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Journal of Medicine and Pharmacy","Tạp chí Y Dược học Cần Thơ",{"EN":487,"VI":488},"\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">04\u002F10\u002F2015 Ministry of Information and Communications allowed Can Tho journal of medicine and pharmacy to operate (102 \u002FGP-BTTTT)\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">07\u002F16\u002F2015 Can Tho journal of medicine and pharmacy is internationally recognized: ISSN 2354-1210\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">In 2016, The journal has been included in the list of medical science journals by The State Council for professorship which is awarded a work score of 0-0.5 points for a published article.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Can Tho Journal of Medicine and Pharmacy welcome original works that haven’t been submitted or published in other medical journals. Posts must contain content related to one of the journal’s categories.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">The content published\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">The journal is divided into 3 categories:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Scientific research article: are valuable scientific works, which have been researched and accepted.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Overview of medicine, biology and pharmacy: serving the objective of continuing training in the fields of medicine, biology and pharmacy; to systematize classical and modern knowledge.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Update information on new knowledge about medicine, biology, pharmacy in the country and in the world.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Scope\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Publication and introduction of scientific research in the fields:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">+ Medicine (internal medicine, surgery, pediatrics, obstetrics and gynecology, odonto-stomatology, laboratory, oncology, traditional medicine, nursing).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">+ Biology (genetics, biotechnology).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">+ Pharmacology (pharmaceutics, drug quality analysis-control, synthetic pharmaceutical chemistry, biochemistry, pharmacognosy, botany, clinical pharmacy).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- To enhance the quality of undergraduate, postgraduate education, scientifically researching and meet the necessary treatment in hospital.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Introducing the updated domestic and oversea information about science technology to promote scientific research and exchanging technology in local, other universities.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Exchanging pharmaceutical and medical information for social health developing in the Mekong Delta and Vietnam.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">The object\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Postgraduate students, student of Can Tho University of Medicine and Pharmacy, scientists from schools, research institutes, hospitals, health centers, pharmaceutical companies of the Mekong Delta; other provinces and regions in Vietnam and other country.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Address\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Headquarters of Can Tho Journal of Medicine and Pharmacy, located Scientific Research and International Cooperation Office: 179 Nguyen Van Cu Street, An Khanh Ward, Ninh Kieu District, Can Tho City, Vietnam.\u003C\u002Fspan>\u003C\u002Fp>","\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Ngày 16\u002F7\u002F2015, Tạp chí Y Dược học Cần Thơ được cấp chỉ số quốc tế: ISSN 2354-1210.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Từ tháng 4\u002F2016, Tạp chí đã được Hội đồng Giáo sư ngành Y đưa vào danh sách các tạp chí khoa học Y học được tính điểm công trình 0-0,5 điểm cho một bài báo đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Năm 2020 Tạp chí Y Dược học Cần Thơ đã được phê duyệt vào danh mục của các Hội đồng Giáo sư ngành Dược học được tính điểm công trình 0-0,5 điểm cho một bài báo đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ ra 12 số\u002Fnăm, 180-200 trang\u002Fsố.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Từ tháng 12\u002F2022 Tạp chí Y Dược học Cần Thơ là thành viên của hệ thống Crossref và từ tháng 01\u002F2023 tạp chí thực hiện bình duyệt online kín 2 chiều nhằm tăng tính minh bạch, tin cậy của các công trình nghiên cứu khoa học và đảm bảo tốt nhất chất lượng khoa học của bài viết.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tôn chỉ, mục đích và phạm vi của tạp chí\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tôn chỉ và mục đích hoạt động của tạp chí: xuất bản nhằm mục đích phổ biến kết quả từ các đề tài nghiên cứu khoa học; giao lưu trao đổi khoa học, chia sẻ kinh nghiệm, học tập, đồng thời cập nhật thông tin khoa học mới trong các lĩnh vực y, sinh, dược học trong và ngoài nước.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Phạm vi của tạp chí: Tạp chí xuất bản được chia thành 3 chuyên mục: (i) Bài báo nghiên cứu khoa học là kết quả công trình nghiên cứu khoa học có giá trị đã được triển khai nghiên cứu, (ii) Bài tổng quan y, sinh, dược học: phục vụ mục tiêu đào tạo liên tục trong lĩnh vực y, sinh, dược học; nhằm hệ thống hóa những kiến thức kinh điển và hiện đại; (iii) Thông tin cập nhật kiến thức mới về y, sinh, dược học trong nước và trên thế giới.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Chính sách truy cập mở\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ áp dụng chính sách truy cập mở đối với các bài báo đã xuất bản đến với độc giả, nhằm mở rộng cơ hội tiếp cận các kết quả nghiên cứu chất lượng cao và tăng cường trao đổi kiến thức. Tạp chí đăng tải trực tuyến (miễn phí) toàn văn các bài báo được công bố trên website của Tạp chí (https:\u002F\u002Ftapchi.ctump.edu.vn).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đạo đức xuất bản\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ cam kết tuân thủ đạo đức xuất bản phù hợp với các hướng dẫn và tiêu chuẩn của the Committee on Publication Ethics (COPE), tuân thủ các nguyên tắc của COPE’s Core Practices, Best Practices Guidelines for Journal Editors và Guidelines on Good Publication Practices.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Bản thảo bài báo chỉ được chấp nhận khi được tác giả chịu trách nhiệm chính cam kết các nội dung sau: Các nội dung của bản thảo chưa được đăng tải toàn bộ hoặc một phần ở các tạp chí khác; Tất cả các tác giả đều có đóng góp một cách đáng kể vào quá trình nghiên cứu hoặc chuẩn bị bản thảo và cùng chịu trách nhiệm về các nội dung của bản thảo; Tuân thủ các biện pháp đảm bảo đạo đức nghiên cứu (ví dụ thỏa thuận đồng ý tham gia nghiên cứu).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Cam kết bảo mật\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí cam kết thực hiện và tuân thủ các quy định của luật và các văn bản hướng dẫn liên quan đến bảo mật thông tin cá nhân trên không gian mạng. Các thông tin mà người dùng (tác giả, độc giả, biên tập viên, người phản biện) nhập vào các biểu mẫu trên Hệ thống Quản lý xuất bản trực tuyến của tạp chí chỉ được sử dụng vào các mục đích đã được tuyên bố rõ ràng và sẽ không được cung cấp cho bất kỳ bên thứ ba nào khác, hay dùng vào bất kỳ mục đích nào khác.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Phí gửi bài\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Lệ phí gửi đăng bài: 1.000.000đ\u002Fbài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Lệ phí gửi đăng nhanh: 1.500.000đ\u002Fbài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đối với tác giả là cán bộ viên chức thuộc Trường Đại học Y Dược Cần Thơ thì được hỗ trợ 50% lệ phí gửi đăng bài.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đối với sinh viên thực hiện đề tài nghiên cứu khoa học cấp trường được hỗ trợ 100% lệ phí đăng bài ( Tác giả gửi đính kèm “ Quyết định về việc giao tổ chức thực hiện đề tài nghiên cứu khoa học cấp Trường của sinh viên”).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Hình thức nộp lệ phí:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Tiền mặt:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Nộp trực tiếp tại Phòng Tài chính - Kế toán, Trường Đại học Y Dược Cần Thơ, số 179 Nguyễn Văn Cừ, P. An Khánh, Q. Ninh Kiều, thành phố Cần Thơ.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Chuyển khoản:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tên Tài khoản: Trường ĐHYD Cần Thơ, Số TK: 0111000115668, tại ngân hàng Vietcombank chi nhánh Cần Thơ.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Thời gian: Áp dụng từ ngày 01\u002F02\u002F2023.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">* Phí gửi bài không được hoàn trả khi bài viết bị từ chối hoặc tác giả xin rút bài viết.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Quy trình phản biện bài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ thực hiện quy trình phản biện kín hai chiều nghiêm ngặt. Danh tính của những người phản biện không được tiết lộ cho các tác giả và ngược lại. Quy trình thẩm định bài báo đăng gồm các bước sau:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tiếp nhận bản thảo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tác giả liên hệ gửi bản thảo đến Tạp chí qua hệ thống trực tuyến tại website: https:\u002F\u002Ftapchi.ctump.edu.vn. Hướng dẫn về cách đăng ký, gửi bài và chuẩn bị bản thảo được cung cấp trên website của Tạp chí.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Sàng lọc sơ bộ\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Sau khi Tòa soạn nhận được bài báo của tác giả, Ban Thư ký sẽ tiến hành kiểm tra sơ bộ bài báo (các yêu cầu về nội dung và hình thức). Những bài báo không đúng quy cách hoặc có nội dung không phù hợp hoặc vi phạm bản quyền sẽ bị từ chối (Ban Thư ký thông báo phản hồi đến tác giả trong vòng 1 tuần). Những bài báo đủ điều kiện, được Ban Thư ký tòa soạn chuyển đến Ban Biên tập có cùng chuyên môn với nội dung bài báo để đề xuất người phản biện. Thời gian kể từ khi Ban Biên tập nhận bài báo đến khi đề xuất người phản biện bài báo chậm nhất là 5 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Vòng phản biện\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Ban Thư ký gửi bài và yêu cầu phản biện đến 02 phản biện độc lập.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Các phản biện gởi nhận xét cho Ban Thư ký. Thời gian từ khi gửi bài cho phản biện đến khi nhận ý kiến của phản biện tối đa là 20 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Xử ký kết quả phản biện\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Nếu ý kiến đồng ý cho đăng và không cần chỉnh sửa, Ban Thư ký tiếp tục đăng bài theo qui trình.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Nếu ý kiến đồng ý đăng và cần chỉnh sửa, Ban Thư ký sẽ thông tin đến tác giả chỉnh sửa theo yêu cầu của người phản biện. Thời gian chỉnh sửa và gửi lại kéo dài không quá 2 tuần, từ khi tác giả bài báo nhận được thông tin (Quá trình này có thể lặp lại tối đa 2 lần\u002F1 bài báo). Khi có sự thống nhất, đồng ý của người phản biện; bài báo được tiếp tục đăng theo qui trình.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">3. Những bài báo có chất lượng không đạt yêu cầu, cả 2 phản biện không đồng ý cho đăng sẽ bị Tòa soạn từ chối đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Xuất bản\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Ban Thư ký tổng hợp các bản thảo đã được tác giả hoàn thiện sau thẩm định trình Ban Biên tập xem xét, Tổng Biên tập phê duyệt, quyết định bài đăng theo các tiêu chí: sự phù hợp nội dung với tôn chỉ và mục đích, thể loại bài viết (ưu tiên các bài có bài có nghiên cứu chuyên sâu, hàm lượng khoa học cao), đóng góp mới bài báo, bài báo được ưu tiên đăng trong số gần nhất của Tạp chí theo thứ tự: tính thời sự, chất lượng bài báo và thời gian gửi bài.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Ban Biên tập và Ban Thư ký biên tập bản thảo, chế bản, đọc rà soát lỗi. Thời gian hoàn thành từ 10-15 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">3. Ban Thư ký có trách nhiệm thông báo cho tác giả bài báo (bằng e-mail) về tình hình phê duyệt bài báo, thời gian, số kỳ, tập xuất bản bài báo theo qui định.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">4. Danh sách bài báo theo số Tạp chí được in ấn và phát hành trong năm định kỳ được công bố chính thức trên website: https:\u002F\u002Ftapchi.ctump.edu.vn\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>",{"VOID":490},"wcQ1uqwAAAAJ","2023-05-30T08:17:21.868+00:00",[],[494],{"id":495,"createTime":28,"updateTime":28,"relativeEntities":496,"slug":28,"properties":497,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":507,"parentIds":508,"statistic":28},"6413896b-eca9-442b-a73f-182a58a0ce40",[],{"title":498,"address":501,"country":504,"abbreviation":505},{"EN":499,"VI":500},"Can Tho University of Medicine and Pharmacy","Trường Đại học Y Dược Cần Thơ",{"EN":502,"VI":503},"No 179, Nguyen Van Cu street, An Khanh ward, Ninh Kieu district, Can Tho city, Vietnam","Số 179, đường Nguyễn Văn Cừ, phường An Khánh, quận Ninh Kiều, thành phố Cần Thơ, Việt Nam",{"VOID":15},{"VOID":506},"ctump","http:\u002F\u002Fwww.ctump.edu.vn\u002F",[],[],"https:\u002F\u002Ftapchi.ctump.edu.vn\u002Findex.php\u002Fctump",{"impactFactor":32,"impactFactorByYear":512,"i10Index":32,"i10IndexLast5Year":32,"totalPublication":514,"totalPublicationByYear":515,"totalCitation":520,"totalCitationByYear":521,"totalCitationPerPublication":108,"totalCitationPerPublicationByYear":523,"hindexLast5Year":45,"hindex":45},{"2022":513,"2023":111,"2024":106},0.01,1556,{"2020":47,"2021":516,"2022":517,"2023":518,"2024":519,"2025":122},57,306,801,358,161,{"2021":146,"2022":280,"2023":522},99,{"2021":524,"2022":318,"2023":104},0.23,{"impactFactor":28,"impactFactorByYear":28,"i10Index":123,"i10IndexLast5Year":123,"totalPublication":526,"totalPublicationByYear":527,"totalCitation":526,"totalCitationByYear":528,"totalCitationPerPublication":40,"totalCitationPerPublicationByYear":531,"hindexLast5Year":49,"hindex":49},476,{"0":205,"2019":123,"2021":139,"2022":459,"2023":451,"2024":357,"2025":49,"2026":48},{"2021":42,"2022":123,"2023":161,"2024":529,"2025":360,"2026":530},136,83,{"2021":105,"2022":513,"2023":532,"2024":127,"2025":533,"2026":534},0.62,25.43,13.83,{"id":536,"createTime":537,"updateTime":382,"relativeEntities":538,"slug":539,"properties":540,"entityType":25,"verifyStatus":26,"verifyTime":28,"verifyNote":28,"languages":552,"translateLanguages":28,"viewCount":133,"subjectFields":553,"manageAffiliations":554,"indexDatabases":555,"url":556,"thumbnailPath":557,"statistic":558,"gsStatistic":594,"type":55,"analyzePriority":28},"6984a56a-db70-403b-9cc4-4013e1ceaffa","2023-05-09T06:47:40.346+00:00",[],"T%E1%BA%A1p%20ch%C3%AD%20Nghi%C3%AAn%20c%E1%BB%A9u%20n%C6%B0%E1%BB%9Bc%20ngo%C3%A0i",{"country":541,"issn":542,"title":544,"introduce":547,"gsId":550},{"VOID":15},{"VOID":543},"25252445",{"EN":545,"VI":546},"VNU Journal of Foreign Studies","Tạp chí Nghiên cứu nước ngoài",{"EN":548,"VI":549},"{\"ops\":[{\"insert\":\"\\n\\nThe \\n\"},{\"attributes\":{\"italic\":true},\"insert\":\"VNU Journal of Science\"},{\"insert\":\"\\n was established in 1985 for the publication of national and international research papers in all fields of natural sciences and technology, social sciences and humanities. 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In addition, articles published in Drugs may be accompanied by plain language summaries to assist readers who have some knowledge of, but not in-depth expertise in, the area to understand important medical advances.","PENDING",[885],{"id":886,"createTime":28,"updateTime":28,"relativeEntities":887,"label":888,"description":890,"parentId":28,"standard":28,"scholarHubFieldId":28},"8d3ee16d-8f93-4e34-b94e-cd3a00dde338",[],{"EN":889},"Pharmacology (medical)",{},[892,899],{"id":893,"createTime":28,"updateTime":28,"relativeEntities":894,"slug":28,"properties":895,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":898,"statistic":28},"f74aea9c-129f-4619-b592-43cb4b0ecb7b",[],{"title":896},{"EN":897},"Adis International Ltd",[],{"id":900,"createTime":28,"updateTime":28,"relativeEntities":901,"slug":28,"properties":902,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":905,"statistic":28},"67d8862b-59d0-444b-ba15-7c029e652853",[],{"title":903},{"EN":904},"ADIS INT LTD",[],[907,919],{"id":908,"indexDatabase":909,"url":914,"indexYears":915,"academicFieldIds":916,"indexDatabaseRanking":918},"cf5643a1-5f24-42a7-bdad-f74b908e017b",{"id":775,"createTime":28,"updateTime":28,"relativeEntities":910,"label":911,"description":912,"key":781,"publicationTags":913,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],"https:\u002F\u002Fwww.scopus.com\u002Fsourceid\u002F21239","1971-2025",[917],"46eddd1f-e049-4237-8609-9d60083086ad","SCOPUS__Q1",{"id":920,"indexDatabase":921,"url":932,"indexYears":28,"academicFieldIds":933,"indexDatabaseRanking":28},"d4d30112-eff1-4a0f-82fb-a5da0bc9f854",{"id":922,"createTime":28,"updateTime":28,"relativeEntities":923,"label":924,"description":926,"key":929,"publicationTags":930,"standard":28},"a4921856-b128-4d9f-8f1f-e80813d3bbd4",[],{"EN":925,"VI":925},"ISI\u002FSCIE - Science Citation Index Expanded",{"EN":927,"VI":928},"SCIE database","Cơ sở dữ liệu SCIE","scie",[931,813],"SCIE","https:\u002F\u002Fmjl.clarivate.com\u002Fsearch-results?issn=0012-6667",[934,935],"1ff2b686-ac7f-4d79-91fb-d25180fb47ca","2b943d65-24a8-4546-9232-a1e32c12cb6c","https:\u002F\u002Fwww.springer.com\u002Fjournal\u002F40265",{"impactFactor":32,"impactFactorByYear":938,"i10Index":32,"i10IndexLast5Year":32,"totalPublication":939,"totalPublicationByYear":940,"totalCitation":32,"totalCitationByYear":942,"totalCitationPerPublication":32,"totalCitationPerPublicationByYear":943,"hindexLast5Year":32,"hindex":32},{},273,{"1993":40,"2012":941,"2013":357,"2014":48,"2015":49,"2016":123,"2017":49,"2018":46,"2019":46,"2020":48,"2021":357,"2022":46,"2023":145},204,{},{},{"meta":945,"data":947},{"total":946},"6255",[948,1160,1245,1349,1484,1591,1674,1754,1833,1927],{"id":949,"createTime":950,"updateTime":951,"relativeEntities":952,"slug":953,"properties":954,"entityType":963,"verifyStatus":26,"verifyTime":951,"verifyNote":964,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":965,"fullTextUrl":28,"authors":966,"publicationType":1106,"publisherRelationship":1107,"citationCount":28,"citationInfo":28,"publishDate":1156,"publishYear":1157,"citationAnalyzeStatus":883,"lastCitationAnalyze":28,"indexDatabases":1158,"openAccess":28,"references":28,"isForceReanalyzing":1159},"00273887-acb5-4f09-ac18-3183868205c3","2024-01-13T19:51:14.737+00:00","2025-02-11T19:50:03.048+00:00",[],"Are-Biosimilars-the-Future-of-Oncology-and-Haematology-",{"abstract":955,"title":957,"references":959,"doi":961},{"EN":956},"Biological drugs are vital but often high-cost components of cancer treatment. Several biosimilar versions of these drugs have been approved in Europe and\u002For the USA, with many more in development. However, there is some disconnect between the biosimilars that are approved for use and those accessible in clinical practice, with availability impacted by factors including patent litigation and complex healthcare insurance policies, particularly in the USA. Provided the barriers to widespread uptake can be overcome, biosimilars offer potential benefits including cost savings and improved patient access versus the reference product (RP). This article provides an up-to-date and focused perspective on the development and use of biosimilars in the haemato-oncology setting. European and US regulatory pathways governing biosimilar licensing demand that there are no clinically meaningful differences between a biosimilar and its RP. Pathways are rigorously enforced and involve comprehensive non-clinical evaluations and clinical trials in selected indications to establish the equivalence or non-inferiority of efficacy, and the comparability of safety, of the biosimilar versus its RP. ‘Indication extrapolation’ is only permitted if scientifically justifiable considering mechanism(s) of action, pharmacokinetics, immunogenicity and safety in relevant patient populations. Switching treatment from RP to biosimilar is supported by most available data, predominantly from indications other than cancer, and post-marketing pharmacovigilance programmes are warranted. Notably, the potential benefits of biosimilar cancer treatment may extend beyond direct cost savings: for example, the availability of biosimilars of common regimen components may help incentivise the evaluation and\u002For clinical use of new treatment approaches and novel drugs.",{"EN":958},"Are Biosimilars the Future of Oncology and Haematology?",{"VOID":960},"Gulácsi L, Brodszky V, Baji P, Rencz F, Péntek M. The rituximab biosimilar CT-P10 in rheumatology and cancer: a budget impact analysis in 28 European countries. Adv Ther. 2017;34(5):1128–44. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs12325-017-0522-y.\nLee S-M, Jung J-H, Suh D, Jung Y-S, Yoo S-L, Kim D-W, et al. Budget impact of switching to biosimilar trastuzumab (CT-P6) for the treatment of breast cancer and gastric cancer in 28 European countries. BioDrugs. 2019;33(4):423–36. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs40259-019-00359-0.\nEuropean Medicines Agency. 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Accessed 02 Sep 2019.\nYang YT, Chen B, Bennett CL. Biosimilars—curb your enthusiasm. JAMA Oncol. 2017;3(11):1467–8. https:\u002F\u002Fdoi.org\u002F10.1001\u002Fjamaoncol.2017.1530.\nQuintilesIMS. The impact of biosimilar competition in Europe. 2017. https:\u002F\u002Fwww.medicinesforeurope.com\u002Fwp-content\u002Fuploads\u002F2017\u002F05\u002FIMS-Biosimilar-2017_V9.pdf. Accessed 02 Sep 2019.\nBuske C, Ogura M, Kwon HC, Yoon SW. An introduction to biosimilar cancer therapeutics: definitions, rationale for development and regulatory requirements. Future Oncol. 2017;13(15s):5–16. https:\u002F\u002Fdoi.org\u002F10.2217\u002Ffon-2017-0153.\nNational Comprehensive Cancer Network. NCCN clinical practice guidelines in oncology. Myeloid growth factors. Version 2.2018. https:\u002F\u002Fwww.nccn.org\u002Fprofessionals\u002Fphysician_gls\u002Fpdf\u002Fmyeloid_growth.pdf. Accessed 02 Sep 2019.\nChen B, Nagai S, Armitage JO, Witherspoon B, Nabhan C, Godwin AC, et al. Regulatory and clinical experiences with biosimilar filgrastim in the US, the European Union, Japan, and Canada. Oncologist. 2019;24(4):537–48. https:\u002F\u002Fdoi.org\u002F10.1634\u002Ftheoncologist.2018-0341.\nGrewal S, Ramsey S, Balu S, Carlson JJ. Cost-savings for biosimilars in the United States: a theoretical framework and budget impact case study application using filgrastim. Expert Rev Pharmacoecon Outcomes Res. 2018;18(4):447–54. https:\u002F\u002Fdoi.org\u002F10.1080\u002F14737167.2018.1476142.\nMcBride A, Balu S, Campbell K, Bikkina M, MacDonald K, Abraham I. Expanded access to cancer treatments from conversion to neutropenia prophylaxis with biosimilar filgrastim-sndz. Future Oncol. 2017;13(25):2285–95. https:\u002F\u002Fdoi.org\u002F10.2217\u002Ffon-2017-0374.\nEuropean Medicines Agency. Omnitrope. https:\u002F\u002Fwww.ema.europa.eu\u002Fen\u002Fmedicines\u002Fhuman\u002FEPAR\u002Fomnitrope. Accessed 02 Sep 2019.\nUnited States Food and Drug Administration. Zarxio BLA approval letter. https:\u002F\u002Fwww.accessdata.fda.gov\u002Fdrugsatfda_docs\u002Fappletter\u002F2015\u002F125553Orig1s000ltr.pdf. Accessed 02 Sep 2019.\nGoldsmith D, Dellanna F, Schiestl M, Krendyukov A, Combe C. Epoetin biosimilars in the treatment of renal anemia: what have we learned from a decade of European experience? Clin Drug Investig. 2018;38(6):481–90. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs40261-018-0637-1.\nIQVIA. The impact of biosimilar competition in Europe. 2018. https:\u002F\u002Fec.europa.eu\u002Fdocsroom\u002Fdocuments\u002F31642. Accessed 02 Sep 2019.\nUnited States Food and Drug Administration. Retacrit: Prescribing Information. 2018. https:\u002F\u002Fwww.accessdata.fda.gov\u002Fdrugsatfda_docs\u002Flabel\u002F2019\u002F125545s003lbl.pdf. Accessed 02 Sep 2019.\nPharmaceuticals and Medical Devices Agency. New drugs approved in FY 2018. https:\u002F\u002Fwww.pmda.go.jp\u002Ffiles\u002F000229856.pdf. Accessed 02 Sep 2019.\nPharmaceuticals and Medical Devices Agency. New drugs approved in FY 2017. https:\u002F\u002Fwww.pmda.go.jp\u002Ffiles\u002F000229079.pdf. Accessed 02 Sep 2019.\nGenerics and Biosimilars Initiative. Biosimilars approved in South Korea. http:\u002F\u002Fwww.gabionline.net\u002FBiosimilars\u002FGeneral\u002FBiosimilars-approved-in-South-Korea. Accessed 02 Sep 2019.\nHealth Canada. Product monograph including patient medication information: Truxima (submission control no: 227399). 2019. https:\u002F\u002Fpdf.hres.ca\u002Fdpd_pm\u002F00052298.PDF. Accessed 02 Sep 2019.\nHealth Canada. Product monograph including patient medication information: Truxima (submission control no: 208204). 2019. https:\u002F\u002Fpdf.hres.ca\u002Fdpd_pm\u002F00050545.PDF. Accessed 02 Sep 2019.\nHealth Canada. Product monograph including patient medication information: Ogivri. 2019. https:\u002F\u002Fpdf.hres.ca\u002Fdpd_pm\u002F00051011.PDF. Accessed 02 Sep 2019.\nHealth Canada. Product monograph including patient medication information: Mvasi. 2019. https:\u002F\u002Fpdf.hres.ca\u002Fdpd_pm\u002F00051712.PDF. Accessed 02 Sep 2019.\nHealth Canada. Product monograph including patient medication information: Zirabev. 2019. https:\u002F\u002Fpdf.hres.ca\u002Fdpd_pm\u002F00051821.PDF. Accessed 02 Sep 2019.\nRak Tkaczuk KH, Jacobs IA. Biosimilars in oncology: from development to clinical practice. Semin Oncol. 2014;41(Suppl 3):S3–12. https:\u002F\u002Fdoi.org\u002F10.1053\u002Fj.seminoncol.2014.03.008.\nWeise M, Bielsky MC, De Smet K, Ehmann F, Ekman N, Giezen TJ, et al. Biosimilars: what clinicians should know. Blood. 2012;120(26):5111–7. https:\u002F\u002Fdoi.org\u002F10.1182\u002Fblood-2012-04-425744.\nUnited States Food and Drug Administration. Biological product definitions. https:\u002F\u002Fwww.fda.gov\u002Fdownloads\u002FDrugs\u002FDevelopmentApprovalProcess\u002FHowDrugsareDevelopedandApproved\u002FApprovalApplications\u002FTherapeuticBiologicApplications\u002FBiosimilars\u002FUCM581282.pdf. Accessed 02 Sep 2019.\nUnited States Food and Drug Administration. Biosimilar product regulatory review and approval. https:\u002F\u002Fwww.fda.gov\u002Fdownloads\u002FDrugs\u002FDevelopmentApprovalProcess\u002FHowDrugsareDevelopedandApproved\u002FApprovalApplications\u002FTherapeuticBiologicApplications\u002FBiosimilars\u002FUCM581309.pdf. Accessed 02 Sep 2019.\nVulto AG, Jaquez OA. The process defines the product: what really matters in biosimilar design and production? Rheumatology (Oxford). 2017;56:414–29. https:\u002F\u002Fdoi.org\u002F10.1093\u002Frheumatology\u002Fkex278.\nChapman K, Adjei A, Baldrick P, da Silva A, De Smet K, DiCicco R, et al. Waiving in vivo studies for monoclonal antibody biosimilar development: national and global challenges. mAbs. 2016;8:427–35. https:\u002F\u002Fdoi.org\u002F10.1080\u002F19420862.2016.1145331.\nEuropean Medicines Agency. Guideline on immunogenicity assessment of therapeutic proteins. 2017. https:\u002F\u002Fwww.ema.europa.eu\u002Fen\u002Fdocuments\u002Fscientific-guideline\u002Fguideline-immunogenicity-assessment-therapeutic-proteins-revision-1_en.pdf. Accessed 02 Sep 2019.\nEuropean Medicines Agency. Guideline on similar biological medicinal products containing biotechology-derived proteins as active substance: non-clinical and clinical issues (Rev1). 2014. https:\u002F\u002Fwww.ema.europa.eu\u002Fdocuments\u002Fscientific-guideline\u002Fguideline-similar-biological-medicinal-products-containing-biotechnology-derived-proteins-active_en-2.pdf. Accessed 02 Sep 2019.\nUnited States Food and Drug Administration. Guidance for industry: E9 statistical principles for clinical trials. 1998. https:\u002F\u002Fwww.fda.gov\u002Fmedia\u002F71336\u002Fdownload. Accessed 02 Sep 2019.\nEuropean Medicines Agency. Note for guidance on statistical principles for clinical trials. 1998. https:\u002F\u002Fwww.ema.europa.eu\u002Fen\u002Fdocuments\u002Fscientific-guideline\u002Fich-e-9-statistical-principles-clinical-trials-step-5_en.pdf. Accessed 02 Sep 2019.\nEuropean Medicines Agency. Guideline on similar biological medicinal products containing monoclonal antibodies—non-clinical and clinical issues. 2012. https:\u002F\u002Fwww.ema.europa.eu\u002Fdocuments\u002Fscientific-guideline\u002Fguideline-similar-biological-medicinal-products-containing-monoclonal-antibodies-non-clinical_en.pdf. Accessed 02 Sep 2019.\nIsakov L, Jin B, Jacobs IA. Statistical primer on biosimilar clinical development. Am J Ther. 2016;23(6):e1903–10. https:\u002F\u002Fdoi.org\u002F10.1097\u002FMJT.0000000000000391.\nThatcher N, Thomas M, Paz-Ares L, Ostoros G, Pan Z, Goldschmidt JH et al. Randomized, double-blind, phase 3 study evaluating efficacy and safety of ABP 215 compared with bevacizumab in patients with non-squamous NSCLC. J Clin Oncol 2016;34(15 Suppl.):Abstract 9095. https:\u002F\u002Fdoi.org\u002F10.1200\u002Fjco.2016.34.15_suppl.9095.\nEuropean Medicines Agency. Mvasi: EPAR - Public assessment report. EMA\u002F798844\u002F2017. 2017. https:\u002F\u002Fwww.ema.europa.eu\u002Fdocuments\u002Fassessment-report\u002Fmvasi-epar-public-assessment-report_en.pdf. Accessed 02 Sep 2019.\nvon Minckwitz G, Colleoni M, Kolberg HC, Morales S, Santi P, Tomasevic Z, et al. Efficacy and safety of ABP 980 compared with reference trastuzumab in women with HER2-positive early breast cancer (LILAC study): a randomised, double-blind, phase 3 trial. Lancet Oncol. 2018;19(7):987–98. https:\u002F\u002Fdoi.org\u002F10.1016\u002FS1470-2045(18)30241-9.\nStebbing J, Baranau Y, Baryash V, Manikhas A, Moiseyenko V, Dzagnidze G, et al. CT-P6 compared with reference trastuzumab for HER2-positive breast cancer: a randomised, double-blind, active-controlled, phase 3 equivalence trial. Lancet Oncol. 2017;18(7):917–28. https:\u002F\u002Fdoi.org\u002F10.1016\u002FS1470-2045(17)30434-5.\nRugo HS, Barve A, Waller CF, Hernandez-Bronchud M, Herson J, Yuan J, et al. Effect of a proposed trastuzumab biosimilar compared with trastuzumab on overall response rate in patients with ERBB2 (HER2)-positive metastatic breast cancer: a randomized clinical trial. JAMA. 2017;317(1):37–47. https:\u002F\u002Fdoi.org\u002F10.1001\u002Fjama.2016.18305.\nPivot X, Bondarenko I, Nowecki Z, Dvorkin M, Trishkina E, Ahn JH, et al. 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J Clin Oncol. 1999;17(4):1244. https:\u002F\u002Fdoi.org\u002F10.1200\u002Fjco.1999.17.4.1244.\nCheson BD, Pfistner B, Juweid ME, Gascoyne RD, Specht L, Horning SJ, et al. Revised response criteria for malignant lymphoma. J Clin Oncol. 2007;25(5):579–86. https:\u002F\u002Fdoi.org\u002F10.1200\u002FJCO.2006.09.2403.",{"VOID":962},"10.1007\u002Fs40265-019-01193-y","PUBLICATION","Auto Verify","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs40265-019-01193-y",[967,983,998,1013,1037,1052,1067,1082],{"id":968,"sortIndex":32,"researcher":28,"roles":969,"affiliations":971,"properties":980,"displayName":982,"givenName":28,"familyName":28},"467baa1a-0ae7-417f-a507-aac93b57d32c",[970],"AUTHOR",[972],{"id":973,"sortIndex":32,"affiliation":974,"properties":28},"7e694e9c-6a60-43b6-8fac-308d6bd50974",{"id":973,"createTime":28,"updateTime":28,"relativeEntities":975,"slug":28,"properties":976,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":979,"statistic":28},[],{"title":977},{"VI":978},"Institute of Hematology Seragnoli, University of Bologna, Bologna, Italy",[],{"title":981},{"VI":982},"Pier Luigi Zinzani",{"id":984,"sortIndex":40,"researcher":28,"roles":985,"affiliations":986,"properties":995,"displayName":997,"givenName":28,"familyName":28},"19b3f5b7-76a0-4e88-8477-3deadc8d57d2",[970],[987],{"id":988,"sortIndex":32,"affiliation":989,"properties":28},"04419d8c-ef06-4f18-a051-cf17d502c19e",{"id":988,"createTime":28,"updateTime":28,"relativeEntities":990,"slug":28,"properties":991,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":994,"statistic":28},[],{"title":992},{"VI":993},"Medizinische Klinik III, Klinikum der Universitat Munchen, LMU Munich, Munich, Germany",[],{"title":996},{"VI":997},"Martin Dreyling",{"id":999,"sortIndex":123,"researcher":28,"roles":1000,"affiliations":1001,"properties":1010,"displayName":1012,"givenName":28,"familyName":28},"9591b501-7847-44e3-86c9-b6db9afc8295",[970],[1002],{"id":1003,"sortIndex":32,"affiliation":1004,"properties":28},"ba163d9c-3fe1-480d-8df5-c7da940db677",{"id":1003,"createTime":28,"updateTime":28,"relativeEntities":1005,"slug":28,"properties":1006,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1009,"statistic":28},[],{"title":1007},{"VI":1008},"Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, USA",[],{"title":1011},{"VI":1012},"William Gradishar",{"id":1014,"sortIndex":42,"researcher":28,"roles":1015,"affiliations":1016,"properties":1034,"displayName":1036,"givenName":28,"familyName":28},"537537b7-7ba5-4658-9572-78c3f23e9592",[970],[1017,1025],{"id":1018,"sortIndex":32,"affiliation":1019,"properties":28},"f9a0f91c-83e2-4a6e-9963-dc2859b75738",{"id":1018,"createTime":28,"updateTime":28,"relativeEntities":1020,"slug":28,"properties":1021,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1024,"statistic":28},[],{"title":1022},{"VI":1023},"Universite Catholique de Louvain, CHU UCL Namur, Yvoir, Belgium",[],{"id":1026,"sortIndex":40,"affiliation":1027,"properties":1033},"6cc9042b-5116-4d7e-bfb7-63b1e81c51a9",{"id":1026,"createTime":28,"updateTime":28,"relativeEntities":1028,"slug":28,"properties":1029,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1032,"statistic":28},[],{"title":1030},{"VI":1031},"Pôle de Recherche Mont, Institut de Recherche Expérimentale et Clinique, Université Catholique de Louvain, Yvoir, Belgium",[],{},{"title":1035},{"VI":1036},"Marc Andre",{"id":1038,"sortIndex":45,"researcher":28,"roles":1039,"affiliations":1040,"properties":1049,"displayName":1051,"givenName":28,"familyName":28},"e1c301ef-c3fd-4c42-90db-66aec7f8b052",[970],[1041],{"id":1042,"sortIndex":32,"affiliation":1043,"properties":28},"01853ae8-40f2-412a-9201-54f6b3692988",{"id":1042,"createTime":28,"updateTime":28,"relativeEntities":1044,"slug":28,"properties":1045,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1048,"statistic":28},[],{"title":1046},{"VI":1047},"Perlmutter Cancer Center at NYU Langone Health, New York, USA",[],{"title":1050},{"VI":1051},"Francisco J. 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Barca",{"id":1083,"sortIndex":49,"researcher":28,"roles":1084,"affiliations":1085,"properties":1103,"displayName":1105,"givenName":28,"familyName":28},"28521863-ca5d-4a75-988e-cb324db0a8db",[970],[1086,1094],{"id":1087,"sortIndex":32,"affiliation":1088,"properties":28},"27ea3eb2-7f56-4063-a4b3-207791080afa",{"id":1087,"createTime":28,"updateTime":28,"relativeEntities":1089,"slug":28,"properties":1090,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1093,"statistic":28},[],{"title":1091},{"VI":1092},"Department of Oncology and Hemato-Oncology, University of Milano, Milano, Italy",[],{"id":1095,"sortIndex":40,"affiliation":1096,"properties":1102},"2f19b524-13f4-4e73-b4d7-9b2d3557f026",{"id":1095,"createTime":28,"updateTime":28,"relativeEntities":1097,"slug":28,"properties":1098,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1101,"statistic":28},[],{"title":1099},{"VI":1100},"European Institute of Oncology, IRCCS, Milano, Italy",[],{},{"title":1104},{"VI":1105},"Giuseppe 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(Lyfnua®; Merck & Co.) is a first-in-class, non-narcotic, selective P2X3 receptor antagonist being developed for the treatment of refractory chronic cough or unexplained chronic cough. Marketing approval for gefapixant is being sought in the EU and USA, and the drug was recently approved for marketing in Japan as treatment for refractory or unexplained chronic cough. This article summarizes the milestones in the development of gefapixant leading to this first approval.",{"EN":1170},"Gefapixant: First Approval",{"VOID":1172},"Muccino D, Green S. Update on the clinical development of gefapixant, a P2X3 receptor antagonist for the treatment of refractory chronic cough. Pulm Pharmacol Ther. 2019;56:75–8.\nKyorin. MSD K.K. receives manufacturing and marketing approval of LYFNUA® tablets, world's first selective P2X3 receptor antagonist for the treatment of chronic cough [media release]. 20 Jan 2022. http:\u002F\u002Fwww.kyorin-pharm.com.\nMerck AG. Merck Provides U.S. and Japan regulatory update for gefapixant [media release]. 24 Jan 2022. http:\u002F\u002Fwww.merck.com.\nFord AP, Dillon MP, Kitt MM, et al. The discovery and development of gefapixant. Auton Neurosci. 2021;235:102859.\nMartinez FJ, Afzal AS, Smith JA, et al. Treatment of persistent cough in subjects with idiopathic pulmonary fibrosis (IPF) with gefapixant, a P2X3 antagonist, in a randomized, placebo-controlled clinical trial. Pulm Ther. 2021;7(2):471–86.\nRoche. Roche licenses first-in-class treatments for chronic pain to afferent pharmaceuticals; afferent secures $23 million in series A financing [media release]. 17 Dec 2009. http:\u002F\u002Fwww.roche.com.\nMerck Co. Merck announces second-quarter 2016 financial results [media release]. 29 Jul 2016. http:\u002F\u002Fwww.merck.com.\nKyorin. MSD and KYORIN conclude distribution agreement of gefapixant citrate, a treatment for chronic cough, in Japan [media release]. 26 Apr 2021. http:\u002F\u002Fwww.kyorin-pharm.com.\nRichards D, Gever JR, Ford AP, et al. Action of MK-7264 (gefapixant) at human P2X3 and P2X2\u002F3 receptors and in vivo efficacy in models of sensitisation. Br J Pharmacol. 2019;176(13):2279–91.\nMSD. Lyfnua® tablets 45 mg [Japanese prescribing information]. 2022. https:\u002F\u002Fwww.pmda.go.jp\u002FPmdaSearch\u002FiyakuDetail\u002FResultDataSetPDF\u002F170050_22900A0F1027_1_02. Accessed 7 Mar 2022.\nNussbaum JC, Hussain A, Ma B, et al. Characterization of the absorption, metabolism, excretion, and mass balance of gefapixant in humans. Pharmacol Res Perspect. 2022;10(1):e00924.\nMcCrea JB, Hussain A, Ma B, et al. Assessment of pharmacokinetic interaction between gefapixant (MK-7264), a P2X3 receptor antagonist, and the OATP1B1 drug transporter substrate pitavastatin. Clin Pharmacol Drug Dev. 2021;11:406–12. https:\u002F\u002Fdoi.org\u002F10.1002\u002Fcpdd.1047.\nNussbaum JC, Hussain A, Ma B, et al. Assessment of the effect of pyrimethamine, a potent inhibitor of multidrug and toxin extrusion protein 1\u002F2K, on the pharmacokinetics of gefapixant (MK-7264), a P2X3 receptor antagonist. Clin Pharmacol Drug Deliv. 2022;11(1):123–8.\nMcGarvey L, Birring S, Morice A, et al. Efficacy and safety of gefapixant, a P2X3 receptor antagonist, in refractory chronic cough and unexplained chronic cough (COUGH-1 and COUGH-2): results from two double-blind, randomised, parallel-group, placebo-controlled, phase 3 trials. Lancet. 2022. https:\u002F\u002Fdoi.org\u002F10.1016\u002FS0140-6736(21)02348-5.\nDicpinigaitis P, Birring SS, Morice A, et al. Patient-reported chronic cough severity over 52 weeks in two phase 3 trials of gefapixant. Eur Respir J. 2021;58(suppl 65):OA1588.\nSmith JA, Kitt MM, Morice AH, et al. Gefapixant, a P2X3 receptor antagonist, for the treatment of refractory or unexplained chronic cough: a randomised, double-blind, controlled, parallel-group, phase 2b trial. Lancet Respir Med. 2020;8(8):775–85.\nSmith JA, Kitt MM, Butera P, et al. Gefapixant in two randomised dose-escalation studies in chronic cough. Eur Respir J. 2020;55(3):1901615. https:\u002F\u002Fdoi.org\u002F10.1183\u002F13993003.01615-2019.\nBirring S, Cardozo L, Dmochowski R, et al. A phase 3b trial evaluating the efficacy of gefapixant in reducing stress urinary incontinence in women with chronic cough. Am J Respir Crit Care Med Conf Am Thorac Soc Int Conf ATS. 2020;201(1):A7776.",{"VOID":1174},"10.1007\u002Fs40265-022-01700-8","2024-12-15T05:01:16.342+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs40265-022-01700-8",[1178],{"id":1179,"sortIndex":32,"researcher":28,"roles":1180,"affiliations":1181,"properties":1190,"displayName":1192,"givenName":28,"familyName":28},"08713f93-e8c4-492f-8d67-f1e2532ba99a",[970],[1182],{"id":1183,"sortIndex":32,"affiliation":1184,"properties":28},"19c469a0-3aa4-4667-97a5-0fc6b2bc9be4",{"id":1183,"createTime":28,"updateTime":28,"relativeEntities":1185,"slug":28,"properties":1186,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1189,"statistic":28},[],{"title":1187},{"VI":1188},"Springer Nature, Auckland, New Zealand",[],{"title":1191},{"VI":1192},"Anthony Markham",{"url":1176,"publisher":1194,"properties":1237},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1195,"slug":872,"properties":1196,"entityType":25,"verifyStatus":883,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":47,"subjectFields":1201,"manageAffiliations":1206,"indexDatabases":1217,"url":936,"thumbnailPath":28,"statistic":1232,"gsStatistic":28,"type":28,"analyzePriority":28},[],{"country":1197,"eissn":1198,"issn":1199,"title":1200},{"VOID":875},{"VOID":877},{"VOID":879},{"EN":872},[1202],{"id":886,"createTime":28,"updateTime":28,"relativeEntities":1203,"label":1204,"description":1205,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":889},{},[1207,1212],{"id":893,"createTime":28,"updateTime":28,"relativeEntities":1208,"slug":28,"properties":1209,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1211,"statistic":28},[],{"title":1210},{"EN":897},[],{"id":900,"createTime":28,"updateTime":28,"relativeEntities":1213,"slug":28,"properties":1214,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1216,"statistic":28},[],{"title":1215},{"EN":904},[],[1218,1225],{"id":908,"indexDatabase":1219,"url":914,"indexYears":915,"academicFieldIds":1224,"indexDatabaseRanking":918},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":1220,"label":1221,"description":1222,"key":781,"publicationTags":1223,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],[917],{"id":920,"indexDatabase":1226,"url":932,"indexYears":28,"academicFieldIds":1231,"indexDatabaseRanking":28},{"id":922,"createTime":28,"updateTime":28,"relativeEntities":1227,"label":1228,"description":1229,"key":929,"publicationTags":1230,"standard":28},[],{"EN":925,"VI":925},{"EN":927,"VI":928},[931,813],[934,935],{"impactFactor":32,"impactFactorByYear":1233,"i10Index":32,"i10IndexLast5Year":32,"totalPublication":939,"totalPublicationByYear":1234,"totalCitation":32,"totalCitationByYear":1235,"totalCitationPerPublication":32,"totalCitationPerPublicationByYear":1236,"hindexLast5Year":32,"hindex":32},{},{"1993":40,"2012":941,"2013":357,"2014":48,"2015":49,"2016":123,"2017":49,"2018":46,"2019":46,"2020":48,"2021":357,"2022":46,"2023":145},{},{},{"pages":1238,"volume":1240},{"VOID":1239},"691-695",{"VOID":1241},"82","2022-03-28",2022,[931,918],{"id":1246,"createTime":1247,"updateTime":1248,"relativeEntities":1249,"slug":1250,"properties":1251,"entityType":963,"verifyStatus":883,"verifyTime":1248,"verifyNote":1259,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1260,"fullTextUrl":28,"authors":1261,"publicationType":1106,"publisherRelationship":1297,"citationCount":28,"citationInfo":28,"publishDate":1346,"publishYear":1347,"citationAnalyzeStatus":883,"lastCitationAnalyze":28,"indexDatabases":1348,"openAccess":28,"references":28,"isForceReanalyzing":1159},"0034849c-4245-4501-9e4f-c26b9ce97cc1","2023-12-21T07:00:17.459+00:00","2025-01-19T11:53:02.320+00:00",[],"Clarithromycin",{"abstract":1252,"title":1254,"references":1255,"doi":1257},{"EN":1253},"Results from noncomparative and placebo-controlled studies demonstrate the efficacy of clarithromycin in the treatment of disseminated Mycobacterium avium-intracellulare complex (MAC) infection in patients with acquired immune deficiency syndrome (AIDS), Whether given alone or in combination with other antimycobacterial treatments, doses of 500 to 2000mg (typically 1000mg) administered twice daily are effective in controlling bacteraemia in these patients. Clarithromycin has also been shown to improve clinical symptoms of infection and may improve quality of life in AIDS patients with MAC infection. Clarithromycin is generally well tolerated when used in the doses typically required for the treatment of MAC infection (1000 or 2000 mg\u002Fday). Gastrointestinal disturbances are the most commonly occurring adverse events and occur most frequently at dosages of 4000 mg\u002Fday. Thus, clarithromycin, as monotherapy or in combination with other antimycobacterial agents, is well tolerated and effectively eradicates MAC from the blood in the short term in patients with AIDS; however, short term monotherapy may lead to bacterial resistance, underscoring the importance of long term treatment with a combination of antimycobacterial agents. While the optimal combination regimen to prevent the development of resistance to antimycobacterial agents by MAC remains to be determined, clarithromycin will almost certainly be a valuable agent in any such combination. Until recently, infection due to the intracellular bacteria Mycobacterium avium and Mycobacterium intracellulare was rarely observed and was generally restricted to pulmonary sites in patients with underlying pulmonary pathology. Disseminated disease is now common in patients with acquired immune deficiency syndrome (AIDS), and is the most frequently occurring bacterial infection in this patient population in the US. Patients with AIDS-related disseminated mycobacterial disease have a shorter median survival, and increased morbidity, compared with patients with AIDS who do not have mycobacterial disease; however, it is unclear whether shortened survival is attributable to the mycobacterial infection per se. The minimum inhibitory concentration of clarithromycin against MAC depends on both pH and the medium used for in vitro testing. At pH 7.4 clarithromycin is active against MAC in vitro, with minimum concentrations inhibitory to 90% of tested isolates ranging from 0.85 to 8 mg\u002FL. The minimum bactericidal concentration of clarithromycin against MAC ranged from ⩽6 to >256 mg\u002FL; some investigators suggested clarithromycin would have bactericidal activity in vivo only if it accumulated within phagocytic cells. Clarithromycin does accumulate in leucocytes and polymorphonuclear cells and, at concentrations which are achievable in the serum, it appears that clarithromycin may have bactericidal activity against M. avium-intracellulare complex located within macrophages. The 14-hydroxy metabolite of clarithromycin also has activity against MAC in vitro and against MAC growing within macrophages. Clarithromycin is well absorbed after oral administration, but undergoes first-pass metabolism, principally to an active metabolite, reducing its systemic bioavailability. As the major metabolite of clarithromycin has some antimicrobial activity, the bioavailability of the parent compound may underestimate the bioavailability of active compounds. Tissue concentrations of clarithromycin are generally higher than those achieved in the serum, and clarithromycin penetrates into human phagocytic cells to a greater extent than does erythromycin. Clarithromycin has been studied alone or in combination with other antimycobacterial drugs in the treatment of patients with AIDS and disseminated MAC infection, and initial results have been encouraging. All 23 evaluable patients in 2 noncomparative studies responded clinically and had negative blood cultures for MAC after 8 weeks of combined antimycobacterial treatment, which included clarithromycin 2000 mg\u002Fday with either clofazimine or ciprofloxacin plus amikacin. Dose-ranging studies involving larger numbers of patients found clarithromycin in daily doses of 1000 to 2000mg to be effective in the treatment of MAC infection, although dosages of 1500 to 2000 mg\u002Fday may produce a therapeutic response more quickly or more effectively than dosages of ⩽1000 mg\u002Fday. Preliminary results of quality-of-life analyses using the Medical Outcomes Study (MOS)-HIV scale indicated that, compared with pretreatment values, clarithromycin produced significant improvements in quality-of-life parameters such as overall health, social functioning and energy level. Small placebo-controlled studies showed that clarithromycin 1000mg twice daily, with or without a 3-drug combination of isoniazid, ethambutol and clofazimine for 6 weeks, achieved consistent bacteriological and clinical response in patients with AIDS and disseminated MAC infection. However, relapse of AIDS-related MAC infection has been documented with clarithromycin, either when given as monotherapy or when used in combination with other antimycobacterial agents. More studies are required to establish the optimal therapeutic regimens for preventing the emergence of resistant organisms. Data from patients with AIDS receiving clarithromycin 500 to 2000mg twice daily for the treatment of disseminated MAC infection suggest that adverse events, particularly gastrointestinal problems, are dosage-related. An unpublished analysis revealed that gastrointestinal adverse events occurred with a similar frequency in patients receiving clarithromycin 1000 or 2000 mg\u002Fday, but occurred considerably more often in patients receiving 4000 mg\u002Fday. Similarly, patients receiving clarithromycin 4000 mg\u002Fday were more likely to have their treatment with clarithromycin discontinued because of drug-related adverse gastrointestinal events. Furthermore, the drug was well tolerated in other trials using similar dosage regimens in this clinical setting. Other adverse events associated with higher clarithromycin dosages have included minor temporary elevations in liver function test parameters and dysphoric sensations. Pooled data from phase II\u002FIII clinical trials undertaken in 3437 patients, the majority of whom had respiratory tract infections, demonstrated that clarithromycin 250 to 500mg twice daily is well tolerated with few severe adverse events. Approximately 20% of clarithromycin recipients reported 1 or more adverse event, the most frequent of which were gastrointestinal problems. Overall, 3% of patients receiving clarithromycin discontinued treatment due to adverse events. Furthermore, discontinuation of therapy because of adverse effects was less likely with clarithromycin than with older macrolides (3 vs 6%). The most common dosage of clarithromycin used in clinical trials undertaken in patients with AIDS and disseminated MAC infection has been 1000mg twice daily either alone or in combination with other antimycobacterial agents. Efficacy appears to be dosage-related, but dosages of between 1000 and 2000 mg\u002Fday were effective in this patient population. Dosage reduction may be required in the presence of severe renal impairment, and in elderly patients dosages should be based on bodyweight and renal function and may need to be reduced to 1000 mg\u002Fday.",{"EN":1250},{"VOID":1256},"Agins BD, Berman DS, Spicehandler D, El-Sadr W, Simberkoff MS, et al. Effect of combined therapy with ansamycin, clofazimine, ethambutol, and isoniazid for Mycobacterium avium infection in patients with AIDS. Journal of Infectious Diseases 159: 784–787, 1989.\nAlbani F, Riva R, Baruzzi A. Clarithromycin-carbamazepine interaction. Case report. Epilepsia 34: 161–162, 1993.\nAnderson R, Joone G, van Rensburg CEJ. An in-vitro evaluation of the cellular uptake and intraphagocytic bioactivity of clarithromycin (A-56268, TE-031), a new macrolide antimicrobial agent. Journal of Antimicrobial Chemotherapy 22: 923–933, 1988.\nBakhtiar M, Selwyn S. Combination of aztreonam with anti-staphylococcal antibiotics. Journal of Antimicrobial Chemotherapy 22: 773–774, 1988.\nBeavis KG, Hall GS. In vitro activity of two macrolides, clarithromycin and azithromycin, against M. avium-intracellulare. Abstract. The First International Conference on the Macrolides, Azalides and Streptogramins, Santa Fe, New Mexico, January 1992.\nBerlin OGW, Young LS, Floyd-Reising SA, Bruckner DA. Comparative in vitro activity of the new macrolide A-56268 against mycobacteria. European Journal of Clinical Microbiology 6: 486–487, 1987.\nBessesen MT, Berry CD, Johnson MA, Klaus B, Blaser MJ, et al. Site of origin of disseminated MAC infection in AIDS. Abstract. 30th Interscience Conference on Antimicrobial Agents and Chemotherapy. Washington DC, American Society for Microbiology, p. 297, 1990.\nBrown ST, Edwards FF, Bernard EM, Armstrong D. Inhibition of Mycobacterium avium complex (MAC) by single agents and combinations. Abstract. Interscience Conference on Antimicrobial Agents and Chemotherapy, American Society for Microbiology, 1991.\nBrown BA, Wallace Jr RJ, Onyi GO. Activities of clarithromycin against eight slowly growing species of nontuberculous mycobacteria, determined by using a broth microdilution MIC system. Antimicrobial Agents and Chemotherapy 36: 1987–1990, 1992.\nChaisson RE. Mycobacterial infection and HIV. Current Opinion in Infectious Diseases, in press, 1993.\nChaisson RE, Benson C, Dube M, Korvick J, Wu A, et al. Clarithromycin therapy for disseminated Mycobacterium avium-complex (MAC) in AIDS. Abstract. 32nd Interscience Conference on Antimicrobial Agents and Chemotherapy, American Society for Microbiology, Anaheim, California, 11–14 October, 1992.\nChaisson RE, Hopewell PC. Mycobacteria and AIDS mortality. Editorial. American Review of Respiratory Disease 139: 1–3, 1989.\nChiu J, Nussbaum J, Bozzette S, Tilles JG, Young LS, et al. Treatment of disseminated Mycobacterium avium complex infection in AIDS with amikacin, ethambutol, rifampin, and ciprofloxacin. Annals of Internal Medicine 113: 358–361, 1990.\nChu S-y. Wilson DS, Guay DRP, Craft C. Clarithromycin pharmacokinetics in healthy young and elderly volunteers. Journal of Clinical Pharmacology 32: 1045–1049, 1992a.\nChu S-Y, Sennello LT, Bunnell ST, Varga LL, Wilson DS, et al. Pharmacokinetics of clarithromycin, a new macrolide, after single ascending oral doses. Antimicrobial Agents and Chemotherapy 36: 2447–2453, 1992b.\nCohen Y, Perronne C, Truffot-Pernot C, Grosset J, Vilde JL, et al. Activities of WIN-57273, minocycline, clarithromycin, and 14-hydroxy-clarithromycin against Mycobacterium avium complex in human macrophages. Antimicrobial Agents and Chemotherapy 36 (10): 2104–2107, 1992.\nCynamon MH, Klemens SP. Activity of azithromycin against Mycobacterium avium infection in beige mice. Antimicrobial Agents and Chemotherapy 36: 1611–1613, 1992.\nCynamon MH, Klemens SP, Swenson CE. TLC G-65 in combination with other agents in the therapy of Mycobacterium avium infection in beige mice. Journal of Antimicrobial Chemotherapy 29: 693–699, 1992.\nDautzenberg B, Hazebroucq J, Chauvin JP. Clarithromycin in 100 AIDS patients with disseminated M. avium infection. Abstract. 32nd Interscience Conference on Antimicrobial Agents and Chemotherapy, American Society for Microbiology, Anaheim, California, 11–14 October, 1992.\nDautzenberg B, Saint Marc T, Meyohas MC, Eliaszewitch M, Haniez F, et al. Clarithromycin and other antimicrobial agents in the treatment of disseminated Mycobacterium avium infections in patients with acquired immunodeficiency syndrome. Archives of Internal Medicine 153: 368–372, 1993.\nDautzenberg B, Truffot C, Legris S, Meyohas M-C, Berlie HC, et al. Activity of clarithromycin against Mycobacterium avium infection in patients with the acquired immune deficiency syndrome. American Review of Respiratory Disease 144: 564–569, 1991.\nde Lalla F, Maserati R, Scarpellini P, Marone P, Nicolin R, et al. Clarithromycin-ciprofloxacin-amikacin for therapy of Mycobacterium avium-Mycobacterium intracellulare bacteremia in patients with AIDS. Antimicrobial Agents and Chemotherapy 36: 1567–1569, 1992.\nde Wit S, D’Abraccio M, de Mol P, Clumeck N. Acquired resistance to clarithromycin as combined therapy in Mycobacterium avium intracellulare infection. Correspondence. Lancet 341: 53–54, 1993.\nEllner JJ, Goldberger MJ, Parenti DM. Mycobacterium avium infection and AIDS: a therapeutic dilemma in rapid evolution. Journal of Infectious Diseases 163: 1326–1335, 1991.\nFernandes PB, Hardy DJ, McDaniel D, Hanson CW, Swanson RN. In vitro and in vivo activities of clarithromycin against Mycobacterium avium. Antimicrobial Agents and Chemotherapy 33: 1531–1534, 1989.\nGan VN, Chu S-Y, Kusmiesz HT, Craft JC. Pharmacokinetics of a clarithromycin suspension in infants and children. Antimicrobial Agents and Chemotherapy 36: 2478–2480, 1992.\nGreene JB, Sidhu GS, Lewin S, Levine JF, Masur H, et al. Mycobacterium avium-intracellulare: a cause of disseminated life-threatening infection in homosexuals and drug abusers. Annals of Internal Medicine. 97: 539–546, 1982.\nGrubman SD, Hoyt L, Schramm RJ, Picardi J, Oleske J. Clarithromycin for the treatment of MAI in an HIV-infected child. Annals of Allergy 68: 99, 1992.\nGuay DRP, Patterson DR, Seipman N, Craft JC. Overview of the tolerability profile of clarithromycin in preclinical and clinical trials. Drug Safety 8: 350–364, 1993.\nGupta S, Blahunka K, Dellerson M, Craft JC, Smith T. Interim results of safety and efficacy of clarithromycin (C) in the treatment of disseminated Mycobacterium avium complex (MAC) infection in patients (Pts) with AIDS. Abstract. 32nd Interscience Conference on Antimicrobial Agents and Chemotherapy, American Society for Microbiology, Anaheim, California, 11–14 October, 1992.\nGustavson LE, Chu S-y, Mackenthum A, Gupta SD, Craft JC. Drug interaction between clarithromycin and oral zidovudine in HIV-1 infected patients. Abstract. Clinical Pharmacology and Therapeutics 53: 163, 1993.\nHavlik Jr JA, Horsburgh Jr CR, Metchock B, Williams PP, Fann SA, et al. Disseminated Mycobacterium avium complex infection: clinical identification and epidemiological trends. Journal of Infectious Diseases 165: 577–580, 1992.\nHawkins CC, Gold JWM, Whimbey E, Kiehn TE, Brannon P, et al. Mycobacterium avium complex infections in patients with the acquired immunodeficiency syndrome. Annals of Internal Medicine 105: 184–188, 1986.\nHeifets LB. Antituberculosis drugs: antimicrobial activity in vitro. In Heifets LB (Ed.) Drug susceptibility in the chemotherapy of mycobacterial infections, pp. 13–57, CRC Press, Florida 1991a.\nHeifets LB. Dilemmas and realities in drug susceptibility testing of M. avium — M. intracellulare and other slowly growing non-tuberculous mycobacteria. In Heifets LB (Ed.). Drug susceptibility in the chemotherapy of mycobacterial infections, pp. 123–196, CRC Press, Florida, 1991b.\nHeifets L, Lindholm-Levy P, Constock D. MICs and MBCs of clarithromycin for M. avium isolated from AIDS patients. Abstract. American Society of Microbiologists, Dallas, Texas, 5–9 May, 1991.\nHeifets LB, Lindholm-Levy PJ, Comstock RD. Clarithromycin minimal inhibitory and bactericidal concentrations against Mycobacterium avium. American Review of Respiratory Disease 145: 856–858, 1992a.\nHeifets LB, Lindholm-Levy PJ, Comstock RD. Bacteriostatic and bactericidal activities of gentamicin alone and in combination with clarithromycin against Mycobacterium avium. Antimicrobial Agents and Chemotherapy 36: 1695–1698, 1992b.\nHonig P, Wortham D, Zamani K, Conner D, Cantilena L. Effect of erythromycin, clarithromycin and azithromycin on the pharmacokinetics of terfenadine. Abstract. Clinical Pharmacology and Therapeutics 53: 161, 1993.\nHorsburgh Jr CR, Caldwell MB, Simonds RJ. Epidemiology of disseminated nontuberculous mycobacterial disease in children with acquired immunodeficiency syndrome. Pediatric Infectious Diseases Journal 12: 219–222, 1993.\nHorsburgh Jr CR, Havlik JA, Ellis DA, Kennedy E, Fann SA, et al. Survival of patients with acquired immune deficiency syndrome and disseminated Mycobacterium avium complex infection with and without antimycobacterial chemotherapy. American Review of Respiratory Disease 144: 557–559, 1991.\nHorsburgh Jr CR, Selik RM. The epidemiology of disseminated nonturberculous mycobacterial infection in the acquired immunodeficiency syndrome (AIDS). American Review of Respiratory Disease 139: 4–7, 1989.\nHoy J, Mijch A, Sandland M, Grayson L, Lucas R, et al. Quadruple-drug therapy for Mycobacterium avium-intracellulare bacteremia in AIDS patients. Journal of Infectious Diseases 161: 801–805, 1990.\nHoyt L, Oleske J, Holland B, Connor E. Nontuberculous mycobacteria in children with acquired immunodeficiency syndrome. Pediatric Infectious Disease Journal 11: 354–360, 1992.\nInderlied CB, Sandoval FG, Peters J, Young LS. In vitro susceptibility of the Mycobacterium avium complex (MAC) to clarithromycin, (CRM) and WIN 57273 (WIN). Abstract 1195. The 29th Interscience Conference on Antimicrobial Agents and Chemotherapy, Houston, p 304, 1989.\nIseman MD, Corpe RF, O’Brien RJ, Rosenzwieg DY, Wolinsky E. Disease due to Mycobacterium avium-intracellulare. Chest 87 (Suppl.): 139S–149S, 1985.\nIshiguro M, Koga H, Kohno S, Hayashi T, Yamaguchi K, et al. Penetration of macrolides into human polymorphonuclear leucocytes. Journal of Antimicrobial Chemotherapy 24: 719–729, 1989.\nJi B, Lounis N, Truffot-Pernot C, Grosset JH. Susceptibility of the immunocompetent, beige and nude mice to Mycobacterium avium infection and response to clarithromycin. Abstract. The 31st Interscience Conference on Antimicrobial Agents and Chemotherapy, American Society for Microbiology, Chicago, Illinois, 1991.\nJi B, Lounis N, Truffot-Pernot C, Grosset JH. In vitro activities of clarithromycin-containing double- or triple-drug combinations against Mycobacterium avium complex. Abstract. The First International Conference on the Macrolides, Azalides and Streptogramins, Santa Fe, New Mexico, January, 1992a.\nJi B, Lounis N, Truffot-Pernot C, Grosset J. Selection of resistant mutants of Mycobacterium avium in beige mice by clarithromycin monotherapy. Antimicrobial Agents and Chemotherapy 36: 2839–2840, 1992b.\nJi B, Lounis N, Truffot-Pernot C, Grosset JH. Bactericidal activities of multidrug regimens against M. avium in beige mice. Abstract. The 32nd Interscience Conference on Antimicrobial Agents and Chemotherapy, American Society for Microbiology, Anaheim, California, 11–14 October, 1992c.\nKemper CA, Chiu J, Meng TC, Nussbaum J, Bartok AE, et al. Microbiologie and clinical response of patients with AIDS and MAC bacteremia to a four oral drug regimen. Abstract, p. 297 30th Interscience Conference on Antimicrobial Agents and Chemotherapy, American Society for Microbiology, Washington DC, October 21–24, 1990.\nKent RJ, Bakhtiar M, Shanson DC. The in-vitro bactericidal activities of combinations of antimicrobial agents against clinical isolates of Mycobacterium avium-intracellulare. Journal of Antimicrobial Chemotherapy 30: 643–650, 1992.\nKhardori N, Rolston K, Rosenbaum B, Hayat S, Bodey GP. Comparative in-vitro activity of twenty antimicrobial agents against clinical isolates of Mycobacterium avium complex. Journal of Antimicrobial Chemotherapy 24: 667–673, 1989.\nKiehn TE, Edwards FF, Brannon P, Tsang AY, Maio M, et al. Infections caused by Mycobacterium avium complex in immunocompromised patients: diagnosis by blood culture and fecal examination, antimicrobial susceptibility tests, and morphological and seroagglutination characteristics. Journal of Clinical Microbiology 21: 168–173, 1985.\nKlemens SP, DeStefano MS, Cynamon MH. Activity of clarithromycin against Mycobacterium avium complex infection in beige mice. Antimicrobial Agents and Chemotherapy 36: 2413–2417, 1992.\nKohno S, Koga H, Yamaguchi K, Masaki M, Inoue Y, et al. A new macrolide, TE-031 (A-56268), in treatment of experimental Legionnaires’ disease. Journal of Antimicrobial Chemotherapy 24: 397–405, 1989.\nKohno Y, Yoshida H, Suwa T, Suga T. Uptake of clarithromycin by rat lung cells. Journal of Antimicrobial Chemotherapy 26: 503–513, 1990.\nMizushima Y, Hiratsuka H. General clinical study on TE-031 (A-56268). Chemotherapy 36: 452–499, 1988.\nMor N, Heifets L. MICs and MBCs of clarithromycin against Mycobacterium avium within human macrophages. Antimicrobial Agents and Chemotherapy 37: 111–114, 1993.\nMurray JF, Felton CP, Garay SM, Gottlieb MS, Hopewell PC, et al. Pulmonary complications of the acquired immunodeficiency syndrome. New England Journal of Medicine 310: 1682–1688, 1984.\nNaik S, Ruck R. In vitro activities of several new macrolide antibiotics against Mycobacterium avium complex. Antimicrobial Agents and Chemotherapy 33: 1614–1616, 1989.\nNational Committee for Clinical Laboratory Standards, Jorgensen JH et al. (Eds) Performance standards for antimicrobial susceptibility testing. National Committee for Clinical Laboratory Standards publication M100-S4, Villanova, Pennsylvania, 1992.\nNightingale SD, Byrd LT, Southern PM, Kockusch JD, Cal SX, et al. Incidence of Mycobacterium avium intracellulare complex bacteremia in human immunodeficiency virus-positive patients. Journal of Infectious Disease 165: 1082–1085, 1992.\nNogita T, Ishibashi Y. The penetration of sparfloxacin into human plasma and skin tissues. Correspondence. Journal of Antimicrobial Chemotherapy 28: 313–314, 1991.\nPerronne C, Gikas A, Truffot-Pernot C, Grosset J, Vilde J-L, et al. Activities of sparfloxacin, azithromycin, temafloxacin, and rifapentine compared with that of clarithromycin against multiplication of Mycobacterium avium complex within human macrophages. Antimicrobial Agents and Chemotherapy 35: 1356–1359, 1991.\nPerronne C, Gikas A, Truffot-Pernot C, Grosset J, Pocidalo J-J, et al. Activities of clarithromycin, sulfisoxazole, and rifabutin against Mycobacterium avium complex multiplication within human macrophages. Antimicrobial Agents and Chemotherapy 34: 1508–1511, 1990.\nPeters DH, Clissold SP. Clarithromycin. A review of its antimicrobial activity, pharmacokinetic properties and therapeutic potential. Drugs 44: 117–164, 1992.\nPetty B, Polis M, Haneiwich S, Dellerson M, Craft JC, et al. Pharmacokinetic assessment of clarithromycin plus zidovudine in HIV patients. Abstract. 32nd Intersciences Conference on Antimicrobial Agents and Chemotherapy, Anaheim, California, 11–14th October, 1992.\nPolis MA, Haneiwich S, Kovacs JA, Davey RT, Walker RE, et al. Dose escalation study to determine the safety, maximally tolerated dose (MTD) and pharmacokinetics of clarithromycin (clari) with zidovudine (zdv) in HIV-infected patients. International Congress on Antimicrobial Agents and Chemotherapy, 1991.\nProkocimer P, Dellerson M, Craft C, Pernet A, Ruff B, et al. Effect of clarithromycin (C) on blood cultures (BC) positive for Mycobacterium avium complex (MAC) in HIV + patients (Pts). Abstract. 30th Intersciences Conference on Antimicrobial Agents and Chemotherapy, Atlanta, Georgia, 1990.\nRastogi N, Goh KS. Effect of pH on radiometric MICs of clarithromycin against 18 species of mycobacteria. Antimicrobial Agents and Chemotherapy 36: 2841–2842, 1992 Rastogi N, Labrousse V. Extracellular and intracellular activities of clarithromycin used alone and in association with ethambutol and rifampin against Mycobacterium avium complex. Antimicrobial Agents and Chemotherapy 35: 462–470, 1991.\nRastogi N, Labrousse V, Goh KS, Carvalho de Sousa JP. Antimycobacterial spectrum of sparfloxacin and its activities alone and in association with other drugs against Mycobacterium avium complex growing extracellularly and intracellularly in murine and human macrophages. Antimicrobial Agents and Chemotherapy 35: 2473–2480, 1991.\nRastogi N, Labrousse V, Goh KS, Carvalho de Sousa JP. Spectrum of activity of clarithromycin against atypical mycobacteria: evidence that it is bactericidal against intracellular Mycobacterium avium and M. paratuberculosis both in murine and human macrophages and that its activity is further enhanced by ethambutol. Abstract. The First International Conference on the Macrolides, Azalides and Streptogramins, Santa Fe, New Mexico, January, 1992.\nRathbun RC, Martin III ES, Eaton VE, Matthew EB. Current and investigational therapies for AIDS-associated Mycobacterium avium complex disease. Clinical Pharmacy 10: 280–291, 1991.\nRuf B, Schürmann D, Mauch H, Jautzke G, Fehrenbach FJ, et al. Effectiveness of the macrolide clarithromycin in the treatment of Mycobacterium avium complex infection in HIV-infected patients. Infection 20: 267–272, 1992a.\nRuf B, Schürmann D, Mauch H. Acquired resistance of MAI to clarithromycin. Correspondence. American Review of Respiratory Disease 145: 1241, 1992b.\nSaint-Marc T, Touraine JL. Clinical experience with a combination of clarithromycin and clofazimine in the treatment of disseminated M. avium infections in AIDS patients. Abstract. 31st Intersciences Conference on Antimicrobial Agents and Chemotherapy, Chicago, Illinois, 1991.\nSiegal FP, Chaisson R, Stern J, Bernstein B, Lamarca A, et al. Clinical manifestations of M. avium complex (MAC) bacteremia in patients with AIDS. Abstract. VIII International Conference on AIDS\u002FIII STD World Congress, Amsterdam, The Netherlands 19–24 July, 1992.\nSnider Jr DE, Hopewell PC, Mills J, Reichman LB. Mycobacterioses and the acquired immunodeficiency syndrome. American Review of Respiratory Disease 136: 492–496, 1987.\nSteinberg TH, Hand WL. Effects of phagocytosis on antibiotics and nucleoside uptake by human polymorphonuclear leukocytes. Journal of Infectious Diseases 149: 397–403, 1984.\nSteinberg TH, Hand WL. Effect of phagocyte membrane stimulation on antibiotic uptake and intracellular bactericidal activity. Antimicrobial Agents and Chemotherapy 31: 660–662, 1987.\nTruffot-Pernot C, Ji B, Grosset JH. Effect of pH on in vitro potency of clarithromycin against Mycobacterium avium complex. Antimicrobial Agents and Chemotherapy, 35: 1677–1678, 1991.\nWallace Jr RJ, Brown BA, Onyi GO. Activity of clarithromycin against slow-growing nontuberculous mycobacteria using a broth microdilution MIC system. Abstract. The First International Conference on the Macrolides, Azalides and Streptogramins, Santa Fe, New Mexico, January, 1992.\nWallace Jr RJ, Brown BA, Griffith DE. Drug intolerance to highdose clarithromycin among elderly patients. Diagnostic Microbiological Infectious Diseases 16: 215–221, 1993.\nWood MJ. The tolerance and toxicity of clarithromycin. Journal of Hospital Infection 19 (suppl. A): 39–46, 1991.\nWu AW, Lichter SL, Richardson W, Urbanski PA, Benson C, et al. Quality of life in patients receiving clarithromycin for Mycobacterium avium complex infection and AIDS. Abstract PoB 3550. VIII International Conference on AIDS\u002FIII STD World Congress, Amsterdam, The Netherlands, 19–24 July, 1992.\nYajko DM. In vitro activity of antimicrobial agents against the Mycobacterium avium complex inside macrophages from HIV1-infected individuals: the link to clinical response to treatment. Research in Microbiology 143: 411–419, 1992.\nYajko DM, Nassos PS, Hadley WK. Therapeutic implications of inhibition versus killing of Mycobacterium avium complex by antimicrobial agents. Antimicrobial Agents and Chemotherapy 31: 117–120, 1987.\nYajko DM, Nassos PS, Sanders CA, Gonzalez PC, Hadley WK. Comparison of the intracellular activities of clarithromycin and erythromycin against Mycobacterium avium complex strains in J774 cells and in alveolar macrophages from human immunodeficiency virus type 1-infected individuals. Antimicrobial Agents and Chemotherapy 36: 1163–1165, 1992.\nYajko DM, Nassos PS, Sanders CA, Hadley WK. Killing by antimicrobial agents of AIDS-derived strains of Mycobacterium avium complex inside cells of the mouse macrophage cell line J774. American Review of Respiratory Disease 140: 1198–1203, 1989.\nYakrus MA, Good RC. Geographic distribution, frequency, and specimen source of Mycobacterium avium complex serotypes isolated from patients with acquired immunodeficiency syndrome. Journal of Clinical Microbiology 28: 926–929, 1990.\nYoung LS, Inderlied CB, Berlin OG, Gottlieb MS. Mycobacterial infections in AIDS patients, with an emphasis on the Mycobacterium avium complex. Reviews of Infectious Diseases 8: 1024–1033, 1986.\nZakowski P, Fligiel S, Berlin GW, Johnson Jr BL. Disseminated Mycobacterium avium-intracellulare infection in homosexual men dying of acquired immunodeficiency. Journal of the American Medical Association 248: 2980–2982, 1982.",{"VOID":1258},"10.2165\u002F00003495-199346020-00007","Author affiliation is blank","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.2165\u002F00003495-199346020-00007",[1262,1269,1284],{"id":1263,"sortIndex":32,"researcher":28,"roles":1264,"affiliations":1265,"properties":1266,"displayName":1268,"givenName":28,"familyName":28},"e33117ef-9637-437f-9ebd-afb5268dbfd0",[970],[],{"title":1267},{"VI":1268},"Lee B. 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Published data have indicated that metoclopramide assists radiological identification of lesions in the small intestine, facilitates duodenal intubation and small intestine biopsy, and eases emergency endoscopy in upper gastro-intestinal haemorrhage. Metoclopramide reduces post-operative vomiting and radiation sickness, and ameliorates some types of drug-induced vomiting. It may provide symptomatic relief in dyspepsia and possibly in vertigo, reflux oesophagitis and hiccups, but further controlled trials are needed to confirm the efficacy of metoclopramide in these proposed areas of use. It promotes gastric emptying prior to anaesthesia. Its effects in healing gastric ulcer and preventing relapse of duodenal ulcer remain unproven. Side-effects are few and transient, though alarming extrapyramidal reactions can occur in a small proportion of patients receiving therapeutic doses but more usually following excessive doses in young subjects. They respond rapidly to withdrawal of the drug. \n                        Pharmacodynamic studies in man and in a variety of experimental animals have established that metoclopramide, after oral or intravenous administration, rapidly affects the motility of the gastro-intestinal tract. Its effects include improved resting tone of the oesophageal sphincter, improved tone and peristalsis of the stomach with accelerated gastric emptying (but with slowing in some cases), enhanced pyloric activity, distension of the duodenal bulb, and increased peristalsis of the duodenum with accelerated transit through the duodenum and jejunum. It has comparatively little overall effect on colonic motor activity in vivo. The actions of metoclopramide on motility are blocked by atropine and can be reproduced in vitro on animal and human smooth muscle. It is unclear whether the drug is effective in all post-vagotomy patients. Metoclopramide has no effect on gastric secretion, and may sensitise gut muscle to the action of endogenous acetylcholine. The accelerated gastric emptying usually produced by metoclopramide is reflected in its effects on the absorption of other drugs. Intramuscular metoclopramide promoted the absorption of salicylate from the depressed levels associated with attacks of migraine to those characteristic of normal subjects. Paracetamol absorption was both accelerated and enhanced in normal subjects. Metoclopramide also accelerated absorption of tetracycline and pivampicillin, ethanol, and levodopa, but did not affect that of isoniazid. The absorption of digoxin from slow-release tablets was depressed by multiple doses of metoclopramide given to patients on maintenance digoxin therapy. Metoclopramide is effective in preventing apomorphine-induced vomiting in man, and appears to be equipotent with prochlorperazine but superior to trimethobenzamide. In animals it is a potent antagonist of vomiting induced by apomorphine, hydergine, reserpine, tetrodotoxin and copper sulphate. Metoclopramide has behavioural properties in animals which suggest that it is a central dopaminergic antagonist, and it may exert its anti-emetic effects by blocking the chemoreceptor trigger zone for vomiting. In cats, spontaneous electrical discharges from this part of the central nervous system were abolished by metoclopramide and stimulated by apomorphine. Other effects of metoclopramide on the central nervous system include typical neuroleptic properties in animals; catalepsy and reversal of the behavioural stereotypies produced by apomorphine or amphetamine. In man, however, metoclopramide is without significant antipsychotic or sedative properties. Metoclopramide lacks significant cardiovascular effects, and large intravenous doses in patients with heart disease had no marked influence on haemodynamic parameters. Intracardiac conduction is unaffected by metoclopramide, though large doses prevent experimentally-induced cardiac arrhythmias in animals and produce a slight and transient decrease in blood pressure. Metoclopramide has a negligible effect on blood pressure responses in animals to acetylcholine, adrenaline, histamine and noradrenaline but it blocks the hypotensive action of dopamine. \n                        Pharmacokinetic studies of metoclopramide in man are limited, but animal experiments suggest that the drug is well absorbed and rapidly excreted, with a short half-life and only partial metabolism by O-demethylation, N-de-ethylation and amide hydrolysis. Maximum plasma levels occur within 30 to 120 minutes of oral dosage, and human studies indicate that levels of 0.2gmg\u002Fml are achieved following intramuscular doses of 40mg. Plasma half-life in animals is 1 to 2 hours, and metoclopramide is distributed principally to the intestinal mucosa, liver, biliary tract, and salivary glands. Within the central nervous system the drug is localised at the area postrema, which contains the chemoreceptor trigger zone for vomiting. Metoclopramide binds only moderately to human plasma protein and 24% of the dose was excreted unchanged in the first 24 hours following an intramuscular dose of 40mg in human volunteers. \n                        Therapeutic trials under controlled conditions have shown that metoclopramide in intramuscular doses of 10 to 20mg is significantly better than placebo in controlling postoperative vomiting. Metoclopramide was also slightly more effective than prochlorperazine (10mg, im) in one study and significantly superior to perphenazine (5mg, im) in one of two studies but there was no significant difference between metoclopramide (20mg, iv) and trimethobenzamide (300mg, iv). The effects of metoclopramide seem to be independent of either the type of anaesthetic or the premedicant used but for optimum effect may need to be given towards the end of the operation. Controlled trials have demonstrated that 10mg intramuscular metoclopramide is significantly superior to placebo, perphenazine (5mg, im), or prochlorperazine (10mg, im) in preventing vomiting due to pethidine or morphine. The drug was effective in women during labour, in the elderly, and in surgical patients, and it abolished pre-operative vomiting associated with pethidine administration. Clinical experience suggests that daily doses of 30 to 80mg metoclopramide are effective in controlling nausea and vomiting in Parkinsonian patients receiving levodopa, without compromising the therapeutic efficacy of levodopa. However, controlled trials show that the drug has no place in relieving emesis induced by some cytostatic drugs or by iodipamide. Radiation sickness was ameliorated by daily metoclopramide, which was not significantly different in its effect from prochlorperazine. Metoclopramide was indistinguishable from prochlorperazine and significantly superior to placebo in a controlled trial in the relief of vomiting of pregnancy, without apparent deleterious effects on the fetus. Clinical experience confirms these effects, but like all new drugs metoclopramide should probably not be given to women during the first 3 months of pregnancy since its safety in use has not been established, despite the lack of dysmorphogenic effects in animals. Limited controlled trials show that metoclopramide may be useful in providing symptomatic relief, particularly from nausea and vomiting, in patients with a variety of disorders. Further controlled trials in large groups of selected patients are needed to confirm these effects. Results of a controlled study indicate that metoclopramide may be effective in treating nausea and vomiting of vertigo and certain associated disorders, but it appears to have no place in the treatment of seasickness. Migraine may respond to the drug, but in the studies to date patients have continued to take their usual analgesic medication, the absorption of which is promoted by metoclopramide. The lack of sufficient controlled trials, however, leaves the role of metoclopramide in these disorders uncertain. Dyspepsia responds to metoclopramide, which was significantly superior to placebo or the anticholinergic drug pipenzolate in controlled trials. Metoclopramide was more effective in controlling nausea, vomiting, epigastric burning, heartburn, and regurgitation of sour fluid than the flatulent symptoms of belching, bloating, and abdominal distension. Nevertheless, there is still some debate as to whether metoclopramide is effective in preventing gastro-oesophageal reflux. Metoclopramide may be useful in treating hiccup. Limited controlled trials suggest that metoclopramide provides symptomatic relief and may accelerate the healing of gastric ulcer and prevent relapse of duodenal ulcer, but its role remains unproven. Some functional gastro-intestinal disorders appear to respond to metoclopramide. In controlled trials, it was significantly more effective than carbachol or placebo in relieving post-vagotomy gastric stasis, superior to placebo in alleviating gastritis and gastroptosis, and as effective as isopropamide plus haloperidol against irritable colon and spastic constipation. It has been used successfully in the conservative management of complete pyloric obstruction due to duodenal ulcer, in order to avoid emergency surgery but it probably should not be used in pyloric stenosis due to carcinoma or severe fibrosis. The dual action of metoclopramide in preventing emesis and accelerating gastric emptying, has established its use in anaesthetic practice. It is especially useful in emergency anaesthesia, including during labour, when rapid clearance of gastric contents is required. \n                        Diagnostic uses: In diagnostic radiology or cineradiology, metoclopramide given before barium meal provides excellent conditions for the diagnosis of lesions in the duodenum, jejunum and ileum, and prevents vomiting of barium in nauseated patients such as those with jaundice. It significantly increases the rate of gastric emptying and reduces the transit time for barium to reach the caecum. Controlled trials have shown that small intestine examinations are complete within 1 hour in over 80% of metoclopramide-treated patients compared with in less than 20% of untreated patients. Both oral and intravenous metoclopramide were superior to placebo in speeding gastric emptying and reducing the number of films needed for complete visualisation of the small intestine, but in one study oral metoclopramide gave an increased number of radiographically poor examinations. Metoclopramide is useful in facilitating duodenal intubation ad permitting rapid and successful biopsy of the small intestine, in the absence of significant side-effects. It speeds the passage of biopsy capsules across the pylorus, and was significantly superior to both placebo and pharyngeal anaesthesia in controlled trials. In patients with functional pyloric stenosis, metoclopramide facilitated endoscopic observation of the duodenal bulb. Emergency endoscopy of upper gastro-intestinal haemorrhage is facilitated by the administration of metoclopramide, which clears the viewing area of blood. However, it is possible that the increased stomach activity may in itself cause further haemorrhage. \n                        Side-effects with metoclopramide are usually mild, transient, and readily reversed by withdrawal of drug. A review of one published trial suggests that they occur in about 11% of patients, but the incidence may be different in clinical practice. They consist principally of drowsiness and lassitude, bowel disturbances, and dizziness and faintness. Metoclopramide may increase lactation by stimulating the release of prolactin. Extrapyramidal effects are alarming but uncommon (in about 1% of patients). They consist of dystonic reactions such as trismus, torticollis, facial spasms, opisthotonos, and oculogyric crises, but Parkinsonian-like symptoms are absent. Metoclopramide-induced dystonia occurs more often in females and in the young patient; when it occurs it is usually following excessive doses, but may also occur at normal therapeutic dosage, and resembles in many respects the dyskinesias induced by the phenothiazines. It responds readily to withdrawal of drug, but severe cases may benefit from intramuscular benztropin or diazepam. Children are particularly susceptible, but restriction of the daily dose to 0.5mg\u002Fkg usually prevents overdosage in young patients. Signs of overdosage in children usually include extreme irritability and agitation, with muscle hypertonia. Two adult cases of attempted suicide with 360 and 800mg metoclopramide recovered uneventfully following gastric lavage and observation; somnolence and disorientation were reported, but there were no extrapyramidal signs. \n                        Contra-indications and precautions: Metoclopramide should neither be given with, or within 2 weeks of treatment with monoamine oxidase inhibitors, tricyclic antidepressants, or sympathomimetic drugs, nor to women in the first 3 months of pregnancy, as the safety of use of such associations has not been established. It may potentiate the central action of some antipyschotic drugs, and its own action on the gastro-intestinal tract may be potentiated by acetylcholine-like drugs and blocked by atropine-like agents. It should not be given with phenothiazines. The ability of metoclopramide to provide symptomatic relief in gastro-intestinal disorders does not replace proper investigation and diagnosis of the patient’s symptoms. Metoclopramide should not be given to patients with epilepsy or extrapyramidal syndromes, though it may be safely used in Parkinsonian patients to control vomiting. The dosage for children should be carefully adjusted from initially low levels. Increasing the adult dosage beyond the recommended level does not normally lead to a corresponding enhancement of therapeutic effects. \n                        Dosage: Metoclopramide is given before or just after meals, or 20 minutes before symptoms are likely to occur, in oral, intramuscular, or intravenous doses of 10mg, up to 3 times daily, in adults, and 5 to 10mg 2 to 3 times daily in young adults. Children under 14 should receive 1 to 5mg, 2 to 3 times daily, according to age and body weight. The total daily dose in children and young adults should not exceed 0.5mg\u002Fkg. For diagnostic purposes, the adult dose is 20mg orally, 20 minutes before examination, or 10 to 20mg by injection 5 minutes before examination. Children receive, according to age and body weight, 1 to 5mg, 5 to 10 minutes before examination.",{"EN":1359},"Metoclopramide: A Review of its Pharmacological Properties and Clinical Use",{"VOID":1361},"Ahtee, L. and Buncombe, G.: Metoclopramide induces catalepsy and increases striatal homovanillic acid content in mice. Acta Pharmacologica et Toxicologica 35: 429 (1974).\nArita, T.; Hori, R.; Ito, K.; Ichikawa, K. and Uesugi, T.: Transformation and excretion of drugs in biological systems. II. Transformation of metoclopramide in rabbits. Chemical and Pharmaceutical Bulletin 18: 1663 (1970a).\nArita, T.; Hori, R.; Ito, K. and Ichikawa, K.: Transformation and excretion of drugs in biological systems. III. Separatory determination of metoclopramide and its N4-glucuronide and N4-sulfenate in rabbit urine and bile. Chemical and Pharmaceutical Bulletin 18: 1670 (1970b).\nArita, T.; Hori, R.; Ito, K. and Sekikawa, H.: Transformation and excretion of drugs in biological systems. IV. Reabsorption of biliary metoclopramide-N4 4-glucuronide and -N4-sulfonate from rabbit intestine. Chemical and Pharmaceutical Bulletin 18: 1675 (1970c).\nArmstrong, R.F.: Metoclopramide and gastric emptying. British Journal of Anaesthesia 45: 123 (1973).\nArvanitakis, C; Gonzales, G. and Rhodes, J.B.: The role of metoclopramide in peroral jejunal biopsy —a controlled, randomised trial. Gastroenterology 68: 859 (1975).\nAssaf, R.A.E.; Clarke, R.S.J. and Dundee, J.W.: Studies of drugs given before anaesthesia. XXIV. Metoclopramide with morphine and pethidine. British Journal of Anaesthesia 46: 514 (1974a).\nAssaf, R.A.E.; Dundee, J.W. and Samuel, I.O.: The efficacy of metoclopramide against narcotic-induced emetic symptoms. British Journal of Clinical Pharmacology 1: 1778 (1974b).\nBader, E.: Metoclopramide and emergency endoscopy for upper gastro-intestinal bleeding. Lancet 1: 101 (1973).\nBakke, O.M. and Segura, J.: The absorption and elimination of metoclopramide in three animal species. Journal of Pharmacy and Pharmacology 28: 32 (1976).\nBanke, L.: Research on the action of metoclopramide in the gastro-intestinal tract. In Modern Gastroenterology (Proceedings of VIII International Congress on Gastroenterology, Prague, July 1968), pp 571–572 (Schattauer, Stuttgart 1969).\nBanke, L.; Mahnstrom, J. and Heltberg, J.: The influence of metoclopramide (Primperan) and neostigmine upon early postvagotomy motor disturbances. Scandinavian Journal of Gastroenterology 7: 33 (1972).\nBar, J.: A propos d’une tentative de suicide sans consequence facheuse, avec le métoclopramide. Therapie 21: 349 (1966).\nBastos, W.P.: Action of metoclopramide in arrhythmias provoked by a bensol-adrenaline association. Ciencia e Cultura 20: 389 (1968).\nBaumann, H.W.; McCallum, R.W. and Strudevant, R.A.L.: Metoclopramide. A possible antagonist of dopamine in the esophagus of man. Gastroenterology 70: 862 (1976).\nBeani, L.; Bianchi, C. and Crema, C: Effects of metoclopramide on isolated guinea-pig colon. 1) Peripheral sensitisation to acetylcholine. European Journal of Pharmacology 12: 320 (1970).\nBeckett, A.H. and Huizing, G.: In vitro metabolism of metoclopramide. Journal of Pharmacy and Pharmacology 27 (Suppl.): 42P (1975).\nBehar, J. and Biancani, P.: Effect of oral metoclopramide on gastroesophageal reflux in the post-cibal state. Gastroenterology 70: 331 (1976).\nBhaduri, T. and Bradley, G.W.: The effect of metoclopramide (Maxolon) on intragastric pressure and gastric motility. Clinical Trials Journal 6: 13 (1969).\nBianchi, C; Beani, L. and Crema, C: Effects of metoclopramide on isolated guinea-pig colon. 2) Interference with ganglionic stimulant drugs. European Journal of Pharmacology 12: 332 (1970).\nBirtley, R.D.N. and Baines, M.W.: The effects of metoclopramide on some isolated intestinal preparations. Postgraduate Medical Journal 49 (Suppl.4): 13 (1973).\nBloch, A.: Incorrect use of metoclopramide. Harefuah 86: 411 (1974).\nBoissier, J.R.; Simon, P.; Lwoff, J.M. and Fichelle-Pagny, J.: Action psycholeptique du métoclopramide. Comptes Rendus des Séances de la Société de Biologie de Paris 158: 1859 (1964).\nBoisson, J. and Albot, G: Sur l’intérét thérapeutique du métoclopramide. A propos de 2,300 observations. Revue critique et indications de son emploi. Cahiers du Collège de Médecine 7: 45 (1966).\nBolin, T.D.: The facilitation of duodenal intubation with metoclopramide. Med. J. Aust. 1: 1078 (1969).\nBonechi, I.; Biagini, M. and Giagnoni, P.: Azione antiemetica delia Metoclopramide nell’uremia. Riforma Medica 82 (Suppl.): 1691 (1968).\nBorenstein, P. and Bles, G.: Effets cliniques et électroencéphalographiques du metoclopramide en psychiatrie. Thérapie 20: 975 (1965).\nBreivik, H. and Lind, B.: Anti-emetic and propulsive peristaltic properties of metoclopramide. British Journal of Anaesthesia 43: 400 (1971).\nBremner, CG. and Bremner, C.H.: Augmentation of lower oesophageal sphincter tone with metoclopramide (maxolon) in normals and in patients with sphincter incompetence. South African Journal of Surgery 10: 211 (1972).\nBrownlee, M. and Kroopf, S.S.: Metoclopramide for gastroparesis diabeticorum. New England Journal of Medicine 291: 1257 (1974).\nBuckingham, M.; Welphy, G.; Miller, J.F. and Elstein, M.: Gastro-intestinal absorption and transplacental transfer of amoxycillin during labour and the influence of metoclopramide. Current Medical Research and Opinion 3: 392 (1975).\nCannon, J.G.: Chemistry of dopaminergic agonists. Advances in Neurology 9: 177 (1975).\nCarnevali, G.; Roncoroni, L.; Bissanti, A. and Mainardi, L.: Action du metoclopramide sur l’evacuation gastrique. Échos de la Médecine 39: 8 (1968).\nCasteels-Van Daele, M.; Jaeken, J.; Van Der Schueren, P.; Zimmerman, A. and Van Den Bon, P.: Dystonic reactions in children caused by metoclopramide. Archives of Diseases of Children 45: 130 (1970).\nCecco, L. de; Ragni, N.; Sbernini, R.; Uleri, G. and Molinaroli, P.: Effect of metoclopramide on intestinal motility in pregnancy and the puerperium. Riforma Medica 82 (Suppl.): 1786 (1968).\nClark, M.M. and Storrs, J.A.; The prevention of postoperative vomiting after abortion: metoclopramide. British Journal of Anaesthesia 41: 890 (1969).\nClarke, R.S.J. and Dundee, J.W.: Side-effects of antiemetics: Results of a class experiment. European Journal of Pharmacology 14: 291 (1971).\nCochlin, D.L.: Dystonic reactions due to metoclopramide and phenothiazines resembling tetanus. British Journal of Clinical Practice 28: 201 (1974).\nConnell, A.M. and George, J.D.: Effect of metoclopramide on gastric function in man. Gut 10: 678 (1969).\nCostall, B. and Naylor, R.J.: The nucleus amygdaloideus centralis and neuroleptic activity in the rat. European Journal of Pharmacology 25: 138 (1974).\nCostall, B. and Naylor, R.J.: Neuroleptic and non-neuroleptic catalepsy. Arzneimittel-Forschung 23: 674 (1973).\nCousin, J.; Katende, G.; Pauli, A. and Fournier, A.: L’intoxication par le métoclopramide chez l’enfant. Journal des Sciences Médicates de Lille 91: 1 (1973).\nDavies, J.A.H. and Howells, T.H.: Management of anaesthesia for the full stomach case in the casualty department. Postgraduate Medical Journal 49 (Suppl. 4): 58 (1973).\nDay, M.D.: Cardiovascular dopamine receptor stimulation antagonised by metoclopramide. Journal of Pharmacy and Pharmacology 27: 276 (1975).\nDe Silva, K.L.; Muller, P.J. and Pearce, J.: Acute drug-induced extrapyramidal syndromes. Practitioner 211: 316 (1973).\nDe Vries, P.M.: A double-blind crossover clinical evaluation of metoclopramide and a combination of haloperidol and isopropamide iodide in gastroenterology. Arzneimittel-Forschung 19: 1766 (1969).\nDias Martins, A.: Metoclopramida nas nauseas e vomitos da gravidez. O’Hospital (Rio de Janeiro) 71: 1631 (1967).\nDilawari, J.B. and Misiewicz, J.J.: Does oral metoclopramide increase cardiac sphincter pressure? Gut 13: 856 (1972).\nDiliwari, J.B. and Misiewicz, J.J.: Action of oral metoclopramide on the gastro-oesophageal junction in man. Gut 14: 380 (1973).\nDippy, J.E.; Rhodes, J. and Cross, S.: Bile reflux in gastric ulcer: The effect of smoking, metoclopramide and carbenoxolone sodium. Current Medical Research and Opinion 1: 569 (1973).\nDobkin, A.E.; Evers, W. and Israel, J.S.: Double-blind evaluation of metoclopramide (MK 745, Sinemet), trimethobenzamide (Tigan), and a placebo as postanaesthetic anti-emetics following methoxyflurane anaesthesia. Canadian Anaesthetist’s Society Journal 15: 80 (1968).\nDougan, D.F.H.; Mearrick, P.T. and Wade, D.N.: Metoclopramide as a dopamine antagonist in the heart and gut of the mollusc Tapes Watlingi Clinical and Experimental Pharmacology and Physiology 1: 473 (1974).\nDouthwaite, A.H.: Hiccup. Lancet 1: 144 (1968).\nDundee, J.W. and Clarke, R.S.J.: The premedicant and anti-emetic action of metoclopramide. Postgraduate Medical Journal 49 (Suppl.4): 34 (1973).\nDundee, J.W.; Clarke, R.S.J. and Howard, P.J.: Studies of drugs given before anaesthesia. XXIII. Metoclopramide. British Journal of Anaesthesia 46: 509 (1974).\nDundee, J.W.; Kirwan, M.J. and Clarke, R.S.J.: Anaesthesia and premedication as factors in postoperative vomiting. Acta Anaesthetica Scandinavica 9: 223 (1965).\nDolphin, A.; Jenner, P.; Marsden, CD.; Pycock, C. and Tarsy, D.: Pharmacological evidence for cerebral dopamine receptor blockade by metoclopramide in rodents. Psychopharmacologia 41: 133 (1975).\nEditorial: Hiccup. British Medical Journal 2: 234 (1971).\nEisner, M.: Gastro-intestinal effects of metoclopramide in man. In vitro experiments with human smooth muscle preparations. British Medical Journal 4: 679 (1968).\nEisner, M.: Effect of metoclopramide on gastro-intestinal motility in man. Digestive Diseases 16: 409 (1971).\nEllis, F.R. and Spence, A.A.: Clinical trials of metoclopramide (Maxolon) as an anti-emetic in anaesthesia. Anaesthesia 25: 368 (1970).\nFanelli, A.: The use of metoclopramide in obstetrics and gynaecology. Riforma Medica 82 (Suppl.): 1806 (1968).\nFischer, P.A.; Schneider, E.; Jacobi, P. and Maxion, H.: Kombinationsbehandlung des Parkinson-Syndroms mit 1-Dopa und einem Decarboxylasehemmer. Medizin-ische Welt 24: 1742 (1973).\nFlavell Matts, S.G.: Metoclopramide in the treatment of migraine. Practitioner 212: 887 (1974).\nFontaine, J. and Reuse, J.J.: Transmural stimulation of isolated guinea-pig ileum: action of metoclopramide and sulpiride. Archives Internationales de Pharmaco-dynamie et de Thérapie 197: 396 (1972).\nFournier, A.; Pauli, A.; Ducoulombier, M. and Cousin, J.: Effets du surdosage en metoclopramide chez l’enfant. Pédiatrie 24: 799 (1969).\nFritel, D.; Meyer, P.; Rey, L.P. and Grivaux, M.: Les troubles gastriques de l’insuffisance renale et leur traitement par le metoclopramide. Semaine des Hôpitaux, Therapeutique 41: 217 (1965).\nFry, E.N.S.: Metoclopramide and drinking before general anaesthesia. Anaesthesia 29: 754 (1974).\nFry, E.N.S.: Metoclopramide and oral premedication. Anaesthesia 30: 690 (1975).\nGaletti, A.; De Santis, L. and Famularo, L.: Three cases of metoclopramide poisoning (two iatrogenic and one accidental). Gaslini 6: 173 (1974).\nGalindo, F. and Mahmud, H.R.: Acción de la metoclopramida sobre la secreción pancréatica externa y el esfinter de Oddi. La Prensa Médica Argentina 59: 1615 (1972).\nGibbons, D.O. and Lant, A.F.: Effects of intravenous and oral propantheline and metoclopramide on ethanol absorption. Clinical Pharmacology and Therapeutics 17: 578 (1975).\nGiger, M.: Toxische Wirkungen von Metoclopramid. Schweizerische Rundschau fur Medizin (Praxis) 64: 930 (1975).\nGlanville, J.N. and Walls, W.D.: Effect of intravenous metoclopramide on gastro-oesophagealreflux. Gut 13: 31 (1972).\nGothoni, G.; Pentikäinen, P.; Vapaatalo, H.I.; Hackman, R. and Af Björksten, K.: Absorption of antibiotics: Influence of metoclopramide and atropine on serum levels of pivampicillin and tetracycline. Annals of Clinical Research 4: 228 (1972).\nGuelrud, M.: Effect of intravenous metoclopramide on the incompetent lower oesophageal sphincter. American Journal of Gastroenterology 61: 119 (1974).\nHackman, R.; Pentikäinen, P.; Neuvonen, P.J. and Vapaatalo, H.: Inhibition of the apomorphine gnawing compulsion by amphetamine. Experientia 34: 1524 (1973).\nHancock, B.D.; Bowen-Jones, E.; Dixon, R.; Dymock, I.W. and Cowley, DJ.: The effect of metoclopramide on gastric emptying of solid meals. Gut 15: 462 (1974).\nHandley, A.J.: Metoclopramide in the prevention of postoperative nausea and vomiting. British Journal of Clinical Practice 21: 460 (1967).\nHarris, M.J.; Harrington, G. and Beveridge, J.: Modification to the technique for small bowel biopsy in children. American Journal of Diseases in Children 115: 43 (1968).\nHay, A.M.: The mechanism of action of metoclopramide. Gut 16: 403 (1975).\nHeading, R.C.; Nimmo, J.; Prescott, L.F. and Tothill, P.: The dependence of paracetamol absorption on the rate of gastric emptying. British Journal of Pharmacology 47: 415 (1973).\nHeitmann, P. and Möller, N.: The effect of metoclopramide on the gastro-oesophageal junctional zone and the distal oesophagus in man. Scandinavian Journal of Gastroenterology 5: 621 (1970).\nHerranz-Fernandez, J.L.; Monfort-Marti, A.; Moreno-Rubio, J.A. and Perez-Santos, J.L.: Efectos secundarios de la metoclopramida en pediatria. Revista Espanola de Pediatria 31: 99 (1975).\nHoskins, E.O.L.: Metoclopramide in benign gastric ulceration. Postgrad, med. J. 49 (Suppl. 4): 95 (1973).\nHoward, F.A. and Sharp, D.S.: Effect of metoclopramide on gastric emptying during labour. British Medical Journal 1: 446 (1973).\nHowarth, F.H.; Cockel, R.; Roper, B.W. and Hawkins, CF.: The effect of metoclopramide upon gastric motility and its value in barium progress meals. Clinical Radiology 20: 294 (1969).\nHowells, T.H.; Khanam, T.; Kreel, L.; Seymour, C; Oliver, B. and Davies, J.A.H.: Pharmacological emptying of the stomach with metoclopramide. British Medical Journal 2: 558 (1971).\nHradsky, M. and Stockbrügger, R.: The effect of metoclopramide (Primperan) during gastroscopic observation of the antrum and pylorus. Gastrointestinal Endo-scopy 21: 55 (1974).\nHucker, H.B.; Hochberg, A.; Hoffman, E.A. and Miller, J.K.: Studies on the physiological distribution of metoclopramide. Pharmacologist 8: 220 (1966).\nHukuhara, T.; Nakayama, S.; Fukuda, H.; Siina, H. and Neya, T.: Effects of N-(diethylamineethyl)-2-methoxy-4-amino-5-chlorobenzamide dihydrochloride (metoclopramide) upon the movements of the stomach and small intestine of dogs. Japanese Journal of Smooth Muscle Research 2: 15 (1966).\nIngrand, J. and Boulu, R.: Study of the distribution of tritiated metoclopramide in the mouse. Thérapie 25: 741 (1970).\nJacoby, H.I. and Brodie, D.A.: Gastro-intestinal actions of metoclopramide. An experimental study. Gastroenterology 52: 676 (1967).\nJames, W.B. and Hume, R.: Action of metoclopramide on gastric emptying and small bowel transit time. Gut 9: 203 (1968).\nJames, W.B. and Melrose, A.G.: Metoclopramide in gastrointestinal radiology. Clinical Radiology 20: 57 (1969).\nJanssen, P.A.J.; Niemegeers, C.J.E.; Schellekens, K.H.L. and Lenaerts, F.M.: Is it possible to predict the clinical effects of neuroleptic drugs (major tranquillisers) from animal data? Arzneimittel-Forschung 17: 841 (1967).\nJohnson, A.G.: The action of metoclopramide on the canine stomach, duodenum, and gall-bladder. British Journal of Surgery 56: 696 (1969).\nJohnson, A.G.: The effect of metoclopramide on gastro-duodenal and gallbladder contractions. Gut 12: 158 (1971a).\nJohnson, A.G.: The action of metoclopramide on human gastroduodenal motility. Gut 12: 421 (1971b).\nJohnson, A.G.: Controlled trial of metoclopramide in the treatment of flatulent dyspepsia. British Medical Journal 2: 25 (1971c).\nJohnson, A.G.: Gastroduodenal motility and synchronisation. Postgraduate Medical Journal 49 (Suppl.4): 29 (1973a).\nJohnson, A.G.: Flatulent dyspepsia. Postgraduate Medical Journal 49 (Suppl.4): 104 (1973b).\nJones, C.T.: Metoclopramide in the treatment of nausea. A double-blind trial. New Zealand Medical Journal 68: 388 (1968).\nJustin-Besancon, L. and Laville, C: Action antiémétique du métoclopramide vis-á-vis de l’apomorphine et de l’hydergine. Comptes Rendus des Séances de la Société de Biologie de Paris 158: 723 (1964a).\nJustin-Besancon, L. and Laville, C: Action du métoclopramide sur le systeme nerveux autonome. Comptes Rendus des Séances de la Société de Biologie de Paris 158: 1016 (1964b).\nKatevuo, K.; Kanto, J. and Pihlajamaki, K.: The effect of metoclopramide on the contraction of the human gallbladder. Investigative Radiology 10: 197 (1975).\nKelly, J.M.: Metoclopramide in the vagotomised stomach. Part II —In dog. Postgraduate Medical Journal 49 (Suppl.4): 83 (1973).\nKennedy, T.: Metoclopramide in the vagotomised stomach. Part I —In man. Postgraduate Medical Journal 49 (Suppl.4): 81 (1973a).\nKennedy, T.: In discussion. Postgraduate Medical Journal 49 (Suppl.4): 98 (1973b).\nKlein, R.L.; Militello, T.E. and Ballinger, C.M.: Antiemetic effect of metoclopramide... Evaluation in humans. Anaesthesia and Analgesia 47: 259 (1968).\nKocian, J. and Kocianova, J.: Klinische Erfahrungen mit Paspertin in der Gastroenterologie. Medizinische Welt 26: 1939 (1975).\nKorczyn, A.D.: Hiccup. British Medical Journal 2: 590 (1971).\nKreel, L.: The use of oral metoclopramide in the barium meal and follow-through examination. British Journal of Radiology 43: 31 (1970).\nKreel, L.: The use of metoclopramide in radiology. Postgraduate Medical Journal 49 (Suppl. 4): 42 (1973).\nKreel, L.; Trott, M. and Howells, T.H.: The influence of oral metoclopramide on gastric emptying after a fixed water load. Clinical Radiology 23: 213 (1972).\nKumada, S.: Details on the discovery of Primperan, its security and destiny in a living body. First Symposium on Therapy with New Drugs, Nagoya, 1965, pp. 23–26.\nLa Barre, J.: A propos du mode d’action du métoclopramide en thérapeutique gastro-intestinale. Pathologie et Biologie 17: 663 (1969).\nLaville, C: Protection exercée par le métoclopramide contre les effets vomitifs du sulfate de cuivre. Pathologie et Biologie 12: 577 (1964).\nLind, B. and Breivik, H.: Metoclopramide and perphenazine in the prevention of postoperative nausea and vomiting. A double-blind comparison. British Journal of Anaesthesia 42: 614 (1970).\nMcCallum, R.; Ippoliti, A.; Cooney, C and Sturdevant, R.A.L.: A double-blind trial of metoclopranide in symptomatic gastro-oesophageal reflux. Gastroenterology 70: 962 (1976).\nMcCallum, R.W.; Kline, M.M.; Curry, N. and Sturdevant, R.A.L.: Comparative effects of metoclopramide and bethanechol on lower oesophageal sphincter pressure in reflux patients. Gastroenterology 68: 1114 (1975).\nMcGarry, J.M.: A double-blind comparison of the antiemetic effect during labour of metoclopramide and perphenazine. British Journal of Anaesthesia 43: 613 (1971).\nMcMurray, G.N.: An evaluation of metoclopramide as an anti-emetic in seasickness. Postgraduate Medical Journal 49 (Suppl.4): 38 (1973).\nMcNeilly, A.S.; Thomer, M.O.; Volans, G. and Besser, G.M.: Metoclopramide and prolactin. British Medical Journal 2: 729 (1974).\nMadanagopolan, N.: Metoclopramide in hiccup. Current Medical Research and Opinion 3: 371 (1975).\nMalméjac J. and Laville, C: Effets cardiovasculaires du métoclopramide. Pathologie et Biologie 12: 1074 (1964).\nManninen, V.; Apajalahti, A.; Melin, J. and Karesoja, M.: Altered absorption of digoxin in patients given propantheline and metoclopramide. Lancet 1: 398 (1973a).\nManninen, V.; Apajalahti, A.; Simonen, H. and Reissei, P.: Effect of propantheline and metoclopramide on absorption of digoxin. Lancet 1: 1118 (1973b).\nMargieson, G.R.; Sorby, A. and Williams, H.B.L.: The action of metoclopramide on gastric emptying: A radiological assessment. Medical Journal of Australia 2: 1272 (1966).\nMargieson, G.R. and Williams, H.B.L.: Radiopharmacology of the stomach with special reference to the effects of metoclopramide. Australian Radiology 12: 239 (1968).\nMarino, A.; Girone, E.; Battista, O. and De Marino, V.: Effetti della metoclopramide sul comportamento spontaneo e condiazionato, sulla convulsivita da cardiazolo e sull’elettrocardiogramma. Antologia di Medicina e Igiene 6: 1173 (1968).\nMarmo, E.; Di Giacomo, S. and Imperatore, A.: Metoclopramid und electrokardiographische Veranderungen-durch KCl, BaCl2, CaCl2, MgCl2, Aconitin, k-Strophanthosid, Vasopressin und durch Asphyxie. Arzneimittel-Forschung 20: 12 (1970a).\nMarmo, E.; Di Mezza, F.; Imperatore, A. and Di Giacomo, S.: Metoclopramid und die Muskulatur von Ösophagus, Magen, Darm, Milz, Trachea, Gallen- und Harnblase: Untersuchungen in vitro. Arzneimittel-Forschung 20: 18 (1970b).\nMarmo, E.; Imperatore, A. and di Giacomo, S.: Effects of metoclopramide on the cardiovascular apparatus and on the relative autonomic nervous system. La Clinica Terapeutica 51: 509 (1969).\nMarshall, N.W.: A double-blind trial of metoclopramide and prochlorperazine in general practice. British Journal of Clinical Practice 24: 25 (1970).\nMartin, P.D. and Scobie, B.A.: Metoclopramide and gastric emptying. New Zealand Medical Journal 67: 494 (1967).\nMatuchansky, C; Huet, P.M.; Mary, J.Y.; Rambaud, J.C. and Bernier, J.J.: Effects of cholecystokinin and metoclopramide on jejunal movements of water and electrolytes and on the transit time of luminal fluid in man. European Journal of Clinical Investigation 2: 169 (1972).\nMearrick, P.T.; Wade, D.N.; Birkett, D.J. and Morris, J.: Metoclopramide, gastric emptying and l-dopa absorption. Australian and New Zealand Journal of Medicine 4: 144 (1974).\nMedin, S. and Nyberg, L.: Effect of propantheline and metoclopramide on absorption of digoxin. Lancet 1: 1393 (1973).\nMeeroff, J.C.: The effect of metoclopramide on human gastric emptying and secretion. Acta Gastroenterologica Latin America 6: 55 (1974).\nMiddleton, R.S.W.: The use of metoclopramide in the elderly. Postgraduate Medical Journal 49 (Suppl. 4): 90 (1973).\nMetzger, W.; Cano, R. and Sturdevant, R.A.L.: Effect of metoclopramide in chronic gastric retention after gastric surgery. Gastroenterology 68: 954 (1975).\nMitchell, A.B.S. and Parkins, R.A.: Metoclopramide as an adjunct to small bowel intubation. Gut 10: 690 (1969).\nMiyake, T.; Yamamoto, Y.; Ariyoshi, J.; Suzaki, T.; Hajiro, K.; Todo, A.; Ohishi, M.; Hoshino, T. and Yanagihara, K.: Clinical evaluation of metoclopramide (Primperan) —a double-blind controlled trial. Japanese Archives of Internal Medicine 19: 249 (1972).\nModica, G.; Sorrentino, F.; Gulisano, G. and Bortoli, M.G.de.: Effects of metoclopramide on the motility of the biliary ducts. Riforma Medica 84: 817 (1970).\nMoertel, CG. and Reitemeier, R.J.: Controlled clinical studies of orally administered antiemetic drugs. Gastroenterology 57: 262 (1969).\nMoshal, M.G.: The propulsive action of metoclopramide (Maxolon). South African Medical Journal 46: 1871 (1972).\nMoshal, M.G.: Trials with metoclopramide in duodenal ulceration. Postgraduate Medical Journal 49 (Suppl. 4): 100 (1973).\nMuller, J.M.; Denis, B.; Schaerer, R. and Cordonnier, D.: Utilisation clinique du Métoclopramide dans le traitement des nausées, des vomissements et du hoquet des insuffisants renaux chroniques. Grenoble Medico-Chirurgical 6: 73 (1968).\nMur Linares, J. and Llorca, V.: La metoclopramide en el ulcus gastroduodenal. Cinco anos de observacion clinico-biologico-radiologica. Medizinishce Klinik (Edicion en Espanol) 8: 38 (1968).\nNakra, B.R.S.; Bond, A.J. and Lader, M.H.: Comparative psychotropic effects of metoclopramide and prochlorperazine in normal subjects. Journal of Clinical Pharmacology 15: 449 (1975).\nNatale, L.: Trattamento di alcuni disturbi funzionali dell’apparato digerente: sperimentazione clinica di confronto fra un preparato d’associazione di medazepam e metoclopramide ed uno d’associazione di medazepam con un anticolinergico. La Clinica Terapeutica 72: 141 (1975).\nNimmo, J.: The influence of metoclopramide on drug absorption. Postgraduate Medical Journal 49 (Suppl. 4): 25 (1973).\nNimmo, J.; Heading, R.C.; Tothill, P. and Prescott, L.F.: Pharmacological modification of gastric emptying: Effects of propantheline and metoclopramide on paracetamol absorption. British Medical Journal 1: 587 (1973).\nÖigaard, A.: The motor-stimulating effect of metoclopramide and pyridostigmine bromide in normal man and laparotomised patients. Scandinavian Journal of Gastroenterology 10: 65 (1975).\nPagnini, G. and Di Carlo, R.: Investigations on the interaction of 2-methoxy-5-chloroprocainamide (metoclopramide) with serum proteins. Arzneimittel-Forschung 22: 780 (1972).\nPauli, A. and Kerr Grant, A.: A controlled trial of meto-clopramide in reflux oesophagitis. Medical Journal of Australia 2: 627 (1974).\nPearson, M.C.; Edwards, D.; Tate, A.; Gilkes, R.; Saxton, H.M. and Rowland, C: Comparison of the effects of oral and intravenous metoclopramide on the small bowel. Postgraduate Medical Journal 49 (Suppl. 4): 47 (1973).\nPeringer, E.; Jenner, P. and Marsden, CD.: Effect of metoclopramide on turnover of brain dopamine, noradrenaline and 5-hydroxytryptamine. Journal of Pharmacy and Pharmacology 27: 442 (1975).\nPirola, R.C.: Rapid duodenal intubation with metoclopramide. American Journal of Digestive Diseases 12: 913 (1967).\nPoignant, J.C.; Laubie, M.; Tsoucaris-Kupfer, D. and Schmitt, H.M.: The effect of various pharmacological agents on the stereotyped movements produced in the rat by injection of l-(2″-pyrimidyl)-4-piperonylpiperazine (piribedil). Comptes Rendus Hebdomadaires des seances de l’Academie des Sciences, Paris, Series D 275: 715 (1972).\nRamos, A.O.; Bastos, W.P. and Sakata, M.: Influence of metoclopramide in experimental arrhythmias induced by barium or by chloroform and adrenaline. Medecina et Pharmacologia Experimentalis 17: 385 (1967).\nRamsbottom, N. and Hunt, J.N.: Studies of the effect of metoclopramide and apomorphine on gastric emptying and secretion in man. Gut 11: 989 (1970).\nRentzhog, L. and Wikstrom, S.: Pharmacological effects of gastric emptying following laparotomy in the rat. Acta Chirurgica Scandinavic 141: 649 (1975).\nRobinson, O.P.W.: Metoclopramide —a new pharmacological approach? Postgraduate Medical Journal 49 (Suppl. 4): 77 (1973b).\nSalas, J.R.: Metoclopramide for vertigo. New Zealand Medical Journal 66: 870 (1967).\nSavio, E. and Pontiggia, P.: Metoclopramide e assorbimento intestinale di isoniazide. Annali di Medicina Sondalol 3: 402 (1965).\nScalabrino, R. and Pasquariello, G.: Effeti indesideriabili da farmaci. Esperienze con metoclopramide. Riforma Medica 82 (Suppl.): 1562 (1968).\nScarzella, R.; Gario, S. and Ferrari, G.: Nota preliminare sull’azione di alte dosi di metoclopramide nell’uomo. Riforma Medica 82 (Suppl.): 2010 (1968).\nSchmid, E. and Ritter, U.: Enfluss von rektal appliziertem Hyoscin-N-butylbromide auf die Dündarnmotilitat. Arzneimittel-Forschung 22: 2149 (1972).\nSchütz, E.: Fortschritte in der Therapie des Ulcus duodeni. de Verkürzte Heildauer unter hohen Gaben von Paspertin. Münchener Medizinische Wochenshrift 118: 231 (1976).\nSethobhakdi, S.; Sricharoen, V. and Wilairatana, S.: The effect of metoclopramide on gastric emptying. American Journal of Proctology 26: 51 (1975).\nShah, Z.P. and Wilson, J.: An evaluation of metoclopramide (Maxolon) as an anti-emetic in minor gynaecological surgery. British Journal of Anaesthesia 44: 865 (1972).\nShaklai, M.; Pinkhas, J. and De Vries, A.: Metoclopramide and cardiac arrhythmia. British Medical Journal 2: 385 (1974).\nSicard, J.-P.; Reignier, A. and Bakouche, P. Manifestations extrapyramidales dues au métoclopramide. A propos de 6 observations. La Nouvelle Presse Médicale 2: 31 (1973).\nSingh, M.S. and Lean, T.H.: The use of metoclopramide (Maxolon) in hyperemesis gravidarum. Proceedings of the Obstetrical and Gynaecological Society, Singapore 1: 43 (1970).\nSousa, P.L.R.: Metoclopramide and breast-feeding. British Medical Journal 1: 512 (1975).\nStadaas, J. and Aune, S.: The effect of metoclopramide (Primperan) on gastric motility before and after vagotomy in man. Scandinavian Journal of Gastroenterology 6: 17 (1971).\nStadaas, J.O. and Aune, S.: Clinical trial of metoclopramide in postvagotomy gastric stasis. Archives of Surgery 104: 684 (1972).\nStanciu, C. and Bennett, J.R.: Metoclopramide in gastro-oesophageal reflux. 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Journal of Neurology, Neurosurgery, and Psychiatry 38: 331 (1975).\nThompson, W.G.: Altered absorption of digoxin in patients given propantheline and metoclopramide. Lancet 1: 783 (1973).\nThorburn, C.W. and Sowton, E.: The haemodynamic effects of metoclopramide. Postgraduate Medical Journal 49 (Suppl. 4): 22 (1973).\nTinker, J. and Cox, A.G.: Effect of metoclopramide on transport in the small intestine of the dog. Gut 10: 986 (1969).\nTornetta, F.J.: Clinical studies with the new antiemetic, metoclopramide. Anesthesia and Analgesia 48: 198 (1969).\nTrafford, J.A.P.; Fisher, A.M.H.: Marshall, S. and Douth-waite, A.H.: Metoclopramide (Maxolon) —A new anti-emetic. British Journal of Clinical Practice 21: 457 (1967).\nUzeta Mejia, S.: Estudio doble ciego con metoclopramida y placebo en diversos trastomos dispepticos. Revista Faculdad Medica 14: 367 (1971).\nValenzuela, J.E.; Defilippi, C. and Csendes, A.: Manometric studies on the human pyloric sphincter. Effect of cigarette smoking, metoclopramide, and atropine. Gastroenterology 70: 481 (1976).\nVenables, C.W.; Bell, D. and Eccleston, D.: A double-blind study of metoclopramide in symptomatic peptic oesophagitis. Postgraduate Medical Journal 49 (Suppl. 4): 73 (1973).\nVialatte, J. and Paupe, J.: Applications du métoclopramide aux vomissements du nourisson et de l’enfant. Semaine des Hôpitaux de Paris 40: 2367 (1964).\nVolans, G.N.: The effect of metoclopramide on the absorption of effervescent aspirin in migraine. British Journal of Clinical Pharmacology 2: 57 (1975).\nWard, H.W.C.: Metoclopramide and prochlorperazine in radiation sickness. British Medical Journal 2: 52 (1973).\nWard, H.W.C.: Metoclopramide and prolactin. British Medical Journal 3: 169 (1974).\nWatanabe, N.; Nakai, T.; Iwanami, K. and Fujii, T.: Studies on the subchronic and chronic toxicity of metoclopramide. Yakugaku Kenkyu (Japanese Journal of Pharmaceutical Chemistry) 39: 75 (1968a).\nWatanabe, N.; Iwanami, K. and Nakahara, N.: Teratogenicity of metoclopramide Yakugaku Kenkyu (Japanese Journal of Pharmaceutical Chemistry) 39: 92 (1968b).\nWeisbrodt, N.W.; Wiley, J.N.; Overholt, CF. and Bass, P.: A relation between gastroduodenal muscle contractions and gastric emptying. Gut 10: 543 (1969).\nZer, M. and Dintsman, M.: The use of metoclopramide in acute pyloric obstruction. 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Speight",{"id":1421,"sortIndex":45,"researcher":28,"roles":1422,"affiliations":1423,"properties":1430,"displayName":1432,"givenName":28,"familyName":28},"cbef5677-fad8-46c4-9707-10595acd8860",[970],[1424],{"id":1371,"sortIndex":32,"affiliation":1425,"properties":28},{"id":1371,"createTime":28,"updateTime":28,"relativeEntities":1426,"slug":28,"properties":1427,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1429,"statistic":28},[],{"title":1428},{"VI":1376},[],{"title":1431},{"VI":1432},"G. S. Avery",{"url":1364,"publisher":1434,"properties":1477},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1435,"slug":872,"properties":1436,"entityType":25,"verifyStatus":883,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":47,"subjectFields":1441,"manageAffiliations":1446,"indexDatabases":1457,"url":936,"thumbnailPath":28,"statistic":1472,"gsStatistic":28,"type":28,"analyzePriority":28},[],{"country":1437,"eissn":1438,"issn":1439,"title":1440},{"VOID":875},{"VOID":877},{"VOID":879},{"EN":872},[1442],{"id":886,"createTime":28,"updateTime":28,"relativeEntities":1443,"label":1444,"description":1445,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":889},{},[1447,1452],{"id":893,"createTime":28,"updateTime":28,"relativeEntities":1448,"slug":28,"properties":1449,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1451,"statistic":28},[],{"title":1450},{"EN":897},[],{"id":900,"createTime":28,"updateTime":28,"relativeEntities":1453,"slug":28,"properties":1454,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1456,"statistic":28},[],{"title":1455},{"EN":904},[],[1458,1465],{"id":908,"indexDatabase":1459,"url":914,"indexYears":915,"academicFieldIds":1464,"indexDatabaseRanking":918},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":1460,"label":1461,"description":1462,"key":781,"publicationTags":1463,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],[917],{"id":920,"indexDatabase":1466,"url":932,"indexYears":28,"academicFieldIds":1471,"indexDatabaseRanking":28},{"id":922,"createTime":28,"updateTime":28,"relativeEntities":1467,"label":1468,"description":1469,"key":929,"publicationTags":1470,"standard":28},[],{"EN":925,"VI":925},{"EN":927,"VI":928},[931,813],[934,935],{"impactFactor":32,"impactFactorByYear":1473,"i10Index":32,"i10IndexLast5Year":32,"totalPublication":939,"totalPublicationByYear":1474,"totalCitation":32,"totalCitationByYear":1475,"totalCitationPerPublication":32,"totalCitationPerPublicationByYear":1476,"hindexLast5Year":32,"hindex":32},{},{"1993":40,"2012":941,"2013":357,"2014":48,"2015":49,"2016":123,"2017":49,"2018":46,"2019":46,"2020":48,"2021":357,"2022":46,"2023":145},{},{},{"pages":1478,"volume":1480},{"VOID":1479},"81-131",{"VOID":1481},"12","2012-11-15",[931,918],{"id":1485,"createTime":1486,"updateTime":1487,"relativeEntities":1488,"slug":1489,"properties":1490,"entityType":963,"verifyStatus":26,"verifyTime":1487,"verifyNote":964,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1498,"fullTextUrl":28,"authors":1499,"publicationType":1106,"publisherRelationship":1540,"citationCount":28,"citationInfo":28,"publishDate":1589,"publishYear":1347,"citationAnalyzeStatus":883,"lastCitationAnalyze":28,"indexDatabases":1590,"openAccess":28,"references":28,"isForceReanalyzing":1159},"004fb2da-c951-4efe-8f87-81cd2484cb37","2024-01-09T05:18:24.890+00:00","2024-12-25T23:01:08.033+00:00",[],"Ticlopidine",{"abstract":1491,"title":1493,"references":1494,"doi":1496},{"EN":1492},"Ticlopidine inhibits platelet aggregation induced by adenosine diphosphate (ADP) and most other platelet agonists in ex vivo studies of human platelets. The drug also improves other abnormalities of platelet function seen in patients with cerebrovascular disease, peri-pheral arterial disease, ischaemic heart disease or other conditions involving platelet hyperaggregation. Abnormal platelet activity has been implicated in a variety of clinical conditions in which patients are at high risk of thromboembolic events, and thus the effectiveness of ticlopidine has been investigated in such patients. Since the initial review of the drug appeared in the Journal, data from several large multicentre studies have shown that ticlopidine has a substantial benefit to offer patients who have experienced transient ischaemic attacks or stroke, and in those with peripheral arterial disease or ischaemic heart disease. Ticlopidine reduces the incidence of further stroke, myocardial infarction or vascular death, and is superior to placebo and aspirin in this regard in studies of patients with recent stroke or transient ischaemic attacks, or intermittent claudication. Ticlopidine is equally effective in both men and women and also improves symptoms of claudication in patients with peripheral arterial disease, and appears to reduce anginal pain. Patients with subarachnoid haemorrhage and sickle cell disease have shown some improvement with ticlopidine administration. The drug reduces thromboembolic events and re-stenosis in patients undergoing haemodialysis and cardiac surgery, and appears to prevent the progression of nonproliferative diabetic retinopathy. Ticlopidine in large clinical trials is associated with a higher incidence of adverse effects than placebo and an overall incidence similar to aspirin. Most adverse effects do not require withdrawal of treatment. Gastrointestinal symptoms (particularly diarrhoea) are most common, occurring almost twice as frequently with ticlopidine as with aspirin. Other adverse effects associated with ticlopidine include skin rash, haemorrhagic disorders, and haematological effects; these latter effects require careful monitoring of patients during the initial weeks of therapy. In conclusion, ticlopidine is a valuable addition to the prophylactic treatments available for the management of patients with cerebrovascular disease, peripheral arterial disease or ischaemic heart disease, who present a high risk of thromboembolic events. Although tolerability may be a problem for some patients, the overall benefit conferred by the drug would appear to outweigh this potential disadvantage. Because of its antiplatelet activity, ticlopidine has a promising role in other disorders mediated by platelet dysfunction. However, the precise role of the drug in these additional therapeutic indications awaits clarification with wider clinical experience. Ticlopidine is a thienopyridine derivative which has a broad spectrum antiaggregating activity. In ex vivo studies of platelets obtained from healthy volunteers and patients with cerebrovascular disease, peripheral arterial disease, ischaemic heart disease, or other conditions associated with platelet hyperaggregation, ticlopidine inhibits ADP-induced platelet aggregation. A maximal effect was seen 3 to 5 days after repeated administration in healthy volunteers and this can be seen for up to 10 days after withdrawal of drug treatment. Inhibition of ex vivo platelet aggregation induced by other platelet agonists such as arachidonic acid, collagen, thrombin and platelet activating factor (PAF)-acether has also been reported, although this may not be a direct effect but rather a result of the inhibitory effect of ticlopidine on aggregation produced by ADP released by low concentrations of these agonists. Other ticlopidine-induced effects resulting from its interaction with ADP and platelets include a decrease in platelet deposition on atheromatous plaque in patients with cerebrovascular disease, reduced fibrinogen levels and blood viscosity in patients with peripheral arterial disease, and normalised platelet adhesiveness, erythrocyte deformability and β-thromboglobulin release in diabetic patients. Ticlopidine also prolongs bleeding time, with a maximal effect seen after 5 to 6 days in volunteers. The influence of ticlopidine on a variety of platelet agonists suggests a common site of action at an early stage of the platelet activating process. No comprehensive mechanism of action has been proposed, but inhibition of the ADP-induced exposure of the fibrinogen-binding site of the glycoprotein IIb-IIIa complex has been demonstrated. About 80 to 90% of an oral ticlopidine dose is absorbed, with plasma concentrations peaking at 1 to 3 hours. Steady-state peak and trough plasma concentrations of 0.9 mg\u002F L and 0.2 mg\u002FL, respectively, have been achieved after ticlopidine 250mg twice daily for 14 days. Ticlopidine is rapidly and extensively metabolised, with 1 metabolite more active than the parent drug. A terminal elimination half-life of 96h at steady-state has been reported in healthy volunteers. In the elderly the AUC and half-life of ticlopidine are significantly prolonged compared with younger volunteers after a single dose but this was not significant at steady-state. No studies evaluating the pharmacokinetics of ticlopidine in patients with major organ dysfunction have been published. Since the initial review of ticlopidine appeared in the Journal, attention has focused on the effectiveness of the drug in patients at high risk of thromboembolic events, i.e. those with transient ischaemic attacks and stroke, peripheral arterial disease or ischaemic heart disease. A large multicentre trial, the Canadian-American Ticlopidine Study (CATS) completed since the first review, has demonstrated that ticlopidine administered as a 250mg dose twice daily in patients who had had a recent stroke reduced the incidence of stroke, myocardial infarction or vascular death by 30.2% compared with placebo. Another large trial in more than 3000 patients [the Ticlopidine Aspirin Stroke Study (TASS)] has shown that ticlopidine has a more pronounced preventative effect on death from all causes or nonfatal stroke compared with aspirin. This was statistically significant within 1 year and was maintained over a 5-year period. Ticlopidine appears to be equally effective in women and men. Major clinical trials in patients with intermittent claudication resulting from peripheral arterial disease demonstrate that ticlopidine 250mg twice daily improves walking ability during treatment periods of 6 to 21 months. A reduction in the total mortality rate (by 29.1% compared with placebo), mainly because of its marked effect on ischaemic heart disease mortality, was seen in the Swedish Ticlopidine Multicentre Study (STIMS). In the same trial, the incidence of acute myocardial infarction, stroke, or transient ischaemic attack was significantly lowered by ticlopidine during an average period of 5.6 years. Results of another multicentre study show that ticlopidine 500 mg\u002Fday begun within 48 hours of admission reduces the risk of acute myocardial infarction, myocardial infarction and sudden death, and vascular mortality in patients with unstable angina. Ticlopidine also appears to reduce anginal pain to a similar extent to aspirin if administered within 24 hours of acute myocardial infarction. Other indications in which ticlopidine shows some benefit include the following: prevention of thrombotic events in patients undergoing haemodialysis, coronary artery bypass surgery, carotid endarterectomy or extracorporeal circulation; prevention of nonproliferative diabetic retinopathy; and prevention of cerebral vasospasm following subarachnoid haemorrhage. The effectiveness of the drug in Raynaud’s phenomenon, sickle cell disease, ocular vein occlusion, glomerulonephritis and the prevention of postoperative thrombosis and bleeding remains uncertain. The findings of a large placebo-controlled study in 1053 patients with a recent thromboembolic stroke show a higher incidence of adverse effects associated with ticlopidine compared with placebo: 54% of ticlopidine recipients and 34% of placebo recipients experienced an adverse symptom over a 3-year period. Of these patients, 12 and 3%, respectively, required withdrawal of treatment. The incidence of adverse effects was roughly similar in patients treated with ticlopidine or aspirin over a 2-to 6-year period, although ticlopidine recipients had almost twice the incidence of diarrhoea and skin rash whereas more peptic ulcers were reported in the aspirin group. The most common adverse effects associated with ticlopidine are gastrointestinal symptoms: diarrhoea is the most frequently reported, affecting about 20% of treated patients. Other effects are skin reactions (urticaria, pruritus, erythema), haemorrhagic disorders (epistaxis, ecchymoses, menorrhagia), and haematological disorders (leucopenia, thrombocytopenia, pancytopenia). These effects are generally not severe and resolve on discontinuation of ticlopidine treatment. The most potentially serious symptoms are haematological disturbances and close monitoring is therefore essential for at least the first 12 weeks of ticlopidine therapy. Abnormal liver function is rare with ticlopidine therapy but in instances where a definite causal relationship was determined, abnormal effects disappeared on withdrawal of treatment. Ticlopidine has also been associated with an increase in total cholesterol levels. A daily dosage of ticlopidine 500mg, administered orally as two 250mg tablets with food, is recommended. Up to 4 tablets (daily dosage 1000mg) can be administered for short term treatment but patients require careful monitoring. All patients receiving ticlopidine should be monitored during at least the first 12 weeks because of the risk of haematological disturbances. Ticlopidine is contraindicated in patients receiving high dose heparin, those with a history of bleeding disorders, gastroduodenal ulcer or those in the acute phase of haemorrhagic cerebral vascular accident.",{"EN":1489},{"VOID":1495},"Apollonio A, Castignani P, Magrini L, Angeletti R. Ticlopidinepentoxifylline combinaton in the treatment of atherosclerosis and the prevention of cerebrovascular accidents. Journal of International Medical Research 17: 28–35, 1989\nArcan JC, Blanchard J, Boissel JP, Destors JM, Panak E. Multicenter double-blind study of ticlopidine in the treatment of intermittent claudication and the prevention of its complications. Angiology 39(9): 802–811, 1988\nArcan JC, Destors JM. Controlled clinical trial of ticlopidine in patients suffering from intermittent claudication. Abstract. Thrombosis Research (Suppl. 6): 159, 1986\nArcan JC, Panak E. Ticlopidine in the treatment of peripheral occlusive arterial disease. Seminars in thrombosis and nemostasis 15: 167–170, 1989\nAukland A, Hurlow RA, George AJ, Stuart J. Platelet inhibition with ticlopidine in atherosclerotic intermittent claudication. Journal of Clinical Pathology 35: 740–743, 1982\nAvellone G, Di Garbo V, Panno AV, Longo B, Accardo MA, et al. Valutazione di alcuni farmaci emoreologici nella ischemia del microcircolo. Abstract. Clinical Therapeutics 122(2): 121–127, 1987\nBalsano F, Coccheri S, Libretti A, Nenci GG, Catalano M, et al. Ticlopidine in the treatment of intermittent claudication: a 21-month double-blind trial. Journal of Laboratory and Clinical Medicine 114: 84–91, 1989\nBalsano F, Rizzon P, Violi F, Scrutinio D, Cimminiello C, et al. Antiplatelet treatment with ticlopidine in unstable angina, a controlled multicenter clinical trial. Circulation, in press, 1990\nBarcellini W, Borghi MO, Lazzaroni E, Vismara A, Ferraro G, et al. Study on the interference of ticlopidine on the immune system. International Journal of Tissue Reactions 10(3): 183–188, 1988\nBerglund U, Lassvik C, Wallentin L. Effects of the platelet inhibitor ticlopidine on exercise tolerance in stable angina pectoris, European Heart Journal 8: 25–30, 1987\nBerglund U, von Schenck H, Wallentin L. Effects of ticlopidine of platelet function in men with stable angina pectoris. Thrombosis and Haemostasis 54(4): 808–812, 1985\nBoberg M. Ticlopidine in patients with intermittent claudication: The Swedish Ticlopidine Multicentre Study (STIMS). Ticlopidine Satellite Symposium, Ljubljana, Yugoslavia, pp. 24–27, June 27, 1990\nBoissel JP, Peyrieux JC, Destors JM. Is it possible to reduce the risk of cardiovascular events in subjects suffering from intermittent claudication of the lower limbs? Thrombosis and Haemostasis 62(2): 681–685, 1989\nBokarev IN, Velikov VK, Zelenchuk NM, Yarovaya LD, Polunin GS, et al. Effect of ticlopidine on hemostasis in diabetic microangiopathy. Klinicheskaya Meditsina 66(1): 58–61, 1988\nBortolani E, Vandone PL, Ghilardi G, Agrati AM, Ambrosi G, et al. Ticlopidine treatment after carotid endarterectomy: a one year follow up in one hundred patients. Angiologie 5 (Suppl): 42–46, 1988\nBourde C, Eschwège E, Verry M. Controlled clinical trial of an antiaggregating agent: ticlopidine, in vascular ulcers of the leg. Abstract. Thrombosis and Haemostasis 46(1): 91, 1981\nBowles MJ, Khurmi NS, O’Hara MJ, Raftery EB. An evaluation of objective indices of myocardial ischaemia for clinical trials of anti-anginal drugs. British Journal of Clinical Pharmacology 17: 213P, 1984\nBrommer EJP. The effect of ticlopidine upon platelet function, haemorrhage and post-operative thrombosis in patients undergoing suprapubic prostatectomy. Journal of International Medical Research 9(3): 203–210, 1981\nBruno JJ, Molony BA. In Scriabine (Ed.) New drugs annual: cardiovascular drugs, pp. 295–316, Raven Press, New York, 1983\nCabannes R, Lonsdorfer J, Castaigne JP, Ondo A, Plassard A, et al. Clinical and biological double-blind-study of ticlopidine in preventive treatment of sickle-cell disease crises. Agents and Actions Supplements 15: 199–211, 1984\nCalenda E, Papion H, Borg JY, Menguy E, Delaunay T, et al. Normalisation du temps de saignement, après administration de desmopressine chez un femme traitée par la ticlopidine. Presse Médicale 40: 2143, 1988\nCanadian Cooperative Study Group. A randomized trial of aspirin and sulfmpyrazone in threatened stroke. New England Journal of Medicine 299: 53–59, 1978\nCastelli P, Basellini A, Agus GB, Ippolito E, Pogliani EM, et al. Thrombosis prevention with ticlopidine after femoropopliteal thromboendarterectomy. Angiologie 5 (Suppl. 77): 34–37, 1988\nChignard M, Lalau Keraly C, Delautier D, Sebag C, Bouloux C, et al. Reduced sensitivity of human platelets to PAF-acether following ticlopidine intake. Haemostasis 19: 213–218, 1989\nCimminiello C, Bernasconi P, Chianese R, Uberti T, Pietra A, et al. Ticlopidine administration to patients does not inhibit the ability of their monocytes to form rosettes and to phagocytize erythrocytes in vitro. International Journal of Tissue Reactions 9(3): 251–253, 1987\nCimminiello C, Violi F, Balsano F, STAI Group. Antiplatelet treatment with ticlopidine in unstable angina: a controlled multicentre clinical trial. Ticlopidine Satellite Symposium, Ljubljana, Yugoslavia, June 27, pp. 20–33, 1990\nCloarec M, Arcean JC, Caillard Ph, Gouraud B, Mouren X. Double-blind clinical trial of ticlopidine versus placebo in peripheral atherosclerotic disease of the legs. Angiologie 5 (Suppl. 77): 14–20, 1988\nCohn M, Matzner Y, Eldor A. Effect of ticlopidine on neutrophil chemotaxis in rats. Haemostasis 15: 114–118, 1985\nColli A, Buccino G, Cocciolo M, Parravicini R, Elli GM, et al. Ticlopidine-theophylline interaction. Clinical Pharmacology and Therapeutics 41: 358–362, 1987\nCospite M, Ferrara F, Milio G, Scrivano V, Meli F. Ticlopidine in the treatment of multiple atherosclerotic arteriopathy: a strain gauge plethysmography and Döppler spectrum analysis evaluation. Journal of International Medical Research 15: 303–311, 1987\nCriado A, Juflfe A, Carmona J, Otero C, Avello F. Ticlopidine as a hemorrhagic risk factor in coronary surgery. Drug Intelligence and Clinical Pharmacy 19(9): 673–676, 1985\nD’Addato M, Pedrini L. Effects of ticlopidine in carotid thromboendarterectomy: a double-blind placebo controlled study using indium labeled platelets. Angiologie 5 (Suppl. 77): 38–41, 1988\nDavid JL, Legrand V, Kulbertus HE. Relevance of free platelet count ratio (PCR) to circulating platelet aggregates (CPA) and to the release of B-thromboglobulin (β-tg) induced by exercise in patients with coronary heart disease (CHD). Effects of ticlopidine (T) treatment. Thrombosis and Haemostasis 58(227): 67, 1987\nDavid JL, Monfort F, Herion F, Raskinet R. Compared effects of three dose-levels of ticlopidine on platelet function in normal subjects. Thrombosis Research 14: 35–49, 1979\nDefreyn G, Bernat A, Delebassee D, Maffrand JP. Pharmacology of ticlopidine: a review. Seminars in Thrombosis and Hemostasis 15: 159–166, 1989\nDerian CK, Friedman PA. Effect of ticlopidine ex vivo on platelet intracellular calcium mobilization. Thrombosis Research 50: 65–76, 1988\nDe Scalzi M, De Leonardis V, Anichini P, Borghi G, Cinelli P. Effects of ticlopidine therapy on platelet function in patients with increased platelet activation. Current Therapeutic Research 42: 106–110, 1987\nDestors JM, Gauthier E, Lelong S, Boissel JP. Failure of a pure anti-platelet drug to decrease the number of attacks more than placebo in patients with Raynaud’s phenomenon. Angiology 37(8): 565–569, 1986\nDi Minno G, Cerbone AM, Iride C, Mattioli PL, Postiglione A, et al. Platelet fibrinogen binding in familial hypercholesterolemia. Advances in Experimental Medicine and Biology 210: 233–236, 1987\nDi Minno G, Cerbone AM, Mattioli PL, Turco S, Iovine C, et al. Functionally thrombasthenic state in normal platelets following the administration of ticlopidine. Journal of Clinical Investigation 75: 328–338, 1985a\nDi Minno G, Palladino M, Pannain M, Scillitani A, Turco S, et al. Normalization by ticlopidine of the abnormally high fibrinogen binding to platelets from retinopathic diabetics. Abstract 0380. Thrombosis and Haemostasis 54(1): 64, 1985b\nEll S, Mihindukulasuriya JCL, O’Brien JR, Polak A, Vernham G, Ticlopidine in the prevention of blockage of fistulae and shunts. 7th International Congress on Thrombosis, Valencia, October 13–16, Abstract 332, p. 180, 1982\nEllis DJ. Treatment of intermittent claudication with ticlopidine. Abstract. 32nd Annual Meeting of the International Committee on Thrombosis and Haemostasis and the 9th Congress of the Mediterranean League Against Thrombembolic Diseases, Jerusalem, Jun 1–6, 1986\nEllis DJ, Roe RL, Bruno JJ, Cranston BJ, McSpadden MM. The effects of ticlopidine hydrochloride on bleeding time and platelet function in man. Thrombosis and Haemostasis 46: 176, 1987\nFéliste R, Delebassée D, Simon AMF, Chap H, Defreyn G, et al. Broad spectrum and platelet activity of ticlopidine and PCR 4099 involves the suppression of the effects of released ADP. Thrombosis Research 48: 403–415, 1987\nFiskerstrand CE, Thompson IW, Burnet ME, Williams P, Anderton JL, et al. Double-blind randomized trial of the effect of ticlopidine in arteriovenous fistulas for hemodialysis. Artificial Organs 2(1): 61–63, 1985\nFox KM, Jonathan A, Selwyn AP. Effects of platelet inhibition on myocardial ischaemia. Lancet II (8301) 2: 727–730, 1982\nGent M. Ticlopidine after completed thromboembolic stroke: the Canadian-American Ticlopidine Study (CATS). Ticlopidine Satellite Symposium, Ljubljana, Yugoslavia, pp. 8–11, June 27, 1990\nGent M, Blakely JA, Easton JD, Ellis DJ, Hachinski VC, et al. The Canadian American Ticlopidine Study (CATS) in thromboembolic stroke. Lancet: 1215–1220, 1989\nGould RJ, Derian CK, Friedman PA. Epinephrine overcomes ticlopidine inhibition of platelet aggregation. Federation Proceedings 46(3): 723, 1987\nGragnoli G, Signorini AM, Tanganelli I. The effects of ticlopidine on plasma values of β-thromboglobulin and thromboxane β2 in diabetics (Types 1 and 2). Minerva Medica 75: 1791–1796, 1984\nGrekas D, Alivanis P, Kalekou H, Syrganis C, Tourkantonis A. Are antiplatelet agents of value in the treatment of chronic glomerular disease? Correspondence. Nephrology Dialysis Transplantation 2(5); 377–379, 1987\nGröntoft K-Ch, Mulec H, Gutierrez A, Olander R. Thromboprophylactic effect of ticlopidine in arteriovenous fistulas for haemodialysis. Scandinavian Journal of Urology and Nephrology 19: 55–57, 1985\nHass WK, Easton JD, Adams Jr HP, Pryse-Phillips W, Molony BA, et al. A randomized trial comparing ticlopidine hydrochloride with aspirin for the prevention of stroke in high-risk patients. New England Journal of Medicine 321: 501–507, 1989\nHoutsmuller AJ, Vermeulen JACM, Klompe M, Zahn KJ, Henkes HE, Baarsma GS, et al. The influence of ticlopidine on the natural course of retinal vein occlusion. Agents and Actions Supplements 15: 219–229, 1984\nIkeda Y, Kikuchi M, Murakami H, Satoh K, Murata M, et al. Comparison of the inhibitory effects of cilostazol, acetylsalicylic acid and ticlopidine on platelet functions ex vivo. A randomised, double-blind cross-over study. Arzneimittel-Forschung 37(1): 563–566, 1987\nInstalle E, Gonzalez M, Schoevaerdts JC, Tremouroux J. Prevention by ticlopidine of platelet consumption during extracorporeal circulation for heart surgery and lack of effect on operative and postoperative bleeding. Journal of Cardiovascular Pharmacology 3: 1174–1183, 1981\nIsaka Y, Kimura K, Etani H, Uehara A, Uyama O, et al. Effect of aspirin and ticlopidine on platelet deposition in carotid atherosclerosis: assessment by Indium-111 platelet scintigraphy. Stroke 17: 1215–1220, 1986\nJanzon L, Bergqvist D, Boberg J, Boberg M, Eriksson I, et al. Prevention of myocardial infarction and stroke in patients with intermittent claudication: effects of ticlopidine. Journal of Internal Medicine 227: 301–308, 1990\nKarpatkin S, Pearlstein E, Ambrogio C, Coller BS. Role of adhesive proteins in platelet tumor interaction in vitro and metastasis formation in vivo. Journal of Clinical Investigation 81: 1012–1019, 1988\nKatsumura T, Mishima Y, Kamiya K, Sakaguchi S, Tanabe T, et al. Therapeutic effect of ticlopidine, a new inhibitor of platelet aggregation, on chronic arterial occlusive diseases, a double-blind study versus placebo. Angiology 33: 357–367, 1982\nKawagoe S, Seino Y, Tei H, Munakata J, Yamaguchi A, et al. Platelet TXA2 synthesizing activity in ischemic heart disease and effect of ticlopidine. Abstract P397. Thrombosis and Haemostasis 54(1): 67, 1985\nKhurmi NS, Bowles MJ, Raftery EB. Are antiplatelet drugs of value in the management of patients with chronic stable angina? A study with ticlopidine. Clinical Cardiology 9: 493–498, 1986\nKikuchi M, Ikeda Y, Murakami H, Watanabe K, Ando Y. Effects of cilostazol, a new antithrombotic agent, on platelet function ex vivo: randomized double-blind, crossover study with aspirin and ticlopidine. Thrombosis and Haemostasis 54(1): 136, 1985\nKnudsen JB, Gormsen J. The effect of ticlopidine on platelet function in normal volunteers and in patients with platelet hyperaggreagability in vitro. Thrombosis Research 16: 663–671, 1979\nKnudsen JB, Kjøller E, Gormsen J. The effect of ticlopidine, propranolol, and verapamil on stress induced platelet activation. Abstract 1469. Thrombosis and Haemostasis 50(1): 458, 1983\nKnudsen JB, Kjøller E, Skagen K, Gormsen J. The effect of ticlopidine on platelet functions in acute myocardial infarction, a double blind controlled trial. Thrombosis and Haemostasis 53(3): 332–336, 1985\nKobayashi I, Takeuchi M, Takemiya T, Osawa M, Maruyama S. Enhancement of platelet function in ischemic cerebrovascular disorders (CVD) and its effect on ticlopidine treatment. Abstract 1491. Thrombosis and Haemostasis 50: 463, 1983\nKobayashi K, Maeda K, Koshikawa S, Kawaguchi Y, Shimizu N, et al. Antithrombotic therapy with ticlopidine in chronic renal failure patients on maintenance haemodialysis — a multicentre collaborative double blind study. Thrombosis Research 20: 255–261, 1980\nKumada M, Dohi K, Fujii Y, Hanatani M, Ishikawa H. The effects of anti-platelet agents on renal functions and the modes of their anti-platelet action in primary glomerulonephritis. Abstract 79. Japanese Journal of Medicine 24(4): 335, 1985\nLalé A, Delebassée D, Savi P, Vallée E, Roncucci R, et al. Ticlopidine and leukocyte functions in rats. Abstract P1189. Thrombosis and Haemostasis 54(1): 201, 1985\nLandi G, Guidotti M. An open study with ticlopidine in cerebral reversible ischemia. Acta Neurologica (Naples) 9(5–6): 346–353, 1987\nLimet R, David J-L, Magotteaux P, Larock MP, Rigo P. Prevention of aorta-coronary bypass graft occlusion. Journal of Thoracic and Cardiovascular Surgery 94: 773–783, 1987\nLonsdorfer J, Castaigne JP, Lenormand E, Otayeck A, Bogui P, et al. Beneficial effects of ticlopidine on cardiopulmonary function of sickle cell patients not in crisis. Agents and Actions Supplements 15: 213–219, 1984\nMaeda K, Usuda M, Kawaguchi S, Shinzato T, Saito A, et al. Effects of ticlopidine on thrombotic obstruction of AV shunts and on dialysance of artificial kidneys. Artificial Organs 4: 30–33, 1980\nMaffrand JP, Bernat A, Delebassée D, Defreyn G, Cazenave JP, et al. ADP plays a key role in thrombogenesis in rats. Thrombosis and Haemostasis 59(2): 225–230, 1988\nManucci PM, Vicente V, Vianello L, Cattaneo M, Alberca I, et al. Controlled trial of desmopressin in liver cirrhosis and other conditions associated with a prolonged bleeding time. Blood 4: 1148–1153, 1986\nMaruyama S, Katayama S. Therapeutic effects of anti-platelet drugs towards TIA, RIND. An open comparative study of ticlopidine versus aspirin. Japanese Journal of Clinical and Experimental Medicine 58: 3617–3626, 1981\nMcKenna R, Galante J, Molony B, Kamm B. Failure of ticlopidine hydrochloride to prevent DVT in orthopaedic patients. Blood 62: 304a, 1983\nMontecchio GP, Custodi P, Carbone S, Bendotti C, Piovella F. Ticlopidine and indobufen: effects on haemostatic functions. Thrombosis and Haemostasis 58(1): 169, 1987\nNechaev DD, Bochko II, Martynov IV, Kuz’mina LF. Advantages and shortcomings of platelet antiaggregants in the treatment of myocardial infarction. Terapevticheskii Arkhiv 60(8): 59–63, 1988\nNeumann V, Cove DH, Shapiro LM, George AJ, Kenny MW, et al. Effect of ticlopidine on platelet function and blood rheology in diabetes mellitus. Clinical Hemorheology 3: 13–21, 1983\nNunn B, Lindsay R. Effect of ticlopidine on human platelet responsiveness ex vivo: comparison with aspirin. Thrombosis Research 18: 807–813, 1980\nNyberg G, Larsson O, Westberg NG, Aurell M, Jagenburg R, et al. A platelet aggregation inhibitor — ticlopidine — in diabetic nephropathy: a randomized double blind study. Clinical Nephrology 21: 184–187, 1984\nOgawa J, Inoue H, Tsurumi T, Onoue H, Koide S, et al. Interactions between UFT and anticoagulants in lung cancer patients. Japanese Journal of Surgery 18: 243–251, 1988\nOgawa S, Naruse T. Effects of various antiplatelet drugs and a defibrinating agent on experimental glomerulonephritis in rats. Journal of Laboratory and Clinical Medicine 99: 428–441, 1982\nOno H, Mizukami M, Kitamura K, Kikuchi H. Subarachnoid hemorrhage. Agents and Actions Supplements 15: 259–272, 1984\nOno S, Ashida S, Abiko Y. Hemorheological effect of ticlopidine in the rat. Thrombosis Research 31: 549–556, 1983\nOrlando E, Cortelazzo S, Nosari I, Lepore G, Pagani G, et al. Inhibition by ticlopidine of platelet adhesion to human venous subendothelium in patients with diabetes. Journal of Laboratory and Clinical Medicine 112: 583–588, 1988\nPalareti G, Poggi M, Torricelli P, Balestra V, Coccheri S. Longterm effects of ticlopidine on fibrinogen and haemorheology in patients with peripheral arterial disease. Thrombosis Research 52: 621–629, 1988\nPanak E, Blanchard J, Roe RL. Evaluation of the antithrombotic efficacy of ticlopidine in man. Agents and Actions Supplements 15: 148–166, 1984\nPanak E, Maffrand JP, Picard-Fraire C, Vallée E, Blanchard J, et al. Ticlopidine: a promise for the prevention and treatment of thrombosis and its complications. Haemostasis 13 (Suppl. 1): 1–54, 1983\nPicard-Fraire C. Pharmacokinetic and metabolic characteristics of ticlopidine in relation to its inhibitory properties on platelet function. Agents and Actions Supplements. Ticlopidine: Quo Vadis? 15: 68–75, 1984\nPotevin F, Lecompte T, Lecrubier C, Samama M. Administration of ticlopidine impedes ADP-induced activation but does not induce a thrombasthenic state. Abstract 1053. Thrombosis and Haemostasis 58(1): 289, 1987\nPryse-Phillips W. Efficacy of ticlopidine hydrochloride in the management of patients at high risk of stroke. Ticlopidine Satellite Symposium, Ljubljana, Yugoslavia, pp. 12–18, June 27, 1990\nRandi ML, Fabris F, Crociani ME, Battocchio F, Girolami A. Effects of ticlopidine on blood fibrinogen and blood viscosity in peripheral atherosclerotic disease. Arzneimittel-Forschung 35: 1847–1849, 1985\nRenner C, Guilmet D, Curtet JM. Ticlopidine in cardiac surgery with extracorporeal circulation. Nouvelle Presse Medicale 9: 3249–3521, 1980\nRothlin ME, Pfluger N, Speiser K, Goebel N, Krayenbühl H-P, et al. Platelet inhibitors versus anticoagulants for prevention of aorto-coronary bypass graft occlusion. European Heart Journal 6(2): 168475, 1985\nRuan C, Destelle G, Wang Z, Wan H, He Y, et al. Ticlopidine in China: comparative study on the effect of two dose levels on bleeding time and platelet function in healthy volunteers. Haemostasis 19: 94–99, 1989\nSablayrolles M, Wajcman H, Castaigne J-P, Labie D. Membrane expansion as a mechanism explaining the antisickling action of ticlopidine observed in vitro. American Journal of Hematology 18: 121–130, 1985\nSakata E. Therapy of vertigo — with clinical trial of ticlopidine. Yakuri to Chipyo 16: 1385–1395, 1989\nSaltiel E, Ward A. Ticlopidine: a review of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy in platelet-dependent disease states. Drugs 34: 222–262, 1987\nShapiro LM, Cove DH, Trethowan N, Neumann V. Clinical trials of an antiplatelet agent, ticlopidine, in diabetes mellitus. Current Medical Research and Opinion 8: 518–523, 1983\nShintani M. Clinical effect of combination therapy of ticlopidine and cinepazide on closed cerebrovascular diseases. Yakuri to Chiyo 16: 107–114, 1988\nSmith SA, Ellis DJ, Reitman MA, Teitelbaum PJ. Metabolic fate of ticlopidine hydrochloride in humans. Abstract 4459. Drug Absorption, Distribution and Excretion 2(5): 4457–4462, 1988\nSolvay H, Kahn M, Garreyn S, Cloarec M, Sneppe R. Glucose and erythrocyte ATP: distinctive effects of dipyridamole and of ticlopidine. Angiology 38(11): 815–823, 1987\nStiegler H, Hess H, Trampisch HJ. The course of peripheral obliterative arterial disease under the influence of the platelet function inhibitor ticlopidine. Abstract 594. European Heart Journal (Suppl.): 138, 1984\nTakegoshi T, Ono K, Matsubayashi K, Hashimoto F, Sano M. Metabolic disposition of ticlopidine hydrochloride, a new antithrombotic agent in rats. Pharmacometrics 19(3): 349–361, 1980\nTeitelbaum P, Gabuzda TG, Koretz SH, Massey I, Molony B. Pharmacokinetics of ticlopidine hydrochloride in young and old normal adult subjects following single and multiple dosing. Abstract. Journal of Pharmaceutical Sciences 76: 599, 1987\nThébault J, Blatrix CE, Blanchard JF, Panak EA. The interactions of ticlopidine and aspirin in normal subjects. Journal of International Medical Research 5: 405–411, 1977\nThébault J, Blatrix C, Blanchard J, Panak E. A possible method to control prolongations of bleeding time under antiplatelet therapy with ticlopidine. Thrombosis and Haemostasis 48(1): 6–8, 1982\nTIMAD Study Group. Ticlopidine treatment reduces the progression of nonproliferative diabetic retinopathy. Archives of Ophthalmology, in press, 1990\nTohgi H. The Japanese ticlopidine study in transient ischaemic attack. Sang Thrombose Vaisseaux 4(2): 19–22, 1990\nTohgi H, Murakami M. The effect of ticlopidine on TIA compared with aspirin: a double-blind, twelve-month follow-up study and open 24-month follow-up study. Japanese Journal of Medicine 26: 117–119, 1987\nTraietti P, Chiappini MG, Belfiglio A, Bartoli R, Bologna E. Effect of ticlopidine treatment in haemodialysis patients. La Clinica Therapeutica 127: 27–35, 1988\nUchiyama S, Sone R, Shibagaki Y, Nagayama T, Tsutsumi Y, et al. Antiplatelet effects of combination therapy with low doses of aspirin and ticlopidine in cerebral ischemia. Abstract. Blood Vessels 19: 390–393, 1988\nUgarte M, de Teresa E, Lorenz P, Marin MC, de Artaza M, et al. Intracoronary platelet activation in ischemic heart disease: effects of ticlopidine. American Heart Journal 109: 738–743, 1985\nUK-TIA Study Group. United Kingdom Transient Ischaemic Attack (UK-TIA) aspirin trial: interim results. British Medical Journal 296: 316–320, 1988\nValentin LI, Sicard GA, Freeman MB, Allen BT, McGoff MA, et al. Combined arachidonic acid and ADP platelet inhibition maximises patency of small-diameter vascular grafts. Surgery 104: 178–184, 1988\nVargas R, Reitman M, Teitelbaum P, Ryan JR, McMahon FG, et al. Study of the effect of ticlopidine on digoxin blood levels. Abstract. Clinical Pharmacology and Therapeutics 43(2): 176, 1988\nYamazaki H, Kawagoe S, Yamaguchi A, Munakata J, Kuroki S, et al. Thromboxane A2synthesizing activity of platelets in coronary artery diseases. Japanese Circulation Journal 51: 451–458, 1987\nZorzon M, Monti F, Del Pio Luogo T, Cazzato G. Ticlopidine and pentoxifylline in the treatment of acute non-embolic cerebral infarct: clinical study on 151 patients. Journal of Clinical Medicine 11: 569–572, 1987",{"VOID":1497},"10.2165\u002F00003495-199040020-00006","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.2165\u002F00003495-199040020-00006",[1500,1514,1527],{"id":1501,"sortIndex":32,"researcher":28,"roles":1502,"affiliations":1503,"properties":1512,"displayName":1296,"givenName":28,"familyName":28},"6b8d080d-b12a-41cc-9e16-f57a685be8d1",[970],[1504],{"id":1505,"sortIndex":32,"affiliation":1506,"properties":28},"4b0cc847-1b60-4418-b48e-1bb4ec1f719e",{"id":1505,"createTime":28,"updateTime":28,"relativeEntities":1507,"slug":28,"properties":1508,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1511,"statistic":28},[],{"title":1509},{"VI":1510},"ADIS Drug Information Services, Auckland, New Zealand",[],{"title":1513},{"VI":1296},{"id":1515,"sortIndex":40,"researcher":28,"roles":1516,"affiliations":1517,"properties":1524,"displayName":1526,"givenName":28,"familyName":28},"68fc96f5-3fcd-40a4-a27b-51e26c5d63db",[970],[1518],{"id":1505,"sortIndex":32,"affiliation":1519,"properties":28},{"id":1505,"createTime":28,"updateTime":28,"relativeEntities":1520,"slug":28,"properties":1521,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1523,"statistic":28},[],{"title":1522},{"VI":1510},[],{"title":1525},{"VI":1526},"Diana Faulds",{"id":1528,"sortIndex":123,"researcher":28,"roles":1529,"affiliations":1530,"properties":1537,"displayName":1539,"givenName":28,"familyName":28},"32bbd020-2ef0-416a-bc23-5fe7673257bf",[970],[1531],{"id":1505,"sortIndex":32,"affiliation":1532,"properties":28},{"id":1505,"createTime":28,"updateTime":28,"relativeEntities":1533,"slug":28,"properties":1534,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1536,"statistic":28},[],{"title":1535},{"VI":1510},[],{"title":1538},{"VI":1539},"Karen L. Goa",{"url":1498,"publisher":1541,"properties":1584},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1542,"slug":872,"properties":1543,"entityType":25,"verifyStatus":883,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":47,"subjectFields":1548,"manageAffiliations":1553,"indexDatabases":1564,"url":936,"thumbnailPath":28,"statistic":1579,"gsStatistic":28,"type":28,"analyzePriority":28},[],{"country":1544,"eissn":1545,"issn":1546,"title":1547},{"VOID":875},{"VOID":877},{"VOID":879},{"EN":872},[1549],{"id":886,"createTime":28,"updateTime":28,"relativeEntities":1550,"label":1551,"description":1552,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":889},{},[1554,1559],{"id":893,"createTime":28,"updateTime":28,"relativeEntities":1555,"slug":28,"properties":1556,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1558,"statistic":28},[],{"title":1557},{"EN":897},[],{"id":900,"createTime":28,"updateTime":28,"relativeEntities":1560,"slug":28,"properties":1561,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1563,"statistic":28},[],{"title":1562},{"EN":904},[],[1565,1572],{"id":908,"indexDatabase":1566,"url":914,"indexYears":915,"academicFieldIds":1571,"indexDatabaseRanking":918},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":1567,"label":1568,"description":1569,"key":781,"publicationTags":1570,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],[917],{"id":920,"indexDatabase":1573,"url":932,"indexYears":28,"academicFieldIds":1578,"indexDatabaseRanking":28},{"id":922,"createTime":28,"updateTime":28,"relativeEntities":1574,"label":1575,"description":1576,"key":929,"publicationTags":1577,"standard":28},[],{"EN":925,"VI":925},{"EN":927,"VI":928},[931,813],[934,935],{"impactFactor":32,"impactFactorByYear":1580,"i10Index":32,"i10IndexLast5Year":32,"totalPublication":939,"totalPublicationByYear":1581,"totalCitation":32,"totalCitationByYear":1582,"totalCitationPerPublication":32,"totalCitationPerPublicationByYear":1583,"hindexLast5Year":32,"hindex":32},{},{"1993":40,"2012":941,"2013":357,"2014":48,"2015":49,"2016":123,"2017":49,"2018":46,"2019":46,"2020":48,"2021":357,"2022":46,"2023":145},{},{},{"pages":1585,"volume":1587},{"VOID":1586},"238-259",{"VOID":1588},"40","2012-10-23",[931,918],{"id":1592,"createTime":1593,"updateTime":1594,"relativeEntities":1595,"slug":1596,"properties":1597,"entityType":963,"verifyStatus":26,"verifyTime":1594,"verifyNote":964,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1606,"fullTextUrl":28,"authors":1607,"publicationType":1106,"publisherRelationship":1623,"citationCount":28,"citationInfo":28,"publishDate":1672,"publishYear":1347,"citationAnalyzeStatus":883,"lastCitationAnalyze":28,"indexDatabases":1673,"openAccess":28,"references":28,"isForceReanalyzing":1159},"007e1bc6-7738-4455-94b2-5bec3ab33a7d","2024-01-17T06:53:49.521+00:00","2025-01-03T14:06:42.905+00:00",[],"Use-of-Nitrates-in-the-Treatment-of-Unstable-and-Variant-Angina",{"abstract":1598,"title":1600,"references":1602,"doi":1604},{"EN":1599},"Unstable angina is a clinical syndrome that includes patients with new onset of angina, a change in a previous stable pattern, or the development of chest pain at rest. Generally, more than 90% of patients with this syndrome have significant fixed atherosclerotic coronary artery disease. Other complex, interacting pathophysiological mechanisms may include coronary vasoconstriction, plaque rupture and thrombosis. Therapeutic strategies aim at either reduction of myocardial oxygen demand or restoration of coronary blood flow. Both alternatives have been suggested as treatment of choice. However, as long as the pathophysiological mechanism(s) is unknown in the individual case, the treatment will mainly be empirical or based on results from clinical trials of heterogeneous groups of patients with unstable angina with probably varying aetiology. The results from such studies indicate that some strategies may be of value, but others may even be harmful in treatment of patients with this unstable syndrome. In this situation nitrates seem to be a safe drug which may be used in most forms of angina irrespective of the underlying pathophysiological mechanism(s).",{"EN":1601},"Use of Nitrates in the Treatment of Unstable and Variant Angina",{"VOID":1603},"Alison HW, Russell RO, Mantle JA, Kouchoukos NT, Moraski RE, et al. Coronary anatomy and arteriography in patients with unstable angina pectoris. American Journal of Cardiology 41: 204–209, 1978\nBertrand ME, LaBlanche JM, Tilmant PY, Thieuleux FA, Delforge MR, et al. Frequency of provoked coronary arterial spasm in 1089 consecutive patients undergoing coronary arteriography. Circulation 65: 1299–1306, 1982\nBorn GVR. Arterial thrombosis and its prevention. In Hayase, Murao (Eds) Proceedings of the VIII World Congress of: Cardiology, pp. 81–91, Excerpta Medica, Amsterdam, 1979\nBresnahan DR, Davis JL, Holmes DR, Smith HC. Angiographic incidence and clinical correlates of intra-luminal coronary thrombus. 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New England Journal of Medicine 309: 685–689, 1983\nMuller JE, Turi ZG, Pearle DL. Nifedipine and conventional therapy for unstable angina pectoris: a randomized, double-blind comparison. Circulation 69: 728–739, 1984\nNordlander R, Orinius E. Ergonovine testing in patients with exertional angina. Acta Medica Scandinavica, in press\nPage A, Gateau P, Ohayon J, et al. Intravenous nitroglycerin in unstable angina. In Lichtlen et al. (Eds) Nitrate III, cardiovascular effects, pp. 371–376, Springer Verlag, New York, 1981\nParodi O, Maseri A, Simonetti I. Management of unstable angina at rest by verapamil. A double-blind, cross-over study in coronary care unit. British Heart Journal 41: 167–174, 1979\nPucillo AL, Reison DS, Cannon PJ, Powers ER. Systemic and coronary hemodynamics during intravenous nitroglycerin infusion in patients with unstable angina. Journal of the American College of Cardiology 5: 505, 1985\nRackley CE. Role of isosorbide dinitrate in patients with unstable angina pectoris. American Heart Journal 110: 269–272, 1985\nRobertson RM, Wood AJ, Vaughn WK, Robertson D. Exacerbation of vasotonic angina pectoris by propranolol. Circulation 65: 281–285, 1982\nRoubin GS, Harris PJ, Eckhardt I, Hensley W, Kelly DT. Intravenous nitroglycerin in refractory unstable angina pectoris. Australian and New Zealand Journal of Medicine 12: 598–602, 1982\nSquire A, Cantor R, Packer M. Limitations of confusuous intravenous nitroglycerin prophylaxis in patients with refractory angina at rest. Circulation 66: 11–120, 1982\nTelford AM, Wilson C. Trial of heparin versus atenolol in prevention of myocardial infarction in intermediate coronary syndrome. Lancet 1: 1225–1228, 1981\nThéroux P, Taeymans Y, Morissette D, Bosch X, Pelletier GB, et al. A randomized study comparing propranolol and diltiazem in the treatment of unstable angina. Journal of the American College of Cardiology 5: 717–722, 1985\nVetrovec GW, Cowley MJ, Overtou H, Richardson DW. Intracoronary thrombus in syndrome of unstable myocardial ischemia. American Heart Journal 102: 1202–1208, 1981",{"VOID":1605},"10.2165\u002F00003495-198700334-00025","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.2165\u002F00003495-198700334-00025",[1608],{"id":1609,"sortIndex":32,"researcher":28,"roles":1610,"affiliations":1611,"properties":1620,"displayName":1622,"givenName":28,"familyName":28},"c54efaa8-e69b-4207-b1a9-1260fe2dd7f5",[970],[1612],{"id":1613,"sortIndex":32,"affiliation":1614,"properties":28},"6ced0dea-0294-4392-80b4-ca20ef476adf",{"id":1613,"createTime":28,"updateTime":28,"relativeEntities":1615,"slug":28,"properties":1616,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1619,"statistic":28},[],{"title":1617},{"VI":1618},"Division of Cardiology, Department of Medicine, Thoracic Clinics, Karolinska Hospital, Stockholm, Sweden",[],{"title":1621},{"VI":1622},"Rolf Nordlander",{"url":1606,"publisher":1624,"properties":1667},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1625,"slug":872,"properties":1626,"entityType":25,"verifyStatus":883,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":47,"subjectFields":1631,"manageAffiliations":1636,"indexDatabases":1647,"url":936,"thumbnailPath":28,"statistic":1662,"gsStatistic":28,"type":28,"analyzePriority":28},[],{"country":1627,"eissn":1628,"issn":1629,"title":1630},{"VOID":875},{"VOID":877},{"VOID":879},{"EN":872},[1632],{"id":886,"createTime":28,"updateTime":28,"relativeEntities":1633,"label":1634,"description":1635,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":889},{},[1637,1642],{"id":893,"createTime":28,"updateTime":28,"relativeEntities":1638,"slug":28,"properties":1639,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1641,"statistic":28},[],{"title":1640},{"EN":897},[],{"id":900,"createTime":28,"updateTime":28,"relativeEntities":1643,"slug":28,"properties":1644,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1646,"statistic":28},[],{"title":1645},{"EN":904},[],[1648,1655],{"id":908,"indexDatabase":1649,"url":914,"indexYears":915,"academicFieldIds":1654,"indexDatabaseRanking":918},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":1650,"label":1651,"description":1652,"key":781,"publicationTags":1653,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],[917],{"id":920,"indexDatabase":1656,"url":932,"indexYears":28,"academicFieldIds":1661,"indexDatabaseRanking":28},{"id":922,"createTime":28,"updateTime":28,"relativeEntities":1657,"label":1658,"description":1659,"key":929,"publicationTags":1660,"standard":28},[],{"EN":925,"VI":925},{"EN":927,"VI":928},[931,813],[934,935],{"impactFactor":32,"impactFactorByYear":1663,"i10Index":32,"i10IndexLast5Year":32,"totalPublication":939,"totalPublicationByYear":1664,"totalCitation":32,"totalCitationByYear":1665,"totalCitationPerPublication":32,"totalCitationPerPublicationByYear":1666,"hindexLast5Year":32,"hindex":32},{},{"1993":40,"2012":941,"2013":357,"2014":48,"2015":49,"2016":123,"2017":49,"2018":46,"2019":46,"2020":48,"2021":357,"2022":46,"2023":145},{},{},{"pages":1668,"volume":1670},{"VOID":1669},"131-139",{"VOID":1671},"33","2012-11-22",[931,918],{"id":1675,"createTime":1676,"updateTime":1677,"relativeEntities":1678,"slug":1679,"properties":1680,"entityType":963,"verifyStatus":26,"verifyTime":1677,"verifyNote":964,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1687,"fullTextUrl":28,"authors":1688,"publicationType":1106,"publisherRelationship":1704,"citationCount":28,"citationInfo":28,"publishDate":1482,"publishYear":1347,"citationAnalyzeStatus":883,"lastCitationAnalyze":28,"indexDatabases":1753,"openAccess":28,"references":28,"isForceReanalyzing":1159},"007e9a46-2573-4e95-b377-50f536a8088a","2023-12-18T03:43:46.727+00:00","2025-02-24T00:41:30.839+00:00",[],"Prophylactic-Agents-for-Thrombosis",{"title":1681,"references":1683,"doi":1685},{"EN":1682},"Prophylactic Agents for Thrombosis",{"VOID":1684},"Harker, L.A. and Slichter, S.J.: Studies of platelet and fibrinogen kinetics in patients with prosthetic heart valves. New England Journal of Medicine 283: 1302–1305 (1970).\nDodman, B.; Conliffe, W.J.; Roberts, B.E. and Sibbald, R.: Clinical and laboratory double-blind investigation on effect of fibrinolytic therapy in patients with cutaneous vasculitis. British Medical Journal 2: 82–84 (1973).\nBoston Collaborative Drug Surveillance Group: Regular aspirin intake and acute myocardial infarction. British Medical Journal 1: 440–443 (1974).\nElwood, P.C.; Cochrane, A.L.; Burr, M.L.; Sweetman, P.M.; Williams, G.; Welsby, E.; Hughes, S.J. and Renton, R.: A randomised controlled trial of acetyl salicylic acid in the secondary prevention of mortality from myocardial infarction. British Medical Journal 1: 436–440 (1974).",{"VOID":1686},"10.2165\u002F00003495-197509010-00001","http:\u002F\u002Flink.springer.com\u002F10.2165\u002F00003495-197509010-00001",[1689],{"id":1690,"sortIndex":32,"researcher":28,"roles":1691,"affiliations":1692,"properties":1701,"displayName":1703,"givenName":28,"familyName":28},"68e8b57a-392d-4e49-8d48-132ca9aedf77",[970],[1693],{"id":1694,"sortIndex":32,"affiliation":1695,"properties":28},"4b0b4e01-350d-427c-84e1-27e8c1dcc128",{"id":1694,"createTime":28,"updateTime":28,"relativeEntities":1696,"slug":28,"properties":1697,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1700,"statistic":28},[],{"title":1698},{"VI":1699},"Department of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Australia",[],{"title":1702},{"VI":1703},"P. A. 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Allergic rhinitis. N Engl J Med 1991; 325: 860–9",{"VOID":1764},"10.2165\u002F00003495-199855020-00013","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.2165\u002F00003495-199855020-00013",[1767],{"id":1768,"sortIndex":32,"researcher":28,"roles":1769,"affiliations":1770,"properties":1779,"displayName":1781,"givenName":28,"familyName":28},"228731bb-440b-45ab-b2b3-9699ddaec34d",[970],[1771],{"id":1772,"sortIndex":32,"affiliation":1773,"properties":28},"2e18f11a-a47d-4bb3-81b6-419016c16224",{"id":1772,"createTime":28,"updateTime":28,"relativeEntities":1774,"slug":28,"properties":1775,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1778,"statistic":28},[],{"title":1776},{"VI":1777},"Asthma and Allergy Research Center, Orange, USA",[],{"title":1780},{"VI":1781},"Stanley P. 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In clinical trials in patients with rheumatic diseases or pain arising from other conditions, it was as effective an analgesic as standard piroxicam, and showed a faster onset of action on the first day of treatment. In short term pharmacodynamic studies in healthy volunteers, piroxicam-β-cyclodextrin was equivalent to or tended to show less gastrointestinal mucosal toxicity than standard piroxicam, as assessed by endoscopy and faecal blood loss. However, no data are available on its comparative gastrointestinal mucosal effects from long term clinical trials using similar measures. Preliminary findings from a clinical study suggest piroxicam-β-cyclodextrin caused fewer gas-troduodenal lesions than tenoxicam. As with other NSAIDs, the majority of adverse events associated with piroxicam-β-cyclodextrin in clinical trials were gastrointestinal in origin, with epigastric pain, heartburn and nausea the most common. Thus, piroxicam-β-cyclodextrin is an effective agent in patients with rheumatic diseases or other pain states. When rapid analgesia is required in the initial treatment of acute pain, the faster onset of action of piroxicam-β-cyclodextrin may be an advantage over the parent compound; however, this is unlikely to be important during long term therapy. The results of further long term trials are awaited before firm conclusions can be reached regarding the gastrointestinal tolerability of piroxicam-β-cyclodextrin compared with that of standard piroxicam and other NSAIDs. Piroxicam-β-cyclodextrin is a NSAID with anti-inflammatory, analgesic and antipyretic properties. Limited data available on the analgesic and anti-inflammatory effects of piroxicam-β-cyclodextrin suggest that it is equivalent to piroxicam in animal and human models of pain. The effects of piroxicam-β-cyclodextrin on the gastrointestinal mucosa have been more extensively studied. Findings from endoscopy and faecal blood loss studies suggest that piroxicam-β-cyclodextrin is equivalent to, or shows a trend to be less toxic than, the parent molecule in healthy volunteers aged 20 to 50 years. However, none of these trends reached statistical significance. In these studies, total endoscopy scores were similar for both drugs. In 2 studies of 1 month’s duration, piroxicam-β-cyclodextrin 20 mg\u002Fday tended to cause less cumulative faecal blood loss than piroxicam 20 mg\u002Fday after 2 to 4 weeks’ treatment. In all studies piroxicam-β-cyclodextrin showed a trend towards greater gastric mucosal damage, or significantly more damage, than placebo. Administration of piroxicam-β-cyclodextrin as a single dose in fasting volunteers resulted in mean plasma piroxicam concentrations 0.25 and 0.5 hours after administration that were, respectively, 3 to 10 and 1.3 to 3 times higher than after standard piroxicam administration in 2 comparative studies. Although food slowed the absorption from both products, plasma concentrations of piroxicam were still 2 to 4 and 1.3 to 1.4 times higher 0.5 and 2 hours after administration of piroxicam-β-cyclodextrin than after standard piroxicam. However, after multiple-dose administration the only difference was at 0.25 hours after administration, when the plasma concentration of piroxicam was 1.3 times higher after piroxicam-β-cyclodextrin than piroxicam. The area under the plasma concentration-time curve was similar for piroxicam-β-cyclodextrin 20mg and Piroxicam 20mg, demonstrating a comparable overall extent of absorption. Post-absorption pharmacokinetic parameters were similar for piroxicam-β-cyclodextrin and piroxicam. The volume of distribution was 0.14 L\u002Fkg and the mean terminal elimination half-life was 40 to 63 hours. The main route of elimination of piroxicam is metabolism, with only trace amounts of unchanged drug excreted in the urine. In patients with acute pain resulting from arthritis and other rheumatic disease, the analgesic efficacy of piroxicam-β-cyclodextrin was equivalent to that of piroxicam when both were administered once daily at a dose of 20mg for up to 12 weeks. Anti-inflammatory effects of the 2 agents were also equivalent in the study that assessed this. In 2 studies measuring the onset of analgesic effect, piroxicam-β-cyclodextrin was significantly more effective, or showed a trend towards greater efficacy, than piroxicam in the 4 hours after the first dose. In a further 2 studies the analgesic effects of piroxicam-β-cyclodextrin and piroxicam on the second or third day of administration were similar. In other comparative studies in patients with rheumatic pain, piroxicam-β-cyclodextrin 20 mg\u002Fday was superior in analgesic efficacy to dipyrone 500mg 3 times daily, at least as effective as etodolac 200mg twice daily, and equivalent in efficacy to tenoxicam 20 mg\u002Fday and nabumetone 1000 mg\u002Fday. In studies also investigating the onset of analgesia in the first few hours after the first dose, piroxicam-β-cyclodextrin 20mg appeared to show a faster onset of action than tenoxicam 20mg, nabumetone 1000mg, etodolac 200mg and dipyrone 500mg. Orally administered piroxicam-β-cyclodextrin 20mg as a granule formulation was equivalent in analgesic effect over 12 hours to diclofenac 75mg and ketoprofen 100mg, both administered by deep intramuscular injection. In patients with postoperative pain or pain arising from acute musculoskeletal disorders, piroxicam-β-cyclodextrin 20 mg\u002Fday was equivalent to piroxicam 20 mg\u002Fday in relieving pain but the onset of its effect was generally faster in the first hour after the first dose. Piroxicam-β-cyclodextrin has also demonstrated efficacy in the treatment of pain arising from primary dysmenorrhoea, headache or dental extraction. Piroxicam-β-cyclodextrin would be expected to demonstrate a tolerability profile similar to that of standard piroxicam. However, it has been postulated that reducing the time piroxicam spends in the gastrointestinal tract by complexation with β-cyclodextrin may result in less direct mucosal damage and hence better gastrointestinal tolerability. Short term studies in healthy volunteers suggest a possible trend towards less gastrointestinal toxicity for piroxicam-β-cyclodextrin, but this hypothesis has not been adequately studied in clinical trials. Long term studies comparing piroxicam-β-cyclodextrin with piroxicam in terms of endoscopy score and\u002For faecal blood loss measurement are awaited. Data from clinical trials indicate that the principal adverse events involve the gastrointestinal tract. In 2 large short term phase IV studies, 11.3 and 13.5% of patients receiving piroxicam-β-cyclodextrin 20 mg\u002Fday reported an adverse event; 67 and 77% of these were gastrointestinal in origin, including epigastric pain, heartburn and nausea. Severe adverse reactions such as gastrointestinal bleeding or gastroduodenal ulcer were seen in 0.2% of 9105 patients. The pattern of adverse events from a longer term trial (3 to 6 months) was broadly similar. In a double-blind comparative trial in 203 patients with rheumatic disease, the number of gastrointestinal adverse events in piroxicam-β-cyclodextrin recipients was 16 and that in piroxicam recipients was 24; 5 and 8 patients, respectively, withdrew because of the adverse event. In 1 study, piroxicam-β-cyclodextrin 20 mg\u002Fday caused fewer upper gastrointestinal tract lesions than tenoxicam 20 mg\u002Fday over 8 weeks. For the treatment of pain and inflammation, the recommended dosage of piroxicam-β-cyclodextrin is 20mg administered once daily as a tablet or granules. Higher dosages of 30 to 40 mg\u002Fday may be required in some patients, but these are expected to be associated with a greater incidence of gastrointestinal adverse effects. A maintenance dosage of 10 mg\u002Fday may be appropriate in some patients, particularly the elderly. As with other NSAIDs, the use of piroxicam-β-cyclodextrin is contraindicated in patients with active peptic ulceration, and the drug should be used cautiously in patients with a history of upper gastrointestinal tract disease.",{"EN":1843},"Piroxicam-β-Cyclodextrin",{"VOID":1845},"Szejtli J. Cyclodextrins: properties and applications. Drag Invest 1990; 2 Suppl.4: 11–21\nRainsford KD. NSAID gastropathy: novel physicochemical approaches for reducing gastric mucosal injury by drug com-plexation with cyclodextrins. Drug Invest 1990; 2 Suppl.4: 3–10\nGerlóczy A, Fónagy A, Keresztes P, et al. Absorption, distribution, excretion and metabolism of orally administered 14C-β-cyclodextrin in rat. Arzneimittel Forschung 1985; 35: 1042–7\nCadel S, Bongrani S. Toxicological profile of piroxicam-β-cyclodextrin. Drug Invest 1990; 2 Suppl.4: 37–41\nBrogden RN, Heel RC, Speight TM, et al. Piroxicam: a reappraisal of its pharmacology and therapeutic efficacy. Drugs 1984; 28: 292–323\nCadel S, Bongrani S. β-Cyclodextrin complexation improves absorption and gastric tolerability of piroxicam [abstract]. Acta Physiol Hung 1990; 75 Suppl: 45-6\nLister RE, Acerbi D, Cadel S. Supermolecular inclusion of piroxicam with β-cyclodextrin: a review of its pharmacological properties in laboratory animals. Eur J Rheumatol Inflamm 1993; 12(4):6-11\nDolci G, Gatto R, Malagnino V. Effetto analgesico piroxicam-β-cyclodestrina sul dolore dentale indotto. Studio controllato in doppio cieco. Odontostomatol Implantoprotesi 1989 (1 Suppl.): 3-6\nRainsford KD. Mechanisms of gastrointestinal toxicity of nonsteroidal anti-inflammatory drugs. Scand J Gastroenterol 1989; 24 Suppl.163: 9–16\nWallace JL. Pathogenesis of nonsteroidal anti-inflammatory drug gastropathy: recent advances. Eur J Gastroenterol Hepatol 1993; 5: 403–7\nHayllar J, Macpherson A, Bjarnason I. Gastroprotection and nonsteroidal anti-inflammatory drugs (NSAIDs). Rationale and clinical implications. Drug Saf 1992; 7: 86–105\nLevi S, Shaw-Smith C. Non-steroidal anti-inflammatory drugs: how do they damage the gut?. Br J Rheumatol 1994; 33: 605–12\nNuutinen LS, Laitinen JO, Salomäki TE. A risk-benefit appraisal of injectable NSAIDs in the management of postoperative pain. Drug Saf 1993; 9: 380–93\nAabakken L. NSAID-associated gastrointestinal damage: methodological considerations and a review of the experience with enteric coated naproxen. Eur J Rheumatol Inflamm 1992; 12 (2): 9–20\nNervetti A, Ambanelli U, Ugolotti G. Assessment of gastric mucosal damage by a new inclusion complex of piroxicam with β-cyclodextrin: a functional study by a scintigraphic method. J Drug Dev 1991; 4 Suppl.1: 39–42\nPatoia L, Clausi G, Farroni F, et al. Comparison of faecal blood loss, upper gastrointestinal mucosal integrity and symptoms after piroxicam beta-cyclodextrin, piroxicam and placebo administration. Eur J Clin Pharmacol 1989; 36: 599–604\nSantucci L, Fiorucci S, Chiucchiu S, et al. Placebo-controlled comparison of piroxicam-β-cyclodextrin piroxicam and indo-methacin on gastric potential difference and mucosal injury in humans. Dig Dis Sci 1992; 37: 1825–32\nWarrington S, Debbas N, Farthing M, et al. Piroxicam-beta-cyclodextrin: effects on gastrointestinal blood loss and gastric mucosal appearance in healthy men. Int J Tissue React 1991; 13 (5): 243–8\nWarrington S. Effects of piroxicam-beta-cyclodextrin on the gastrointestinal tract. Eur J Rheumatol Inflamm 1993; 12 (4): 29–37\nData on file, Creemers MCW, Van Riel PLCM, et al. Gastro-intestinal toxicity during non-steroidal antiinflammatory drugs in ankylosing spondylitis: increased fecal blood loss, and evidence for gastric adaptation in a 48-week clinical trial. Chiesi Farmaceutici S.p.A, 1993.\nMcCormack K, Brune K. Dissociation between the antinociceptive and anti-inflammatory effects of the nonsteroidal anti-inflammatory drugs: a survey of their analgesic efficacy. Drugs 1991; 41: 533–47\nAbramson S, Weissmann G. The mechanism of action of nonsteroidal antiinflammatory drugs. Clin Exp Rheumatol 1989; 7 Suppl.3: 163–70\nUrquhart E. Central analgesic activity of nonsteroidal antiinflammatory drugs in animal and human pain models. Semin Arthritis Rheum 1993; 23: 198–205\nBannwarth B, Demotes-Mainard F, Schæverbeke T, et al. Where are peripheral analgesics acting? [leader]. Ann Rheum Dis 1993; 52: 1–4\nOlkkola KT, Brunetto AV, Mattila MJ. Pharmacokinetics of oxicam nonsteroidal anti-inflammatory agents. Clin Phar-macokinet 1994; 26: 107–20\nRichardson CJ, Ross SG, Bloka K, et al. High-performance liquid chromatographic analysis of piroxicam and it major metabolite 5′-hydroxypiroxicam in human plasma and urine. J Chromatogr 1986; 382: 382–8\nWoodcock BG, Acerbi D, Merz PG, et al. Supermolecular inclusion of piroxicam with β-cyclodextrin: pharmaokinetic properties in man. Eur J Rheumatol Inflamm 1993; 12: 12–28\nPiroxicam-β-cyclodextrin prescribing information. Chiesi Farmaceutici SpA, Parma, Italy, 1993.\nAcerbi D. Pharmacokinetic profile of piroxicam-β-cyclodextrin. Drug Invest 1990; 2 Suppl.4: 42–9\nAcerbi D, Bovis G, Carli F, et al. Biopharmaceutical optimisation of β-cyclodextrin inclusion compounds. Drug Invest 1990; 2 Suppl.4: 29–36\nAcerbi D, Bonati C, Boscarino G, et al. Pharmacokinetic study on piroxicam at the steady-state in elderly subjects and younger adults after administration of piroxicam beta-cyclo-dextrin. Int J Clin Pharmacol Res 1988; 8: 175–80\nAcerbi D, Lebacq Jr E, Rondelli I, et al. Rapid oral absorption profile of piroxicam from its β-cyclodextrin complex. Drug Invest 1990; 2 Suppl.4: 50–5\nOral bioavailability of CHF1194, an inclusion complex of piroxicam and β-cyclodextrin, in healthy subjects under single dose and steady-state conditions [editorial]. Eur J Clin Pharmacol. In press\nData on file, Biopharma S.A. Bioavailability comparison study of CHF1194 fast-disintegration tablets and Feldene capsules (20mg piroxicam) in 12 healthy volunteers. Study reference 88.129. Data on file. Chiesi Farmaceutici S.p.A, Italy, 1988.\nMichelacci M, Boscarino G, Acerbi D, et al. Analgesic effect and pharmacokinetics of a piroxicam beta-cyclodextrin oral formulation in post-surgical pain. A controlled study vs. an injectable piroxicam formulation. Clin Trials J 1990; 27 (3): 176–86\nNetter P, Bannwarth B, Royer-Morrot M-J. Recent findings on the pharmacokinetics of nonsteroidal anti-inflammatory drugs in synovial fluid. Clin Pharmacokinet 1989; 17: 145–62\nWoolf TF, Radulovic LL. Oxicams: metabolic disposition in man and animals. Drug Metab Rev 1989; 21: 255–76\nBufalino L, Oliani C, Gardini F, et al. Studio multicentrico sugli effetti di piroxicam-beta-ciclodestrina nel trattamento delgi stati dolorosi acuti a diversa etiologia. Basi Raz Ter 1990; 20: 227–39\nAmbanelli U, Nervetti A, Colombo B, et al. Piroxicam-beta-cyclodextrin in the treatment of rheumatic diseases: a prospective study. Curr Ther Res 1990; 48: 58–68\nGiungi F. Tollerabilità ed efficacia di un trattamento a base di piroxicam beta-ciclodestrina in patologie osteoartrosiche con elevata risposta algica studio controllato contro piroxicam. Med Praxis 1987; 8 (2): 1–12\nManzini CU, Mascia MT, Oliani C, et al. Analgesic activity of piroxicam-beta-cyclodextrin complex (granulate formulation) in the treatment of osteoarthritic pain [in Italian]. Arch Med Interna 1989; 41: 189–99\nMinisola G, Dardano B. Valutazione dell’attività antalgica e delia tollerabilità del piroxicam nel dolore crónico da cervicoartrosi e da lombartrosi. Clin Ter 1989; 131: 73–82\nReginster JY, Franchimont P. Piroxicam-beta-cyclodextrin in the treatment of acute pain of rheumatic disease. Eur J Rheumatol Inflamm 1990; 12 (4): 38–46\nData on file, Nardelli P, Marino G, et al. Piroxicam-β-cyclodextrin in the treatment of rheumatic pain. A controlled trial vs piroxicam capsules. Data on file. Cheisi Farmacuetici S.p.A, 1990.\nAbate G, Zito M, Guarino F, et al. Il dolore osteoartritico: terapia con oxicam-derivati. Eur Rev Med Pharmacol Sci 1990; 12: 273–81\nBonardelli P, Oliani C, Preti PAM, et al. Efficacy and gastrointestinal tolerability of beta-cyclodextrin-piroxicam and ten-oxicam in the treatment of chronic osteoarthritis. Clin Ther 1990; 12: 547–55\nGhirardini M, Betelemme L, Fatti F. Studio di confronto tra droxicam e β-ciclodestrina-piroxicam nel trattamento dell’osteoartrosi e del reumatismo extra-articolare. Reumatologo 1993; 14: 145–7\nCasale G, Oricchio P, Alfonsi A. Attività antalgica del complesso β-ciclodestrina-Piroxicam nelle forme croniche. Arch Med Interna 1991; 43: 157–64\nDavoli L, Ciotti G, Biondi M, et al. Piroxicam-beta-cyclodextrin in the treatment of low-back pain. Curr Ther Res 1989; 46: 940–7\nGospodinoff A, Minisola G. β-Ciclodestrina-piroxicam vs meclofenamato sódico nel dolore osteoartrosico. Algos 1990; 7 (4): 49–55\nLa Montagna G, Parenti M, Oliani C, et al. Beta-ciclodestrina-piroxicam nel trattamento delle fasi attive della patologia osteoartrosica. Eur Rev Med Pharmacol Sci 1990; 12: 265–72\nPortioli RI, Casoli P, Tumiati B. II complesso piroxicam-beta-ciclodestrina nel trattamento dell’osteoartrosi e del reumatismo extra-articolare: studio clinico controllato. Reumatologo 1989; 10: 104–7\nRiccieri V, Spadaro A, Zoppini A. Utilizzo del complesso beta-ciclodestrina piroxicam nella patologia osteoartrosica: studio controllato vs diclofenac sódico. Arch Med Interna 1990; 42: 189–99\nRossetti A, Musiari L, Bonati PL, et al. Trattamento del dolore osteoartrosico con PBC. Studio clinico controllato verso metamizolo. Algos 1988; 5 (4): 30–5\nTamburro P, Galasso G. Studio clinico controllato sull’effetto antalgico del complesso piroxicam-beta-ciclodestrina nel dolore acuto muscolo-scheletrico e\u002Fo articulare. Reumatologo 1989; 10: 237–41\nSimone C, Oliani C. Beta-cyclodextrin-piroxicam: efficacy and tolerability in the treatment of pain after bone and joint surgery. Curr Ther Res 1990; 47: 541–7\nZezza AR, Cosco Mazzuca R, Giuntini C, et al. Valutazione dell’effetto analgesico del piroxicam-betaciclodestrina per os nel trattamento del dolore traumatologico e post-operatorio in ortopedia. Studio controllato vs piroxicam iniettabile. Orto-ped Traumatol Oggi 1988; 8: 255–61\nDi Matteo L, Fratelli V, Oliani C, et al. Shoulder rotator cuff tendinitis: efficacy and tolerability of piroxicam-beta-cyclodextrin complex [in Italian]. Arch Med Interna 1989; 41: 261–72\nGalasso G, Tamburro P, Vecchiet L. Analgesic activity of beta-cyclodextrin-piroxicam and tenoxicam in acute soft tissue injuries. Adv Ther 1990; 7: 43–50\nTamburro P, Galasso G. Efficacia e tollerabilità del piroxicam-beta-ciclodestrina nel trattamento del dolore muscolo-scheletrico. Reumatologo 1989; 10: 104–7\nTamburro P, Galasso G. A controlled trial of β-cyclodextrin-piroxicam versus tiaprofenic acid in the treatment of painful states from inflammation or trauma of periarticular soft-tissues [in Italian]. Arch Med Interna 1990; 42: 73–82\nZarotti F, Boscarino G, Serra G, et al. Trattamento del dolore muscolo-scheletrico a diversa etiologia con complesso piroxicam beta-ciclodestrina. Ortoped Traumatol Oggi 1988; 8: 305–12\nCosta S, Mioli M, Ravaioli R, et al. Prostaglandin synthetase inhibitor piroxicam beta-cyclodextrin in the treatment of primary dysmenorrhea. Curr Ther Res 1987; 42: 156–64\nData on file, Di Renzo GC, Gori F, et al. Efficacy and tolerability of piroxicam-beta-cyclodextrin in the treatment of primary dysmenorrhea. Report 20.00\u002FCT\u002F01\u002F90. Data on file. Cheisi Farmaceutici S.p.A, 1990.\nGualdi F, Pagliani A, Dessanti L, et al. Trattamento della dismenorrea primaria con il complesso piroxicam-betaciclodestrina. Giorn It Ost Gin 1989; 11: 77–82\nZinelli G, Dessanti L, Ventura A, et al. It trattamento farmacológico della dismenorrea primaria: studio clinico controllato con piroxicam beta-ciclodestrina. Giorn It Ost Gin 1986; 8: 679–87\nBruno E, Porcellini A, Farronato GP, et al. Il dolore post-es-trattivo, trattamento analgesico con piroxicam. Dental Cadmos 1987; 14: 61–8\nData on file, Umile A, Monici Preti PA, et al. Double-blind parallel comparison of single oral doses of piroxicam-β-cyclodextrin, piroxicam, paracetamol and placebo with moderate to severe pain following oral surgery (3rd molar extraction). Clinical trial no. 20.00\u002FCT\u002F06\u002F91. Chiesi Farmaceutici S.p.A., 1993.\nDolci G, Ripari M, Pacifici L, et al. Analgesic efficacy and tolerability of piroxicam-β-cyclodextrin in comparison with piroxicam, paracetamol and placebo in the treatment of postsurgical dental pain [in Italian]. Minerva Stomatol 1993; 42: 235–41\nMarcucci M, Panelli G, Cambini S. Clinical experience in the treatment of dental pain. Clin J Pain 1991; 7 Suppl. 1: S72-6\nGiacovazzo M, Martelletti P, Zaurito V, et al. Effetto antalgico acuto del complesso piroxicam-beta-ciclodestrina nel trattamento della cefalea. G Neuropsicofarmacol 1989; 11: 31–55\nGiacovazzo M, Martelletti P, Zaurito V. Piroxicam-beta-ciclodestrina nel trattamento della cefalea: effetto antalgico acuto e prevenzione dell’insorgenza delle crisi cefalalgiche. G Neuropsicofarmacol 1990; 12: 27–33\nGranella F, Dadatti A, Bizzi P, et al. Trattamento dell’emicrania comune con il complesso piroxicam-beta-ciclodestrina. G Neuropsicofarmacol 1989; 11: 253–8\nMicieli C, Iannacchero R, Tassorelli C, et al. Effetto antalgico del complesso piroxicam-beta-ciclodestrina nel trattamento dell’emicrania comune. G Neuropsicofarmacol 1989; 11: 170–3\nLemmel EM. Gastrointestinal tolerability of piroxicam-β-cyclodextrin in the treatment of painful joint and spine complaints due to osteoarthritis or inflammatory rheumatism [abstract no. V9]. Klinische Pharmakologie aktuell 1993 (2): 39\nData on file, Dreiser RL, Umile A, et al. Piroxicam-beta-cyclodextrin in the treatment of rheumatic disease. A multicentric, long-term (6 months), open study in Belgium, France and The Netherlands. Clinical trial no. 20.00\u002FCT\u002F09\u002F90. Chiesi Farmaceutici S.p.A. 1993.\nPiroxicam prescribing information. Pfizer Ltd, UK, 1993.\nDel Favero A. Anti-inflammatory analgesics and drugs used in rheumatiod arthritis and gout. In: Dukes MNG, Beeley L, editors. Side effects of drugs annual, v. 12. Amsterdam: Elsevier Science Publishers B.V., 1988: 91-100\nLaporte J-R, Carne X, Vidal X, et al. Upper gastrointestinal bleeding in relation to previous use of analgesics and non-steroidal anti-inflammatory drugs. Lancet 1991; 337: 85–9\nGabriel SE, Jaakkimainen L, Bombardier C. Risk for serious gastrointestinal complications related to use of nonsteroidal anti-inflammatory drugs: a meta-analysis. Ann Intern Med 1991; 115: 787–96\nSavage RL, Moller PW, Ballantyne CL, et al. Variation in the risk of peptic ulcer complications with nonsteroidal antiinflammatory drug therapy. Arthritis Rheum 1993; 36: 84–90\nKaufman DW, Kelly JP, Sheehan JE, et al. Nonsteroidal anti-inflammatory drug use in relation to major upper gastrointestinal bleeding. Clin Pharmacol Ther 1993; 53: 485–94\nGarcía Rodríguez LA, Jick H. Risk of upper gastrointestinal bleeding and perforation associated with individual non-steroidal anti-inflammatory drugs. Lancet 1994; 343: 769–72\nLangman MJS, Weil J, Wainwright P, et al. Risks of bleeding peptic ulcer associated with individual non-steriodal anti-inflammatory drugs. Lancet 1994; 343: 1075–8\nHawkey CJ. Non-steroidal anti-inflammatory drugs and peptic ulcers. Facts and figures multiply but do they add up. BMJ 1990; 300: 278–84\nBarradell LB, Whittington R, Benfield P. Misoprostol: pharmacoeconomics of its use as prophylaxis against gastroduodenal damage induced by nonsteroidal anti-inflammatory drugs. PharmacoEconomics 1993; 3: 140–70\nFriedel HA, Langtry HD, Buckley MM. Nabumetone: a reappraisal of its pharmacology and therapeutic use in rheumatic diseases. Drugs 1993; 45: 131–56\nBalfour JA, Buckley MM-T. Etodolac: a reappraisal of its pharmacology and therapeutic use in rheumatic diseases and pain states. Drugs 1991; 42: 274–99\nLanza FL. Gastrointestinal toxicity of newer NSAIDs. Am J Gastroenterol 1993; 88: 1318–23\nSkeith KJ, Wright M, Davis P. Differences in NSAID tolerability profiles: fact or fiction?. Drug Saf 1994; 10: 183–95\nRees Willet L, Carson JL, Strom BL. Epidemiology of gastrointestinal damage associated with nonsteroidal anti-inflammatory drugs. Drug Saf 1994; 10: 170–81",{"VOID":1847},"10.2165\u002F00003495-199448060-00007","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.2165\u002F00003495-199448060-00007",[1850,1863],{"id":1851,"sortIndex":32,"researcher":28,"roles":1852,"affiliations":1853,"properties":1860,"displayName":1862,"givenName":28,"familyName":28},"53d98d40-3dfd-499a-8add-2056e52dbc22",[970],[1854],{"id":1274,"sortIndex":32,"affiliation":1855,"properties":28},{"id":1274,"createTime":28,"updateTime":28,"relativeEntities":1856,"slug":28,"properties":1857,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1859,"statistic":28},[],{"title":1858},{"VI":1279},[],{"title":1861},{"VI":1862},"C. Rhoda Lee",{"id":1864,"sortIndex":40,"researcher":28,"roles":1865,"affiliations":1866,"properties":1873,"displayName":1875,"givenName":28,"familyName":28},"2e72007d-d46b-42d3-b669-c2dd5380722c",[970],[1867],{"id":1274,"sortIndex":32,"affiliation":1868,"properties":28},{"id":1274,"createTime":28,"updateTime":28,"relativeEntities":1869,"slug":28,"properties":1870,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1872,"statistic":28},[],{"title":1871},{"VI":1279},[],{"title":1874},{"VI":1875},"Julia A. Balfour",{"url":1848,"publisher":1877,"properties":1920},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1878,"slug":872,"properties":1879,"entityType":25,"verifyStatus":883,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":47,"subjectFields":1884,"manageAffiliations":1889,"indexDatabases":1900,"url":936,"thumbnailPath":28,"statistic":1915,"gsStatistic":28,"type":28,"analyzePriority":28},[],{"country":1880,"eissn":1881,"issn":1882,"title":1883},{"VOID":875},{"VOID":877},{"VOID":879},{"EN":872},[1885],{"id":886,"createTime":28,"updateTime":28,"relativeEntities":1886,"label":1887,"description":1888,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":889},{},[1890,1895],{"id":893,"createTime":28,"updateTime":28,"relativeEntities":1891,"slug":28,"properties":1892,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1894,"statistic":28},[],{"title":1893},{"EN":897},[],{"id":900,"createTime":28,"updateTime":28,"relativeEntities":1896,"slug":28,"properties":1897,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1899,"statistic":28},[],{"title":1898},{"EN":904},[],[1901,1908],{"id":908,"indexDatabase":1902,"url":914,"indexYears":915,"academicFieldIds":1907,"indexDatabaseRanking":918},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":1903,"label":1904,"description":1905,"key":781,"publicationTags":1906,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],[917],{"id":920,"indexDatabase":1909,"url":932,"indexYears":28,"academicFieldIds":1914,"indexDatabaseRanking":28},{"id":922,"createTime":28,"updateTime":28,"relativeEntities":1910,"label":1911,"description":1912,"key":929,"publicationTags":1913,"standard":28},[],{"EN":925,"VI":925},{"EN":927,"VI":928},[931,813],[934,935],{"impactFactor":32,"impactFactorByYear":1916,"i10Index":32,"i10IndexLast5Year":32,"totalPublication":939,"totalPublicationByYear":1917,"totalCitation":32,"totalCitationByYear":1918,"totalCitationPerPublication":32,"totalCitationPerPublicationByYear":1919,"hindexLast5Year":32,"hindex":32},{},{"1993":40,"2012":941,"2013":357,"2014":48,"2015":49,"2016":123,"2017":49,"2018":46,"2019":46,"2020":48,"2021":357,"2022":46,"2023":145},{},{},{"pages":1921,"volume":1923},{"VOID":1922},"907-929",{"VOID":1924},"48","2012-10-31",[931,918],{"id":1928,"createTime":1929,"updateTime":1930,"relativeEntities":1931,"slug":1932,"properties":1933,"entityType":963,"verifyStatus":26,"verifyTime":1930,"verifyNote":964,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1944,"fullTextUrl":28,"authors":1945,"publicationType":1106,"publisherRelationship":1976,"citationCount":28,"citationInfo":28,"publishDate":2020,"publishYear":1347,"citationAnalyzeStatus":883,"lastCitationAnalyze":28,"indexDatabases":2021,"openAccess":28,"references":28,"isForceReanalyzing":1159},"00c130b7-6cd1-4a9d-b2a4-90035a6fb3ad","2024-04-05T17:56:14.573+00:00","2025-02-22T14:22:53.638+00:00",[],"The-Calcium-Antagonist-Isradipine-in-the-Therapy-of-Hypertension",{"abstract":1934,"title":1936,"keywords":1938,"references":1940,"doi":1942},{"EN":1935},"The calcium antagonists of the dihydropyridine group, isradipine and nifedipine, were compared in 64 patients with mild to moderate hypertension (diastolic blood pressure 95 to 110mm Hg). A 2-week placebo run-in phase was followed by a double-blind crossover trial comprising two 3-week treatment periods with either calcium antagonist. The (fixed) dosages were isradipine 2.5mg twice daily and nifedipine retard 20mg twice daily. Blood pressure (systolic\u002Fdiastolic) at baseline was 155\u002F101mm Hg and decreased significantly by 14%\u002F15% on isradipine and by 11%\u002F12% on nifedipine (difference between treatments not significant). The drugs differed significantly with regard to incidence of adverse effects (mostly flushing and headache); the total rates were 16% on isradipine and 36% on nifedipine. At the end of the trial, patients were asked which drug or treatment phase they preferred. Isradipine was preferred by 50% of patients; only 20% preferred nifedipine. Thus, it is concluded that isradipine, administered in an equally effective antihypertensive dosage regimen is superior to nifedipine with regard to the incidence of adverse effects, resulting in greater patient satisfaction with treatment.",{"EN":1937},"The Calcium Antagonist Isradipine in the Therapy of Hypertension",{"EN":1939},"",{"VOID":1941},"Collins R, Peto R, MacMahon S, Hebert P, Fiebach NH, et al. Blood pressure, stroke and coronary heart disease. Part 2. Short-term reduction in blood pressure: overview of randomised drug trials in their epidemiological context. Lancet 335: 827–838, 1990\nDoyle AE. Comparison of calcium antagonists with other antihypertensive agents. Journal of Hypertension 3(Suppl. 3): S531–S533, 1985\nKirch W, Burger KJ, Weidinger G, Welzel D. Efficacy and tolerability of the new calcium antagonist isradipine in essential hypertension. Journal of Cardiovascular Pharmacology 15(Suppl. 1): S55–S59, 1989\nLund-Johansen P. The hemodynamics of essential hypertension. In Robertson JIS (Ed.) Handbook of hypertension. Clinical aspects of hypertension, Vol. I, pp. 151–173, Elsevier, Amsterdam, 1983\nMan in’t Veld A. Calcium antagonists in hypertension. American Journal of Medicine 86(Suppl. 4A): 6–14, 1989\nMauser M, Voelker W, Ickrath O, Karsch KR. Differences of the myocardial properties of the new dihydropyridine calcium channel blocker isradipine as compared to nifedipine with or without additional beta blockade in patients with coronary artery disease. American Journal of Cardiology 63: 40–44, 1988b\nMauser M, Voelker W, Karsch KR. Isradipin (PN 200-110), ein neuer Dihydropyridin-Kalziumantagonist mit geringeren negativ inotropen Eigenschaften im Vergleich zu Nifedipin. Zeitschrift für Kardiologie 77: 373–377, 1988a\nSaltiel E, Ellrodt AG, Monk JP, Langley MS. Felodipine — a review of its pharmacodynamic and pharmacokinetic properties and therapeutic use in hypertension. Drugs 36: 387–428, 1988\nvon Zerssen D, Koeller DM, Rey ER. Die Befindlichkeitsskala (B-S) — ein einfaches Instrument zur Objektivierung von Befindlichkeitsstörungen, insbesondere im Rahmen von Längsschnitt-Untersuchungen. Arzneimittel Forschung 20: 915–918, 1970\nWelzel D, Burger KJ, Weidinger G. Calcium antagonists as first-line antihypertensive agents: a placebo-controlled, comparative trial of isradipine and nifedipine. 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