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Absolute bioavailability was determined by comparing pharmacokinetic data after administration of single oral and intravenous 50‐mg doses of sildenafil (\u003Cjats:italic>n\u003C\u002Fjats:italic>=12 subjects). Food effects were examined by comparing pharmacokinetic data for sildenafil and its primary circulating metabolite, UK‐103,320, after administration of a single oral 100‐mg dose in the fasted and fed states (\u003Cjats:italic>n\u003C\u002Fjats:italic>=34 subjects). Dose proportionality was assessed from pharmacokinetic data obtained after administration of four single oral doses of sildenafil (25, 50, 100 and 200 mg) to 32 subjects. The safety and tolerability of sildenafil were also assessed in all of these studies.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Results \u003C\u002Fjats:bold> The calculated absolute oral bioavailability of sildenafil was 41% (90% CI: 36–47). Food slowed the rate of absorption, delaying mean \u003Cjats:italic>t\u003C\u002Fjats:italic>\u003Cjats:sub>max\u003C\u002Fjats:sub> by approximately 1 h and reducing \u003Cjats:italic>C\u003C\u002Fjats:italic>\u003Cjats:sub>max\u003C\u002Fjats:sub> by 29% (90% CI: 19–38). Systemic exposure, as assessed by the mean area under the plasma concentration–time curve (AUC), was reduced by 11% (90% CI: 6–16). These food effects were not considered to be of clinical significance. There was statistical evidence of nonproportionality in \u003Cjats:italic>C\u003C\u002Fjats:italic>\u003Cjats:sub>max\u003C\u002Fjats:sub> and AUC over the dose range 25–200 mg. However the degree of nonproportionality was small, with predicted increases in \u003Cjats:italic>C\u003C\u002Fjats:italic>\u003Cjats:sub>max\u003C\u002Fjats:sub> and AUC of 2.2‐ and 2.1‐fold, respectively, for a doubling in dose, and was thought to be clinically nonsignificant. Sildenafil was well tolerated in the three studies; the majority of adverse events were mild and transient.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Conclusions \u003C\u002Fjats:bold> Sildenafil had a mean absolute bioavailability of 41%. Food caused small reductions in the rate and extent of systemic exposure; these reductions are unlikely to be of clinical significance. Across the dose range of 25–200 mg, systemic exposure increased in a slightly greater than dose‐proportional manner.\u003C\u002Fjats:p>","\u003Cjats:p>\u003Cjats:bold>Mục tiêu \u003C\u002Fjats:bold> Xác định sinh khả dụng tuyệt đối, tỷ lệ liều và tác động của thực phẩm lên dược động học của các liều đơn uống sildenafil citrate.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Phương pháp \u003C\u002Fjats:bold> Ba nghiên cứu chéo ngẫu nhiên, không mù đã được thực hiện trên các đối tượng nam giới khỏe mạnh. Sinh khả dụng tuyệt đối được xác định bằng cách so sánh dữ liệu dược động học sau khi cho uống và truyền tĩnh mạch 50 mg sildenafil (\u003Cjats:italic>n\u003C\u002Fjats:italic>=12 đối tượng). Tác động của thực phẩm được khảo sát bằng cách so sánh dữ liệu dược động học của sildenafil và chất chuyển hóa tuần hoàn chính của nó, UK-103,320, sau khi cho một liều uống đơn 100 mg trong trạng thái nhịn ăn và đã ăn (\u003Cjats:italic>n\u003C\u002Fjats:italic>=34 đối tượng). Tỷ lệ liều được đánh giá từ dữ liệu dược động học thu được sau khi cho ba liều uống đơn của sildenafil (25, 50, 100 và 200 mg) cho 32 đối tượng. Độ an toàn và khả năng chịu đựng của sildenafil cũng được đánh giá trong tất cả các nghiên cứu này.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Kết quả \u003C\u002Fjats:bold> Sinh khả dụng đường uống tuyệt đối của sildenafil được tính toán là 41% (Khoảng tin cậy 90%: 36–47). Thực phẩm làm chậm tốc độ hấp thu, làm trì hoãn thời gian \u003Cjats:italic>t\u003C\u002Fjats:italic>\u003Cjats:sub>max\u003C\u002Fjats:sub> trung bình khoảng 1 giờ và giảm \u003Cjats:italic>C\u003C\u002Fjats:italic>\u003Cjats:sub>max\u003C\u002Fjats:sub> đi 29% (Khoảng tin cậy 90%: 19–38). Sự tiếp xúc toàn thân, được đánh giá thông qua vùng dưới đường cong nồng độ-plasma theo thời gian (AUC) trung bình, bị giảm 11% (Khoảng tin cậy 90%: 6–16). Những tác động của thực phẩm này không được coi là có ý nghĩa lâm sàng. Có bằng chứng thống kê cho thấy sự không tỷ lệ ở \u003Cjats:italic>C\u003C\u002Fjats:italic>\u003Cjats:sub>max\u003C\u002Fjats:sub> và AUC trong khoảng liều từ 25–200 mg. Tuy nhiên, mức độ không tỷ lệ là nhỏ, với sự gia tăng dự đoán về \u003Cjats:italic>C\u003C\u002Fjats:italic>\u003Cjats:sub>max\u003C\u002Fjats:sub> và AUC lần lượt là 2.2- và 2.1-lần, cho sự gia tăng gấp đôi liều, và được coi là không có ý nghĩa lâm sàng. Sildenafil được dung nạp tốt trong ba nghiên cứu; phần lớn các sự kiện không mong muốn là nhẹ và tạm thời.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Kết luận \u003C\u002Fjats:bold> Sildenafil có sinh khả dụng tuyệt đối trung bình là 41%. Thực phẩm gây ra các giảm nhẹ trong tốc độ và mức độ tiếp xúc toàn thân; những giảm nhẹ này không có khả năng có ý nghĩa lâm sàng. Trong khoảng liều từ 25–200 mg, mức độ tiếp xúc toàn thân tăng lên một cách hơi lớn hơn tỷ lệ liều.",{"EN":199,"VI":200},"Pharmacokinetics of sildenafil after single oral doses in healthy male subjects: absolute bioavailability, food effects and dose proportionality","Dược động học của sildenafil sau liều uống đơn ở nam giới khỏe mạnh: sinh khả dụng tuyệt đối, tác động của thực phẩm và tỷ lệ liều",{"VOID":202},"11879254",{"VOID":204},"10.1046\u002Fj.0306-5251.2001.00027.x","PUBLICATION","VERIFIED","2025-01-03T04:16:29.306+00:00","Auto Verify",[210],"EN",[212],"VI","https:\u002F\u002Fbpspubs.onlinelibrary.wiley.com\u002Fdoi\u002F10.1046\u002Fj.0306-5251.2001.00027.x",[215,232,247],{"id":216,"sortIndex":25,"researcher":24,"roles":217,"affiliations":218,"properties":227,"displayName":229,"givenName":24,"familyName":24},"2d3a6d1a-ef65-425d-99e9-edf699b0c4b7",[],[219],{"id":220,"sortIndex":25,"affiliation":221,"properties":24},"1cc5d0ee-aea6-48e8-8bce-1d9f9f2af3e0",{"id":220,"createTime":24,"updateTime":24,"relativeEntities":222,"slug":24,"properties":223,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":226,"statistic":24},[],{"title":224},{"EN":225},"Pfizer Central Research, Sandwich, Kent, UK#TAB#",[],{"title":228,"openalex":230},{"EN":229},"Donald J. 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Abstract, Br J Urol, 79, 66",{},{"id":24,"text":343,"url":24,"identifiers":344},"Boolell M, 1996, Sildenafil: an orally active type 5 cyclic GMP‐specific phosphodiesterase inhibitor for the treatment of penile erectile dysfunction, Int J Impot Res, 8, 47",{},{"id":24,"text":346,"url":24,"identifiers":347},"10.1016\u002FS0002-9149(99)00043-0",{"doi":346},{"id":24,"text":349,"url":24,"identifiers":350},"10.1056\u002FNEJM199805143382001",{"doi":349},{"id":24,"text":352,"url":24,"identifiers":353},"10.1016\u002Fs0090-4295(98)00586-x",{"doi":352},{"id":24,"text":355,"url":24,"identifiers":356},"10.1016\u002FS0378-4347(97)00339-3",{"doi":355},{"id":24,"text":358,"url":24,"identifiers":359},"10.1080\u002F004982599238687",{"doi":358},{"id":24,"text":361,"url":24,"identifiers":362},"Muirhead GJ, 1996, Pharmacokinetics of sildenafil (Viagra®), a selective cGMP PDE5 inhibitor, after single oral doses in fasted and fed healthy volunteers, Br J Clin Pharmacol, 42, 268P",{},{"id":24,"text":364,"url":24,"identifiers":365},"Sjöqvist Borgå O, 1997, Avery's Drug Treatment, 2",{},{"id":24,"text":367,"url":24,"identifiers":368},"10.1046\u002Fj.1365-2125.2001.00318.x",{"doi":367},{"id":24,"text":370,"url":24,"identifiers":371},"10.1038\u002Fsj.ijir.3900354",{"doi":370},{"id":24,"text":373,"url":24,"identifiers":374},"Sadovsky R, 2001, Three‐year update of sildenafil citrate (Viagra®) efficacy and safety, Int J Clin Pract, 55, 115, 10.1111\u002Fj.1742-1241.2001.tb10992.x",{"doi":375},"10.1111\u002Fj.1742-1241.2001.tb10992.x",{"id":24,"text":377,"url":24,"identifiers":378},"Laties A, 1998, Visual function testing in patients and healthy volunteers receiving Viagra®, Ophthalmic Res, 30, 177",{},false,{"id":381,"createTime":382,"updateTime":383,"relativeEntities":384,"slug":385,"properties":386,"entityType":205,"verifyStatus":206,"verifyTime":382,"verifyNote":208,"languages":404,"translateLanguages":405,"viewCount":25,"primaryUrl":406,"fullTextUrl":24,"authors":407,"publicationType":264,"publisherRelationship":575,"citationCount":630,"citationInfo":631,"publishDate":641,"publishYear":632,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":642,"openAccess":24,"references":643,"isForceReanalyzing":379},"3316c36b-8cdd-45ac-afc2-8b58e9f19958","2024-09-03T02:12:34.642+00:00","2025-02-25T16:31:57.382+00:00",[],"Effects-of-renal-impairment-on-the-pharmacokinetics-pharmacodynamics-and-safety-of-rivaroxaban-an-oral-direct-Factor-Xa-inhibitor",{"mag":387,"keywords":389,"pmc":390,"openalex":392,"abstract":394,"title":397,"pm":400,"doi":402},{"VOID":388},"1485772655",{"VI":190},{"VOID":391},"2997310",{"VOID":393},"W1485772655",{"EN":395,"VI":396},"\u003Cjats:sec>\u003Cjats:label \u002F>\u003Cjats:p> \u003Cjats:bold>WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT\u003C\u002Fjats:bold> \u003C\u002Fjats:p>\u003Cjats:p>• Prior to the commencement of this study, it was already known that rivaroxaban is partially cleared via the kidneys and an influence of renal insufficiency on rivaroxaban pharmacokinetics and exposure was anticipated.\u003C\u002Fjats:p>\u003Cjats:p> \u003Cjats:bold>WHAT THIS STUDY ADDS\u003C\u002Fjats:bold> \u003C\u002Fjats:p>\u003Cjats:p>• As many patients in the target indications of rivaroxaban will be elderly, a precise quantitative knowledge of the influence of renal function on rivaroxaban pharmacokinetics and exposure is mandatory for adequate labelling recommendations (in the context of benefit\u002Frisk provided by phase III studies) to guide therapy. This study provided detailed insight on both rivaroxaban pharmacokinetics and pharmacodynamic behaviour in renal impairment including severely renally impaired subjects.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>AIM\u003C\u002Fjats:title>\u003Cjats:p>This study evaluated the effects of impaired renal function on the pharmacokinetics, pharmacodynamics and safety of rivaroxaban (10 mg single dose), an oral, direct Factor Xa inhibitor.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>METHODS\u003C\u002Fjats:title>\u003Cjats:p>Subjects (\u003Cjats:italic>n\u003C\u002Fjats:italic>= 32) were stratified based on measured creatinine clearance: healthy controls (≥80 ml min\u003Cjats:sup>−1\u003C\u002Fjats:sup>), mild (50–79 ml min\u003Cjats:sup>−1\u003C\u002Fjats:sup>), moderate (30–49 ml min\u003Cjats:sup>−1\u003C\u002Fjats:sup>) and severe impairment (<30 ml min\u003Cjats:sup>−1\u003C\u002Fjats:sup>).\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>RESULTS\u003C\u002Fjats:title>\u003Cjats:p>Renal clearance of rivaroxaban decreased with increasing renal impairment. Thus, plasma concentrations increased and area under the plasma concentration–time curve (AUC) LS‐mean values were 1.44‐fold (90% confidence interval [CI] 1.1, 1.9; mild), 1.52‐fold (90% CI 1.2, 2.0; moderate) and 1.64‐fold (90% CI 1.2, 2.2; severe impairment) higher than in healthy controls. Corresponding values for the LS‐mean of the AUC for prolongation of prothrombin time were 1.33‐fold (90% CI 0.92, 1.92; mild), 2.16‐fold (90% CI 1.51, 3.10 moderate) and 2.44‐fold (90% CI 1.70, 3.49 severe) higher than in healthy subjects, respectively. Likewise, the LS‐mean of the AUC for Factor Xa inhibition in subjects with mild renal impairment was 1.50‐fold (90% CI 1.07, 2.10) higher than in healthy subjects. In subjects with moderate and severe renal impairment, the increase was 1.86‐fold (90% CI 1.34, 2.59) and 2.0‐fold (90% CI 1.44, 2.78) higher than in healthy subjects, respectively.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>CONCLUSIONS\u003C\u002Fjats:title>\u003Cjats:p>Rivaroxaban clearance is decreased with increasing renal impairment, leading to increased plasma exposure and pharmacodynamic effects, as expected for a partially renally excreted drug. However, the influence of renal function on rivaroxaban clearance was moderate, even in subjects with severe renal impairment.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>","\u003Cjats:sec>\u003Cjats:label \u002F>\u003Cjats:p> \u003Cjats:bold>NHỮNG ĐIỀU ĐÃ BIẾT VỀ CHỦ ĐỀ NÀY\u003C\u002Fjats:bold> \u003C\u002Fjats:p>\u003Cjats:p>• Trước khi bắt đầu nghiên cứu này, đã biết rằng rivaroxaban được thải trừ một phần qua thận và ảnh hưởng của suy thận đến dược động học và phơi nhiễm với rivaroxaban đã được dự đoán.\u003C\u002Fjats:p>\u003Cjats:p> \u003Cjats:bold>CÁI GÌ NHIÊN CỨU NÀY ĐEM LẠI\u003C\u002Fjats:bold> \u003C\u002Fjats:p>\u003Cjats:p>• Do nhiều bệnh nhân trong các chỉ định mục tiêu của rivaroxaban sẽ là người cao tuổi, kiến thức định lượng chính xác về ảnh hưởng của chức năng thận đến dược động học và phơi nhiễm với rivaroxaban là điều cần thiết cho các khuyến nghị ghi nhãn phù hợp (trong bối cảnh lợi ích\u002Frủi ro được cung cấp bởi các nghiên cứu giai đoạn III) để hướng dẫn điều trị. Nghiên cứu này đã cung cấp cái nhìn chi tiết về cả dược động học và hành vi dược lực học của rivaroxaban trong tình trạng suy thận, bao gồm cả những đối tượng suy thận nặng.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>MỤC TIÊU\u003C\u002Fjats:title>\u003Cjats:p>Nghiên cứu này đã đánh giá tác động của chức năng thận suy yếu đến dược động học, dược lực học và an toàn của rivaroxaban (liều đơn 10 mg), một chất ức chế trực tiếp yếu tố Xa qua đường uống.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>PHƯƠNG PHÁP\u003C\u002Fjats:title>\u003Cjats:p>Các chủ thể (\u003Cjats:italic>n\u003C\u002Fjats:italic>= 32) được phân loại dựa trên độ thanh thải creatinine đo được: nhóm chứng khỏe mạnh (≥80 ml phút\u003Cjats:sup>−1\u003C\u002Fjats:sup>), suy thận nhẹ (50–79 ml phút\u003Cjats:sup>−1\u003C\u002Fjats:sup>), suy thận trung bình (30–49 ml phút\u003Cjats:sup>−1\u003C\u002Fjats:sup>) và suy thận nặng (<30 ml phút\u003Cjats:sup>−1\u003C\u002Fjats:sup>).\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>KẾT QUẢ\u003C\u002Fjats:title>\u003Cjats:p>Độ thanh thải thận của rivaroxaban giảm dần với tình trạng suy thận gia tăng. Do đó, nồng độ trong huyết tương tăng lên và giá trị trung bình LS của diện tích dưới đường cong nồng độ–thời gian (AUC) cao hơn lần lượt 1.44 lần (khoảng tin cậy [CI] 90% 1.1, 1.9; nhẹ), 1.52 lần (90% CI 1.2, 2.0; trung bình) và 1.64 lần (90% CI 1.2, 2.2; suy thận nặng) so với nhóm chứng khỏe mạnh. Các giá trị tương ứng cho trung bình LS của AUC cho sự kéo dài thời gian prothrombin lần lượt cao hơn 1.33 lần (90% CI 0.92, 1.92; nhẹ), 2.16 lần (90% CI 1.51, 3.10 trung bình) và 2.44 lần (90% CI 1.70, 3.49 nặng) so với các chủ thể khỏe mạnh. Tương tự, trung bình LS của AUC cho sự ức chế yếu tố Xa ở các đối tượng có suy thận nhẹ cao hơn 1.50 lần (90% CI 1.07, 2.10) so với các đối tượng khỏe mạnh. Ở các chủ thể có suy thận trung bình và nặng, sự gia tăng lần lượt đạt 1.86 lần (90% CI 1.34, 2.59) và 2.0 lần (90% CI 1.44, 2.78) so với những đối tượng khỏe mạnh.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>KẾT LUẬN\u003C\u002Fjats:title>\u003Cjats:p>Độ thanh thải của rivaroxaban giảm với tình trạng suy thận gia tăng, dẫn đến tăng cường phơi nhiễm trong huyết tương và các tác động dược động học, như dự kiến đối với một loại thuốc được thải trừ một phần qua thận. Tuy nhiên, ảnh hưởng của chức năng thận đến độ thanh thải rivaroxaban là trung bình, ngay cả ở những đối tượng có suy thận nặng.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>",{"EN":398,"VI":399},"Effects of renal impairment on the pharmacokinetics, pharmacodynamics and safety of rivaroxaban, an oral, direct Factor Xa inhibitor","Ảnh hưởng của suy thận đến dược động học, dược lực học và an toàn của rivaroxaban, một chất ức chế trực tiếp yếu tố Xa qua đường 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Available athttp:\u002F\u002Fwww.medicines.org.uk\u002Femc\u002Fmedicine\u002F15123(Updated 25 March 2009; last accessed 24 August 2010).",{},{"id":24,"text":727,"url":24,"identifiers":728},"10.2165\u002F00129784-200505050-00002",{"doi":727},{"id":24,"text":730,"url":24,"identifiers":731},"10.2165\u002F0003088-200948010-00001",{"doi":730},{"id":24,"text":733,"url":24,"identifiers":734},"10.1160\u002FTH07-12-0714",{"doi":733},{"id":736,"createTime":737,"updateTime":738,"relativeEntities":739,"slug":740,"properties":741,"entityType":205,"verifyStatus":206,"verifyTime":759,"verifyNote":208,"languages":760,"translateLanguages":761,"viewCount":25,"primaryUrl":762,"fullTextUrl":24,"authors":763,"publicationType":264,"publisherRelationship":830,"citationCount":143,"citationInfo":884,"publishDate":891,"publishYear":885,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":892,"openAccess":24,"references":893,"isForceReanalyzing":379},"35ada1ff-3cc4-40a9-b57a-35f1b0148c65","2024-09-21T03:37:01.571+00:00","2025-02-25T16:30:52.079+00:00",[],"Medical-management-of-paraquat-ingestion",{"mag":742,"keywords":744,"pmc":745,"openalex":747,"abstract":749,"title":752,"pm":755,"doi":757},{"VOID":743},"1765661487",{"VI":190},{"VOID":746},"3243009",{"VOID":748},"W1765661487",{"EN":750,"VI":751},"\u003Cjats:p>Poisoning by paraquat herbicide is a major medical problem in parts of Asia while sporadic cases occur elsewhere. The very high case fatality of paraquat is due to inherent toxicity and lack of effective treatments. We conducted a systematic search for human studies that report toxicokinetics, mechanisms, clinical features, prognosis and treatment. Paraquat is rapidly but incompletely absorbed and then largely eliminated unchanged in urine within 12–24 h. Clinical features are largely due to intracellular effects. Paraquat generates reactive oxygen species which cause cellular damage via lipid peroxidation, activation of NF‐κB, mitochondrial damage and apoptosis in many organs. Kinetics of distribution into these target tissues can be described by a two‐compartment model. Paraquat is actively taken up against a concentration gradient into lung tissue leading to pneumonitis and lung fibrosis. Paraquat also causes renal and liver injury. Plasma paraquat concentrations, urine and plasma dithionite tests and clinical features provide a good guide to prognosis. Activated charcoal and Fuller's earth are routinely given to minimize further absorption. Gastric lavage should not be performed. Elimination methods such as haemodialysis and haemoperfusion are unlikely to change the clinical course. Immunosuppression with dexamethasone, cyclophosphamide and methylprednisolone is widely practised, but evidence for efficacy is very weak. Antioxidants such as acetylcysteine and salicylate might be beneficial through free radical scavenging, anti‐inflammatory and NF‐κB inhibitory actions. However, there are no published human trials. The case fatality is very high in all centres despite large variations in treatment.\u003C\u002Fjats:p>","\u003Cjats:p>Ngộ độc do thuốc diệt cỏ paraquat là một vấn đề y tế lớn ở một số vùng của châu Á, trong khi các trường hợp đơn lẻ xảy ra ở nơi khác. Tỷ lệ tử vong rất cao của paraquat là do độc tính vốn có của nó và sự thiếu hụt điều trị hiệu quả. Chúng tôi đã tiến hành tìm kiếm hệ thống cho các nghiên cứu trên người báo cáo về độc tính, cơ chế, đặc điểm lâm sàng, tiên lượng và điều trị. Paraquat được hấp thụ nhanh chóng nhưng không hoàn toàn và chủ yếu bị loại bỏ không thay đổi qua nước tiểu trong vòng 12-24 giờ. Các đặc điểm lâm sàng chủ yếu là do ảnh hưởng bên trong tế bào. Paraquat tạo ra các loài oxy phản ứng đẩy mạnh tổn thương tế bào thông qua quá trình peroxy hóa lipid, kích hoạt NF-κB, tổn thương ti thể và apoptosis ở nhiều cơ quan. Động học phân phối vào các mô mục tiêu này có thể được mô tả bằng mô hình hai ngăn. Paraquat được hấp thu tích cực chống lại độ chênh lệch nồng độ vào mô phổi dẫn đến viêm phổi và xơ phổi. Paraquat cũng gây tổn thương thận và gan. Nồng độ paraquat trong plasma, các bài kiểm tra dithionite trong nước tiểu và plasma cùng các đặc điểm lâm sàng cung cấp một hướng dẫn tốt về tiên lượng. Than hoạt tính và đất Fuller thường được sử dụng để giảm thiểu sự hấp thu thêm. Rửa dạ dày không nên được thực hiện. Các phương pháp loại bỏ như thẩm phân máu và thẩm phân tế bào máu được cho là không có khả năng thay đổi tiến trình lâm sàng. Ức chế miễn dịch với dexamethasone, cyclophosphamide và methylprednisolone được thực hiện rộng rãi, nhưng bằng chứng về hiệu quả rất yếu. Các chất chống oxy hóa như acetylcysteine và salicylate có thể có lợi thông qua việc thu dọn gốc tự do, hành động chống viêm và ức chế NF-κB. Tuy nhiên, không có các thử nghiệm trên người đã được công bố. 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693",{},{"id":24,"text":1179,"url":24,"identifiers":1180},"Redetzki HM, 1980, Vitamin E and paraquat poisoning, Vet Hum Toxicol, 22, 395",{},{"id":24,"text":1182,"url":24,"identifiers":1183},"10.1007\u002Fs002040050270",{"doi":1182},{"id":24,"text":1185,"url":24,"identifiers":1186},"10.1016\u002Fj.tiv.2007.11.008",{"doi":1185},{"id":24,"text":1188,"url":24,"identifiers":1189},"10.3109\u002F10715769809097880",{"doi":1188},{"id":24,"text":1191,"url":24,"identifiers":1192},"10.1016\u002FS0378-4274(01)00431-3",{"doi":1191},{"id":24,"text":1194,"url":24,"identifiers":1195},"10.1016\u002Fj.tox.2006.03.019",{"doi":1194},{"id":24,"text":1197,"url":24,"identifiers":1198},"10.1006\u002Ftaap.1993.1080",{"doi":1197},{"id":24,"text":1200,"url":24,"identifiers":1201},"10.1016\u002FS0891-5849(96)00385-1",{"doi":1200},{"id":24,"text":1203,"url":24,"identifiers":1204},"10.1016\u002F0378-4274(95)03446-3",{"doi":1203},{"id":24,"text":1206,"url":24,"identifiers":1207},"Lugo‐Vallin N, 2003, Thirty‐five cases of S‐carboxymethylcysteine use in paraquat poisoning, Vet Hum Toxicol, 45, 45",{},{"id":24,"text":1209,"url":24,"identifiers":1210},"Korbashi P, 1986, Iron mediates paraquat toxicity in Escherichia coli, J Biol Chem, 261, 12472, 10.1016\u002FS0021-9258(18)67111-X",{"doi":1211},"10.1016\u002FS0021-9258(18)67111-X",{"id":24,"text":1213,"url":24,"identifiers":1214},"10.1016\u002F0006-2952(85)90659-8",{"doi":1213},{"id":24,"text":1216,"url":24,"identifiers":1217},"Hoffer E, 1992, The administration of desferrioxamine to paraquat‐intoxicated rats, Vet Hum Toxicol, 34, 300",{},{"id":24,"text":1219,"url":24,"identifiers":1220},"10.3109\u002F00498258809041682",{"doi":1219},{"id":24,"text":1222,"url":24,"identifiers":1223},"10.1021\u002Fjf0513819",{"doi":1222},{"id":24,"text":1225,"url":24,"identifiers":1226},"10.1016\u002Fj.bcp.2006.04.012",{"doi":1225},{"id":24,"text":1228,"url":24,"identifiers":1229},"10.1038\u002F23948",{"doi":1228},{"id":24,"text":1231,"url":24,"identifiers":1232},"10.1097\u002F01.cmr.0000195698.58013.53",{"doi":1231},{"id":24,"text":1234,"url":24,"identifiers":1235},"10.1016\u002FS0197-0186(03)00170-0",{"doi":1234},{"id":24,"text":1237,"url":24,"identifiers":1238},"Manjula TS, 1993, Effect of aspirin on mitochondrial lipids in experimental myocardial infarction in rats, Biochem Mol Biol Int, 29, 921",{},{"id":24,"text":1240,"url":24,"identifiers":1241},"10.1182\u002Fblood.V97.6.1742",{"doi":1240},{"id":24,"text":1243,"url":24,"identifiers":1244},"10.1124\u002Fjpet.106.102251",{"doi":1243},{"id":1246,"createTime":1247,"updateTime":1248,"relativeEntities":1249,"slug":1250,"properties":1251,"entityType":205,"verifyStatus":23,"verifyTime":1269,"verifyNote":1270,"languages":1271,"translateLanguages":1272,"viewCount":25,"primaryUrl":1273,"fullTextUrl":24,"authors":1274,"publicationType":264,"publisherRelationship":1310,"citationCount":1365,"citationInfo":1366,"publishDate":1371,"publishYear":1367,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":1372,"openAccess":24,"references":1373,"isForceReanalyzing":379},"77267cb3-1d49-4b12-a661-0f8f180d2808","2024-09-03T12:44:25.149+00:00","2025-02-25T16:29:53.672+00:00",[],"Pharmaceutical-innovation-by-the-seven-UK-owned-pharmaceutical-companies-1964-1985-",{"mag":1252,"keywords":1254,"pmc":1255,"openalex":1257,"abstract":1259,"title":1262,"pm":1265,"doi":1267},{"VOID":1253},"2117753715",{"VI":190},{"VOID":1256},"1386364",{"VOID":1258},"W2117753715",{"EN":1260,"VI":1261},"\u003Cjats:p>1 A total of three hundred and nineteen new chemical entities (NCEs) were investigated in man for the first time between 1964 and 1985 by seven UK‐owned pharmaceutical companies. The majority (96.2%), were self‐originated by the UK company or one of its overseas subsidiaries. 2 There was an increase in the number of NCEs investigated each year in man, doubling from an average of 12 per year up to 1980, to over 20 per year between 1981 and 1985. The majority of first drug evaluations in human volunteers were carried out in the UK (92.2%), in contrast to evaluation of new medicines in patients, where 42.9% were first tested outside the UK. 3 The majority of NCEs evaluated in man (78%), were in four therapeutic classes: anti‐infectives (32%), anti‐allergics (22%), drugs acting on the central nervous system (13%) and cardiovascular system agents (11%). 4 By the end of 1985, 49 (15.4%) of these NCEs had been marketed in the UK and 198 (62.0%) discontinued from further development. The main reasons for termination were inappropriate pharmacokinetics in man (39.4%), and lack of clinical efficacy (29.3%). 5 Average development times increased from less than 2 years between 1964 and 1965, to around 8 years in the 1980s with a consequent reduction in the effective patent life.\u003C\u002Fjats:p>","\u003Cjats:p>1 Tổng cộng có ba trăm mười chín thực thể hóa học mới (NCEs) đã được điều tra trên người lần đầu tiên từ năm 1964 đến 1985 bởi bảy công ty dược phẩm sở hữu tại Vương quốc Anh. Phần lớn (96,2%) là sản phẩm tự phát triển từ công ty Vương quốc Anh hoặc một trong những công ty con ở nước ngoài của nó. 2 Số lượng NCEs được điều tra mỗi năm trên người đã tăng lên, gấp đôi từ trung bình 12 NCEs mỗi năm cho đến năm 1980, lên hơn 20 NCEs mỗi năm trong khoảng thời gian từ 1981 đến 1985. Phần lớn các đánh giá thuốc đầu tiên trên tình nguyện viên người được thực hiện tại Vương quốc Anh (92,2%), trái ngược với việc đánh giá các loại thuốc mới trên bệnh nhân, tại đó 42,9% được thử nghiệm lần đầu bên ngoài Vương quốc Anh. 3 Phần lớn NCEs được đánh giá trên người (78%) thuộc bốn nhóm điều trị: thuốc chống nhiễm trùng (32%), thuốc chống dị ứng (22%), thuốc tác động lên hệ thần kinh trung ương (13%) và tác nhân hệ tim mạch (11%). 4 Đến cuối năm 1985, 49 (15,4%) trong số các NCE này đã được đưa ra thị trường tại Vương quốc Anh và 198 (62,0%) đã bị ngừng phát triển hơn nữa. Lý do chính cho việc chấm dứt là do dược động học không thích hợp trên người (39,4%) và thiếu hiệu quả lâm sàng (29,3%). 5 Thời gian phát triển trung bình đã tăng lên từ dưới 2 năm trong khoảng thời gian từ 1964 đến 1965, lên khoảng 8 năm trong những năm 1980, dẫn đến giảm thời gian có hiệu lực của bằng sáng chế.\u003C\u002Fjats:p>",{"EN":1263,"VI":1264},"Pharmaceutical innovation by the seven UK‐owned pharmaceutical companies (1964‐1985).","Đổi mới dược phẩm của bảy công ty dược phẩm sở hữu tại Vương quốc Anh (1964-1985)",{"VOID":1266},"3358900",{"VOID":1268},"10.1111\u002Fj.1365-2125.1988.tb03318.x","2024-09-03T12:44:25.148+00:00","Author affiliation is blank",[210],[212],"https:\u002F\u002Fbpspubs.onlinelibrary.wiley.com\u002Fdoi\u002F10.1111\u002Fj.1365-2125.1988.tb03318.x",[1275,1292,1301],{"id":1276,"sortIndex":25,"researcher":24,"roles":1277,"affiliations":1278,"properties":1287,"displayName":1289,"givenName":24,"familyName":24},"e3558ac9-933b-493d-ab29-b49f902fc54f",[],[1279],{"id":1280,"sortIndex":25,"affiliation":1281,"properties":24},"03770d51-0892-4c70-8663-4b87a6c33a3a",{"id":1280,"createTime":24,"updateTime":24,"relativeEntities":1282,"slug":24,"properties":1283,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1286,"statistic":24},[],{"title":1284},{"EN":1285},"Centre for Medicines Research, Carshalton, Surrey.",[],{"title":1288,"openalex":1290},{"EN":1289},"R A Prentis",{"VOID":1291},"A5091740710",{"id":1293,"sortIndex":109,"researcher":24,"roles":1294,"affiliations":1295,"properties":1296,"displayName":1298,"givenName":24,"familyName":24},"eddd4d5f-07b1-4f88-a340-28898d4436d3",[],[],{"title":1297,"openalex":1299},{"EN":1298},"Y. 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M. W., 1978, Treatment—a handbook of drug therapy",{},{"id":24,"text":1381,"url":24,"identifiers":1382},"10.1111\u002Fj.1365-2125.1981.tb01251.x",{"doi":1381},{"id":24,"text":1384,"url":24,"identifiers":1385},"10.1111\u002Fj.1365-2125.1982.tb01374.x",{"doi":1384},{"id":24,"text":1387,"url":24,"identifiers":1388},"Hass A. E., 1985, New drugs: Their market life and safety, Pharm. J., 234, 235",{},{"id":24,"text":1390,"url":24,"identifiers":1391},"Lumley C. E., 1987, Trends in research and development expenditure by the UK pharmaceutical industry (1982–84), Pharm. Med.",{},{"id":24,"text":1393,"url":24,"identifiers":1394},"10.1016\u002F0273-2300(84)90038-2",{"doi":1393},{"id":24,"text":1396,"url":24,"identifiers":1397},"Mattison N. Trimble A. G.&Lasagna L.(1987).New drug development in the United States 1963–1984.Clin. Pharmac. Ther..",{"doi":1398},"10.1038\u002Fclpt.1988.35",{"id":24,"text":1400,"url":24,"identifiers":1401},"10.1111\u002Fj.1365-2125.1986.tb05219.x",{"doi":1400},{"id":24,"text":1403,"url":24,"identifiers":1404},"Reis‐Arndt E., 1975, New pharmaceutical agents 1961–1973, Drugs made in Germany, 18, 123",{},{"id":24,"text":1406,"url":24,"identifiers":1407},"Reis‐Arndt E., 1982, 20 Jahre Arzneimittelentwick — lung — Neue pharmazeutische Wirkstoffe 1961–1980, Pharmac. Ind., 44, 1115",{},{"id":24,"text":1409,"url":24,"identifiers":1410},"10.1111\u002Fj.1365-2125.1983.tb01545.x",{"doi":1409},{"id":24,"text":1412,"url":24,"identifiers":1413},"Speirs C. J. Saunders R. M.&Griffin J. P.(1984).The UK Clinical Trial Exemption scheme — its effects on investment in researchPharm. Int. Oct. 254–256.",{},{"id":24,"text":1415,"url":24,"identifiers":1416},"10.1038\u002F284118a0",{"doi":1415},{"id":24,"text":1418,"url":24,"identifiers":1419},"Walker S. R., 1982, Innovation and drug development — Can the process be expedited, BIRA Journal, 1, 34",{},{"id":24,"text":1421,"url":24,"identifiers":1422},"Walker S. R., 1985, Drug Research & Pharmaceutical Patents, Pharm. J., 234, 11",{},{"id":24,"text":1424,"url":24,"identifiers":1425},"Walker S. R. Prentis R. A.&Ravenscroft M. K.(1986).Innovation as assessed by new pharmaceutical compounds marketed in the United Kingdom between 1960–1983Pharm. Int. June 135–7.",{},{"id":24,"text":1427,"url":24,"identifiers":1428},"10.1002\u002Fcpt1978242133",{"doi":1427},{"id":24,"text":1430,"url":24,"identifiers":1431},"10.1002\u002Fj.1552-4604.1980.tb01660.x",{"doi":1430},{"id":24,"text":1433,"url":24,"identifiers":1434},"Wardell W. M.&Sheck L. E.(1982).Is pharmaceutical innovation declining?: interpreting measures of pharmaceutical innovation and regulatory impact in the USA 1950–1980Presentation at the Arne Ryde Symposium on Pharmaceutical Economics.Helsingborg Sweden.",{},{"id":1436,"createTime":1437,"updateTime":1438,"relativeEntities":1439,"slug":1440,"properties":1441,"entityType":205,"verifyStatus":23,"verifyTime":1459,"verifyNote":1270,"languages":1460,"translateLanguages":1461,"viewCount":25,"primaryUrl":1462,"fullTextUrl":24,"authors":1463,"publicationType":264,"publisherRelationship":1519,"citationCount":1573,"citationInfo":1574,"publishDate":1586,"publishYear":1575,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":1587,"openAccess":24,"references":1588,"isForceReanalyzing":379},"ab3fd6ec-6cd5-49b0-9782-5efd12eb2df8","2024-09-04T01:09:04.882+00:00","2025-02-25T16:28:54.926+00:00",[],"The-pharmacokinetics-pharmacodynamics-and-tolerability-of-dabigatran-etexilate-a-new-oral-direct-thrombin-inhibitor-in-healthy-male-subjects",{"mag":1442,"keywords":1444,"pmc":1445,"openalex":1447,"abstract":1449,"title":1452,"pm":1455,"doi":1457},{"VOID":1443},"2124882231",{"VI":190},{"VOID":1446},"2000643",{"VOID":1448},"W2124882231",{"EN":1450,"VI":1451},"\u003Cjats:sec>\u003Cjats:title>Aims\u003C\u002Fjats:title>\u003Cjats:p>The novel direct thrombin inhibitor (DTI), dabigatran etexilate (Boehringer Ingelheim Pharma GmbH & Co. KG), shows potential as an oral antithrombotic agent. Two double‐blind, randomized trials were undertaken to investigate the pharmacokinetics (PK), pharmacodynamics (PD) and tolerability of orally administered dabigatran etexilate in healthy male subjects.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Methods\u003C\u002Fjats:title>\u003Cjats:p>Dabigatran etexilate or placebo was administered orally at single doses of 10–400 mg (\u003Cjats:italic>n\u003C\u002Fjats:italic> = 40) or at multiple doses of 50–400 mg three times daily for 6 days (\u003Cjats:italic>n\u003C\u002Fjats:italic> = 40). Plasma and urine samples were collected over time to determine the PK profile of dabigatran. PD activity was assessed by its effects on blood coagulation parameters: activated partial thromboplastin time (aPTT), prothrombin time (PT), reported as international normalized ratio (INR), thrombin time (TT), and ecarin clotting time (ECT). All adverse events were recorded.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Results\u003C\u002Fjats:title>\u003Cjats:p>Dabigatran etexilate was rapidly absorbed with peak plasma concentrations of dabigatran reached within 2 h of administration. This was followed by a rapid distribution\u002Felimination phase and a terminal phase, with associated estimated half‐lives of 8–10 h and 14–17 h with single and multiple dose administrations, respectively. Dabigatran exhibited linear PK characteristics with dose‐proportional increases observed in maximum plasma concentration and area under the curve. Steady‐state conditions were reached within 3 days with multiple dosing. The mean apparent volume of distribution during the terminal phase (\u003Cjats:italic>V\u003C\u002Fjats:italic>\u003Cjats:sub>\u003Cjats:italic>z\u003C\u002Fjats:italic>\u003C\u002Fjats:sub>\u002F\u003Cjats:italic>F\u003C\u002Fjats:italic>) of 1860 l (range 1430–2400 l) and the apparent total clearance after oral administration (CL\u003Cjats:sub>tot\u003C\u002Fjats:sub>\u002F\u003Cjats:italic>F\u003C\u002Fjats:italic>) of 2031 ml min\u003Cjats:sup>−1\u003C\u002Fjats:sup> (range 1480–2430), were dose independent. Time curves for aPTT, INR, TT and ECT paralleled plasma concentration–time curves with values increasing rapidly and in a dose‐dependent manner. At the highest dose of 400 mg administered three times daily, maximum prolongations over baseline of 3.1 (aPTT), 3.5 (INR), 29 (TT) and 9.5‐fold (ECT) were observed. Dabigatran underwent conjugation with glucuronic acid to form pharmacologically active conjugates that accounted for approximately 20% of total dabigatran in plasma. Overall, variability in PK parameters was low to moderate, with an average interindividual coefficient of variation (CV) of approximately 30% and variability in PD parameters was low, with CV < 10%. Of the four assays, TT and ECT exhibited the greatest sensitivity and precision within the anticipated therapeutic dose range. Bleeding events were few and were mild‐to‐moderate in intensity, occurring only in the higher, multiple dose groups.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Conclusions\u003C\u002Fjats:title>\u003Cjats:p>These data suggest that dabigatran etexilate is a promising novel oral DTI with predictable PK and PD characteristics and good tolerability. Further investigation of dabigatran etexilate for the treatment and prophylaxis of patients with arterial and venous thromboembolic disorders, acute coronary syndromes and other medical conditions is warranted.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>","\u003Cjats:sec>\u003Cjats:title>Mục tiêu\u003C\u002Fjats:title>\u003Cjats:p>Chất ức chế thrombin trực tiếp mới (DTI), dabigatran etexilate (Boehringer Ingelheim Pharma GmbH & Co. KG), cho thấy tiềm năng như một tác nhân kháng đông uống. Hai thử nghiệm ngẫu nhiên mù đôi đã được thực hiện để điều tra dược động học (PK), dược lý học (PD) và khả năng dung nạp của dabigatran etexilate được sử dụng uống ở các đối tượng nam khỏe mạnh.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Phương pháp\u003C\u002Fjats:title>\u003Cjats:p>Dabigatran etexilate hoặc giả dược được uống với liều đơn từ 10–400 mg (\u003Cjats:italic>n\u003C\u002Fjats:italic> = 40) hoặc với liều nhiều lần từ 50–400 mg ba lần mỗi ngày trong 6 ngày (\u003Cjats:italic>n\u003C\u002Fjats:italic> = 40). Mẫu huyết tương và nước tiểu được thu thập theo thời gian để xác định hồ sơ PK của dabigatran. Hoạt động PD được đánh giá qua các tác động của nó lên các thông số đông máu: thời gian thromboplastin từng phần hoạt hóa (aPTT), thời gian prothrombin (PT), được báo cáo dưới dạng tỉ lệ chuẩn hóa quốc tế (INR), thời gian thrombin (TT), và thời gian đông máu ecarin (ECT). Tất cả các sự kiện bất lợi đều được ghi nhận.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Kết quả\u003C\u002Fjats:title>\u003Cjats:p>Dabigatran etexilate được hấp thu nhanh chóng với nồng độ huyết tương tối đa của dabigatran đạt được sau 2 giờ uống. Điều này được theo sau bởi một giai đoạn phân phối\u002F loại bỏ nhanh và một giai đoạn cuối, với các thời gian bán hủy ước tính liên quan từ 8–10 giờ và 14–17 giờ với việc sử dụng liều đơn và nhiều lần, tương ứng. Dabigatran biểu hiện các đặc điểm PK tuyến tính với sự gia tăng tỷ lệ thuận theo liều trong nồng độ huyết tương tối đa và diện tích dưới đường cong. Các điều kiện trạng thái ổn định được đạt được trong vòng 3 ngày với liều dùng nhiều lần. Thể tích phân bố rõ ràng trung bình trong giai đoạn cuối (\u003Cjats:italic>V\u003C\u002Fjats:italic>\u003Cjats:sub>\u003Cjats:italic>z\u003C\u002Fjats:italic>\u003C\u002Fjats:sub>\u002F\u003Cjats:italic>F\u003C\u002Fjats:italic>) là 1860 l (khoảng 1430–2400 l) và độ thanh thải tổng rõ ràng sau khi dùng đường uống (CL\u003Cjats:sub>tot\u003C\u002Fjats:sub>\u002F\u003Cjats:italic>F\u003C\u002Fjats:italic>) là 2031 ml phút\u003Cjats:sup>−1\u003C\u002Fjats:sup> (khoảng 1480–2430), là độc lập với liều. Đường cong thời gian cho aPTT, INR, TT và ECT song song với các đường cong nồng độ–thời gian trong huyết tương với các giá trị tăng nhanh và theo liều. Tại liều cao nhất 400 mg dùng ba lần mỗi ngày, độ kéo dài tối đa so với nền tảng trong aPTT, INR, TT và ECT lần lượt là 3.1, 3.5, 29 và 9.5 lần được quan sát thấy. Dabigatran đã trải qua quá trình liên hợp với axit glucuronic để tạo thành các hợp chất hoạt động dược lý chiếm khoảng 20% tổng thể dabigatran trong huyết tương. Tổng thể, sự biến thiên trong các tham số PK từ thấp đến trung bình, với hệ số biến thiên trung bình giữa các cá thể (CV) khoảng 30%, còn sự biến thiên trong các tham số PD thì thấp, với CV \u003C 10%. Trong bốn xét nghiệm, TT và ECT thể hiện độ nhạy và độ chính xác cao nhất trong khoảng liều điều trị dự kiến. Các sự kiện chảy máu thì ít xảy ra, với cường độ từ nhẹ đến trung bình, chỉ xảy ra ở các nhóm liều cao, nhiều lần.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Kết luận\u003C\u002Fjats:title>\u003Cjats:p>Dữ liệu này cho thấy rằng dabigatran etexilate là một DTI uống mới hứa hẹn có các đặc điểm PK và PD có thể dự đoán được cùng với khả năng dung nạp tốt. Cần tiếp tục điều tra dabigatran etexilate cho việc điều trị và phòng ngừa bệnh nhân mắc các rối loạn tắc mạch động mạch và tĩnh mạch, hội chứng vành cấp và các tình trạng y tế khác.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>",{"EN":1453,"VI":1454},"The pharmacokinetics, pharmacodynamics and tolerability of dabigatran etexilate, a new oral direct thrombin inhibitor, in healthy male subjects","Dabigatran etexilate, một chất ức chế thrombin trực tiếp mới, và các đặc điểm dược động, dược lý và khả năng dung nạp của nó trên các đối tượng nam khỏe mạnh",{"VOID":1456},"17506785",{"VOID":1458},"10.1111\u002Fj.1365-2125.2007.02899.x","2024-09-04T01:09:04.881+00:00",[210],[212],"https:\u002F\u002Fbpspubs.onlinelibrary.wiley.com\u002Fdoi\u002F10.1111\u002Fj.1365-2125.2007.02899.x",[1464,1481,1490,1499,1508],{"id":1465,"sortIndex":25,"researcher":24,"roles":1466,"affiliations":1467,"properties":1476,"displayName":1478,"givenName":24,"familyName":24},"9b02dbb7-5f53-433e-9374-eab9d5cb1edd",[],[1468],{"id":1469,"sortIndex":25,"affiliation":1470,"properties":24},"2301aa61-c486-4a10-98b0-88850321f64a",{"id":1469,"createTime":24,"updateTime":24,"relativeEntities":1471,"slug":24,"properties":1472,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1475,"statistic":24},[],{"title":1473},{"VI":1474},"Boehringer Ingelheim Pharma GmbH & Co. KG, Ingelheim, Germany",[],{"title":1477,"openalex":1479},{"EN":1478},"Joachim Stangier",{"VOID":1480},"A5002133662",{"id":1482,"sortIndex":109,"researcher":24,"roles":1483,"affiliations":1484,"properties":1485,"displayName":1487,"givenName":24,"familyName":24},"26536414-b5df-4e95-9eb6-3e15332ac993",[],[],{"title":1486,"openalex":1488},{"EN":1487},"Karin Rathgen",{"VOID":1489},"A5038558228",{"id":1491,"sortIndex":110,"researcher":24,"roles":1492,"affiliations":1493,"properties":1494,"displayName":1496,"givenName":24,"familyName":24},"2136296c-d96c-41cc-adb6-4ee60f79ecc4",[],[],{"title":1495,"openalex":1497},{"EN":1496},"Hildegard Stähle",{"VOID":1498},"A5034309348",{"id":1500,"sortIndex":111,"researcher":24,"roles":1501,"affiliations":1502,"properties":1503,"displayName":1505,"givenName":24,"familyName":24},"e01bc1db-efc9-4599-9e94-cad2fd3f5e57",[],[],{"title":1504,"openalex":1506},{"EN":1505},"Dietmar 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P, 1993, TopFit: a PC‐based pharmacokinetic\u002Fpharmacodynamic data analysis program, Int J Clin Pharmacol Ther Toxicol, 31, 514",{},{"id":24,"text":1614,"url":24,"identifiers":1615},"Weitz J, 2003, Orally active direct thrombin inhibitors, Sem Cardiovasc Med, 3, 131",{},{"id":24,"text":1617,"url":24,"identifiers":1618},"10.1111\u002Fj.1538-7836.2004.01100.x",{"doi":1617},{"id":24,"text":1620,"url":24,"identifiers":1621},"Kher A, 1997, Laboratory assessment of antithrombotic therapy: what tests and if so why?, Haemostasis, 27, 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Abstract",{},{"id":1653,"createTime":1654,"updateTime":1655,"relativeEntities":1656,"slug":1657,"properties":1658,"entityType":205,"verifyStatus":206,"verifyTime":1676,"verifyNote":208,"languages":1677,"translateLanguages":1678,"viewCount":25,"primaryUrl":1679,"fullTextUrl":24,"authors":1680,"publicationType":264,"publisherRelationship":1700,"citationCount":1754,"citationInfo":1755,"publishDate":1764,"publishYear":1756,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":1765,"openAccess":24,"references":1766,"isForceReanalyzing":379},"bc95d1e3-1a49-4dd3-8b2e-5b947b8dc92b","2024-10-13T16:06:48.394+00:00","2025-02-25T16:27:49.528+00:00",[],"Omega-3-polyunsaturated-fatty-acids-and-inflammatory-processes-nutrition-or-pharmacology-",{"mag":1659,"keywords":1661,"pmc":1662,"openalex":1664,"abstract":1666,"title":1669,"pm":1672,"doi":1674},{"VOID":1660},"1596389679",{"VI":190},{"VOID":1663},"3575932",{"VOID":1665},"W1596389679",{"EN":1667,"VI":1668},"\u003Cjats:p>Eicosapentaenoic acid (\u003Cjats:styled-content style=\"fixed-case\">EPA\u003C\u002Fjats:styled-content>) and docosahexaenoic acid (\u003Cjats:styled-content style=\"fixed-case\">DHA\u003C\u002Fjats:styled-content>) are n‐3 fatty acids found in oily fish and fish oil supplements. These fatty acids are able to inhibit partly a number of aspects of inflammation including leucocyte chemotaxis, adhesion molecule expression and leucocyte‐endothelial adhesive interactions, production of eicosanoids like prostaglandins and leukotrienes from the n‐6 fatty acid arachidonic acid, production of inflammatory cytokines and \u003Cjats:styled-content style=\"fixed-case\">T\u003C\u002Fjats:styled-content> cell reactivity. In parallel, \u003Cjats:styled-content style=\"fixed-case\">EPA\u003C\u002Fjats:styled-content> gives rise to eicosanoids that often have lower biological potency than those produced from arachidonioc acid and \u003Cjats:styled-content style=\"fixed-case\">EPA\u003C\u002Fjats:styled-content> and \u003Cjats:styled-content style=\"fixed-case\">DHA\u003C\u002Fjats:styled-content> give rise to anti‐inflammatory and inflammation resolving resolvins and protectins. Mechanisms underlying the anti‐inflammatory actions of \u003Cjats:styled-content style=\"fixed-case\">n\u003C\u002Fjats:styled-content>‐3 fatty acids include altered cell membrane phospholipid fatty acid composition, disruption of lipid rafts, inhibition of activation of the pro‐inflammatory transcription factor nuclear factor kappa \u003Cjats:styled-content style=\"fixed-case\">B\u003C\u002Fjats:styled-content> so reducing expression of inflammatory genes, activation of the anti‐inflammatory transcription factor \u003Cjats:styled-content style=\"fixed-case\">NR1C3\u003C\u002Fjats:styled-content> (i.e. peroxisome proliferator activated receptor γ) and binding to the \u003Cjats:styled-content style=\"fixed-case\">G\u003C\u002Fjats:styled-content> protein coupled receptor \u003Cjats:styled-content style=\"fixed-case\">GPR120\u003C\u002Fjats:styled-content>. These mechanisms are interlinked. In adult humans, an \u003Cjats:styled-content style=\"fixed-case\">EPA\u003C\u002Fjats:styled-content> plus \u003Cjats:styled-content style=\"fixed-case\">DHA\u003C\u002Fjats:styled-content> intake greater than 2 g day\u003Cjats:sup>–1\u003C\u002Fjats:sup> seems to be required to elicit anti‐inflammatory actions, but few dose finding studies have been performed. Animal models demonstrate benefit from \u003Cjats:styled-content style=\"fixed-case\">n\u003C\u002Fjats:styled-content>‐3 fatty acids in rheumatoid arthritis (\u003Cjats:styled-content style=\"fixed-case\">RA\u003C\u002Fjats:styled-content>), inflammatory bowel disease (\u003Cjats:styled-content style=\"fixed-case\">IBD\u003C\u002Fjats:styled-content>) and asthma. Clinical trials of fish oil in patients with \u003Cjats:styled-content style=\"fixed-case\">RA\u003C\u002Fjats:styled-content> demonstrate benefit supported by meta‐analyses of the data. Clinical trails of fish oil in patients with \u003Cjats:styled-content style=\"fixed-case\">IBD\u003C\u002Fjats:styled-content> and asthma are inconsistent with no overall clear evidence of efficacy.\u003C\u002Fjats:p>","\u003Cjats:p>Axit eicosapentaenoic (\u003Cjats:styled-content style=\"fixed-case\">EPA\u003C\u002Fjats:styled-content>) và axit docosahexaenoic (\u003Cjats:styled-content style=\"fixed-case\">DHA\u003C\u002Fjats:styled-content>) là các axit béo n‐3 có trong cá béo và thực phẩm bổ sung dầu cá. Những axit béo này có khả năng ức chế một phần một số khía cạnh của tình trạng viêm, bao gồm hóa ứng động của bạch cầu, biểu hiện phân tử bám dính và tương tác bám dính giữa bạch cầu và nội mô, sản xuất các eicosanoid như prostaglandin và leukotriene từ axit béo n‐6 arachidonic, sản xuất các cytokine viêm và khả năng hoạt động của tế bào \u003Cjats:styled-content style=\"fixed-case\">T\u003C\u002Fjats:styled-content>. Song song đó, \u003Cjats:styled-content style=\"fixed-case\">EPA\u003C\u002Fjats:styled-content> tạo ra các eicosanoid thường có hoạt tính sinh học thấp hơn so với những eicosanoid được sản xuất từ axit arachidonic, và \u003Cjats:styled-content style=\"fixed-case\">EPA\u003C\u002Fjats:styled-content> cùng với \u003Cjats:styled-content style=\"fixed-case\">DHA\u003C\u002Fjats:styled-content> tạo ra các resolvin và protectin có tác dụng chống viêm và giúp giảm thiểu viêm. Các cơ chế dẫn đến tác dụng chống viêm của các axit béo n‐3 bao gồm thay đổi thành phần axit béo phospholipid màng tế bào, gây rối loạn các ‘raft’ lipid, ức chế việc hoạt hóa yếu tố phiên mã gây viêm hạt nhân kappa \u003Cjats:styled-content style=\"fixed-case\">B\u003C\u002Fjats:styled-content>, từ đó giảm sự biểu hiện của các gen viêm, kích hoạt yếu tố phiên mã chống viêm \u003Cjats:styled-content style=\"fixed-case\">NR1C3\u003C\u002Fjats:styled-content> (tức là thụ thể axit béo kích thích phát triển peroxisome γ) và gắn với thụ thể \u003Cjats:styled-content style=\"fixed-case\">G\u003C\u002Fjats:styled-content> protein liên kết \u003Cjats:styled-content style=\"fixed-case\">GPR120\u003C\u002Fjats:styled-content>. Các cơ chế này có liên quan tới nhau. Ở người lớn, việc tiêu thụ \u003Cjats:styled-content style=\"fixed-case\">EPA\u003C\u002Fjats:styled-content> và \u003Cjats:styled-content style=\"fixed-case\">DHA\u003C\u002Fjats:styled-content> lớn hơn 2 g ngày\u003Cjats:sup>–1\u003C\u002Fjats:sup> dường như là cần thiết để phát huy tác dụng chống viêm, nhưng rất ít nghiên cứu xác định liều đã được thực hiện. Các mô hình động vật cho thấy lợi ích từ các axit béo n‐3 trong bệnh thấp khớp dạng thấp (\u003Cjats:styled-content style=\"fixed-case\">RA\u003C\u002Fjats:styled-content>), bệnh viêm ruột (\u003Cjats:styled-content style=\"fixed-case\">IBD\u003C\u002Fjats:styled-content>) và hen suyễn. Các thử nghiệm lâm sàng về dầu cá ở bệnh nhân với \u003Cjats:styled-content style=\"fixed-case\">RA\u003C\u002Fjats:styled-content> cho thấy lợi ích được hỗ trợ bởi các phân tích tổng hợp dữ liệu. Các thử nghiệm lâm sàng về dầu cá ở bệnh nhân mắc \u003Cjats:styled-content style=\"fixed-case\">IBD\u003C\u002Fjats:styled-content> và hen suyễn không nhất quán và không có bằng chứng rõ ràng về hiệu quả tổng thể.\u003C\u002Fjats:p>",{"EN":1670,"VI":1671},"Omega‐3 polyunsaturated fatty acids and inflammatory processes: nutrition or pharmacology?","Các axit béo không bão hòa đa omega-3 và các quá trình viêm: dinh dưỡng hay dược lý?",{"VOID":1673},"22765297",{"VOID":1675},"10.1111\u002Fj.1365-2125.2012.04374.x","2024-10-13T16:06:48.393+00:00",[210],[212],"https:\u002F\u002Fbpspubs.onlinelibrary.wiley.com\u002Fdoi\u002F10.1111\u002Fj.1365-2125.2012.04374.x",[1681],{"id":1682,"sortIndex":25,"researcher":24,"roles":1683,"affiliations":1684,"properties":1693,"displayName":1697,"givenName":24,"familyName":24},"a10adce9-4995-4eeb-b3a7-12d3741132e3",[],[1685],{"id":1686,"sortIndex":25,"affiliation":1687,"properties":24},"485250d2-40bb-4449-85e7-9e46d2933eb5",{"id":1686,"createTime":24,"updateTime":24,"relativeEntities":1688,"slug":24,"properties":1689,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1692,"statistic":24},[],{"title":1690},{"EN":1691},"Human Development and Health Academic Unit, Faculty of Medicine, University of Southampton, MP887 Southampton General Hospital, Southampton, United Kingdom",[],{"orcid":1694,"title":1696,"openalex":1698},{"VOID":1695},"https:\u002F\u002Forcid.org\u002F0000-0002-6038-710X",{"EN":1697},"Philip C. 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Available athttp:\u002F\u002Fwww.ncbi.nlm.nih.gov\u002Fbooks\u002FNBK37146?(last accessed 26 July 2012).",{},{"id":24,"text":2212,"url":24,"identifiers":2213},"Turner D, 2007, Omega 3 fatty acids (fish oil) for maintenance of remission in ulcerative colitis, Cochrane Database Syst Rev",{},{"id":24,"text":2215,"url":24,"identifiers":2216},"10.1002\u002F14651858.CD006320.pub3",{"doi":2215},{"id":24,"text":2218,"url":24,"identifiers":2219},"10.1002\u002F14651858.CD005986.pub2",{"doi":2218},{"id":24,"text":2221,"url":24,"identifiers":2222},"Sperling RI, 1995, Eicosanoids in rheumatoid arthritis, Rheum Dis Clin North Am, 21, 741, 10.1016\u002FS0889-857X(21)00465-8",{"doi":2223},"10.1016\u002FS0889-857X(21)00465-8",{"id":24,"text":2225,"url":24,"identifiers":2226},"10.1046\u002Fj.1365-2222.2003.01637.x",{"doi":2225},{"id":24,"text":2228,"url":24,"identifiers":2229},"Roper RL, 1994, Prostaglandin E2 regulation of the immune response, Adv Prostaglandin Thromboxane Leukot Res, 22, 101",{},{"id":24,"text":2231,"url":24,"identifiers":2232},"10.1183\u002F09031936.97.10010006",{"doi":2231},{"id":24,"text":2234,"url":24,"identifiers":2235},"10.1159\u002F000053645",{"doi":2234},{"id":24,"text":2237,"url":24,"identifiers":2238},"10.1007\u002Fs12016-009-8186-2",{"doi":2237},{"id":24,"text":2240,"url":24,"identifiers":2241},"10.1007\u002FBF00915380",{"doi":2240},{"id":24,"text":2243,"url":24,"identifiers":2244},"10.1136\u002Fthx.43.2.84",{"doi":2243},{"id":24,"text":2246,"url":24,"identifiers":2247},"10.1111\u002Fj.1365-2222.1988.tb02857.x",{"doi":2246},{"id":24,"text":2249,"url":24,"identifiers":2250},"10.1183\u002F09031936.98.11020361",{"doi":2249},{"id":24,"text":2252,"url":24,"identifiers":2253},"10.1183\u002F09031936.00.16586100",{"doi":2252},{"id":24,"text":2255,"url":24,"identifiers":2256},"10.1002\u002F14651858.CD001283",{"doi":2255},{"id":24,"text":2258,"url":24,"identifiers":2259},"Scientific Advisory Committee on Nutrition\u002FCommittee on Toxicity, 2004, Advice on Fish Consumption: Benefits and Risks",{},{"id":24,"text":2261,"url":24,"identifiers":2262},"Food and Agriculture Organisation of the United Nations, 2010, Fats and Fatty Acids in Human Nutrition: Report of an Expert Consultation",{},{"id":24,"text":2264,"url":24,"identifiers":2265},"10.2903\u002Fj.efsa.2010.1461",{"doi":2264},{"id":2267,"createTime":2268,"updateTime":2269,"relativeEntities":2270,"slug":2271,"properties":2272,"entityType":205,"verifyStatus":206,"verifyTime":2268,"verifyNote":208,"languages":2290,"translateLanguages":2291,"viewCount":25,"primaryUrl":2292,"fullTextUrl":24,"authors":2293,"publicationType":264,"publisherRelationship":2573,"citationCount":144,"citationInfo":2627,"publishDate":2638,"publishYear":2628,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":2639,"openAccess":24,"references":2640,"isForceReanalyzing":379},"760cbba0-6b0b-40ae-973e-f95a447ce1c8","2024-07-18T15:24:51.647+00:00","2025-02-25T16:26:48.783+00:00",[],"A-new-taxonomy-for-describing-and-defining-adherence-to-medications",{"mag":2273,"keywords":2275,"pmc":2276,"openalex":2278,"abstract":2280,"title":2283,"pm":2286,"doi":2288},{"VOID":2274},"1741567663",{"VI":190},{"VOID":2277},"3403197",{"VOID":2279},"W1741567663",{"EN":2281,"VI":2282},"\u003Cjats:p>Interest in patient adherence has increased in recent years, with a growing literature that shows the pervasiveness of poor adherence to appropriately prescribed medications. However, four decades of adherence research has not resulted in uniformity in the terminology used to describe deviations from prescribed therapies. The aim of this review was to propose a new taxonomy, in which adherence to medications is conceptualized, based on behavioural and pharmacological science, and which will support quantifiable parameters. A systematic literature review was performed using MEDLINE, EMBASE, CINAHL, the Cochrane Library and PsycINFO from database inception to 1 April 2009. The objective was to identify the different conceptual approaches to adherence research. Definitions were analyzed according to time and methodological perspectives. A taxonomic approach was subsequently derived, evaluated and discussed with international experts. More than 10 different terms describing medication‐taking behaviour were identified through the literature review, often with differing meanings. The conceptual foundation for a new, transparent taxonomy relies on three elements, which make a clear distinction between processes that describe actions through established routines (‘Adherence to medications’, ‘Management of adherence’) and the discipline that studies those processes (‘Adherence‐related sciences’). ‘Adherence to medications’ is the process by which patients take their medication as prescribed, further divided into three quantifiable phases: ‘Initiation’, ‘Implementation’ and ‘Discontinuation’. In response to the proliferation of ambiguous or unquantifiable terms in the literature on medication adherence, this research has resulted in a new conceptual foundation for a transparent taxonomy. The terms and definitions are focused on promoting consistency and quantification in terminology and methods to aid in the conduct, analysis and interpretation of scientific studies of medication adherence.\u003C\u002Fjats:p>","\u003Cjats:p> Sự quan tâm đến sự tuân thủ điều trị của bệnh nhân đã gia tăng trong những năm gần đây, với một lượng tài liệu ngày càng tăng cho thấy tính phổ biến của sự tuân thủ kém đối với các loại thuốc được kê đơn phù hợp. Tuy nhiên, bốn thập kỷ nghiên cứu về sự tuân thủ chưa dẫn đến sự đồng nhất trong thuật ngữ được sử dụng để mô tả các sai lệch khỏi các phương pháp điều trị đã được kê đơn. Mục tiêu của bài tổng quan này là đề xuất một phân loại mới, trong đó sự tuân thủ thuốc được khái niệm hóa dựa trên khoa học hành vi và dược lý học, và sẽ hỗ trợ các tham số có thể đo lường được. Một tổng quan tài liệu có hệ thống đã được thực hiện bằng cách sử dụng MEDLINE, EMBASE, CINAHL, Thư viện Cochrane và PsycINFO từ khi khởi tạo cơ sở dữ liệu đến ngày 1 tháng 4 năm 2009. Mục tiêu là xác định các cách tiếp cận khái niệm khác nhau trong nghiên cứu sự tuân thủ. Các định nghĩa đã được phân tích theo thời gian và quan điểm phương pháp luận. Một cách tiếp cận phân loại sau đó đã được rút ra, đánh giá và thảo luận với các chuyên gia quốc tế. Hơn 10 thuật ngữ khác nhau mô tả hành vi dùng thuốc đã được xác định thông qua tổng quan tài liệu, thường có các ý nghĩa khác nhau. Cơ sở khái niệm cho một phân loại mới, minh bạch dựa trên ba yếu tố, tạo ra sự khác biệt rõ ràng giữa các quy trình mô tả hành động thông qua các thói quen đã thiết lập (‘Tuân thủ thuốc’, ‘Quản lý sự tuân thủ’) và ngành học nghiên cứu các quy trình đó (‘Khoa học liên quan đến sự tuân thủ’). ‘Tuân thủ thuốc’ là quá trình mà bệnh nhân dùng thuốc theo đúng hướng dẫn, được chia thành ba giai đoạn có thể đo lường được: ‘Khởi đầu’, ‘Thực hiện’ và ‘Ngừng lại’. Để đáp ứng với sự phát triển của các thuật ngữ mơ hồ hoặc không thể đo lường trong tài liệu về sự tuân thủ điều trị thuốc, nghiên cứu này đã dẫn đến một cơ sở khái niệm mới cho một phân loại minh bạch. Các thuật ngữ và định nghĩa tập trung vào việc thúc đẩy tính nhất quán và khả năng định lượng trong thuật ngữ và phương pháp để hỗ trợ trong việc thực hiện, phân tích và giải thích các nghiên cứu khoa học về sự tuân thủ điều trị thuốc.\u003C\u002Fjats:p>",{"EN":2284,"VI":2285},"A new taxonomy for describing and defining adherence to medications","Một phân loại mới để mô tả và định nghĩa sự tuân thủ điều trị 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Many pro‐inflammatory mediators such as cytokines and cell adhesion molecules that are responsible for the development of the cerebral infarct are under the control of the transcription factor Nuclear Factor kappa‐B (NF‐κB). The activity of NF‐κB is itself tightly regulated through the multicatalytic enzyme known as the proteasome. PS‐519 is a novel and highly selective small molecule that inhibits the proteasome.   An   \u003Cjats:italic>ex   vivo\u003C\u002Fjats:italic>  assay   of   20S   proteasome   activity   allows   monitoring   of the drug effect in blood. PS‐519 is protective in multiple animal models of cerebral ischaemia over a range of doses that achieve 20S inhibition of 40%−80%.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>\n            \u003Cjats:italic>Methods \u003C\u002Fjats:italic>\n          \u003C\u002Fjats:bold> PS‐519 has been administered to healthy male volunteers as single and repeated doses up to 1.6 mg m\u003Cjats:sup>−2\u003C\u002Fjats:sup>. It was given as an intravenous bolus over 20–30 s in a double blind, randomized, placebo‐controlled phase I study, examining vital signs, safety, tolerability and blood 20S proteasome inhibition.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>\n            \u003Cjats:italic>Results \u003C\u002Fjats:italic>\n          \u003C\u002Fjats:bold> Thirty‐nine subjects received single doses of 0.012 mg m\u003Cjats:sup>−2\u003C\u002Fjats:sup>−1.6 mg m\u003Cjats:sup>−2\u003C\u002Fjats:sup> and 28 subjects received doses of 0.5 mg m\u003Cjats:sup>−2\u003C\u002Fjats:sup>−1.6 mg m\u003Cjats:sup>−2\u003C\u002Fjats:sup> on three consecutive days. The drug was well tolerated. There was no clear treatment‐emergent symptom or abnormality of laboratory tests. Proteasome inhibition in blood samples as measured by 20S assay achieved the intended maximum target level of 70–80% with 1.6 mg m\u003Cjats:sup>−2\u003C\u002Fjats:sup>, and was reproducible with repeated dosing.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>\n            \u003Cjats:italic>Conclusions \u003C\u002Fjats:italic>\n          \u003C\u002Fjats:bold> This study has demonstrated that proteasome inhibition is well tolerated by healthy subjects at levels that are maximally neuroprotective in experimental conditions. 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The attitudes of general practitioners and hospital physicians to the management of hypertension in the elderly, were examined by responses to a postal questionnaire distributed within the Northern Region, concerning the management of a healthy 75 year old male non‐ smoker with sustained diastolic or isolated systolic hypertension. 2. Two hundred and fourteen (64%) general practitioners and 127 (70%) hospital physicians responded to the questionnaire. General practitioners stated they would most commonly measure to the nearest 2 mm Hg (47%) as compared with nearest 5 mm Hg (61%) by physicians; P < 0.05. When measuring diastolic blood pressure 16% general practitioners and 31% physicians would use phase IV sounds; P < 0.01. 3. Median levels of hypertension, confirmed by repeated readings, at which antihypertensive therapy would be commenced were similar: 180 (150‐ 230)\u002F100(90‐120) mm Hg vs 180 (150‐200)\u002F100 (90‐120) mm Hg; median (range). The stated use of non‐pharmacological methods to lower blood pressure before starting drug therapy was similar (74% vs 63%). General practitioners were more likely to prescribe a thiazide diuretic (70% vs 54%) and less likely to prescribe a calcium channel blocker (14% vs 28%) as first line therapy; data for diastolic hypertension, P < 0.001. 4. Considerable variation exists amongst both general practitioners and physicians in their stated assessment and management of a healthy elderly non‐smoking male with sustained hypertension. General practitioners and physicians have similar stated thresholds for treating hypertension but differ in their choice of first line therapy. 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