng có thể sự kết hợp giữa các yếu tố sinh học, sinh lý, xã hội, hành vi, tâm lý và văn hóa là những yếu tố góp phần. Một tỷ lệ đáng kể phụ nữ mắc hen suyễn, viêm khớp, đau nửa đầu, tiểu đường, trầm cảm hoặc động kinh gặp phải tình trạng bệnh nặng hơn trước khi có kinh nguyệt. Cơ chế của tình trạng này chưa được biết đến, nhưng được suy đoán là đa yếu tố do có nhiều tác nhân điều hòa và trung gian nội sinh và ngoại sinh của mỗi bệnh. Như một phần trong liệu pháp chung cho các cơn bùng phát liên quan đến chu kỳ của bất kỳ một trong những rối loạn này, bệnh nhân nên được khuyến khích sử dụng lịch kinh nguyệt để theo dõi các dấu hiệu và triệu chứng trong hai đến ba chu kỳ; nếu phát hiện được xu hướng chu kỳ, phụ nữ nên dự đoán các cơn bùng phát và tránh các yếu tố kích thích. Cần có thể thực hiện điều chỉnh theo chu kỳ bằng liệu pháp dược phẩm. Nếu không thành công, việc thử nghiệm ức chế rụng trứng bằng hormone giải phóng gonadotropin (GnRH) có thể là cần thiết. Nếu điều đó thành công, việc điều trị liên tục bằng hormone GnRH và điều trị bổ sung steroid hoặc các lựa chọn thay thế ít tốn kém hơn có thể có hiệu quả. Nếu liệu pháp dược phẩm không khả thi, cắt bỏ tử cung và cắt bỏ cả hai buồng trứng kèm theo liệu pháp thay thế estrogen sẽ là biện pháp cuối cùng. Những khác biệt theo giới tính và những thay đổi liên quan đến chu kỳ kinh nguyệt là những lĩnh vực quan trọng cần nghiên cứu lâm sàng và cơ chế.","\u003Cjats:p>Pharmacists should be aware of gender‐based differences and menstrual cycle‐related changes in six diseases: asthma, arthritis, migraine, diabetes, depression, and epilepsy. In general, women report symptoms of physical illness at higher rates, visit physicians more frequently, and make greater use of other health care services than men. Whereas reasons for these gender differences are not fully clear, a combination of biologic, physiologic, social, behavioral, psychologic, and cultural factors most likely contributes. A significant percentage of women with asthma, arthritis, migraine, diabetes, depression, or epilepsy experience worsening of their disease premenstrually. The mechanism is unknown, but is speculated to be multifactorial because of many endogenous and exogenous modulators and mediators of each disease. As part of general therapy for cycle‐related exacerbations of any one of these disorders, patients should be encouraged to use a menstrual calendar to track signs and symptoms for two to three cycles; if cyclic trends are identified, the women should anticipate exacerbations and avoid triggering factors. Cyclic modulation with pharmacotherapy may be attempted. If unsuccessful, a trial of medical ovulation suppression with a gonadotropin‐releasing hormone (GnRH) analog may be warranted. If that is successful, continuous therapy with a GnRH analog and steroid add‐back therapy or less expensive alternatives may be effective. If pharmacotherapy is impractical, hysterectomy and bilateral oophorectomy with estrogen replacement therapy is a last resort. Gender differences and menstrual cycle‐related changes are important areas for clinical and mechanistic research.\u003C\u002Fjats:p>",{"EN":664,"VI":665},"Gender‐Based Differences and Menstrual Cycle‐Related Changes in Specific Diseases: Implications for Pharmacotherapy","Sự khác biệt theo giới tính và sự thay đổi liên quan đến chu kỳ kinh nguyệt trong một số bệnh cụ thể: Những hệ quả đối với điều trị bằng thuốc",{"VOID":667},"10809339",{"VOID":669},"10.1592\u002Fphco.20.6.523.35161",[112],[406],"https:\u002F\u002Faccpjournals.onlinelibrary.wiley.com\u002Fdoi\u002F10.1592\u002Fphco.20.6.523.35161",[674],{"id":675,"sortIndex":24,"researcher":23,"roles":676,"affiliations":677,"properties":686,"displayName":690,"givenName":23,"familyName":23},"4e336660-9cb7-4506-8ea8-5a42d5728eae",[],[678],{"id":679,"sortIndex":24,"affiliation":680,"properties":23},"28550091-cfb3-4aaf-a62a-dbfcdeeb9426",{"id":679,"createTime":23,"updateTime":23,"relativeEntities":681,"slug":23,"properties":682,"entityType":23,"verifyStatus":23,"verifyTime":23,"verifyNote":23,"languages":23,"translateLanguages":23,"viewCount":23,"url":23,"parentIds":685,"statistic":23},[],{"title":683},{"EN":684},"Faculty of Pharmaceutical#R#                    Sciences, University of British Columbia, Vancouver, Canada.",[],{"orcid":687,"title":689,"openalex":691},{"VOID":688},"https:\u002F\u002Forcid.org\u002F0000-0002-7802-0939",{"EN":690},"Mary H. 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RU, 1995, Menstrual “asthma”—therapy?, [letter] Fertil Steril, 63, 1131, 10.1016\u002FS0015-0282(16)57563-3",{"doi":1185},"10.1016\u002FS0015-0282(16)57563-3",{"id":23,"text":1187,"url":23,"identifiers":1188},"Gorrell GJ, 1985, Relief of asthma with danazol [letter], Can Med Assoc J, 132, 100",{},{"id":23,"text":1190,"url":23,"identifiers":1191},"Pride SM, 1984, Relief of asthma in two patients receiving danazol for endometriosis, Can Med Assoc J, 131, 763",{},{"id":23,"text":1193,"url":23,"identifiers":1194},"Blumenfeld Z, 1994, Menstrual asthma: use of a gonadotropin‐releasing hormone analogue for the treatment of cyclic aggravation of bronchial asthma, Fertil Steril, 62, 197, 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exchange, drug removal, hemodialysis, pharmacokinetics, plasmapheresis",{"VOID":1343},"W2092328931",{"VI":1345,"EN":1346},"\u003Cjats:p>Trái ngược với tài liệu liên quan đến việc loại bỏ thuốc trong quá trình lọc máu, dữ liệu về việc loại bỏ thuốc trong plasmapheresis còn rất thiếu. Trong vòng 40 năm qua, khoảng 70 công trình nghiên cứu - chủ yếu là các báo cáo trường hợp ngộ độc - đã mô tả tác động của plasmapheresis đối với các tác nhân dược phẩm. Những vấn đề quan trọng bao gồm việc tách thuốc trong quá trình trao đổi huyết tương với hóa trị liệu, cũng như các nhóm thuốc như kháng sinh, thuốc chống đông, thuốc chống động kinh, các tác nhân tim mạch và thuốc ức chế miễn dịch. Những cân nhắc khác là những ưu điểm và nhược điểm của các phương pháp khác nhau được sử dụng trong các báo cáo đã công bố và khuyến nghị cho các nghiên cứu dược động học trong tương lai trong lĩnh vực này.\u003C\u002Fjats:p>","\u003Cjats:p>Contrary to the literature about drug removal during hemodialysis, data regarding drug removal during plasmapheresis are sparse. Over the last 40 years, approximately 70 publications—mostly case reports of overdoses—have described the effects of plasmapheresis on pharmaceutical agents. Important issues are drug extraction during plasma exchange with chemotherapy, as well as drug classes such as antiinfectives, anticoagulants, antiepileptics, cardiovascular agents, and immunosuppressants. 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2000, Clinical pharmacokinetics during plasma exchange, Therapie, 55, 269",{},{"id":23,"text":1821,"url":23,"identifiers":1822},"10.1016\u002FS0003-4975(03)01246-3",{"doi":1821},{"id":23,"text":1824,"url":23,"identifiers":1825},"Fauvelle F., 1991, Extraction of drugs in plasma exchange [in French], Therapie, 46, 109",{},{"id":1827,"createTime":1828,"updateTime":1829,"relativeEntities":1830,"slug":1831,"properties":1832,"entityType":108,"verifyStatus":109,"verifyTime":1848,"verifyNote":110,"languages":1849,"translateLanguages":1850,"viewCount":24,"primaryUrl":1851,"fullTextUrl":23,"authors":1852,"publicationType":230,"publisherRelationship":1923,"citationCount":1969,"citationInfo":1970,"publishDate":1974,"publishYear":1971,"citationAnalyzeStatus":22,"lastCitationAnalyze":23,"indexDatabases":1975,"openAccess":23,"references":1976,"isForceReanalyzing":380},"371af857-8bbe-42e8-befc-f00261969665","2024-12-12T21:58:27.310+00:00","2025-01-26T12:45:40.323+00:00",[],"Use-of-Tissue-Plasminogen-Activator-Alteplase-for-Suspected-Impella-Thrombosis",{"mag":1833,"keywords":1835,"openalex":1836,"abstract":1838,"title":1841,"pm":1844,"doi":1846},{"VOID":1834},"2995222391",{"VI":391},{"VOID":1837},"W2995222391",{"VI":1839,"EN":1840},"\u003Cjats:sec>\u003Cjats:title>Thông tin nền\u003C\u002Fjats:title>\u003Cjats:p>Các thiết bị Impella ngày càng được sử dụng nhiều hơn để điều trị sốc tim. Tần suất hình thành huyết khối và tan máu ở những bệnh nhân đang được hỗ trợ bằng Impella tăng lên theo thời gian sử dụng, và việc quản lý thuyên tắc Impella vẫn chưa rõ ràng.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Phương pháp\u003C\u002Fjats:title>\u003Cjats:p>Trong loạt trường hợp này, chúng tôi mô tả việc sử dụng activator plasminogen tissular (tPA) alteplase của bệnh viện cho dung dịch xả Impella (0,04 hoặc 0,08 mg\u002Fml tPA trong nước tiệt trùng) để quản lý thuyên tắc Impella nghi ngờ ở năm bệnh nhân, mỗi người có lộ trình lâm sàng, điều trị và kết quả khác nhau. Do bằng chứng hạn chế về chẩn đoán thuyên tắc Impella, sự nghi ngờ được thúc đẩy bởi sự hiện diện của tốc độ xả giảm, áp lực xả tăng và các dấu hiệu của tan máu như tăng lactate dehydrogenase và tiểu máu.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Kết quả\u003C\u002Fjats:title>\u003Cjats:p>Trong tất cả các trường hợp, việc sử dụng tPA đã dẫn đến việc phục hồi tốc độ xả thấp và áp lực xả cao. Không có biến chứng chảy máu lớn nào trực tiếp liên quan đến tPA. Hai bệnh nhân đã được cầu nối thành công đến cấy ghép tim, hai bệnh nhân đã trải qua cấy ghép thiết bị hỗ trợ thất trái, và một bệnh nhân đã qua đời sau khi ngừng điều trị.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Kết luận\u003C\u002Fjats:title>\u003Cjats:p>Dựa trên kinh nghiệm của chúng tôi, việc sử dụng tPA có vẻ là một lựa chọn cứu trợ khả thi và an toàn để trì hoãn hoặc ngăn chặn việc thay thế thiết bị trong bối cảnh nghi ngờ thuyên tắc Impella.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>","\u003Cjats:sec>\u003Cjats:title>Background\u003C\u002Fjats:title>\u003Cjats:p>Impella devices are being increasingly used to manage cardiogenic shock. The incidence of thrombosis and hemolysis in patients on Impella support increases with longer durations of use, and the management of Impella thrombosis remains ill‐defined.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Methods\u003C\u002Fjats:title>\u003Cjats:p>In this case series, we describe our institutional use of tissue plasminogen activator (tPA) alteplase in the Impella purge solution (0.04 or 0.08 mg\u002Fml tPA in sterile water) for management of suspected Impella thrombosis in five patients, each with a different clinical course, treatment, and outcome. Given the limited evidence on the diagnosis of Impella thrombosis, suspicion was driven by the presence of decreased purge flow rates, increased purge pressures, and markers of hemolysis such as elevated lactate dehydrogenase and hematuria.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Outcomes\u003C\u002Fjats:title>\u003Cjats:p>In all cases, tPA administration resulted in resolution of low purge flow rates and high purge pressures. No major bleeding complications were directly associated with tPA. Two patients were bridged successfully to heart transplantation, two patients underwent left ventricular assist device implantation, and one patient died after withdrawal of care.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Conclusion\u003C\u002Fjats:title>\u003Cjats:p>Based on our experience, tPA administration appears to be a viable and safe salvage option to delay or prevent device exchange in the setting of suspected Impella thrombosis.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>",{"EN":1842,"VI":1843},"Use of Tissue Plasminogen Activator Alteplase for Suspected Impella Thrombosis","Sử dụng Activator Plasminogen Tissular Alteplase cho Thuyên tắc Impella Nghi ngờ",{"VOID":1845},"31859371",{"VOID":1847},"10.1002\u002Fphar.2356","2024-12-12T21:58:27.309+00:00",[112],[406],"https:\u002F\u002Faccpjournals.onlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fphar.2356",[1853,1872,1887,1904],{"id":1854,"sortIndex":24,"researcher":23,"roles":1855,"affiliations":1856,"properties":1865,"displayName":1869,"givenName":23,"familyName":23},"6c8e14b4-c037-412f-ac97-0b05b2778810",[],[1857],{"id":1858,"sortIndex":24,"affiliation":1859,"properties":23},"46d213de-e5c1-4987-930b-31b02523b6a2",{"id":1858,"createTime":23,"updateTime":23,"relativeEntities":1860,"slug":23,"properties":1861,"entityType":23,"verifyStatus":23,"verifyTime":23,"verifyNote":23,"languages":23,"translateLanguages":23,"viewCount":23,"url":23,"parentIds":1864,"statistic":23},[],{"title":1862},{"VI":1863},"Department of Pharmacy, Houston Methodist Hospital, Houston, Texas",[],{"orcid":1866,"title":1868,"openalex":1870},{"VOID":1867},"https:\u002F\u002Forcid.org\u002F0000-0001-9488-6997",{"EN":1869},"Luma Succar",{"VOID":1871},"A5044487991",{"id":1873,"sortIndex":129,"researcher":23,"roles":1874,"affiliations":1875,"properties":1882,"displayName":1884,"givenName":23,"familyName":23},"bfc6798c-03e5-475d-932b-84a5b7a2b344",[],[1876],{"id":1858,"sortIndex":24,"affiliation":1877,"properties":23},{"id":1858,"createTime":23,"updateTime":23,"relativeEntities":1878,"slug":23,"properties":1879,"entityType":23,"verifyStatus":23,"verifyTime":23,"verifyNote":23,"languages":23,"translateLanguages":23,"viewCount":23,"url":23,"parentIds":1881,"statistic":23},[],{"title":1880},{"VI":1863},[],{"title":1883,"openalex":1885},{"EN":1884},"Kevin R. Donahue",{"VOID":1886},"A5024705426",{"id":1888,"sortIndex":164,"researcher":23,"roles":1889,"affiliations":1890,"properties":1897,"displayName":1901,"givenName":23,"familyName":23},"768e8755-346e-425f-8ec2-6f78196a60e1",[],[1891],{"id":1858,"sortIndex":24,"affiliation":1892,"properties":23},{"id":1858,"createTime":23,"updateTime":23,"relativeEntities":1893,"slug":23,"properties":1894,"entityType":23,"verifyStatus":23,"verifyTime":23,"verifyNote":23,"languages":23,"translateLanguages":23,"viewCount":23,"url":23,"parentIds":1896,"statistic":23},[],{"title":1895},{"VI":1863},[],{"orcid":1898,"title":1900,"openalex":1902},{"VOID":1899},"https:\u002F\u002Forcid.org\u002F0000-0002-8418-3566",{"EN":1901},"Sara Varnado",{"VOID":1903},"A5013985535",{"id":1905,"sortIndex":182,"researcher":23,"roles":1906,"affiliations":1907,"properties":1916,"displayName":1920,"givenName":23,"familyName":23},"5cc69783-35e1-49a8-b6b1-428e27ce9647",[],[1908],{"id":1909,"sortIndex":24,"affiliation":1910,"properties":23},"7b88800e-21c7-4272-85f5-09cba4b339fb",{"id":1909,"createTime":23,"updateTime":23,"relativeEntities":1911,"slug":23,"properties":1912,"entityType":23,"verifyStatus":23,"verifyTime":23,"verifyNote":23,"languages":23,"translateLanguages":23,"viewCount":23,"url":23,"parentIds":1915,"statistic":23},[],{"title":1913},{"EN":1914},"Advanced Heart Failure and Transplant, Methodist DeBakey Cardiology Associates, Houston Methodist Hospital, Houston, Texas",[],{"orcid":1917,"title":1919,"openalex":1921},{"VOID":1918},"https:\u002F\u002Forcid.org\u002F0000-0003-3699-3297",{"EN":1920},"Ju H. 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August2016.http:\u002F\u002Fwww.abiomed.com\u002Fimpella-device-instructions-for-use. Accessed September 11 2019.",{},{"id":23,"text":1987,"url":23,"identifiers":1988},"10.1177\u002F1060028013503623",{"doi":1987},{"id":23,"text":1990,"url":23,"identifiers":1991},"Abiomed®.Impella® Updates. Available fromhttps:\u002F\u002Fwww.abiomedtraining.com\u002Fpdf\u002F1472144471a2a2e47d37d60a8b0ce2b827df735e6f.pdf.Accessed October 9 2016.",{},{"id":23,"text":1993,"url":23,"identifiers":1994},"10.1111\u002Fjoic.12080",{"doi":1993},{"id":23,"text":1996,"url":23,"identifiers":1997},"10.1161\u002FCIRCHEARTFAILURE.112.967224",{"doi":1996},{"id":23,"text":1999,"url":23,"identifiers":2000},"10.1056\u002FNEJMoa1313385",{"doi":1999},{"id":23,"text":2002,"url":23,"identifiers":2003},"10.1016\u002Fj.healun.2013.08.021",{"doi":2002},{"id":23,"text":2005,"url":23,"identifiers":2006},"10.1016\u002Fj.healun.2013.10.005",{"doi":2005},{"id":23,"text":2008,"url":23,"identifiers":2009},"10.1016\u002Fj.jchf.2014.12.001",{"doi":2008},{"id":23,"text":2011,"url":23,"identifiers":2012},"10.1016\u002Fj.healun.2014.01.005",{"doi":2011},{"id":23,"text":2014,"url":23,"identifiers":2015},"Cathflo Activase (alteplase) [package insert].South San Francisco CA:Genentech Inc; February2018.",{},{"id":23,"text":2017,"url":23,"identifiers":2018},"10.1097\u002FMAT.0000000000000877",{"doi":2017},{"id":2020,"createTime":2021,"updateTime":2022,"relativeEntities":2023,"slug":2024,"properties":2025,"entityType":108,"verifyStatus":109,"verifyTime":2021,"verifyNote":110,"languages":2041,"translateLanguages":2042,"viewCount":24,"primaryUrl":2043,"fullTextUrl":23,"authors":2044,"publicationType":230,"publisherRelationship":2139,"citationCount":2184,"citationInfo":2185,"publishDate":2188,"publishYear":2186,"citationAnalyzeStatus":22,"lastCitationAnalyze":23,"indexDatabases":2189,"openAccess":23,"references":2190,"isForceReanalyzing":380},"c1361cb1-2a74-4e9d-85b1-5e9b360b5af8","2024-12-26T12:59:06.255+00:00","2025-01-26T12:44:43.365+00:00",[],"Prophylactic-Magnesium-to-Decrease-the-Arrhythmogenic-Potential-of-Class-III-Antiarrhythmic-Agents-in-a-Rabbit-Model",{"mag":2026,"keywords":2028,"openalex":2029,"abstract":2031,"title":2034,"pm":2037,"doi":2039},{"VOID":2027},"1976025571",{"VI":391},{"VOID":2030},"W1976025571",{"VI":2032,"EN":2033},"\u003Cjats:p>Chúng tôi đã đánh giá hiệu quả dự phòng của magie sulfat tiêm tĩnh mạch đối với sự xuất hiện của torsades de pointes và các pha khử cực sớm, cũng như đối với khoảng QT (QTc) trong một mô hình thỏ đã được thiết lập. Mười con thỏ được tiêm methoxamin qua tĩnh mạch để làm chậm nhịp tim của chúng. Sau 12 phút, năm con được nhận 1 bolus 60 mg\u002Fkg và truyền liên tục magie 0,6 mg\u002Fkg\u002Fphút, và năm con còn lại được nhận dung dịch muối sinh lý đồng lượng cùng với chất chống rối loạn nhịp loại III clofilium 5 mg\u002Fkg trong 30 phút. Điện tâm đồ ở điểm II và điện thế hành động đơn cực đã được ghi liên tục trong suốt cuộc thử nghiệm. Nhóm magie có tần suất torsades de pointes và pha khử cực sớm thấp hơn một cách đáng kể so với nhóm dung dịch muối sinh lý (1\u002F5 và 5\u002F5 cho cả hai tham số, p= 0,048). Không có sự khác biệt giữa các nhóm trong khoảng QT hoặc QTc tại thời điểm cơ bản hoặc tại mức tối đa gia tăng QT hoặc QTc. Magie làm giảm sự xuất hiện của torsades de pointes mà không ảnh hưởng đến khoảng QT hoặc QTc nhưng lại làm giảm sự xuất hiện của các pha khử cực sớm. Các phát hiện này cần được xác thực trong các nghiên cứu trên con người.\u003C\u002Fjats:p>","\u003Cjats:p>We assessed the prophylactic effect of intravenous magnesium sulfate on the occurrence of torsades de pointes and early after‐depolarizations, and on the QT interval (QTc) in an established rabbit model. Ten rabbits were given intravenous methoxamine to slow their heart rates. After 12 minutes five animals received a 60‐mg\u002Fkg bolus and continuous infusion of magnesium 0.6 mg\u002Fkg\u002Fminute, and five received equivolume normal saline concurrently with the class III antiarrhythmic agent clofilium 5 mg\u002Fkg over 30 minutes. Electrocardiogram lead II and the monophasic action potential were recorded continuously throughout the experiment. The magnesium group experienced significantly less torsades de pointes and early after‐depolarizations than the normal saline group (1\u002F5 and 5\u002F5 both parameters, respectively, p= 0.048). There were no differences between groups in QT or QTc interval at baseline or at maximum QT or QTc prolongation. Magnesium decreases the occurrence of torsades de pointes without affecting the QT or QTc interval but does decrease the occurrence of early after‐depolarizations. These findings must be validated in human studies.\u003C\u002Fjats:p>",{"EN":2035,"VI":2036},"Prophylactic Magnesium to Decrease the Arrhythmogenic Potential of Class III Antiarrhythmic Agents in a Rabbit Model","Magnesium Dự Phòng Giảm Tiềm Năng Gây Rối Loạn Nhịp Của Các Chất Chống Rối Loạn Nhịp Loại III Trong Mô Hình Thỏ",{"VOID":2038},"10331827",{"VOID":2040},"10.1592\u002Fphco.19.8.635.31528",[112],[406],"https:\u002F\u002Faccpjournals.onlinelibrary.wiley.com\u002Fdoi\u002F10.1592\u002Fphco.19.8.635.31528",[2045,2072,2095,2114],{"id":2046,"sortIndex":24,"researcher":23,"roles":2047,"affiliations":2048,"properties":2065,"displayName":2069,"givenName":23,"familyName":23},"411f747e-15ed-4e71-8938-90760ef86dec",[],[2049,2057],{"id":2050,"sortIndex":24,"affiliation":2051,"properties":23},"3d883ae3-bec9-41a5-b7a1-21df787acbb4",{"id":2050,"createTime":23,"updateTime":23,"relativeEntities":2052,"slug":23,"properties":2053,"entityType":23,"verifyStatus":23,"verifyTime":23,"verifyNote":23,"languages":23,"translateLanguages":23,"viewCount":23,"url":23,"parentIds":2056,"statistic":23},[],{"title":2054},{"EN":2055},"Connecticut Veterans Administration Medical Center, West Haven, Connecticut",[],{"id":2058,"sortIndex":129,"affiliation":2059,"properties":23},"85f3fb81-7267-46f3-8870-4e16d813f982",{"id":2058,"createTime":23,"updateTime":23,"relativeEntities":2060,"slug":23,"properties":2061,"entityType":23,"verifyStatus":23,"verifyTime":23,"verifyNote":23,"languages":23,"translateLanguages":23,"viewCount":23,"url":23,"parentIds":2064,"statistic":23},[],{"title":2062},{"VI":2063},"University of Connecticut, School of Pharmacy, Storrs, Connecticut",[],{"orcid":2066,"title":2068,"openalex":2070},{"VOID":2067},"https:\u002F\u002Forcid.org\u002F0000-0002-9367-4893",{"EN":2069},"C Michael White",{"VOID":2071},"A5004120573",{"id":2073,"sortIndex":129,"researcher":23,"roles":2074,"affiliations":2075,"properties":2090,"displayName":2092,"givenName":23,"familyName":23},"155aef0d-a175-4465-8e07-a4cd3c6fefb1",[],[2076,2084],{"id":2077,"sortIndex":24,"affiliation":2078,"properties":23},"45552977-7cff-42bf-9f13-53e48476acbe",{"id":2077,"createTime":23,"updateTime":23,"relativeEntities":2079,"slug":23,"properties":2080,"entityType":23,"verifyStatus":23,"verifyTime":23,"verifyNote":23,"languages":23,"translateLanguages":23,"viewCount":23,"url":23,"parentIds":2083,"statistic":23},[],{"title":2081},{"EN":2082},"Drug Information Center, Hartford Hospital, Hartford, Connecticut",[],{"id":2058,"sortIndex":129,"affiliation":2085,"properties":23},{"id":2058,"createTime":23,"updateTime":23,"relativeEntities":2086,"slug":23,"properties":2087,"entityType":23,"verifyStatus":23,"verifyTime":23,"verifyNote":23,"languages":23,"translateLanguages":23,"viewCount":23,"url":23,"parentIds":2089,"statistic":23},[],{"title":2088},{"VI":2063},[],{"title":2091,"openalex":2093},{"EN":2092},"Jianlin Xie",{"VOID":2094},"A5101162219",{"id":2096,"sortIndex":164,"researcher":23,"roles":2097,"affiliations":2098,"properties":2107,"displayName":2111,"givenName":23,"familyName":23},"d6b229f3-41f5-4b3e-a48e-ad2713328e8a",[],[2099],{"id":2100,"sortIndex":24,"affiliation":2101,"properties":23},"7bfcab4f-54f7-48e0-a384-ac08c79d5485",{"id":2100,"createTime":23,"updateTime":23,"relativeEntities":2102,"slug":23,"properties":2103,"entityType":23,"verifyStatus":23,"verifyTime":23,"verifyNote":23,"languages":23,"translateLanguages":23,"viewCount":23,"url":23,"parentIds":2106,"statistic":23},[],{"title":2104},{"VI":2105},"Chinese University of Hong Kong, Shatin, Hong Kong",[],{"orcid":2108,"title":2110,"openalex":2112},{"VOID":2109},"https:\u002F\u002Forcid.org\u002F0000-0001-7794-6214",{"EN":2111},"Moses S.S. 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Connecticut",[],{"id":2127,"sortIndex":129,"affiliation":2128,"properties":23},"6cbd74ff-e260-491e-ab48-f2539dc7412e",{"id":2127,"createTime":23,"updateTime":23,"relativeEntities":2129,"slug":23,"properties":2130,"entityType":23,"verifyStatus":23,"verifyTime":23,"verifyNote":23,"languages":23,"translateLanguages":23,"viewCount":23,"url":23,"parentIds":2133,"statistic":23},[],{"title":2131},{"VI":2132},"University of Connecticut School of Medicine, Farmington, Connecticut",[],{"title":2135,"openalex":2137},{"EN":2136},"Jeffrey 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JS, 1995, Cardiac arrhythmias: their mechanisms, diagnosis, and management, 173",{},{"id":23,"text":2198,"url":23,"identifiers":2199},"10.2165\u002F00003495-199447010-00004",{"doi":2198},{"id":23,"text":2201,"url":23,"identifiers":2202},"Tzoni D, 1988, Treatment of torsades de pointes with magnesium sulfate, Circulation, 77, 292",{},{"id":23,"text":2204,"url":23,"identifiers":2205},"Baai S, 1983, Drug therapy for torsades de pointes, J Cardiovasc Electrophysiol, 4, 206",{},{"id":23,"text":2207,"url":23,"identifiers":2208},"10.1111\u002Fj.1540-8159.1990.tb02131.x",{"doi":2207},{"id":23,"text":2210,"url":23,"identifiers":2211},"Carlsson L, 1993, Attenuation of proarrhythmia related to delayed repolarization by low dose lidocaine in the anesthetized rabbit, J Pharmacol Exp Ther, 267, 1076",{},{"id":23,"text":2213,"url":23,"identifiers":2214},"Buchanan LV, 1993, Comparative assessment of ibutilide, d‐sotalol, clofilium, E‐4031, and UK‐68,798 in a rabbit model of proarrhythmia, J Cardiovasc Pharmacol, 220, 540",{},{"id":23,"text":2216,"url":23,"identifiers":2217},"10.1016\u002F0735-1097(95)00046-7",{"doi":2216},{"id":23,"text":2219,"url":23,"identifiers":2220},"10.1111\u002Fj.1540-8159.1995.tb06990.x",{"doi":2219},{"id":23,"text":2222,"url":23,"identifiers":2223},"Roden DM, 1996, Ionic mechanisms for prolongation of refractoriness and their proarrhythmic and antiarrhythmic correlates, Am J Cardiol, 78, 12",{},{"id":23,"text":2225,"url":23,"identifiers":2226},"10.1161\u002F01.CIR.93.3.407",{"doi":2225},{"id":23,"text":2228,"url":23,"identifiers":2229},"10.1161\u002F01.RES.69.2.519",{"doi":2228},{"id":23,"text":2231,"url":23,"identifiers":2232},"Arena JP, 1988, Block of heart potassium channels by clofilium and its tertiary analogs: relationship between drug structure and type of channel blocked, Molec Pharmacol, 34, 60",{},{"id":23,"text":2234,"url":23,"identifiers":2235},"Lee KS, 1992, Ibutilide, a new compound with potent class III antiarrhythmic activity, activates a slow inward Na current in guinea pig ventricular cells, J Pharmacol Exp Ther, 262, 99",{},{"id":23,"text":2237,"url":23,"identifiers":2238},"10.1161\u002F01.CIR.91.12.3010",{"doi":2237},{"id":23,"text":2240,"url":23,"identifiers":2241},"Roden DM, 1996, Goodman and Gilman's pharmacologic basis of therapeutics, 839",{},{"id":23,"text":2243,"url":23,"identifiers":2244},"10.1016\u002F0006-2952(89)90272-4",{"doi":2243},{"id":23,"text":2246,"url":23,"identifiers":2247},"10.1002\u002Fclc.4960150210",{"doi":2246},{"id":23,"text":2249,"url":23,"identifiers":2250},"10.1007\u002FBF03029780",{"doi":2249},{"id":23,"text":2252,"url":23,"identifiers":2253},"10.1253\u002Fjcj.57.543",{"doi":2252},{"id":23,"text":2255,"url":23,"identifiers":2256},"10.1161\u002F01.CIR.77.6.1395",{"doi":2255},{"id":23,"text":2258,"url":23,"identifiers":2259},"10.1161\u002F01.CIR.86.6.1987",{"doi":2258},{"id":23,"text":2261,"url":23,"identifiers":2262},"10.1016\u002F0002-8703(89)90258-5",{"doi":2261},{"id":23,"text":2264,"url":23,"identifiers":2265},"10.1111\u002Fj.1472-8206.1993.tb00215.x",{"doi":2264},{"id":23,"text":2267,"url":23,"identifiers":2268},"10.1097\u002F00005344-199008000-00014",{"doi":2267},{"id":23,"text":2270,"url":23,"identifiers":2271},"10.1007\u002FBF00265966",{"doi":2270},{"id":23,"text":2273,"url":23,"identifiers":2274},"Critelli G, 1990, Magnesium and cardiac arrhythmias: reappraisal of an old substance, Cardiologia, 35, 39",{},{"id":23,"text":2276,"url":23,"identifiers":2277},"10.1161\u002F01.CIR.82.4.1106",{"doi":2276},{"id":23,"text":2279,"url":23,"identifiers":2280},"10.1111\u002Fj.1540-8167.1997.tb01014.x",{"doi":2279},{"id":23,"text":2282,"url":23,"identifiers":2283},"10.1016\u002FS0140-6736(96)02149-6",{"doi":2282},{"id":23,"text":2285,"url":23,"identifiers":2286},"10.1002\u002Fj.1875-9114.1997.tb03673.x",{"doi":2285},{"id":23,"text":2288,"url":23,"identifiers":2289},"10.1056\u002FNEJM199308123290702",{"doi":2288},{"id":23,"text":2291,"url":23,"identifiers":2292},"10.1016\u002FS0002-9149(96)00453-5",{"doi":2291},{"id":2294,"createTime":2295,"updateTime":2296,"relativeEntities":2297,"slug":2298,"properties":2299,"entityType":108,"verifyStatus":109,"verifyTime":2315,"verifyNote":110,"languages":2316,"translateLanguages":2317,"viewCount":24,"primaryUrl":2318,"fullTextUrl":23,"authors":2319,"publicationType":230,"publisherRelationship":2439,"citationCount":2484,"citationInfo":2485,"publishDate":2488,"publishYear":2486,"citationAnalyzeStatus":22,"lastCitationAnalyze":23,"indexDatabases":2489,"openAccess":23,"references":2490,"isForceReanalyzing":380},"21117450-24ea-4438-be8f-542a6ab3f835","2024-12-29T10:10:37.203+00:00","2025-01-26T12:43:47.170+00:00",[],"The-Effect-of-Prophylactic-Nifedipine-on-Renal-Function-in-Patients-Administered-Contrast-Media",{"mag":2300,"keywords":2302,"openalex":2303,"abstract":2305,"title":2308,"pm":2311,"doi":2313},{"VOID":2301},"1915058917",{"VI":391},{"VOID":2304},"W1915058917",{"VI":2306,"EN":2307},"\u003Cjats:p>\u003Cjats:bold>Mục tiêu nghiên cứu\u003C\u002Fjats:bold>. Xác định xem việc dự phòng bằng nifedipine có thể giảm tần suất suy thận do thuốc cản quang hay không.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Thiết kế\u003C\u002Fjats:bold>. Thử nghiệm lâm sàng ngẫu nhiên, tiềm năng.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Địa điểm\u003C\u002Fjats:bold>. Một bệnh viện liên kết với trường đại học.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Bệnh nhân\u003C\u002Fjats:bold>. Bệnh nhân đang thực hiện các xét nghiệm hình ảnh đã được lên lịch có liên quan đến việc tiêm thuốc cản quang.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Can thiệp\u003C\u002Fjats:bold>. Bốn mươi hai bệnh nhân được ngẫu nhiên nhận nifedipine 10 mg đường uống 1 giờ trước khi thực hiện thủ tục hình ảnh, và 43 bệnh nhân nhận không điều trị.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Đo lường và Kết quả chính\u003C\u002Fjats:bold>. Mức creatinine huyết thanh cơ bản được so sánh với mức tối đa 24 và 48 giờ sau khi sử dụng thuốc cản quang. Không có sự khác biệt có ý nghĩa thống kê nào được thấy ở cả thay đổi trung bình hay thay đổi phần trăm trung bình về mức creatinine huyết thanh giữa nhóm kiểm soát và nhóm nifedipine. Thay đổi trung bình về mức creatinine huyết thanh là +7.4 μmol\u002FL ở nhóm kiểm soát và +2.7 μmol\u002FL ở nhóm nifedipine (p=0.33); thay đổi phần trăm trung bình lần lượt là +10.2% và +4.8% (p=0.54).\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Kết luận\u003C\u002Fjats:bold>. Bất kể phân tích thống kê, có thể không có ý nghĩa lâm sàng khi mức creatinine huyết thanh tăng lên ở mức độ này (< 0.1 mg\u002Fdl). Do đó, chúng tôi kết luận rằng nifedipine dự phòng không có lợi ích lâm sàng trong việc duy trì chức năng thận ở bệnh nhân nhận thuốc cản quang và tác nhân này không nên được sử dụng thường quy cho mục đích này.","\u003Cjats:p>\u003Cjats:bold>Study Objective\u003C\u002Fjats:bold>. To determine if prophylaxis with nifedipine could decrease the frequency of contrast medium‐induced renal impairment.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Design\u003C\u002Fjats:bold>. Prospective, randomized clinical trial.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Setting\u003C\u002Fjats:bold>. A university‐affiliated hospital.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Patients\u003C\u002Fjats:bold>. Patients undergoing scheduled radiologic examinations involving infusion of contrast media.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Interventions\u003C\u002Fjats:bold>. Forty‐two patients were randomized to receive nifedipine 10 mg orally 1 hour before the imaging procedure, and 43 to receive no treatment.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Measurements and Main Results\u003C\u002Fjats:bold>. Baseline serum creatinine levels were compared with maximum levels 24 and 48 hours after administration of contrast medium. No statistically significant difference was seen in either the mean change or mean percentage change in serum creatinine between the control and nifedipine groups. The mean changes in serum creatinine were +7.4 μmol\u002FL in the control group and +2.7 μmol\u002FL in the nifedipine group (p=0.33); the mean percentage changes were +10.2% and +4.8%, respectively (p=0.54).\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Conclusion\u003C\u002Fjats:bold>. Regardless of statistical analysis, it is unlikely that elevations in serum creatinine of this magnitude (< 0.1 mg\u002Fdl) are of clinical significance. We therefore conclude that prophylactic nifedipine is not clinically beneficial in preserving renal function in patients receiving contrast medium and that the agent should not be routinely administered for this purpose.\u003C\u002Fjats:p>",{"EN":2309,"VI":2310},"The Effect of Prophylactic Nifedipine on Renal Function in Patients Administered Contrast Media","Ảnh hưởng của Nifedipine dự phòng đối với chức năng thận ở bệnh nhân sử dụng thuốc cản quang",{"VOID":2312},"7739947",{"VOID":2314},"10.1002\u002Fj.1875-9114.1995.tb04332.x","2024-12-29T10:10:37.202+00:00",[112],[406],"https:\u002F\u002Faccpjournals.onlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fj.1875-9114.1995.tb04332.x",[2320,2339,2356,2373,2388,2403,2420],{"id":2321,"sortIndex":24,"researcher":23,"roles":2322,"affiliations":2323,"properties":2332,"displayName":2336,"givenName":23,"familyName":23},"2f4bb334-7559-46c9-8beb-abea31c6be83",[],[2324],{"id":2325,"sortIndex":24,"affiliation":2326,"properties":23},"04340b82-d435-4164-8698-8bf95b004e72",{"id":2325,"createTime":23,"updateTime":23,"relativeEntities":2327,"slug":23,"properties":2328,"entityType":23,"verifyStatus":23,"verifyTime":23,"verifyNote":23,"languages":23,"translateLanguages":23,"viewCount":23,"url":23,"parentIds":2331,"statistic":23},[],{"title":2329},{"EN":2330},"Departments of Internal Medicine, Pittsburgh Heart Institute, Pittsburgh, Pennsylvania",[],{"orcid":2333,"title":2335,"openalex":2337},{"VOID":2334},"https:\u002F\u002Forcid.org\u002F0000-0003-4190-5853",{"EN":2336},"Ziad El Khoury",{"VOID":2338},"A5013515794",{"id":2340,"sortIndex":129,"researcher":23,"roles":2341,"affiliations":2342,"properties":2351,"displayName":2353,"givenName":23,"familyName":23},"d58b3f4c-8eba-42e3-980f-746defb608a9",[],[2343],{"id":2344,"sortIndex":24,"affiliation":2345,"properties":23},"5dab758c-dc9b-4c15-af2d-3a2f3251d802",{"id":2344,"createTime":23,"updateTime":23,"relativeEntities":2346,"slug":23,"properties":2347,"entityType":23,"verifyStatus":23,"verifyTime":23,"verifyNote":23,"languages":23,"translateLanguages":23,"viewCount":23,"url":23,"parentIds":2350,"statistic":23},[],{"title":2348},{"EN":2349},"Department of Clinical Pharmacy, Duquesne University, Pittsburgh Heart Institute, Pittsburgh, Pennsylvania",[],{"title":2352,"openalex":2354},{"EN":2353},"John R. 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R, 1985, Effects of calcium antagonists on renal hemodynamics, Am J Physiol, 249, F619",{},{"id":23,"text":2501,"url":23,"identifiers":2502},"Epstein M, 1992, Calcium antagonists and renal protection: current status and future perspectives, Arch Intern Med, 152, 1573, 10.1001\u002Farchinte.1992.00400200011003",{"doi":2503},"10.1001\u002Farchinte.1992.00400200011003",{"id":23,"text":2505,"url":23,"identifiers":2506},"10.1159\u002F000185971",{"doi":2505},{"id":23,"text":2508,"url":23,"identifiers":2509},"10.1097\u002F00005344-198303000-00015",{"doi":2508},{"id":23,"text":2511,"url":23,"identifiers":2512},"10.1002\u002Fclc.4960070107",{"doi":2511},{"id":23,"text":2514,"url":23,"identifiers":2515},"Neumayer H‐H, 1989, Prevention of radiocontrast‐media‐induced nephrotoxicity by the calcium channel blocker nitrendipine: a prospective randomised clinical trial, Nephrol Dial Transplant, 4, 1030",{},{"id":23,"text":2517,"url":23,"identifiers":2518},"10.1038\u002Fki.1985.32",{"doi":2517},{"id":23,"text":2520,"url":23,"identifiers":2521},"10.1097\u002F00004424-198610000-00005",{"doi":2520},{"id":23,"text":2523,"url":23,"identifiers":2524},"Humes HD, 1987, Pathogenesis of radiocontrast‐induced renal failure: comparative nephrotoxicity of diatrizoate and iopamidol, Diagn Imaging, 9, 12",{},{"id":23,"text":2526,"url":23,"identifiers":2527},"10.1056\u002FNEJM198901193200304",{"doi":2526},{"id":23,"text":2529,"url":23,"identifiers":2530},"10.1056\u002FNEJM198901193200303",{"doi":2529},{"id":23,"text":2532,"url":23,"identifiers":2533},"10.1148\u002Fradiology.175.3.2343107",{"doi":2532},{"id":23,"text":2535,"url":23,"identifiers":2536},"10.1097\u002F00004424-198303000-00012",{"doi":2535},{"id":23,"text":2538,"url":23,"identifiers":2539},"10.7326\u002F0003-4819-110-2-119",{"doi":2538},{"id":23,"text":2541,"url":23,"identifiers":2542},"10.7326\u002F0003-4819-104-4-501",{"doi":2541},{"id":23,"text":2544,"url":23,"identifiers":2545},"10.7326\u002F0003-4819-86-1-56",{"doi":2544},{"id":23,"text":2547,"url":23,"identifiers":2548},"10.2214\u002Fajr.141.5.1027",{"doi":2547},{"id":23,"text":2550,"url":23,"identifiers":2551},"10.1016\u002F0002-9343(82)90536-8",{"doi":2550},{"id":23,"text":2553,"url":23,"identifiers":2554},"10.1136\u002Fbmj.287.6384.3",{"doi":2553},{"id":23,"text":2556,"url":23,"identifiers":2557},"Messana JM, 1988, Comparison of the toxicity of the radiocontrast agents, iopamidol and diatrizoate, to rabbit renal proximal tubule cells in vitro, J Pharm Exp Ther, 244, 1139",{},{"id":23,"text":2559,"url":23,"identifiers":2560},"Fleming JT, 1987, Calcium antagonists preferentially dilate preglomerular vessels of hydronephrotic kidney, Am J Physiol, 253, 157",{},{"id":23,"text":2562,"url":23,"identifiers":2563},"Sweeney C, 1990, Interactions of the endothelium and mesangium in glomerular injury, J Am Soc Nephrol, 1, S13",{},{"id":23,"text":2565,"url":23,"identifiers":2566},"10.1016\u002F0002-9343(85)90076-2",{"doi":2565},{"id":23,"text":2568,"url":23,"identifiers":2569},"10.1038\u002Fki.1977.8",{"doi":2568},{"id":23,"text":2571,"url":23,"identifiers":2572},"10.1159\u002F000180580",{"doi":2571},{"id":23,"text":2574,"url":23,"identifiers":2575},"McEvoy GK, 1993, AHFS drug information, 978",{},{"id":2577,"createTime":2578,"updateTime":2579,"relativeEntities":2580,"slug":2581,"properties":2582,"entityType":108,"verifyStatus":109,"verifyTime":2578,"verifyNote":110,"languages":2598,"translateLanguages":2599,"viewCount":24,"primaryUrl":2600,"fullTextUrl":23,"authors":2601,"publicationType":230,"publisherRelationship":2621,"citationCount":2665,"citationInfo":2666,"publishDate":2670,"publishYear":741,"citationAnalyzeStatus":22,"lastCitationAnalyze":23,"indexDatabases":2671,"openAccess":23,"references":2672,"isForceReanalyzing":380},"55a51411-1df1-42ff-aa81-133234e5472f","2024-09-19T11:06:15.108+00:00","2025-01-25T05:18:30.043+00:00",[],"Rivastigmine-a-New-Generation-Cholinesterase-Inhibitor-for-the-Treatment-of-Alzheimer-s-Disease",{"mag":2583,"keywords":2585,"openalex":2586,"abstract":2588,"title":2591,"pm":2594,"doi":2596},{"VOID":2584},"2045562525",{"VI":391},{"VOID":2587},"W2045562525",{"VI":2589,"EN":2590},"\u003Cjats:p>Rivastigmine là một chất ức chế cholinesterase (ChEI) với công thức cấu trúc khác biệt so với các ChEI hiện có. Tacrine và donepezil được phân loại là các tác nhân tác động ngắn hoặc có khả năng hồi phục vì sự gắn kết với enzyme acetylcholinesterase (AChE) sẽ bị thủy phân trong vòng vài phút. Rivastigmine được phân loại là tác nhân tác động trung gian hoặc giả không hồi phục do có thời gian ức chế AChE kéo dài lên đến 10 giờ. Các nghiên cứu sinh hóa tiền lâm sàng chỉ ra rằng rivastigmine có tính chọn lọc đối với hệ thần kinh trung ương hơn là ức chế ngoại vi. Nó cải thiện suy giảm trí nhớ ở chuột có tổn thương não trước. Thuốc được hấp thụ nhanh chóng qua đường uống, với độ khả dụng sinh học đạt 0.355 và gắn kết protein thấp (40%). Thời gian bán thải của nó dưới 2 giờ, và thuốc được chuyển đổi thành một chất chuyển hóa không hoạt động tại nơi tác động, không đi qua các con đường chuyển hóa gan. Sự phân bố của nó về cơ bản không thay đổi ở những bệnh nhân suy thận hoặc gan. Nó cũng có các tác động phụ thuộc liều lên ức chế AChE. Trong hai thử nghiệm lâm sàng lớn đa trung tâm (tổng cộng 1324 bệnh nhân) sử dụng một cấu trúc titrat liều bắt buộc, rivastigmine 6–12 mg\u002Fngày đã cho kết quả vượt trội so với giả dược trên ba thang đo nhận thức và chức năng (p<0.001). Các triệu chứng tiêu hóa là các sự kiện không mong muốn được báo cáo thường xuyên nhất. Chúng chủ yếu xảy ra trong giai đoạn titrat liều và giảm dần trong giai đoạn duy trì. Rivastigmine cung cấp cho các bác sĩ lâm sàng một tác nhân điều trị khác để điều trị bệnh Alzheimer.\u003C\u002Fjats:p>","\u003Cjats:p>Rivastigmine is a cholinesterase inhibitor (ChEI) with a structural formula different from that of currently available ChEIs. Tacrine and donepezil are classified as short‐acting or reversible agents since binding to acetylcholinesterase enzyme (AChE) is hydrolyzed within minutes. Rivastigmine is classified as an intermediate‐acting or pseudo‐irreversible agent due to its long inhibition on AChE of up to 10 hours. Preclinical biochemical studies indicated that rivastigmine has central nervous system selectivity over peripheral inhibition. It ameliorated memory impairment in rats with forebrain lesions. The drug is rapidly absorbed orally, with a bioavailability of 0.355 and low protein binding (40%). Its elimination half‐life is less than 2 hours, and it is converted to an inactive metabolite at the site of action, bypassing hepatic metabolic pathways. Its disposition essentially is unaltered in patients with renal or hepatic impairment. It also has dose‐dependent effects on AChE inhibition. In the two large multicenter clinical trials (total 1324 patients) that used a forced‐dosage titration scheme, rivastigmine 6–12 mg\u002Fday was superior to placebo on three cognitive and functioning scales (p<0.001). Gastrointestinal symptoms are the most frequently reported adverse events. They occurred mostly during the dosage titration phase and decreased during the maintenance phase. Rivastigmine offers clinicians another therapeutic agent to treat Alzheimer's disease.\u003C\u002Fjats:p>",{"EN":2592,"VI":2593},"Rivastigmine, a New‐Generation Cholinesterase Inhibitor for the Treatment of Alzheimer's Disease","Rivastigmine, một chất ức chế cholinesterase thế hệ mới cho việc điều trị bệnh Alzheimer",{"VOID":2595},"10641971",{"VOID":2597},"10.1592\u002Fphco.20.1.1.34664",[112],[406],"https:\u002F\u002Faccpjournals.onlinelibrary.wiley.com\u002Fdoi\u002F10.1592\u002Fphco.20.1.1.34664",[2602],{"id":2603,"sortIndex":24,"researcher":23,"roles":2604,"affiliations":2605,"properties":2614,"displayName":2618,"givenName":23,"familyName":23},"43239252-1dd2-4d2e-a9f0-48b68b1e5849",[],[2606],{"id":2607,"sortIndex":24,"affiliation":2608,"properties":23},"8f5e7078-3a40-474b-b69b-230768945d4b",{"id":2607,"createTime":23,"updateTime":23,"relativeEntities":2609,"slug":23,"properties":2610,"entityType":23,"verifyStatus":23,"verifyTime":23,"verifyNote":23,"languages":23,"translateLanguages":23,"viewCount":23,"url":23,"parentIds":2613,"statistic":23},[],{"title":2611},{"EN":2612},"Departments of Pharmacy Practice and Pharmaceutical Sciences, Mercer University, Southern School of Pharmacy, Atlanta, Georgia.",[],{"orcid":2615,"title":2617,"openalex":2619},{"VOID":2616},"https:\u002F\u002Forcid.org\u002F0000-0002-7421-8593",{"EN":2618},"Michael W. 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Therapeutic strategies, 211",{},{"id":23,"text":2705,"url":23,"identifiers":2706},"Weinstock M., 1997, Possible role of the cholinergic system and disease models, J Neural Transm, 49, 93",{},{"id":23,"text":2708,"url":23,"identifiers":2709},"Weinstock M., 1994, Pharmacologic evaluation of phenyl‐carbamates as CNS selective acetylcholinesterase inhibitors, J Neural Transm, 43, 219",{},{"id":23,"text":2711,"url":23,"identifiers":2712},"Anand R., 1996, Efficacy and safety results of the early phase studies with Exelon (ENA 713) in Alzheimer's disease: an overview, J Drug Dev Clin Pract, 8, 1",{},{"id":23,"text":2714,"url":23,"identifiers":2715},"Enz A., 1994, Alzheimer's disease. Therapeutic strategies, 125, 10.1007\u002F978-1-4615-8149-9_22",{"doi":2716},"10.1007\u002F978-1-4615-8149-9_22",{"id":23,"text":2718,"url":23,"identifiers":2719},"10.1016\u002FS0079-6123(08)62429-2",{"doi":2718},{"id":23,"text":2721,"url":23,"identifiers":2722},"Giacobini E., 1994, Alzheimer's disease. Therapeutic strategies, 247, 10.1007\u002F978-1-4615-8149-9",{"doi":2723},"10.1007\u002F978-1-4615-8149-9",{"id":23,"text":2725,"url":23,"identifiers":2726},"10.1111\u002Fj.1600-0404.1998.tb00645.x",{"doi":2725},{"id":23,"text":2728,"url":23,"identifiers":2729},"10.2165\u002F00002512-199914030-00004",{"doi":2728},{"id":23,"text":2731,"url":23,"identifiers":2732},"Games D., 1997, Alzheimer‐type neuropathology in transgenic mice overexpressing V71F β‐amyloid precursor protein, Nature, 336, 523",{},{"id":23,"text":2734,"url":23,"identifiers":2735},"10.1016\u002F0278-5846(94)00113-V",{"doi":2734},{"id":23,"text":2737,"url":23,"identifiers":2738},"10.1111\u002Fj.1749-6632.1991.tb00232.x",{"doi":2737},{"id":23,"text":2740,"url":23,"identifiers":2741},"10.1007\u002FBF01705533",{"doi":2740},{"id":23,"text":2743,"url":23,"identifiers":2744},"10.1016\u002FS0006-8993(97)00982-7",{"doi":2743},{"id":23,"text":2746,"url":23,"identifiers":2747},"Tanaka K., 1993, Effects of the acetylcholinesterase inhibitor ENA‐713 on ischemia‐induced changes in acetylcholine and aromatic amine levels in the gerbil brain, Arch Int Pharmacodyn, 323, 85",{},{"id":23,"text":2749,"url":23,"identifiers":2750},"Schran HF, 1996, The effects of renal and hepatic impairment on the disposition of the acetylcholinesterase inhibitor SDZ ENA 713, Pharm Res, 13, S‐428",{},{"id":23,"text":2752,"url":23,"identifiers":2753},"10.1038\u002Fnpp.1993.10",{"doi":2752},{"id":23,"text":2755,"url":23,"identifiers":2756},"10.1176\u002Fajp.141.11.1356",{"doi":2755},{"id":23,"text":2758,"url":23,"identifiers":2759},"10.1097\u002F00002093-199700112-00004",{"doi":2758},{"id":23,"text":2761,"url":23,"identifiers":2762},"10.1016\u002F0022-3956(75)90026-6",{"doi":2761},{"id":23,"text":2764,"url":23,"identifiers":2765},"DeJong R., 1989, Measurement of quality‐of‐life changes in patients with Alzheimer's disease, Clin Ther, 11, 545",{},{"id":23,"text":2767,"url":23,"identifiers":2768},"10.1056\u002FNEJM199704243361704",{"doi":2767},{"id":23,"text":2770,"url":23,"identifiers":2771},"Cutler NR, 1996, Alzheimer's disease. Therapeutic strategies, 387",{},{"id":23,"text":2773,"url":23,"identifiers":2774},"10.1016\u002F0024-3205(96)00081-1",{"doi":2773},{"id":23,"text":2776,"url":23,"identifiers":2777},"10.1001\u002Farchinte.158.9.1021",{"doi":2776},{"id":23,"text":2779,"url":23,"identifiers":2780},"10.1212\u002FWNL.50.1.136",{"doi":2779},{"id":23,"text":2782,"url":23,"identifiers":2783},"10.1016\u002FS0011-393X(98)85048-0",{"doi":2782},{"id":23,"text":2785,"url":23,"identifiers":2786},"Corey‐Bloom J., 1998, A randomized trial evaluating the efficacy and safety of ENA 713 (rivastigmine tartrate), a new acetylcholinesterase inhibitor, in patients with mild to moderate severe Alzheimer's disease, Int J Geriatr Psychopharmacol, 1, 55",{},{"id":23,"text":2788,"url":23,"identifiers":2789},"10.1136\u002Fbmj.318.7184.633",{"doi":2788},{"id":23,"text":2791,"url":23,"identifiers":2792},"Cutler NR, 1998, Antiemetic therapy for Alzheimer's patients receiving the cholinesterase inhibitor SDZ ENA 713, Clin Pharmacol Ther, 63, 188",{},{"id":23,"text":2794,"url":23,"identifiers":2795},"10.1111\u002Fj.1532-5415.1998.tb01546.x",{"doi":2794},{"id":23,"text":2797,"url":23,"identifiers":2798},"Steele CD, 1999, Recognition and management of early Alzheimer's disease, J Clin Outcomes Manage, 6, 52",{},{"id":23,"text":2800,"url":23,"identifiers":2801},"10.2165\u002F00002018-199819060-00004",{"doi":2800},{"id":23,"text":2803,"url":23,"identifiers":2804},"10.1345\u002Faph.18211",{"doi":2803},{"id":23,"text":2806,"url":23,"identifiers":2807},"10.1016\u002FS0140-6736(05)62221-0",{"doi":2806},{"id":23,"text":2809,"url":23,"identifiers":2810},"10.2165\u002F00023210-199911040-00004",{"doi":2809},{"id":23,"text":2812,"url":23,"identifiers":2813},"Crismon ML, 1998, Pharmacokinetics and drug interactions of cholinesterase inhibitors administered in Alzheimer disease, Pharmacotherapy, 18, 47S, 10.1002\u002Fj.1875-9114.1998.tb03878.x",{"doi":2814},"10.1002\u002Fj.1875-9114.1998.tb03878.x",{"id":23,"text":2816,"url":23,"identifiers":2817},"10.1001\u002Fjama.281.15.1401",{"doi":2816},{"id":23,"text":2819,"url":23,"identifiers":2820},"10.1177\u002F089198879600900101",{"doi":2819},{"id":23,"text":2822,"url":23,"identifiers":2823},"10.4088\u002FJCP.v60n0510",{"doi":2822},{"id":23,"text":2825,"url":23,"identifiers":2826},"10.2165\u002F00023210-199911030-00001",{"doi":2825},{"id":2828,"createTime":2829,"updateTime":2830,"relativeEntities":2831,"slug":2832,"properties":2833,"entityType":108,"verifyStatus":109,"verifyTime":2829,"verifyNote":110,"languages":2849,"translateLanguages":2850,"viewCount":24,"primaryUrl":2851,"fullTextUrl":23,"authors":2852,"publicationType":230,"publisherRelationship":2919,"citationCount":2964,"citationInfo":2965,"publishDate":2968,"publishYear":2966,"citationAnalyzeStatus":22,"lastCitationAnalyze":23,"indexDatabases":2969,"openAccess":23,"references":2970,"isForceReanalyzing":380},"d8b77ddf-29d0-4f36-a026-1b47f3ee84ca","2024-10-04T18:57:53.038+00:00","2025-01-25T05:17:33.212+00:00",[],"Comparison-of-Intramuscular-Ketorolac-Tromethamine-and-Morphine-Sulfate-for-Analgesia-of-Pain-After-Major-Surgery",{"mag":2834,"keywords":2836,"openalex":2837,"abstract":2839,"title":2842,"pm":2845,"doi":2847},{"VOID":2835},"1545823900",{"VI":391},{"VOID":2838},"W1545823900",{"VI":2840,"EN":2841},"\u003Cjats:p>Ketorolac tromethamine là một loại thuốc giảm đau mới không gây nghiện tiêm được. Trong một nghiên cứu song song và mù đôi, hiệu quả giảm đau của các liều tiêm bắp đơn lẻ của ketorolac 10, 30 và 90 mg đã được so sánh với morphine sulfate 6 và 12 mg. Hai trăm bốn mươi một bệnh nhân được phân loại theo loại thủ thuật phẫu thuật và mức độ đau. Cường độ đau và mức độ giảm đau được đánh giá trong vòng 6 giờ bằng cách chấm điểm theo thang đo ngữ nghĩa và thang đo thị giác tương tự tiêu chuẩn. Những bệnh nhân nhận ketorolac 10, 30 hoặc 90 mg hoặc morphine (MS) 12 mg đều có mức độ giảm đau tốt hơn một cách có ý nghĩa thống kê trong hầu hết các phép đo được thực hiện so với những bệnh nhân nhận MS 6 mg (p \u003C 0.05). Ketorolac 10 và 30 mg có hiệu quả tương đương với morphine 12 mg trong suốt thời gian quan sát 6 giờ, và ketorolac 90 mg hiệu quả hơn morphine 12 mg trong toàn bộ 6 giờ. Những bệnh nhân mengalami cơn đau liên quan đến phẫu thuật lớn (ví dụ: cắt bỏ túi mật và cắt tử cung vùng bụng) dễ phân biệt tác động giảm đau của morphine hơn những người tham gia các thủ tục ít chấn thương hơn (ví dụ: sửa chữa gân và dây chằng)\u003C\u002Fjats:p>","\u003Cjats:p>Ketorolac tromethamine is a new injectable nonnarcotic analgesic. In a parallel, double‐blind study, the analgesic efficacies of single intramuscular doses of ketorolac 10, 30 and 90 mg were compared with those of morphine sulfate 6 and 12 mg. Two hundred forty‐one patients were categorized according to type of surgical procedure and severity of pain. Pain intensity and pain relief were assessed for 6 hours by scoring standard verbal and visual analog scales. Patients receiving ketorolac 10, 30 or 90 mg or morphine (MS) 12 mg all had significantly better pain relief in almost all measurements performed than those receiving MS 6 mg (p < 0.05). Ketorolac 10 and 30 mg were as effective as morphine 12 mg during the entire 6‐hour observation period, and ketorolac 90 mg was more effective than morphine 12 mg during the entire 6 hours. Patients with pain related to major surgery (e.g., cholecystectomy and abdominal hysterectomy) were better able to distinguish analgesic potency of morphine than those having less traumatic procedures (e.g., tendon and ligament repairs)\u003C\u002Fjats:p>",{"EN":2843,"VI":2844},"Comparison of Intramuscular Ketorolac Tromethamine and Morphine Sulfate for Analgesia of Pain After Major Surgery","So sánh Ketorolac Tromethamine tiêm bắp và Morphine Sulfate trong giảm đau sau phẫu thuật lớn",{"VOID":2846},"3540877",{"VOID":2848},"10.1002\u002Fj.1875-9114.1986.tb03485.x",[112],[406],"https:\u002F\u002Faccpjournals.onlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fj.1875-9114.1986.tb03485.x",[2853,2870,2885,2902],{"id":2854,"sortIndex":24,"researcher":23,"roles":2855,"affiliations":2856,"properties":2865,"displayName":2867,"givenName":23,"familyName":23},"dec0adab-5ff1-41a9-8d60-838d24eb6f8e",[],[2857],{"id":2858,"sortIndex":24,"affiliation":2859,"properties":23},"5a815838-9b9b-4e1e-b150-535ede46ca72",{"id":2858,"createTime":23,"updateTime":23,"relativeEntities":2860,"slug":23,"properties":2861,"entityType":23,"verifyStatus":23,"verifyTime":23,"verifyNote":23,"languages":23,"translateLanguages":23,"viewCount":23,"url":23,"parentIds":2864,"statistic":23},[],{"title":2862},{"EN":2863},"Research, Institute of Clinical Medicine, Palo Alto, California",[],{"title":2866,"openalex":2868},{"EN":2867},"James Yee",{"VOID":2869},"A5103420507",{"id":2871,"sortIndex":129,"researcher":23,"roles":2872,"affiliations":2873,"properties":2880,"displayName":2882,"givenName":23,"familyName":23},"c0c0c8b1-752f-4ba0-b93d-667da0385717",[],[2874],{"id":2858,"sortIndex":24,"affiliation":2875,"properties":23},{"id":2858,"createTime":23,"updateTime":23,"relativeEntities":2876,"slug":23,"properties":2877,"entityType":23,"verifyStatus":23,"verifyTime":23,"verifyNote":23,"languages":23,"translateLanguages":23,"viewCount":23,"url":23,"parentIds":2879,"statistic":23},[],{"title":2878},{"EN":2863},[],{"title":2881,"openalex":2883},{"EN":2882},"John E. 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Part I, Contem Surg, 20, 85",{},{"id":23,"text":3002,"url":23,"identifiers":3003},"10.1016\u002F0006-8993(82)90894-0",{"doi":3002},{"id":3005,"createTime":3006,"updateTime":3007,"relativeEntities":3008,"slug":3009,"properties":3010,"entityType":108,"verifyStatus":109,"verifyTime":3006,"verifyNote":110,"languages":3026,"translateLanguages":3027,"viewCount":24,"primaryUrl":3028,"fullTextUrl":23,"authors":3029,"publicationType":230,"publisherRelationship":3108,"citationCount":3153,"citationInfo":3154,"publishDate":3158,"publishYear":3155,"citationAnalyzeStatus":22,"lastCitationAnalyze":23,"indexDatabases":3159,"openAccess":23,"references":3160,"isForceReanalyzing":380},"4078dcb9-5943-4031-94ab-9a35dfdad219","2024-10-14T19:27:55.143+00:00","2025-01-25T05:16:37.026+00:00",[],"Statins-and-Liver-Toxicity-A-Meta-Analysis",{"mag":3011,"keywords":3013,"openalex":3014,"abstract":3016,"title":3019,"pm":3022,"doi":3024},{"VOID":3012},"2019519444",{"VI":391},{"VOID":3015},"W2019519444",{"VI":3017,"EN":3018},"\u003Cjats:p>\u003Cjats:bold>Mục tiêu nghiên cứu.\u003C\u002Fjats:bold> Đánh giá nguy cơ bất thường trong các xét nghiệm chức năng gan (LFT) khi sử dụng các chất ức chế HMG-CoA reducase 3-hydroxy-3-methyl (statin) cho việc điều trị tăng lipid máu.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Thiết kế.\u003C\u002Fjats:bold> Phân tích tổng hợp của các thử nghiệm ngẫu nhiên, có đối chứng giả dược về việc sử dụng statin trong điều trị tăng lipid máu hoặc trong phòng ngừa bệnh tim mạch nguyên phát hoặc thứ phát.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Địa điểm.\u003C\u002Fjats:bold> Trung tâm nghiên cứu trường đại học.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Bệnh nhân.\u003C\u002Fjats:bold> Tổng cộng 49.275 bệnh nhân từ 13 thử nghiệm.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Can thiệp.\u003C\u002Fjats:bold> Một tìm kiếm tài liệu về các thử nghiệm lâm sàng đã được công bố được thực hiện trên MEDLINE (tháng 1 năm 1966–tháng 3 năm 2003) và Sổ đăng ký thử nghiệm có kiểm soát Cochrane (quý 1 năm 2003). Các nghiên cứu cũng được xác định từ các tài liệu tham khảo của các thử nghiệm và các đánh giá tổng hợp đã được công bố.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Biện pháp và Kết quả chính.\u003C\u002Fjats:bold> Để một thử nghiệm được đưa vào phân tích tổng hợp, thời gian theo dõi ít nhất phải là 48 tuần và thử nghiệm phải có ít nhất 400 bệnh nhân, trong đó ít nhất 200 bệnh nhân được điều trị bằng statin. Các thử nghiệm được thực hiện trên người nhận ghép được loại trừ. Tỷ lệ bệnh nhân có bất thường trong LFT thấp ở cả hai nhóm (statin 1,14% vs giả dược 1,05%, tỷ lệ odds [OR] 1,26, khoảng tin cậy 95% [CI] 0,99–1,62, p=0,07). Chỉ có fluvastatin liên quan đến sự gia tăng đáng kể nguy cơ có bất thường trong LFT (fluvastatin 1,13% vs giả dược 0,29%, OR 3,54, 95% CI 1,1–11,6, p=0,04) so với giả dược, mặc dù phát hiện này chỉ dựa trên hai thử nghiệm.","\u003Cjats:p>\u003Cjats:bold>Study Objective.\u003C\u002Fjats:bold> To assess the risk of liver function test (LFT) abnormalities with the use of 3‐hydroxy‐3‐methylglutaryl coenzyme A reductase inhibitors (statins) for the treatment of hyperlipidemia.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Design.\u003C\u002Fjats:bold> Meta‐analysis of randomized, placebo‐controlled trials of statins used for the treatment of hyperlipidemia or for primary or secondary prevention of cardiovascular disease.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Setting.\u003C\u002Fjats:bold> University research center.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Patients.\u003C\u002Fjats:bold> A total of 49,275 patients from 13 trials.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Intervention.\u003C\u002Fjats:bold> A literature search of published clinical trials was performed in MEDLINE (January 1966–March 2003) and the Cochrane Controlled Trials Registry (first quarter 2003). Studies also were identified from the references of the trials and of published systematic reviews.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Measurements and Main Results.\u003C\u002Fjats:bold> For a trial to be included in the meta‐analysis, its duration of follow‐up had to be at least 48 weeks and the trial had to include at least 400 patients, with at least 200 treated with a statin. Trials conducted in transplant recipients were excluded. The proportion of patients having LFT abnormalities was low in both groups (statins 1.14% vs placebo 1.05%, odds ratio [OR] 1.26, 95% confidence interval [CI] 0.99–1.62, p=0.07). Only fluvastatin was associated with a significant increase in the odds of having LFT abnormalities (fluvastatin 1.13% vs placebo 0.29%, OR 3.54, 95% CI 1.1–11.6, p=0.04) compared with placebo, although this finding was based on only two trials.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Conclusions.\u003C\u002Fjats:bold> Our results support previous observations that pravastatin, lovastatin, and simvastatin at low‐to‐moderate doses are not associated with a significant risk of LFT abnormalities. 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