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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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One type of MS is factitious Cushing syndrome, an extremely rare clinical situation in which the diagnosis is challenging mainly due to interference of the exogenous medication in cortisol immunoassays. We described a 26-year-old woman who was originally diagnosed with a macroprolactinoma and during follow-up developed clinical and laboratorial hypercortisolism. A transsphenoidal surgery was performed and immunohistochemistry revealed positive and diffuse staining for both hormones. Four years later, her hypercortisolism recurred and the confirmation of factitious Cushing syndrome was delayed due to conflicting laboratorial results. There are few cases in the literature of factitious Cushing syndrome, and only one had a fatal outcome. The diagnosis of this condition is complex and includes cyclic Cushing syndrome in the differential diagnosis. These patients have high morbidity and increased mortality risk and are likely to have other psychiatric disorders. Prednisone was identified as the culprit in the majority of the cases.",{"EN":921},"Fatal factitious Cushing syndrome (Münchhausen’s syndrome) in a patient with macroprolactinoma and silent corticotrophinoma: case report and literature review",{"VOID":923},"Cizza G, Nieman LK, Doppman JL, Passaro MD, Czerwiec FS, Chrousos GP. Factitious Cushing Syndrome. J Clin Endocrinol Metabol. 1996;81:10.\nThynne T, White GH, Morton GB. Factitious Cushing’s syndrome masquerading as a Cushing’s disease. Clin Endocrinol (Oxf). 2013;0:1–5.\nKansagara DL, Tetrault J, Hamill C, Moore C, Olsen B. Fatal factitious Cushing’s syndrome and invasive aspergillosis: case report and review of literature. Endocr Pract. 2006;12:651–5.\nLima L, Alves BB, Paraíba DB, Glezer A, Lopes M, Bronstein MD. Cyclic Cushing’s Disease in a Patient with an ACTH-PRL Secreting Adenoma. In: The Endocrine Society’s 92nd Annual Meeting, 2010. 1st ed. San Diego: The Endocrine Society’s 92nd Annual Meeting Abstracts; 2010. p. 2–321.\nGattaz WF, Dressing H, Hewer H, Nunes P. Síndrome de Munchhausen: diagnostic e manejo clínico. Assoc Med Bras. 2003;49(2):220–4.\nAch K, Khochtali I, Trimech Ajmi S, Maaroufi Beizig A, Chaieb Chadli M, Zaouali A, et al. Le syndrome de Cushing factice : deux observations Factitious Cushing syndrome: two case reports. Rev Med Interne. 2005;26:973–6.\nO’Shaughnessy IM, Haff H, Findling JW. Factitious Cushing’s syndrome: Discovery with use of a sensitite immunoradiometric assay for corticotropin. Endocr Pract. 1995;1:5.\nAzizi F, Jahed A, Hedayati M, Lankarani M, Bejestani HS, Esfahanian F, et al. Outbreak of exogenous Cushing’s syndrome due to unlicensed medications. Clin Endocrinol (Oxf). 2008;69:921–5.\nVillanueva RB, Brett E, Gabrilove JL. A cluster of cases of factitious Cushing’s syndrome. Endocr Pract. 2000;6:143–7.\nWitt ME, Ginsberg-Fellner F. Prednisone-induced Munchausen syndrome. Am J Dis Child. 1981;135:852–3.\nO’Hare JP, Vale JA, Corrall RJM. Factitious Cushing’s Syndrome. Acta Endocrinol. 1986;111:165–7.\nWorkman RJ, Nicholson WE, McCammon DK. Factitious hypercortisoluria. J Clin Endocrinol Metab. 1995;80:3050–1.\nCook DM, Meikle AW. Factitious Cushing’s Syndrome. J Clin Endocrinol Metab. 1985;61:385–7.\nAnderson WA, Galmarini M, Vagnucci A, Horton R. Factitious Cushing’s disease. West J Med. 1993;159:4.",{"VOID":925},"10.1186\u002Fs40842-015-0002-8","PUBLICATION","2025-01-13T00:16:59.074+00:00","Auto Verify","https:\u002F\u002Fclindiabetesendo.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs40842-015-0002-8",[931,947,960,973,988,1001,1014,1029,1042,1055,1068],{"id":932,"sortIndex":32,"researcher":28,"roles":933,"affiliations":935,"properties":944,"displayName":946,"givenName":28,"familyName":28},"c331569e-084e-460b-9959-8aadacbfd4ab",[934],"AUTHOR",[936],{"id":937,"sortIndex":32,"affiliation":938,"properties":28},"25d286ed-b3b6-4f98-aa95-8dd84dd27fc1",{"id":937,"createTime":28,"updateTime":28,"relativeEntities":939,"slug":28,"properties":940,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":943,"statistic":28},[],{"title":941},{"VI":942},"Neuroendocrinology Unit, São Paulo, Brazil",[],{"title":945},{"VI":946},"Carlos André 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University of São Paulo, São Paulo, Brazil",[],{},{"title":1088},{"VI":1089},"Maria Candida Barisson Villares 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model assessment for insulin resistance (HOMA-IR) is a biomarker for type 2 diabetes mellitus (T2DM). However, the role of HOMA-IR in the non-diabetic is unclear. This study aimed to determine whether IR measured HOMA-IR value is associated with new onset diabetes as well as vascular disease and can be used as an early predictor for diabetes and vascular diseases in non-diabetic participants. From a prospective community-based cohort of 10,030 individuals, 4314 individuals younger than 65 years and without diabetes were enrolled and divided into three groups by baseline HOMA-IR tertiles: low (n = 1454), moderate (n = 1414), and high (n = 1446). The primary outcome was new onset T2DM. Secondary outcomes were chronic kidney disease (CKD) and a composite of coronary artery disease, myocardial infarction, and stroke as macrovascular events. The mean age was 51 years. The prevalence of hypertension and cholesterol and HbA1c were higher in the high HOMA-IR group. New onset T2DM (5.8%) and CKD (12.2%) incidence in the high HOMA-IR group was higher than that in the others. The prevalence of macrovascular events did not differ among groups. High-HOMA-IR was an independent risk factor for new onset T2DM (odds ratio 1.86 [1.17–2.96]; p = 0.01) and CKD (1.49 [1.12–1.98]; p = 0.01). High HOMA-IR was an early predictor of new onset T2DM and CKD, regardless of HbA1c in non-diabetic individuals. Further research on the specific cut off value will be needed.",{"EN":1130},"Assessment HOMA as a predictor for new onset diabetes mellitus and diabetic complications in non-diabetic adults: a KoGES prospective cohort study",{"VOID":1132},"Whiting DR, Guariguata L, Weil C, Shaw J. IDF diabetes atlas: global estimates of the prevalence of diabetes for 2011 and 2030. Diabetes Res Clin Pract. 2011;94:311–21.\nCalanna S, Scicali R, Di Pino A, Knop FK, Piro S, Rabuazzo AM, et al. Lipid and liver abnormalities in haemoglobin A1c-defined prediabetes and type 2 diabetes. Nutr Metab Cardiovasc Dis. 2014;24:670–6.\nTang Q, Li X, Song P, Xu L. Optimal cut-off values for the homeostasis model assessment of insulin resistance (HOMA-IR) and pre-diabetes screening: developments in research and prospects for the future. Drug Discov Ther. 2015;9:380–5.\nMorimoto A, Tatsumi Y, Soyano F, Miyamatsu N, Sonoda N, Godai K, et al. Increase in homeostasis model assessment of insulin resistance (HOMA-IR) had a strong impact on the development of type 2 diabetes in Japanese individuals with impaired insulin secretion: the Saku study. PLoS One. 2014;9:e105827.\nChen J, Muntner P, Hamm LL, Fonseca V, Batuman V, Whelton PK, et al. Insulin resistance and risk of chronic kidney disease in nondiabetic US adults. J Am Soc Nephrol. 2003;14:469–77.\nBaek JH, Kim H, Kim KY, Jung J. Insulin resistance and the risk of diabetes and dysglycemia in Korean general adult population. Diabetes Metab J. 2018;42:296–307.\nKhalili D, Khayamzadeh M, Kohansal K, Ahanchi NS, Hasheminia M, Hadaegh F, et al. Are HOMA-IR and HOMA-B good predictors for diabetes and pre-diabetes subtypes? BMC Endocr Disord. 2023;23:1–9.\nKim Y, Han BG, Ko GESg. Cohort profile: the Korean genome and epidemiology study (KoGES). Consortium Int J Epidemiol. 2017;46:e20.\nAmerican Diabetes Association; 2. Classification and Diagnosis of Diabetes: Standards of Medical Care in Diabetes—2019. Diabetes Care. 2019;42(Suppl. 1):S13–28. https:\u002F\u002Fdoi.org\u002F10.2337\u002Fdc19-S002.\nLim S, Jang HC, Lee HK, Kim KC, Park C, Cho NH. A rural-urban comparison of the characteristics of the metabolic syndrome by gender in Korea: the Korean health and genome study (KHGS). J Endocrinol Investig. 2016;29:313–9.\nDiabetes Control and Complications Trial Research Group. The relationship of glycemic exposure (HbA1c) to the risk of development and progression of retinopathy in the diabetes control and complications trial. Diabetes. 1995;44:968–83.\nMatthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and β-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985;28:412–9.\nKatz A, Nambi SS, Mather K, Baron AD, Follmann DA, Sullivan G, et al. Quantitative insulin sensitivity check index: a simple, accurate method for assessing insulin sensitivity in humans. J Clin Endocrinol Metab. 2000;85:2402–10.\nKosmas CE, Silverio D, Tsomidou C, Salcedo MD, Montan PD, Guzman E. The impact of insulin resistance and chronic kidney disease on inflammation and cardiovascular disease. Clin Med Insights Endocrinol Diabetes. 2018;11:1179551418792257.\nFreeman AM. Pennings N. StatPearls Treasure Island (FL): Insulin Resistance; 2019.\nWeir GC, Bonner WS. Five stages of evolving beta-cell dysfunction during progression to diabetes. Diabetes. 2004;53:S16–21.\nWeir GC, Gaglia J, Bonner-Weir S. Inadequate β-cell mass is essential for the pathogenesis of type 2 diabetes. Lancet Diabetes Endocrinol. 2020;8:249–56.\nDiniz M, Beleigoli AMR, Schmidt MI, Duncan BB, Ribeiro ALP, Vidigal PG, et al. Homeostasis model assessment of insulin resistance (HOMA-IR) and metabolic syndrome at baseline of a multicentric Brazilian cohort: ELSA-Brasil study. Cad Saude Publica. 2020;36:e00072120.\nScicali R, Rosenbaum D, Di Pino A, Giral P, Cluzel P, Redheuil A, et al. An increased waist-to-hip ratio is a key determinant of atherosclerotic burden in overweight subjects. Acta Diabetol. 2018;55:741–9.\nFernstrom M, Fernberg U, Hurtig-Wennlof A. Insulin resistance (HOMA-IR) and body fat (%) are associated to low intake of fruit and vegetables in Swedish, young adults: the cross-sectional lifestyle, biomarkers and atherosclerosis study. BMC Nutr. 2019;5:15.\nKlöting N, Fasshauer M, Dietrich A, Kovacs P, Schon MR, Kern M, et al. Am J Physiol Endocrinol Metab. 2010;299:E506–15.\nSchrauben SJ, Jepson C, Hsu JY, Wilson FP, Zhang X, Lash JP, et al. Insulin resistance and chronic kidney disease progression, cardiovascular events, and death: findings from the chronic renal insufficiency cohort study. BMC Nephrol. 2019;20:60.\nSpoto B, Pisano A, Zoccali C. Insulin resistance in chronic kidney disease: a systematic review. Am J Physiol Renal Physiol. 2016;311:F1087–108.\nLiao MT, Sung CC, Hung KC, Wu CC, Lo L, Lu KC. Insulin resistance in patients with chronic kidney disease. J Biomed Biotechnol. 2012;2012:691369.\nHu Y, Shi LX, Zhang Q, Peng NC. Increased risk of chronic kidney diseases in patients with metabolic syndrome: a 3-year prospective cohort study. Curr Med Sci. 2019;39:204–10.\nUK Prospective Diabetes Study (UKPDS) Group. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet. 1998;352:837–53.\nScicali R, Giral P, Gallo A, Di Pino A, Rabuazzo AM, Purrello F, et al. HbA1c increase is associated with higher coronary and peripheral atherosclerotic burden in non diabetic patients. Atherosclerosis. 2016;255:102–8.\nMossmann M, Wainstein MV, Goncalves SC, Wainstein RV, Gravina GL, Sangalli M, et al. HOMA-IR is associated with significant angiographic coronary artery disease in non-diabetic, non-obese individuals: a cross-sectional study. Diabetol Metab Syndr. 2015;7:100.\nBonora E, Kiechl S, Willeit J, Oberhollenzer F, Egger G, Meigs JB, et al. Insulin resistance as estimated by homeostasis model assessment predicts incident symptomatic cardiovascular disease in caucasian subjects from the general population: the Bruneck study. Diabetes Care. 2007;30:318–24.\nBarengo NC, Teuschl Y, Moltchanov V, Laatikainen T, Jousilahti P, Tuomilehto J. Coronary heart disease incidence and mortality, and all-cause mortality among diabetic and non-diabetic people according to their smoking behavior in Finland. Tob Induc Dis. 2017;2(15):12. https:\u002F\u002Fdoi.org\u002F10.1186\u002Fs12971-017-0113-3.",{"VOID":1134},"10.1186\u002Fs40842-023-00156-3","https:\u002F\u002Fclindiabetesendo.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs40842-023-00156-3",[1137,1152,1167,1182],{"id":1138,"sortIndex":32,"researcher":28,"roles":1139,"affiliations":1140,"properties":1149,"displayName":1151,"givenName":28,"familyName":28},"5909b5b2-4563-4b4c-8d0a-6fdc9618eb0f",[934],[1141],{"id":1142,"sortIndex":32,"affiliation":1143,"properties":28},"0ffbf3a8-9e72-4df4-b5bd-8ffc6e37ddea",{"id":1142,"createTime":28,"updateTime":28,"relativeEntities":1144,"slug":28,"properties":1145,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1148,"statistic":28},[],{"title":1146},{"VI":1147},"Department of Biomedical Science and Engineering, Gwangju Institute of Science and Technology, Gwangju, Republic of Korea",[],{"title":1150},{"VI":1151},"Jibeom Lee",{"id":1153,"sortIndex":40,"researcher":28,"roles":1154,"affiliations":1155,"properties":1164,"displayName":1166,"givenName":28,"familyName":28},"84cf1d8c-bf8b-4d2b-a342-827297100acc",[934],[1156],{"id":1157,"sortIndex":32,"affiliation":1158,"properties":28},"59003c70-6b96-43b4-8485-69c6b9869561",{"id":1157,"createTime":28,"updateTime":28,"relativeEntities":1159,"slug":28,"properties":1160,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1163,"statistic":28},[],{"title":1161},{"VI":1162},"Division of Cardiology, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea",[],{"title":1165},{"VI":1166},"Moon-hyun Kim",{"id":1168,"sortIndex":123,"researcher":28,"roles":1169,"affiliations":1170,"properties":1179,"displayName":1181,"givenName":28,"familyName":28},"8cea05b4-2eb6-4d37-8fd0-bc3fb8727d63",[934],[1171],{"id":1172,"sortIndex":32,"affiliation":1173,"properties":28},"1f7bb294-7ea7-41bc-9249-c7c29a206922",{"id":1172,"createTime":28,"updateTime":28,"relativeEntities":1174,"slug":28,"properties":1175,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1178,"statistic":28},[],{"title":1176},{"EN":1177},"Division of Cardiology, National Health Insurance Service Ilsan Hospital, Goyang, Republic of Korea",[],{"title":1180},{"VI":1181},"Ji-Yong Jang",{"id":1183,"sortIndex":42,"researcher":28,"roles":1184,"affiliations":1185,"properties":1192,"displayName":1194,"givenName":28,"familyName":28},"0ea78142-1544-44a7-ba05-959baab392b0",[934],[1186],{"id":1142,"sortIndex":32,"affiliation":1187,"properties":28},{"id":1142,"createTime":28,"updateTime":28,"relativeEntities":1188,"slug":28,"properties":1189,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1191,"statistic":28},[],{"title":1190},{"VI":1147},[],{"title":1193},{"VI":1194},"Chang-Myung Oh",{"url":1135,"publisher":1196,"properties":1215},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1197,"slug":872,"properties":1198,"entityType":25,"verifyStatus":878,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1201,"manageAffiliations":1202,"indexDatabases":1203,"url":892,"thumbnailPath":28,"statistic":1210,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":1199,"title":1200},{"VOID":875},{"EN":877},[],[],[1204],{"id":883,"indexDatabase":1205,"url":889,"indexYears":890,"academicFieldIds":28,"indexDatabaseRanking":891},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":1206,"label":1207,"description":1208,"key":781,"publicationTags":1209,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],{"impactFactor":32,"impactFactorByYear":1211,"i10Index":205,"i10IndexLast5Year":48,"totalPublication":895,"totalPublicationByYear":1212,"totalCitation":897,"totalCitationByYear":1213,"totalCitationPerPublication":900,"totalCitationPerPublicationByYear":1214,"hindexLast5Year":205,"hindex":205},{"2016":109,"2017":105,"2018":223,"2019":346,"2020":228,"2021":820,"2022":347,"2023":167},{"2015":146,"2016":47,"2017":47,"2018":199,"2019":205,"2020":129,"2021":128,"2022":145,"2023":46,"2024":49},{"2015":131,"2016":278,"2017":139,"2018":122,"2019":899,"2020":200,"2021":357,"2022":42},{"2015":902,"2016":903,"2017":904,"2018":363,"2019":905,"2020":906,"2021":346,"2022":169},{"pages":1216,"volume":1218},{"VOID":1217},"1-8",{"VOID":1219},"9","2023-11-16",2023,[891],{"id":1224,"createTime":1225,"updateTime":1226,"relativeEntities":1227,"slug":1228,"properties":1229,"entityType":926,"verifyStatus":26,"verifyTime":1226,"verifyNote":928,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1238,"fullTextUrl":28,"authors":1239,"publicationType":1090,"publisherRelationship":1298,"citationCount":28,"citationInfo":28,"publishDate":1322,"publishYear":1221,"citationAnalyzeStatus":878,"lastCitationAnalyze":28,"indexDatabases":1323,"openAccess":28,"references":28,"isForceReanalyzing":1119},"02c63994-20c4-4613-817e-a9685330f4b6","2024-02-06T00:15:04.874+00:00","2024-09-01T20:16:38.950+00:00",[],"Prevalence-and-risk-factors-of-diabetes-foot-ulcers-in-Kano-northwestern-Nigeria",{"abstract":1230,"title":1232,"references":1234,"doi":1236},{"EN":1231},"Foot complications account for more hospital admissions than any other diabetes mellitus (DM) complications with adverse outcomes being foot ulcers and amputation. To determine the prevalence and risk factors of diabetic foot ulcers in Kano, Northwestern Nigeria. A descriptive cross-sectional study was conducted in the diabetes outpatient clinics and medical and surgical wards of two hospitals in Kano, Nigeria. Data were collected on socio-demographic characteristics, type, and duration of DM. The study subjects were assessed for the presence of and risk factors for foot ulcers. We recruited 394 patients with DM (163 males and 231 females) with a mean (SD) age and duration of DM of 50.8 ± 12.5 years and 7.72 ± 6.65 years respectively. Type 2 DM was present in 95% of the study subjects. Diabetic foot ulcer (DFU) was present in 57 (14.5%) of the patients. Risk factors associated with DFU assessed using univariate analysis were older age, longer duration of DM, presence of peripheral neuropathy (PN), peripheral arterial disease (PAD), diabetic retinopathy, nephropathy, foot deformities, previous DFU, and poor glycemic control. The independent determinants of DFU were previous DFU, foot deformities, retinopathy, PN, PAD, and poor glycemic control. DFU can be found in our setting and the predominant risk factors for DFU are common and remain unchanged in our environment. This study, therefore, buttresses the effect of early detection and treatment of DM in preventing the complications that arise from the disease.",{"EN":1233},"Prevalence and risk factors of diabetes foot ulcers in Kano, northwestern Nigeria",{"VOID":1235},"International Diabetes Federation. Diabetes Atlas, Tenth edition. 2021.\nWHO Study Group on Diabetes Mellitus & World Health Organization. Diabetes mellitus: report of a WHO study group [meeting held in Geneva from 11 to 16 Feb 1985]. World Health Organization; 1985. https:\u002F\u002Fapps.who.int\u002Firis\u002Fhandle\u002F10665\u002F39592. (PubMed)\nBoulton AJ, Vileikyte L, Ragnarson-Tennvall G, Apelqvist J. The global burden of diabetic foot disease. 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PMID: 8933008 (PubMed)",{"VOID":1237},"10.1186\u002Fs40842-023-00155-4","https:\u002F\u002Fclindiabetesendo.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs40842-023-00155-4",[1240,1255,1270,1283],{"id":1241,"sortIndex":32,"researcher":28,"roles":1242,"affiliations":1243,"properties":1252,"displayName":1254,"givenName":28,"familyName":28},"8c796764-ad23-4507-8916-de2a7c3b42c5",[934],[1244],{"id":1245,"sortIndex":32,"affiliation":1246,"properties":28},"db4b2a45-d889-4589-9bc7-a305126b5423",{"id":1245,"createTime":28,"updateTime":28,"relativeEntities":1247,"slug":28,"properties":1248,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1251,"statistic":28},[],{"title":1249},{"VI":1250},"Endocrinology, Diabetes, and Metabolism Unit, Department of Internal Medicine, Federal Teaching Hospital (FTH), Katsina, Nigeria",[],{"title":1253},{"VI":1254},"Raliyatu Aliyu",{"id":1256,"sortIndex":40,"researcher":28,"roles":1257,"affiliations":1258,"properties":1267,"displayName":1269,"givenName":28,"familyName":28},"d1c645f2-0202-4028-92a0-eeac01354b0b",[934],[1259],{"id":1260,"sortIndex":32,"affiliation":1261,"properties":28},"5a5c5a58-5310-4d4b-94aa-bc66305df610",{"id":1260,"createTime":28,"updateTime":28,"relativeEntities":1262,"slug":28,"properties":1263,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1266,"statistic":28},[],{"title":1264},{"VI":1265},"Endocrinology, Diabetes, and Metabolism Unit, Department of Internal Medicine, Bayero University (BUK), Kano, Nigeria",[],{"title":1268},{"VI":1269},"Ibrahim D. Gezawa",{"id":1271,"sortIndex":123,"researcher":28,"roles":1272,"affiliations":1273,"properties":1280,"displayName":1282,"givenName":28,"familyName":28},"08e6ac82-7784-4ba1-b7bd-5410fc4a0fa5",[934],[1274],{"id":1260,"sortIndex":32,"affiliation":1275,"properties":28},{"id":1260,"createTime":28,"updateTime":28,"relativeEntities":1276,"slug":28,"properties":1277,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1279,"statistic":28},[],{"title":1278},{"VI":1265},[],{"title":1281},{"VI":1282},"Andrew E. Uloko",{"id":1284,"sortIndex":42,"researcher":28,"roles":1285,"affiliations":1286,"properties":1295,"displayName":1297,"givenName":28,"familyName":28},"7fb7512e-1741-4839-9d63-c5a0cdbc21e0",[934],[1287],{"id":1288,"sortIndex":32,"affiliation":1289,"properties":28},"bc386c65-a94f-455b-8489-d14aa1bb00b6",{"id":1288,"createTime":28,"updateTime":28,"relativeEntities":1290,"slug":28,"properties":1291,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1294,"statistic":28},[],{"title":1292},{"VI":1293},"Endocrinology, Diabetes, and Metabolism Unit, Department of Internal Medicine, Aminu Kano Teaching Hospital (AKTH), Kano, Nigeria",[],{"title":1296},{"VI":1297},"Mansur A. Ramalan",{"url":1238,"publisher":1299,"properties":1318},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1300,"slug":872,"properties":1301,"entityType":25,"verifyStatus":878,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1304,"manageAffiliations":1305,"indexDatabases":1306,"url":892,"thumbnailPath":28,"statistic":1313,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":1302,"title":1303},{"VOID":875},{"EN":877},[],[],[1307],{"id":883,"indexDatabase":1308,"url":889,"indexYears":890,"academicFieldIds":28,"indexDatabaseRanking":891},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":1309,"label":1310,"description":1311,"key":781,"publicationTags":1312,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],{"impactFactor":32,"impactFactorByYear":1314,"i10Index":205,"i10IndexLast5Year":48,"totalPublication":895,"totalPublicationByYear":1315,"totalCitation":897,"totalCitationByYear":1316,"totalCitationPerPublication":900,"totalCitationPerPublicationByYear":1317,"hindexLast5Year":205,"hindex":205},{"2016":109,"2017":105,"2018":223,"2019":346,"2020":228,"2021":820,"2022":347,"2023":167},{"2015":146,"2016":47,"2017":47,"2018":199,"2019":205,"2020":129,"2021":128,"2022":145,"2023":46,"2024":49},{"2015":131,"2016":278,"2017":139,"2018":122,"2019":899,"2020":200,"2021":357,"2022":42},{"2015":902,"2016":903,"2017":904,"2018":363,"2019":905,"2020":906,"2021":346,"2022":169},{"pages":1319,"volume":1321},{"VOID":1320},"1-10",{"VOID":1219},"2023-11-14",[891],{"id":1325,"createTime":1326,"updateTime":1326,"relativeEntities":1327,"slug":28,"properties":1328,"entityType":926,"verifyStatus":878,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1337,"fullTextUrl":28,"authors":1338,"publicationType":1090,"publisherRelationship":1489,"citationCount":28,"citationInfo":28,"publishDate":1514,"publishYear":1515,"citationAnalyzeStatus":878,"lastCitationAnalyze":28,"indexDatabases":1516,"openAccess":28,"references":28,"isForceReanalyzing":1119},"08ea4096-a122-4734-bd70-0fc7a0c94a4c","2024-02-10T23:44:52.888+00:00",[],{"abstract":1329,"title":1331,"references":1333,"doi":1335},{"EN":1330},"While surgery is the first-line treatment for patients with endogenous hypercortisolism (Cushing syndrome [CS]), mifepristone has been shown to be a beneficial medical treatment option, as demonstrated in the SEISMIC (Study of the Efficacy and Safety of Mifepristone in the Treatment of Endogenous Cushing Syndrome) trial. Mifepristone is a competitive glucocorticoid receptor antagonist and progesterone receptor antagonist that is associated with several treatment effects and adverse events that clinicians need to be aware of when considering its use. The objective of this review was to provide updated clinical management recommendations for patients with CS treated with mifepristone. A panel of endocrinologists from the US with extensive experience in treating patients with CS, including with mifepristone, convened as part of a clinical advisory board to develop a consensus on the practical, real-world clinical management of patients on mifepristone. Comprehensive considerations and recommendations are provided for managing mifepristone-associated effects, including symptoms of cortisol withdrawal, hypokalemia, and change in thyroid function; effects related to its antiprogesterone activity; and rash. Additional management strategies to address concomitant medications and special clinical situations, such as surgery and use in specific populations, are also provided. Safe and effective use of mifepristone requires clinical judgment and close patient monitoring to ensure optimal clinical outcomes. These consensus recommendations provide useful, practical guidance to clinicians using mifepristone.",{"EN":1332},"Clinical management of patients with Cushing syndrome treated with mifepristone: consensus recommendations",{"VOID":1334},"Nieman LK, Biller BM, Findling JW, Murad MH, Newell-Price J, Savage MO, Tabarin A. Endocrine Society. Treatment of Cushing’s syndrome: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2015;100(8):2807–31.\nCarroll TB, Javorsky BR, Findling JW. Postsurgical recurrent Cushing disease: clinical benefit of early intervention in patients with normal urinary free cortisol. Endocr Pract. 2016;22(10):1216–23.\nMinniti G, Osti M, Jaffrain-Rea ML, Esposito V, Cantore G, Maurizi ER. Long-term follow-up results of postoperative radiation therapy for Cushing’s disease. J Neuro-Oncol. 2007;84(1):79–84.\nHamrahian AH, Yuen KCJ, Hoffman AR. AACE neuroendocrine and pituitary scientific committee. AACE\u002FACE disease state clinical review: medical management of Cushing disease. Endocr Pract. 2014;20(7):746–57.\nFleseriu M, Biller BM, Findling JW, Molitch ME, Schteingart DE, Gross C. Mifepristone, a glucocorticoid receptor antagonist, produces clinical and metabolic benefits in patients with Cushing’s syndrome. J Clin Endocrinol Metab. 2012;97(6):2039–49.\nFleseriu M, Findling JW, Koch CA, Schlaffer S-M, Buchfelder M, Gross C. Changes in plasma ACTH levels and corticotroph tumor size in patients with Cushing’s disease during long-term treatment with the glucocorticoid receptor antagonist mifepristone. J Clin Endocrinol Metab. 2014;99(10):3718–27.\nKatznelson L, Loriaux DL, Feldman D, Braunstein GD, Schteingart DE, Gross C. Global clinical response in Cushing’s syndrome patients treated with mifepristone. Clin Endocrinol. 2014;80(4):562–9.\nYuen KC, Williams G, Kushner H, Nguyen D. Association between mifepristone dose, efficacy, and tolerability in patients with Cushing syndrome. Endocr Pract. 2015;21(10):1087–92.\nWallia A, Colleran K, Purnell JQ, Gross C, Molitch ME. Improvement in insulin sensitivity during mifepristone treatment of Cushing syndrome: early and late effects. Diabetes Care. 2013;36(9):e147–e8.\nFein HG, Vaughan TB 3rd, Kushner H, Cram D, Nguyen D. Sustained weight loss in patients treated with mifepristone for Cushing’s syndrome: a follow-up analysis of the SEISMIC study and long-term extension. BMC Endocr Disord. 2015;15:63.\nCarroll T, Findling JW. The use of mifepristone in the treatment of Cushing’s syndrome. Drugs Today (Barc). 2012;48(8):509–18.\nFleseriu M, Molitch ME, Gross C, Schteingart DE, Vaughan TB 3rd, Biller BM. A new therapeutic approach in the medical treatment of Cushing’s syndrome: glucocorticoid receptor blockade with mifepristone. Endocr Pract. 2013;19(2):313–26.\nBhattacharyya A, Kaushal K, Tymms DJ, Davis JR. Steroid withdrawal syndrome after successful treatment of Cushing’s syndrome: a reminder. Eur J Endocrinol. 2005;153(2):207–10.\nRaff H, Sharma ST, Nieman LK. Physiological basis for the etiology, diagnosis, and treatment of adrenal disorders: Cushing’s syndrome, adrenal insufficiency, and congenital adrenal hyperplasia. Compr Physiol. 2014;4(2):739–69.\nSchrier RW. Body water homeostasis: clinical disorders of urinary dilution and concentration. J Am Soc Nephrol. 2006;17(7):1820–32.\nKorlym® (mifepristone) 300 mg tablets [prescribing information]. Menlo Park, CA: Corcept Therapeutics Incorporated; 2019. https:\u002F\u002Fwww.korlym.com\u002Fwp-content\u002Fuploads\u002F2018\u002F01\u002FK-00017-NOV-2019_electronic-PI_r8_FINAL.pdf. Accessed 24 June 2020.\nRushworth RL, Torpy DJ, Falhammar H. Adrenal crisis. N Engl J Med. 2019;381(9):852–61.\nTakasu N, Komiya I, Nagasawa Y, Asawa T, Yamada T. Exacerbation of autoimmune thyroid dysfunction after unilateral adrenalectomy in patients with Cushing’s syndrome due to an adrenocortical adenoma. N Engl J Med. 1990;322(24):1708–12.\nNoguchi Y, Tamai H, Fujisawa K, Nagano J, Mukuta T, Komaki G, Masubayashi S, Kubo C, Torisu M, Nakagaki H, Imayama S. Systemic lupus erythematosus after pituitary adenomectomy in a patient with Cushing’s disease. Clin Endocrinol. 1998;48(5):670–2.\nSenecal JL, Uthman I, Beauregard H. Cushing’s disease-induced remission of severe rheumatoid arthritis. Arthritis Rheum. 1994;37(12):1826.\nTorpy DJ, Mullen N, Ilias I, Nieman LK. Association of hypertension and hypokalemia with Cushing’s syndrome caused by ectopic ACTH secretion: a series of 58 cases. Ann N Y Acad Sci. 2002;970:134–44.\nHowlett TA, Drury PL, Perry L, Doniach I, Rees LH, Besser GM. Diagnosis and management of ACTH-dependent Cushing’s syndrome: comparison of the features in ectopic and pituitary ACTH production. Clin Endocrinol. 1986;24(6):699–713.\nUlick S, Wang JZ, Blumenfeld JD, Pickering TG. Cortisol inactivation overload: a mechanism of mineralocorticoid hypertension in the ectopic adrenocorticotropin syndrome. J Clin Endocrinol Metab. 1992;74(5):963–7.\nUS Department of Health and Human Services, US Department of Agriculture. Dietary Guidelines for Americans, 2015–2020. 8th edition. 2015. https:\u002F\u002Fhealth.gov\u002Fdietaryguidelines\u002F2015\u002Fresources\u002F2015-2020_Dietary_Guidelines.pdf. Accessed July 29, 2019.\nBerger C, Boggavarapu N, Norlin E, Queckborner S, Hornaeus K, Falk A, Engman M, Ramstrom M, Lalitkumar PGL, Gemzell-Danielsson K. Molecular characterization of PRM-associated endometrial changes, PAEC, following mifepristone treatment. Contraception. 2018;98(4):317–22.\nMutter GL, Bergeron C, Deligdisch L, Ferenczy A, Glant M, Merino M, Williams AR, Blithe DL. The spectrum of endometrial pathology induced by progesterone receptor modulators. Mod Pathol. 2008;21(5):591–8.\nCarroll TB, Ioffe O, Spitz IM, Gross C, Cram D, Hamrahian AH. Endometrial effects of long-term mifepristone (MIFE) treatment of Cushing’s syndrome: results from the SEISMIC studies. Endocr Rev. 2013;34(suppl 1):SUN-52.\nFiscella J, Bonfiglio T, Winters P, Eisinger SH, Fiscella K. Distinguishing features of endometrial pathology after exposure to the progesterone receptor modulator mifepristone. Hum Pathol. 2011;42(7):947–53.\nEisinger SH, Meldrum S, Fiscella K, le Roux HD, Guzick DS. Low-dose mifepristone for uterine leiomyomata. Obstet Gynecol. 2003;101(2):243–50.\nEisinger SH, Bonfiglio T, Fiscella K, Meldrum S, Guzick DS. Twelve-month safety and efficacy of low-dose mifepristone for uterine myomas. J Minim Invasive Gynecol. 2005;12(3):227–33.\nBasina M, Liu H, Hoffman AR, Feldman D. Successful long-term treatment of Cushing disease with mifepristone (RU486). Endocr Pract. 2012;18(5):e114–e20.\nGuarda FJ, Findling J, Yuen KCJ, Fleseriu M, Nachtigall LB. Mifepristone increases thyroid hormone requirements in patients with central hypothyroidism: a multicenter study. J Endocr Soc. 2019;3(9):1707–14.\nHeikinheimo O, Ranta S, Grunberg S, Lahteenmaki P, Spitz IM. Alterations in the pituitary-thyroid and pituitary-adrenal axes--consequences of long-term mifepristone treatment. Metabolism. 1997;46(3):292–6.\nGarber JR, Cobin RH, Gharib H, Hennessey JV, Klein I, Mechanick JI, Pessah-Pollack R, Singer PA, Woeber KA. American Association of Clinical Endocrinologists and American Thyroid Association Taskforce on hypothyroidism in adults. Clinical practice guidelines for hypothyroidism in adults: cosponsored by the American Association of Clinical Endocrinologists and the American Thyroid Association. Endocr Pract. 2012;18(6):988–1028.\nBekkering GE, Agoritsas T, Lytvyn L, Heen AF, Feller M, Moutzouri E, Abdulazeem H, Aertgeerts B, Beecher D, Brito JP, Farhoumand PD, Singh Ospina N, Rodondi N, van Driel M, Wallace E, Snel M, Okwen PM, Siemieniuk R, Vandvik PO, Kuijpers T, Vermandere M. Thyroid hormones treatment for subclinical hypothyroidism: a clinical practice guideline. BMJ. 2019;365:l2006.\nUS Center for Drug Evaluation and Research. Clinical review: mifepristone tablets. NDA application number: 202107Orig1s000. 2012. https:\u002F\u002Fwww.accessdata.fda.gov\u002Fdrugsatfda_docs\u002Fnda\u002F2012\u002F202107Orig1s000MedR.pdf. Accessed June 24, 2019.\nEliquis® (apixaban) tablets, for oral use [prescribing information]. Princeton, NJ: Bristol-Myers Squibb Company; 2019. https:\u002F\u002Fpackageinserts.bms.com\u002Fpi\u002Fpi_eliquis.pdf. Accessed 24 June 2020.\nXarelto® (rivaroxaban) tablets, for oral use [prescribing information]. Titusville, NJ: Janssen Pharmaceuticals, Inc.; 2020. http:\u002F\u002Fwww.janssenlabels.com\u002Fpackage-insert\u002Fproduct-monograph\u002Fprescribing-information\u002FXARELTO-pi.pdf. Accessed 24 June 2020.\nJang GR, Wrighton SA, Benet LZ. Identification of CYP3A4 as the principal enzyme catalyzing mifepristone (RU 486) oxidation in human liver microsomes. Biochem Pharmacol. 1996;52(5):753–61.\nHe K, Woolf TF, Hollenberg PF. Mechanism-based inactivation of cytochrome P-450-3A4 by mifepristone (RU486). J Pharmacol Exp Ther. 1999;288(2):791–7.\nGardiner P, Schrode K, Quinlan D, Martin BK, Boreham DR, Rogers MS, Stubbs K, Smith M, Karim A. Spironolactone metabolism: steady-state serum levels of the sulfur-containing metabolites. J Clin Pharmacol. 1989;29(4):342–7.\nCastinetti F, Fassnacht M, Johanssen S, Terzolo M, Bouchard P, Chanson P, Do Cao C, Morange I, Pico A, Ouzounian S, Young J, Hahner S, Brue T, Allolio B, Conte-Devolx B. Merits and pitfalls of mifepristone in Cushing’s syndrome. Eur J Endocrinol. 2009;160(6):1003–10.\nSack PA, Smith JJ. Mifepristone therapy prior to pituitary surgery in Cushing disease prevented need for long-term glucocorticoid replacement. Endocr Pract. 2018;39(2 suppl): SAT-578.\nSaroka RM, Kane MP, Robinson L, Busch RS. No postoperative adrenal insufficiency in a patient with unilateral cortisol-secreting adenomas treated with mifepristone before surgery. Clin Med Insights Endocrinol Diab. 2016;9:31–6.\nMagaji V, Park SY, Mastoris K, Bucciarelli M, Beman S. Mifepristone utilization in Cushing’s from large bilateral adrenal adenoma prior to surgery. J Endocrinol Metab. 2015;5(3):226–8.\nMoraitis AG, Auchus RJ. Clinical and hormonal response to mifepristone therapy in 2 patients with ACTH-independent Cushing syndrome. ACCE Clin Case Rep. 2015;1(3):e204–e7.\nCohan P, East HE, Galati SJ, Mercado JU, Lim PJ, Lamerson M, Smith JJ, Peters AL, Yuen KCJ. Mifepristone treatment in four cases of primary bilateral macronodular adrenal hyperplasia (BMAH). J Clin Endocrinol Metab. 2019;104(12):6279–90.\nDebono M, Chadarevian R, Eastell R, Ross RJ, Newell-Price J. Mifepristone reduces insulin resistance in patient volunteers with adrenal incidentalomas that secrete low levels of cortisol: a pilot study. PLoS One. 2013;8(4):e60984.\nBanerjee RR, Marina N, Katznelson L, Feldman BJ. Mifepristone treatment of Cushing’s syndrome in a pediatric patient. Pediatrics. 2015;136(5):e1377–e81.\nNewfield RS, Spitz IM, Isacson C, New MI. Long-term mifepristone (RU486) therapy resulting in massive benign endometrial hyperplasia. Clin Endocrinol. 2001;54(3):399–404.\nTargher G, Bertolini L, Rodella S, Zoppini G, Zenari L, Falezza G. Associations between liver histology and cortisol secretion in subjects with nonalcoholic fatty liver disease. Clin Endocrinol. 2006;64(3):337–41.\nRagucci E, Nguyen D, Lamerson M, Moraitis AG. Effects of mifepristone on nonalcoholic fatty liver disease in a patient with a cortisol-secreting adrenal adenoma. Case Rep Endocrinol 2017;2017:6161348.\nMoraitis A, Feelders R, Gordon M, Iacuaniello D, Kargi A, Pivonello R. IGF-1 levels in patients with hypercortisolism and effects of medical therapy with relacorilant, a selective cortisol modulator. Endocr Pract. 2018;24(suppl 1):318–9.\nGordon MB, Spiller KL, Bunta R, Gordon MS. Persistent acromegaly controlled on pegvisomant with co-existing non-ACTH dependent Cushing’s syndrome (CS) due to bilateral adrenal adenomas with dramatic clinical response to mifepristone. Endocr Rev. 2016;37(2 suppl 1):SUN 555.\nPage ST, Krauss RM, Gross C, Ishida B, Heinecke JW, Tang C, Amory JK, Schaefer PM, Cox CJ, Kane J, Purnell JQ, Weinstein RL, Vaisar T. Impact of mifepristone, a glucocorticoid\u002Fprogesterone antagonist, on HDL cholesterol, HDL particle concentration, and HDL function. J Clin Endocrinol Metab. 2012;97(5):1598–605.",{"VOID":1336},"10.1186\u002Fs40842-020-00105-4","https:\u002F\u002Fclindiabetesendo.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs40842-020-00105-4",[1339,1354,1369,1384,1399,1414,1429,1444,1459,1474],{"id":1340,"sortIndex":32,"researcher":28,"roles":1341,"affiliations":1342,"properties":1351,"displayName":1353,"givenName":28,"familyName":28},"771a85eb-6d14-45f6-80c5-d8cc1cd0e156",[934],[1343],{"id":1344,"sortIndex":32,"affiliation":1345,"properties":28},"7fd2acae-6376-42d5-bf3f-3e94078d3a47",{"id":1344,"createTime":28,"updateTime":28,"relativeEntities":1346,"slug":28,"properties":1347,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1350,"statistic":28},[],{"title":1348},{"VI":1349},"Private Practice, Endocrinology, Diabetes, and Metabolism, Rockville, USA",[],{"title":1352},{"VI":1353},"David R. Brown",{"id":1355,"sortIndex":40,"researcher":28,"roles":1356,"affiliations":1357,"properties":1366,"displayName":1368,"givenName":28,"familyName":28},"dad51911-c715-4c16-9e06-7381bc0750ca",[934],[1358],{"id":1359,"sortIndex":32,"affiliation":1360,"properties":28},"1f87a00b-46bd-4093-88df-c72c35e1afcc",{"id":1359,"createTime":28,"updateTime":28,"relativeEntities":1361,"slug":28,"properties":1362,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1365,"statistic":28},[],{"title":1363},{"VI":1364},"Metabolic Medicine of Mississippi, Jackson, USA",[],{"title":1367},{"VI":1368},"Honey E. East",{"id":1370,"sortIndex":123,"researcher":28,"roles":1371,"affiliations":1372,"properties":1381,"displayName":1383,"givenName":28,"familyName":28},"50423a39-b911-41d0-993a-901742612b2d",[934],[1373],{"id":1374,"sortIndex":32,"affiliation":1375,"properties":28},"80907c28-e789-4ac6-a3bf-8d28fe619d9a",{"id":1374,"createTime":28,"updateTime":28,"relativeEntities":1376,"slug":28,"properties":1377,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1380,"statistic":28},[],{"title":1378},{"VI":1379},"Regional Diabetes Center, St. Elizabeth Physicians, Covington, USA",[],{"title":1382},{"VI":1383},"Bradley S. Eilerman",{"id":1385,"sortIndex":42,"researcher":28,"roles":1386,"affiliations":1387,"properties":1396,"displayName":1398,"givenName":28,"familyName":28},"49db611d-37d0-456f-b94b-f5a03287e378",[934],[1388],{"id":1389,"sortIndex":32,"affiliation":1390,"properties":28},"7e98d436-54c1-4ec8-af29-e496751ea691",{"id":1389,"createTime":28,"updateTime":28,"relativeEntities":1391,"slug":28,"properties":1392,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1395,"statistic":28},[],{"title":1393},{"VI":1394},"Allegheny Neuroendocrinology Center, Allegheny General Hospital, Pittsburgh, USA",[],{"title":1397},{"VI":1398},"Murray B. Gordon",{"id":1400,"sortIndex":45,"researcher":28,"roles":1401,"affiliations":1402,"properties":1411,"displayName":1413,"givenName":28,"familyName":28},"ab1c22f9-80bb-4e6e-8526-e1c941e44322",[934],[1403],{"id":1404,"sortIndex":32,"affiliation":1405,"properties":28},"a8fa5741-cb34-42b8-b70a-7eace6a0d4ee",{"id":1404,"createTime":28,"updateTime":28,"relativeEntities":1406,"slug":28,"properties":1407,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1410,"statistic":28},[],{"title":1408},{"VI":1409},"Endocrine Associates of Dallas, Dallas, USA",[],{"title":1412},{"VI":1413},"Elizabeth E. King",{"id":1415,"sortIndex":46,"researcher":28,"roles":1416,"affiliations":1417,"properties":1426,"displayName":1428,"givenName":28,"familyName":28},"b8162eb0-1101-43a6-8207-77bc261ebc8a",[934],[1418],{"id":1419,"sortIndex":32,"affiliation":1420,"properties":28},"ed22d099-6de2-4227-aed8-298930b406fc",{"id":1419,"createTime":28,"updateTime":28,"relativeEntities":1421,"slug":28,"properties":1422,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1425,"statistic":28},[],{"title":1423},{"VI":1424},"Midtown Endocrine Associates, Phoenix, USA",[],{"title":1427},{"VI":1428},"Laura A. Knecht",{"id":1430,"sortIndex":48,"researcher":28,"roles":1431,"affiliations":1432,"properties":1441,"displayName":1443,"givenName":28,"familyName":28},"4ef7d4ca-5e62-4625-9dba-817a16319864",[934],[1433],{"id":1434,"sortIndex":32,"affiliation":1435,"properties":28},"df4b5959-c22a-411c-9900-052e097de6ac",{"id":1434,"createTime":28,"updateTime":28,"relativeEntities":1436,"slug":28,"properties":1437,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1440,"statistic":28},[],{"title":1438},{"VI":1439},"Optime Care, Earth City, USA",[],{"title":1442},{"VI":1443},"Brandon Salke",{"id":1445,"sortIndex":49,"researcher":28,"roles":1446,"affiliations":1447,"properties":1456,"displayName":1458,"givenName":28,"familyName":28},"8a8ecf64-f711-4546-996b-69bc46952862",[934],[1448],{"id":1449,"sortIndex":32,"affiliation":1450,"properties":28},"36a165de-34ea-4ed7-8063-562e37b52d57",{"id":1449,"createTime":28,"updateTime":28,"relativeEntities":1451,"slug":28,"properties":1452,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1455,"statistic":28},[],{"title":1453},{"VI":1454},"Pituitary Center, Baylor St. Luke’s Medical Center, Baylor College of Medicine, Houston, USA",[],{"title":1457},{"VI":1458},"Susan L. Samson",{"id":1460,"sortIndex":357,"researcher":28,"roles":1461,"affiliations":1462,"properties":1471,"displayName":1473,"givenName":28,"familyName":28},"dd883e9f-d660-45fc-8370-6cdf2a7e2726",[934],[1463],{"id":1464,"sortIndex":32,"affiliation":1465,"properties":28},"14b08eb4-adb7-4497-9791-04ba75e02c7b",{"id":1464,"createTime":28,"updateTime":28,"relativeEntities":1466,"slug":28,"properties":1467,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1470,"statistic":28},[],{"title":1468},{"VI":1469},"Barrow Neurological Institute and St. Joseph’s Hospital and Medical Center, University of Arizona College of Medicine and Creighton School of Medicine, Phoenix, USA",[],{"title":1472},{"VI":1473},"Kevin C. J. Yuen",{"id":1475,"sortIndex":145,"researcher":28,"roles":1476,"affiliations":1477,"properties":1486,"displayName":1488,"givenName":28,"familyName":28},"ffbdea1c-169d-4a97-a5f1-f294a8ecfb09",[934],[1478],{"id":1479,"sortIndex":32,"affiliation":1480,"properties":28},"0cce2ac4-6b1b-4d16-85e4-6efae26d5a9c",{"id":1479,"createTime":28,"updateTime":28,"relativeEntities":1481,"slug":28,"properties":1482,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1485,"statistic":28},[],{"title":1483},{"VI":1484},"Division of Endocrinology, Diabetes, and Metabolism, The University of Central Florida College of Medicine, Orlando, USA",[],{"title":1487},{"VI":1488},"Hanford Yau",{"url":1337,"publisher":1490,"properties":1509},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1491,"slug":872,"properties":1492,"entityType":25,"verifyStatus":878,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1495,"manageAffiliations":1496,"indexDatabases":1497,"url":892,"thumbnailPath":28,"statistic":1504,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":1493,"title":1494},{"VOID":875},{"EN":877},[],[],[1498],{"id":883,"indexDatabase":1499,"url":889,"indexYears":890,"academicFieldIds":28,"indexDatabaseRanking":891},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":1500,"label":1501,"description":1502,"key":781,"publicationTags":1503,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],{"impactFactor":32,"impactFactorByYear":1505,"i10Index":205,"i10IndexLast5Year":48,"totalPublication":895,"totalPublicationByYear":1506,"totalCitation":897,"totalCitationByYear":1507,"totalCitationPerPublication":900,"totalCitationPerPublicationByYear":1508,"hindexLast5Year":205,"hindex":205},{"2016":109,"2017":105,"2018":223,"2019":346,"2020":228,"2021":820,"2022":347,"2023":167},{"2015":146,"2016":47,"2017":47,"2018":199,"2019":205,"2020":129,"2021":128,"2022":145,"2023":46,"2024":49},{"2015":131,"2016":278,"2017":139,"2018":122,"2019":899,"2020":200,"2021":357,"2022":42},{"2015":902,"2016":903,"2017":904,"2018":363,"2019":905,"2020":906,"2021":346,"2022":169},{"pages":1510,"volume":1512},{"VOID":1511},"1-13",{"VOID":1513},"6","2020-10-29",2020,[891],{"id":1518,"createTime":1519,"updateTime":1519,"relativeEntities":1520,"slug":28,"properties":1521,"entityType":926,"verifyStatus":878,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1530,"fullTextUrl":28,"authors":1531,"publicationType":1090,"publisherRelationship":1575,"citationCount":28,"citationInfo":28,"publishDate":1600,"publishYear":1601,"citationAnalyzeStatus":878,"lastCitationAnalyze":28,"indexDatabases":1602,"openAccess":28,"references":28,"isForceReanalyzing":1119},"0b30600a-b75b-44a9-ba55-eba4d94fa19d","2024-02-21T10:30:49.896+00:00",[],{"abstract":1522,"title":1524,"references":1526,"doi":1528},{"EN":1523},"The prevalence of diabetes in children and adolescents is increasing worldwide, with profound implications on the long-term health of individuals, societies, and nations. The diagnosis and management of diabetes in youth presents several unique challenges. Although type 1 diabetes is more common among children and adolescents, the incidence of type 2 diabetes in youth is also on the rise, particularly among certain ethnic groups. In addition, less common types of diabetes such as monogenic diabetes syndromes and diabetes secondary to pancreatopathy (in some parts of the world) need to be accurately identified to initiate the most appropriate treatment. A detailed patient history and physical examination usually provides clues to the diagnosis. However, specific laboratory and imaging tests are needed to confirm the diagnosis. The management of diabetes in children and adolescents is challenging in some cases due to age-specific issues and the more aggressive nature of the disease. Nonetheless, a patient-centered approach focusing on comprehensive risk factor reduction with the involvement of all concerned stakeholders (the patient, parents, peers and teachers) could help in ensuring the best possible level of diabetes control and prevention or delay of long-term complications.",{"EN":1525},"Challenges in diagnosis and management of diabetes in the young",{"VOID":1527},"International Diabetes Federation. Diabetes Atlas. 6th ed. Brussels: International Diabetes Federation; 2013.\nFazeli Farsani S, Van der Aa MP, et al. Global trends in the incidence and prevalence of type 2 diabetes in children and adolescents: a systematic review and evaluation of methodological approaches. Diabetologia. 2013;56:1471–88.\nPettitt DJ, Talton J, Dabelea D, et al. SEARCH for Diabetes in Youth Study Group. Prevalence of diabetes in U.S. youth in 2009: the SEARCH for diabetes in youth study. Diabetes Care. 2014;37:402–8.\nMa RC, Chan JC. Type 2 diabetes in East Asians: similarities and differences with populations in Europe and the United States. Ann N Y Acad Sci. 2013;1281:64–91.\nAtkinson MA, Eisenbarth GS, Michels AW. Type 1 diabetes. Lancet. 2014;383:69–82.\nMbanya JC, Motala AA, Sobngwi E, Assah FK, Enoru ST. Diabetes in sub-Saharan Africa. Lancet. 2010;375:2254–66.\nZiegler AG, Nepom GT. Prediction and pathogenesis in type 1 diabetes. Immunity. 2010;32:468–78.\nUnnikrishnan AG, Singh SK, Sanjeevi CB. Prevalence of GAD65 antibodies in lean subjects with type 2 diabetes. Ann N Y Acad Sci. 2004;1037:118–21.\nKanungo A, Sanjeevi CB. IA-2 autoantibodies are predominant in latent autoimmune diabetes in adults patients from eastern India. Ann N Y Acad Sci. 2003;1005:390–4.\nRedondo MJ, Jeffrey J, Fain PR, et al. Concordance for islet autoimmunity among monozygotic twins. N Engl J Med. 2008;359:2849–50.\nInsel RA, Dunne JL, Atkinson MA, et al. Staging presymptomatic type 1 diabetes: a scientific statement of JDRF, the Endocrine Society, and the American Diabetes Association. Diabetes Care. 2015;38:1964–74.\nErlich H, Valdes AM, Noble J, et al. Type 1 Diabetes Genetics Consortium. HLA DR-DQ haplotypes and genotypes and type 1 diabetes risk: analysis of the type 1 diabetes genetics consortium families. Diabetes. 2008;57:1084–92.\nPeng H, Hagopian W. Environmental factors in the development of Type 1 diabetes. Rev Endocr Metab Disord. 2006;7:149–62.\nFrederiksen B, Kroehl M, Lamb MM, et al. Infant exposures and development of type 1 diabetes mellitus: The Diabetes Autoimmunity Study in the Young (DAISY). JAMA Pediatr. 2013;167:808–15.\nDabelea D, Bell RA, D’Agostino Jr RB, Writing Group for the SEARCH for Diabetes in Youth Study Group, et al. Incidence of diabetes in youth in the United States. JAMA. 2007;297:2716–24.\nPinhas-Hamiel O, Zeitler P. The global spread of type 2 diabetes mellitus in children and adolescents. J Pediatr. 2005;146:693–700.\nD’Adamo E, Cali AM, Weiss R, Santoro N, Pierpont B, Northrup V, Caprio S. Central role of fatty liver in the pathogenesis of insulin resistance in obese adolescents. Diabetes Care. 2010;33:1817–22.\nTulloch-Reid MK, Boyne MS, Smikle MF, Choo-Kang EG, Parkes RH, Wright-Pascoe RA, Barton EN, Wilks RJ, Williams DE. Clinical and laboratory features of youth onset type 2 diabetes in Jamaica. West Indian Med J. 2010;59(2):131–8.\nPraveen PA, Madhu SV, Mohan V, et al. Registry of Youth Onset Diabetes in India (YDR): Rationale, Recruitment, and Current Status. J Diabetes Sci Technol. 2016;10;1034–41.\nD’Adamo E, Caprio S. Type 2 diabetes in youth: epidemiology and pathophysiology. Diabetes Care. 2011;34 Suppl 2:S161–5.\nNarayan KM, Fagot-Campagna A, Imperatore G. Type 2 diabetes in children: a problem lurking for India? Indian Pediatr. 2001;38:701–4.\nDefronzo RA. Banting Lecture. From the triumvirate to the ominous octet: a new paradigm for the treatment of type 2 diabetes mellitus. Diabetes. 2009;58:773–95.\nMohan V, Amutha A, Ranjani H, et al. Associations of β-cell function and insulin resistance with youth-onset type 2 diabetes and prediabetes among Asian Indians. Diabetes Technol Ther. 2013;15:315–22.\nChan JC, Malik V, Jia W, et al. Diabetes in Asia: epidemiology, risk factors, and pathophysiology. JAMA. 2009;301:2129–40.\nMcKeigue PM, Shah B, Marmot MG. Relation of central obesity and insulin resistance with high diabetes prevalence and cardiovascular risk in South Asians. Lancet. 1991;337:382–6.\nMisra A, Vikram NK. Insulin resistance syndrome (metabolic syndrome) and obesity in Asian Indians: evidence and implications. Nutrition. 2004;20:482–91.\nYajnik CS, Lubree HG, Rege SS, et al. Adiposity and hyperinsulinemia in Indians are present at birth. J Clin Endocrinol Metab. 2002;87:5575–80.\nHattersley A, Bruining J, Shield J, et al. The diagnosis and management of monogenic diabetes in children and adolescents. Pediatr Diabetes. 2009;10 Suppl 12:33–42.\nPihoker C, Gilliam LK, Ellard S, SEARCH for Diabetes in Youth Study Group, et al. Prevalence, characteristics and clinical diagnosis of maturity onset diabetes of the young due to mutations in HNF1A, HNF4A, and glucokinase: results from the SEARCH for Diabetes in Youth. J Clin Endocrinol Metab. 2013;98:4055–62.\nRadha V, Ek J, Anuradha S, et al. Identification of novel variants in the hepatocyte nuclear factor-1alpha gene in South Indian patients with maturity onset diabetes of young. J Clin Endocrinol Metab. 2009;94:1959–65.\nAnuradha S, Radha V, Mohan V. Association of novel variants in the hepatocyte nuclear factor 4A gene with maturity onset diabetes of the young and early onset type 2 diabetes. Clin Genet. 2011;80:541–9.\nTattersall RB, Fajans SS. A difference between the inheritance of classical juvenile-onset and maturity-onset type diabetes of young people. Diabetes. 1975;24:44–53.\nRubio-Cabezas O, Hattersley AT, Njolstad PR, Clinical Practice Consensus Guidelines ISPAD, et al. The diagnosis and management of monogenic diabetes in children and adolescents. Pediatr Diabetes. 2014;15(Suppl20):47–64.\nMurphy R, Ellard S, Hattersley AT. Clinical implications of a molecular genetic classification of monogenic beta-cell diabetes. Nat Clin Pract Endocrinol Metab. 2008;4:200–13.\nHattersley AT, Ashcroft FM. Activating mutations in Kir6.2 and neonatal diabetes: new clinical syndromes, new scientific insights, and new therapy. Diabetes. 2005;54:2503–13.\nBarman KK, Premalatha G, Mohan V. Tropical chronic pancreatitis. Postgrad Med J. 2003;79:606–15.\nPapita R, Nazir A, Anbalagan VP, et al. Secular trends of fibrocalculous pancreatic diabetes and diabetes secondary to alcoholic chronic pancreatitis at a tertiary care diabetes centre in South India. JOP. 2012;13:205–9.\nMohan V, Premalatha G, Pitchumoni CS. Tropical chronic pancreatitis: an update. J Clin Gastroenterol. 2003;36:337–46.\nUnnikrishnan R, Mohan V. Pancreatic diseases and diabetes. In: Holt RIG, Cockram CS, Flyvbjerg A, Goldstein BJ, editors. Textbook of Diabetes. 4th ed. Oxford: Wiley-Blackwell; 2010. p. 298–309.\nMoran A, Becker D, Casella SJ, CFRD Consensus Conference Committee, et al. Epidemiology, pathophysiology, and prognostic implications of cystic fibrosis-related diabetes: a technical review. Diabetes Care. 2010;33:2677–83.\nDabelea D, Rewers A, Stafford JM, et al. Trends in the prevalence of ketoacidosis at diabetes diagnosis: the SEARCH for diabetes in youth study. Pediatrics. 2014;133:e938–45.\nHawa MI, Kolb H, Schloot N, et al. Adult-onset autoimmune diabetes in Europe is prevalent with a broad clinical phenotype. Diabetes Care. 2013;36:908–13.\nBell RA, Meyer-Davis EJ, Beyer JW, et al. Diabetes in non-Hispanic white youth. Diabetes Care. 2009;32(Suppl2):s102–11.\nGilliam LK, Liese AD, Bloch CA, et al. Family history of diabetes, autoimmunity, and risk factors for cardiovascular disease among children with diabetes in the SEARCH for Diabetes in Youth Study. Pediatr Diabetes. 2007;8:354–61.\nHamalainen AM, Knip M. Autoimmunity and familial risk of type 1 diabetes. Curr Diab Rep. 2002;2:347–53.\nMohan V, Chari ST, Hitman GA, et al. Familial aggregation in tropical fibrocalculous pancreatic diabetes. Pancreas. 1989;4:690–3.\nWilkin TJ. The accelerator hypothesis: a review of the evidence for insulin resistance as the basis for type I as well as type II diabetes. Int J Obes. 2009;33:716–26.\nDavis AK, DuBose SN, Haller MJ, et al. Prevalence of detectable C-peptide according to age at diagnosis and duration of type 1 diabetes. Diabetes Care. 2015;38:476–81.\nHillier TA, Pedula KL. Complications in young adults with early-onset type 2 diabetes: losing the relative protection of youth. Diabetes Care. 2003;26:2999–3005.\nAmerican Diabetes Association. Standards of Medical Care in Diabetes – 2015. Diabetes Care. 2015;38:1.\nTamborlane WV, Klingensmith G. Crisis in care: limited treatment options for type 2 diabetes in adolescents and youth. Diabetes Care. 2013;36:1777–8.\nFlannick J, Johansson S, Njølstad PR. Common and rare forms of diabetes mellitus: towards a continuum of diabetes subtypes. Nat Rev Endocrinol. 2016;12:394–406.",{"VOID":1529},"10.1186\u002Fs40842-016-0036-6","https:\u002F\u002Fclindiabetesendo.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs40842-016-0036-6",[1532,1547,1562],{"id":1533,"sortIndex":32,"researcher":28,"roles":1534,"affiliations":1535,"properties":1544,"displayName":1546,"givenName":28,"familyName":28},"76db6e7c-9a10-48c0-996a-71b607cee832",[934],[1536],{"id":1537,"sortIndex":32,"affiliation":1538,"properties":28},"78ce8baf-12b1-4ac6-af9a-41f03f0a0c5d",{"id":1537,"createTime":28,"updateTime":28,"relativeEntities":1539,"slug":28,"properties":1540,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1543,"statistic":28},[],{"title":1541},{"VI":1542},"Madras Diabetes Research Foundation & Dr. Mohan’s Diabetes Specialties Centre, WHO Collaborating Centre for Non-Communicable Diseases Prevention and Control, Chennai, India",[],{"title":1545},{"VI":1546},"Ranjit Unnikrishnan",{"id":1548,"sortIndex":40,"researcher":28,"roles":1549,"affiliations":1550,"properties":1559,"displayName":1561,"givenName":28,"familyName":28},"c40b5c00-60f7-4fef-baa8-cbd5edf9994c",[934],[1551],{"id":1552,"sortIndex":32,"affiliation":1553,"properties":28},"ea52bea0-41fc-4dae-8e20-e27f89440e7c",{"id":1552,"createTime":28,"updateTime":28,"relativeEntities":1554,"slug":28,"properties":1555,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1558,"statistic":28},[],{"title":1556},{"VI":1557},"Barbara Davis Center for Diabetes, University of Colorado Anschutz Campus, Aurora, USA",[],{"title":1560},{"VI":1561},"Viral N. Shah",{"id":1563,"sortIndex":123,"researcher":28,"roles":1564,"affiliations":1565,"properties":1572,"displayName":1574,"givenName":28,"familyName":28},"366cd15a-1283-4c82-8a9f-194ee88aa64f",[934],[1566],{"id":1537,"sortIndex":32,"affiliation":1567,"properties":28},{"id":1537,"createTime":28,"updateTime":28,"relativeEntities":1568,"slug":28,"properties":1569,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1571,"statistic":28},[],{"title":1570},{"VI":1542},[],{"title":1573},{"VI":1574},"Viswanathan Mohan",{"url":1530,"publisher":1576,"properties":1595},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1577,"slug":872,"properties":1578,"entityType":25,"verifyStatus":878,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1581,"manageAffiliations":1582,"indexDatabases":1583,"url":892,"thumbnailPath":28,"statistic":1590,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":1579,"title":1580},{"VOID":875},{"EN":877},[],[],[1584],{"id":883,"indexDatabase":1585,"url":889,"indexYears":890,"academicFieldIds":28,"indexDatabaseRanking":891},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":1586,"label":1587,"description":1588,"key":781,"publicationTags":1589,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],{"impactFactor":32,"impactFactorByYear":1591,"i10Index":205,"i10IndexLast5Year":48,"totalPublication":895,"totalPublicationByYear":1592,"totalCitation":897,"totalCitationByYear":1593,"totalCitationPerPublication":900,"totalCitationPerPublicationByYear":1594,"hindexLast5Year":205,"hindex":205},{"2016":109,"2017":105,"2018":223,"2019":346,"2020":228,"2021":820,"2022":347,"2023":167},{"2015":146,"2016":47,"2017":47,"2018":199,"2019":205,"2020":129,"2021":128,"2022":145,"2023":46,"2024":49},{"2015":131,"2016":278,"2017":139,"2018":122,"2019":899,"2020":200,"2021":357,"2022":42},{"2015":902,"2016":903,"2017":904,"2018":363,"2019":905,"2020":906,"2021":346,"2022":169},{"pages":1596,"volume":1598},{"VOID":1597},"1-9",{"VOID":1599},"2","2016-11-10",2016,[891],{"id":1604,"createTime":1605,"updateTime":1606,"relativeEntities":1607,"slug":1608,"properties":1609,"entityType":926,"verifyStatus":26,"verifyTime":1618,"verifyNote":928,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1619,"fullTextUrl":28,"authors":1620,"publicationType":1090,"publisherRelationship":1758,"citationCount":28,"citationInfo":28,"publishDate":1783,"publishYear":1784,"citationAnalyzeStatus":878,"lastCitationAnalyze":28,"indexDatabases":1785,"openAccess":28,"references":28,"isForceReanalyzing":1119},"11e46a1c-8b17-4441-9448-dcd7eb7e5813","2024-02-12T06:37:47.113+00:00","2025-01-02T17:02:47.128+00:00",[],"The-diagnostic-indicators-of-gestational-diabetes-mellitus-from-second-trimester-to-birth-a-systematic-review",{"abstract":1610,"title":1612,"references":1614,"doi":1616},{"EN":1611},"Gestational diabetes mellitus (GDM) is glucose intolerance first recognised during pregnancy. Both modalities and thresholds of the GDM diagnostic test, the Oral Glucose Tolerance Test (OGTT), have varied widely over time and among countries. Additionally, OGTT limitations include inconsistency, poor patient tolerability, and questionable diagnostic reliability. Many biological parameters have been reported to be modified by GDM and could potentially be used as diagnostic indicators. This study aimed to 1) systematically explore biomarkers reported in the literature as differentiating GDM from healthy pregnancies 2) screen those indicators assessed against OGTT to propose OGTT alternatives. A systematic review of GDM diagnostic indicators was performed according to PRISMA guidelines (PROSPERO registration CRD42020145499). Inclusion criteria were full-text, comprehensible English-language articles published January 2009-January 2021, where a biomarker (from blood, ultrasound, amniotic fluid, placenta) was compared between GDM and normal glucose tolerance (NGT) women from the second trimester onward to immediately postpartum. GDM diagnostic method had to be clearly specified, and the number of patients per study higher than 30 in total or 15 per group. Results were synthesised by biomarkers. Of 13,133 studies identified in initial screening, 174 studies (135,801 participants) were included. One hundred and twenty-nine studies described blood analytes, one amniotic fluid analytes, 27 ultrasound features, 17 post-natal features. Among the biomarkers evaluated in exploratory studies, Adiponectin, AFABP, Betatrophin, CRP, Cystatin-C, Delta-Neutrophil Index, GGT, TNF-A were those demonstrating statistically and clinically significant differences in substantial cohorts of patients (> 500). Regarding biomarkers assessed versus OGTT (i.e. potential OGTT alternatives) most promising were Leptin > 48.5 ng\u002Fml, Ficolin3\u002Fadiponectin ratio ≥ 1.06, Chemerin\u002FFABP > 0.71, and Ultrasound Gestational Diabetes Score > 4. These all demonstrated sensitivity and specificity > 80% in adequate sample sizes (> \u002F = 100). Numerous biomarkers may differentiate GDM from normoglycaemic pregnancy. Given the limitations of the OGTT and the lack of a gold standard for GDM diagnosis, advanced phase studies are needed to triangulate the most promising biomarkers. Further studies are also recommended to assess the sensitivity and specificity of promising biomarkers not yet assessed against OGTT. PROSPERO registration number CRD42020145499.",{"EN":1613},"The diagnostic indicators of gestational diabetes mellitus from second trimester to birth: a systematic review",{"VOID":1615},"Gilmartin AB, Ural SH, Repke JT. Gestational diabetes mellitus. Rev Obstet Gynecol. 2008;1(3):129–34.\nInternational Association of, D, et al. International association of diabetes and pregnancy study groups recommendations on the diagnosis and classification of hyperglycemia in pregnancy. Diabetes Care. 2010;33(3):676–82.\nAmerican Diabetes A. (2) Classification and diagnosis of diabetes. Diabetes Care. 2015;38(Suppl):S8–16.\nHuhn EA, et al. Controversies in screening and diagnostic criteria for gestational diabetes in early and late pregnancy. Front Endocrinol. 2018;9:696.\nCheung NW, Oats JJ, McIntyre HD. Australian carbohydrate intolerance study in pregnant women: implications for the management of gestational diabetes. Aust N Z J Obstet Gynaecol. 2005;45(6):484–5.\nGroup H.S.C.R. Hyperglycemia and adverse pregnancy outcome (HAPO) study: associations with neonatal anthropometrics. Diabetes. 2009;58(2):453–9.\nCastillo-Castrejon M, Powell TL. Placental nutrient transport in gestational diabetic pregnancies. Front Endocrinol. 2017;8:306.\nMarais C, et al. Randomized cross-over trial comparing the diagnosis of gestational diabetes by oral glucose tolerance test and a designed breakfast glucose profile. Int J Gynaecol Obstet. 2018;141(1):85–90.\nSert UY, Ozgu-Erdinc AS. Gestational diabetes mellitus screening and diagnosis. Adv Exp Med Biol. 2020;1307:231–55.\nMansell E, Lunt H, Docherty P. Laboratory diagnosis of gestational diabetes: an in silico investigation into the effects of pre-analytical processing on the diagnostic sensitivity and specificity of the oral glucose tolerance test. Clin Biochem. 2017;50(9):506–12.\nPotter JM, et al. Strict preanalytical oral glucose tolerance test blood sample handling is essential for diagnosing gestational diabetes mellitus. Diabetes Care. 2020;43(7):1438–41.\nProgramme, C.A.S. CASP checklists. 2020 [cited 30 Nov 2020].\nWeinstein S, Obuchowski NA, Lieber ML. Clinical evaluation of diagnostic tests. AJR Am J Roentgenol. 2005;184(1):14–9.\nTantanasis T, et al. Sonographic assessment of fetal subcutaneous fat tissue thickness as an indicator of gestational diabetes. Eur J Obstet Gynecol Reprod Biol. 2010;152(2):157–62.\nTrujillo J, et al. Fasting plasma glucose to avoid a full OGTT in the diagnosis of gestational diabetes. Diabetes Res Clin Pract. 2014;105(3):322–6.\nCarpenter MW, Coustan DR. Criteria for screening tests for gestational diabetes. Am J Obstet Gynecol. 1982;144(7):768–73.\nWHO. Hyperglycaemia in pregnancy. In Diagnostic criteria and classification of hyperglycaemia first detected in pregnancy. WHO, Editor. 2013, WHO: https:\u002F\u002Fwww.who.int\u002Fdiabetes\u002Fpublications\u002FHyperglycaemia_In_Pregnancy\u002Fen\u002F.\nGroup N.-N.D.D. Classification and diagnosis of diabetes mellitus andother categories of glucose intolerance. National Diabetes Data Group.Diabetes. 1979;28(12):1039–57.\nZhao JP, et al. Longitudinal circulating concentrations of long-chain polyunsaturated fatty acids in the third trimester of pregnancy in gestational diabetes. Diabet Med. 2016;33(7):939–46.\nFatima SS, et al. Elevated levels of chemerin, leptin, and interleukin-18 in gestational diabetes mellitus. J Matern Fetal Neonatal Med. 2017;30(9):1023–8.\nZhang Y, et al. Changes in serum adipocyte fatty acid-binding protein in women with gestational diabetes mellitus and normal pregnant women during mid- and late pregnancy. J Diabetes Investig. 2016;7(5):797–804.\nRueangdetnarong H, et al. 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Havard",{"id":1717,"sortIndex":48,"researcher":28,"roles":1718,"affiliations":1719,"properties":1733,"displayName":1735,"givenName":28,"familyName":28},"7e4d83a1-6760-4327-acc7-2fdea88a24f0",[934],[1720,1726],{"id":1626,"sortIndex":32,"affiliation":1721,"properties":28},{"id":1626,"createTime":28,"updateTime":28,"relativeEntities":1722,"slug":28,"properties":1723,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1725,"statistic":28},[],{"title":1724},{"VI":1631},[],{"id":1682,"sortIndex":40,"affiliation":1727,"properties":1732},{"id":1682,"createTime":28,"updateTime":28,"relativeEntities":1728,"slug":28,"properties":1729,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1731,"statistic":28},[],{"title":1730},{"EN":1687},[],{},{"title":1734},{"VI":1735},"Amanda Henry",{"id":1737,"sortIndex":49,"researcher":28,"roles":1738,"affiliations":1739,"properties":1755,"displayName":1757,"givenName":28,"familyName":28},"b04e9fa1-1e35-4a17-b261-ef5a0a5cd0b7",[934],[1740,1746],{"id":1626,"sortIndex":32,"affiliation":1741,"properties":28},{"id":1626,"createTime":28,"updateTime":28,"relativeEntities":1742,"slug":28,"properties":1743,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1745,"statistic":28},[],{"title":1744},{"VI":1631},[],{"id":1747,"sortIndex":40,"affiliation":1748,"properties":1754},"6e00c6dd-d2c4-4e1e-ab34-8fafcaad7f08",{"id":1747,"createTime":28,"updateTime":28,"relativeEntities":1749,"slug":28,"properties":1750,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1753,"statistic":28},[],{"title":1751},{"VI":1752},"Department of Maternal-Fetal Medicine, Royal Hospital for Women, Randwick, Australia",[],{},{"title":1756},{"VI":1757},"Alec Welsh",{"url":1619,"publisher":1759,"properties":1778},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1760,"slug":872,"properties":1761,"entityType":25,"verifyStatus":878,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1764,"manageAffiliations":1765,"indexDatabases":1766,"url":892,"thumbnailPath":28,"statistic":1773,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":1762,"title":1763},{"VOID":875},{"EN":877},[],[],[1767],{"id":883,"indexDatabase":1768,"url":889,"indexYears":890,"academicFieldIds":28,"indexDatabaseRanking":891},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":1769,"label":1770,"description":1771,"key":781,"publicationTags":1772,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],{"impactFactor":32,"impactFactorByYear":1774,"i10Index":205,"i10IndexLast5Year":48,"totalPublication":895,"totalPublicationByYear":1775,"totalCitation":897,"totalCitationByYear":1776,"totalCitationPerPublication":900,"totalCitationPerPublicationByYear":1777,"hindexLast5Year":205,"hindex":205},{"2016":109,"2017":105,"2018":223,"2019":346,"2020":228,"2021":820,"2022":347,"2023":167},{"2015":146,"2016":47,"2017":47,"2018":199,"2019":205,"2020":129,"2021":128,"2022":145,"2023":46,"2024":49},{"2015":131,"2016":278,"2017":139,"2018":122,"2019":899,"2020":200,"2021":357,"2022":42},{"2015":902,"2016":903,"2017":904,"2018":363,"2019":905,"2020":906,"2021":346,"2022":169},{"pages":1779,"volume":1781},{"VOID":1780},"1-15",{"VOID":1782},"7","2021-10-11",2021,[891],{"id":1787,"createTime":1788,"updateTime":1789,"relativeEntities":1790,"slug":1791,"properties":1792,"entityType":926,"verifyStatus":26,"verifyTime":1789,"verifyNote":928,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1801,"fullTextUrl":28,"authors":1802,"publicationType":1090,"publisherRelationship":1888,"citationCount":28,"citationInfo":28,"publishDate":1912,"publishYear":1913,"citationAnalyzeStatus":878,"lastCitationAnalyze":28,"indexDatabases":1914,"openAccess":28,"references":28,"isForceReanalyzing":1119},"127630e1-a772-4222-9e15-2e1525ee87dd","2024-01-18T13:20:59.857+00:00","2025-01-19T06:22:38.873+00:00",[],"A-quality-improvement-project-to-increase-compliance-with-diabetes-measures-in-an-academic-outpatient-setting",{"abstract":1793,"title":1795,"references":1797,"doi":1799},{"EN":1794},"American Diabetes Association (ADA) sets annual guidelines on preventative measures that aim to delay the onset of severe diabetes mellitus complications. Compared to private internal medicine clinics, resident clinics provide suboptimal diabetic preventative care as evidenced by decreased compliance with ADA guidelines. The purpose of our study is to improve diabetic care in resident clinics through quality improvement (QI) projects, with A1C value as primary outcome and other ADA guidelines as secondary outcomes. Our resident clinic at Beaumont Hospital, Royal Oak consists of 76 residents divided in 8 teams. In November 2016, baseline data on ADA guideline measures was obtained on 538 patients with diabetes mellitus. A root cause analysis was conducted. 5 teams developed a QI intervention plan to improve their diabetes care and 3 teams served as comparisons without intervention plans. In November 2017, post-intervention data was collected. Baseline characteristics demonstrate mean age of intervention groups at 60.9 years and of comparison groups at 58.9 years. The change in A1C value from baseline to post-intervention was + 0.09 vs. + 0.322 in the intervention and comparison groups respectively (p = 0.174). As a group, the changes in secondary outcome measures were as follows: eye examinations (+ 5% in intervention vs. -7% in comparison, p \u003C 0.01), foot examinations (+ 13% vs. + 5%, p = 0.09), lipid panel testing (+ 7% vs. -5%, p \u003C 0.01), micro-albumin\u002Fcreatinine ratio testing (+ 4% vs. + 1%, p = 0.03), and A1C testing (+8% vs. + 5%, p = 0.24). While the QI project did not improve A1C value, it did have significant improvement in several secondary outcomes within intervention groups. One resident team implemented an intervention involving protected half-day blocks to identify overdue examinations and consequently had the largest improvements, thus serving as a potential intervention to further study. Given our study results, we believe that QI interventions improve preventative care for patients with diabetes in resident clinics.",{"EN":1796},"A quality improvement project to increase compliance with diabetes measures in an academic outpatient setting",{"VOID":1798},"Centers for Disease Control and Prevention. National Diabetes Statistics Report, 2017. Atlanta: Centers for Disease Control and Prevention, U.S. Dept of Health and Human Services; 2017.\nFowler MJ. Microvascular and macrovascular complications of diabetes. Clinical Diabetes. 2008;26(2):77–82. https:\u002F\u002Fdoi.org\u002F10.2337\u002Fdiaclin.26.2.77.\nNational Center for Chronic Disease Prevention and Health Promotion (NCCDPHP). Centers for Disease Control and Prevention. https:\u002F\u002Fwww.cdc.gov\u002Fdiabetes\u002Fbasics\u002Fdiabetes.html. Accessed 1 Dec 2018.\nStratton IM, Adler AI, Neil HA, et al. Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study. BMJ. 2000;321(7258):405–12.\nStandards of Medical Care in Diabetes—2018 Abridged for Primary Care Providers. Clinical Diabetes. August 2017:cd170119. doi:https:\u002F\u002Fdoi.org\u002F10.2337\u002Fcd17-0119.\nLynn L, Hess BJ, Weng W, Lipner RS, Holmboe ES. Gaps in quality of diabetes care in internal medicine residency clinics suggest the need for better ambulatory care training. Health Aff. 2012;31(1):150–8.\nAIAMC National Initiative III: 2011-2013. Improving Patient Care through Medical Education: A National Initiative of Independent Academic Medical Centers. https:\u002F\u002Fwww.aiamc.org\u002Fni-iii.html. Accessed 1 Dec 2018.\nNasca TJ. Common Program Requirements Section VI Approved. 2017. Memo regarding approved changes to common program requirements for ACGME. http:\u002F\u002Fwww.acgme.org\u002FPortals\u002F0\u002FPDFs\u002FNasca-Community\u002FSection-VI-Memo-3-10-17.pdf?ver=2017-03-10-083926-603. Accessed 1 Dec 2018.\nAli-Ahmed F, Halalau A. The impact of personalized telephone reminders on diabetes core measures and no-show rates in a resident clinic; A crosssectional study. Qual Prim Care. 2016;24(5):231–236.\nLangley GL, Nolan KM, Nolan TW, et al. The improvement guide: a practical approach to enhancing organizational performance. San Francisco: Jossey-Bass; 1996.\nGonzalez JS, Shreck E, Psaros C, Safren SA. Distress and type 2 diabetes-treatment adherence: a mediating role for perceived control. Health Psychol. 2014;34(5):505–13.\nSullivan S, Dalal M, Burke J. The impact of diabetes counseling and education: clinical and cost outcomes from a large population of US managed care patients with type 2 diabetes. Diabetes Educ. 2013;39(4):523–31.\nTricco AC, Ivers NM, Grimshaw JM, et al. Effectiveness of quality improvement strategies on the management of diabetes: a systematic review and meta-analysis. Lancet. 2012;379(9833):2252–61. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fs0140-6736(12)60480-2.\nSzpunar SM, Minnick SE, Dako I, Saravolatz LD. Improving foot Examinations in Patients with Diabetes. Diabetes Educ. 2014;40(3):281–9. https:\u002F\u002Fdoi.org\u002F10.1177\u002F0145721714526789.\nThomas KG, Thomas MR, Stroebel RJ, et al. Use of a registry-generated audit, feedback, and patient reminder intervention in an internal medicine resident clinic—a randomized trial. J Gen Intern Med. 2007;22(12):1740–4. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs11606-007-0431-x.\nAneese N, Halalau A, Muench S, Shelden D, Fett J, Lauster C. Impact of a Pharmacist-Managed Diabetes Clinic on Quality Measures. Am J Manag Care. 2018;24(4 Spec No.):SP116–SP119.\nPousinho S, Morgado M, Falcão A, Alves G. Pharmacist interventions in the management of type 2 diabetes mellitus: a systematic review of randomized controlled trials. J Manag Care Spec Pharm. 2016;22(5):493–515.",{"VOID":1800},"10.1186\u002Fs40842-019-0084-9","https:\u002F\u002Fclindiabetesendo.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs40842-019-0084-9",[1803,1818,1833,1848,1868],{"id":1804,"sortIndex":32,"researcher":28,"roles":1805,"affiliations":1806,"properties":1815,"displayName":1817,"givenName":28,"familyName":28},"e424b965-5c29-4af4-8244-42b448b55b9d",[934],[1807],{"id":1808,"sortIndex":32,"affiliation":1809,"properties":28},"c083f4b6-ac79-4b87-afca-f59ecf0b57a5",{"id":1808,"createTime":28,"updateTime":28,"relativeEntities":1810,"slug":28,"properties":1811,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1814,"statistic":28},[],{"title":1812},{"VI":1813},"Oakland University William Beaumont School of Medicine, Rochester Hills, USA",[],{"title":1816},{"VI":1817},"Subhash Edupuganti",{"id":1819,"sortIndex":40,"researcher":28,"roles":1820,"affiliations":1821,"properties":1830,"displayName":1832,"givenName":28,"familyName":28},"72142606-33d9-4103-894a-511a5c40c14e",[934],[1822],{"id":1823,"sortIndex":32,"affiliation":1824,"properties":28},"bd5e74b4-ecd8-42ee-8a53-b5abe423308f",{"id":1823,"createTime":28,"updateTime":28,"relativeEntities":1825,"slug":28,"properties":1826,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1829,"statistic":28},[],{"title":1827},{"VI":1828},"Department of Internal Medicine, William Beaumont Hospital, Royal Oak, USA",[],{"title":1831},{"VI":1832},"Jordan 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Maditz",{"id":1849,"sortIndex":42,"researcher":28,"roles":1850,"affiliations":1851,"properties":1865,"displayName":1867,"givenName":28,"familyName":28},"e857a442-3ae1-402e-8e18-0b2a91ba9baf",[934],[1852,1858],{"id":1808,"sortIndex":32,"affiliation":1853,"properties":28},{"id":1808,"createTime":28,"updateTime":28,"relativeEntities":1854,"slug":28,"properties":1855,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1857,"statistic":28},[],{"title":1856},{"VI":1813},[],{"id":1823,"sortIndex":40,"affiliation":1859,"properties":1864},{"id":1823,"createTime":28,"updateTime":28,"relativeEntities":1860,"slug":28,"properties":1861,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1863,"statistic":28},[],{"title":1862},{"VI":1828},[],{},{"title":1866},{"VI":1867},"Pradeep 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Halalau",{"url":1801,"publisher":1889,"properties":1908},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1890,"slug":872,"properties":1891,"entityType":25,"verifyStatus":878,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1894,"manageAffiliations":1895,"indexDatabases":1896,"url":892,"thumbnailPath":28,"statistic":1903,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":1892,"title":1893},{"VOID":875},{"EN":877},[],[],[1897],{"id":883,"indexDatabase":1898,"url":889,"indexYears":890,"academicFieldIds":28,"indexDatabaseRanking":891},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":1899,"label":1900,"description":1901,"key":781,"publicationTags":1902,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],{"impactFactor":32,"impactFactorByYear":1904,"i10Index":205,"i10IndexLast5Year":48,"totalPublication":895,"totalPublicationByYear":1905,"totalCitation":897,"totalCitationByYear":1906,"totalCitationPerPublication":900,"totalCitationPerPublicationByYear":1907,"hindexLast5Year":205,"hindex":205},{"2016":109,"2017":105,"2018":223,"2019":346,"2020":228,"2021":820,"2022":347,"2023":167},{"2015":146,"2016":47,"2017":47,"2018":199,"2019":205,"2020":129,"2021":128,"2022":145,"2023":46,"2024":49},{"2015":131,"2016":278,"2017":139,"2018":122,"2019":899,"2020":200,"2021":357,"2022":42},{"2015":902,"2016":903,"2017":904,"2018":363,"2019":905,"2020":906,"2021":346,"2022":169},{"pages":1909,"volume":1910},{"VOID":1511},{"VOID":1911},"5","2019-07-23",2019,[891],{"id":1916,"createTime":1917,"updateTime":1918,"relativeEntities":1919,"slug":1920,"properties":1921,"entityType":926,"verifyStatus":26,"verifyTime":1918,"verifyNote":928,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1930,"fullTextUrl":28,"authors":1931,"publicationType":1090,"publisherRelationship":1947,"citationCount":28,"citationInfo":28,"publishDate":1971,"publishYear":1972,"citationAnalyzeStatus":878,"lastCitationAnalyze":28,"indexDatabases":1973,"openAccess":28,"references":28,"isForceReanalyzing":1119},"1575e194-ea82-4857-a96b-63a426a315be","2023-11-27T08:41:21.938+00:00","2025-02-07T06:29:51.841+00:00",[],"Diabetes-and-its-drivers-the-largest-epidemic-in-human-history-",{"abstract":1922,"title":1924,"references":1926,"doi":1928},{"EN":1923},"The “Diabesity” epidemic (obesity and type 2 diabetes) is likely to be the biggest epidemic in human history. Diabetes has been seriously underrated as a global public health issue and the world can no longer ignore “the rise and rise” of type 2 diabetes. Currently, most of the national and global diabetes estimates come from the IDF Atlas. These estimates have significant limitations from a public health perspective. It is apparent that the IDF have consistently underestimated the global burden. More reliable estimates of the future burden of diabetes are urgently needed. To prevent type 2 diabetes, a better understanding of the drivers of the epidemic is needed. While for years, there has been comprehensive attention to the “traditional” risk factors for type 2 diabetes i.e., genes, lifestyle and behavioral change, the spotlight is turning to the impact of the intra-uterine environment and epigenetics on future risk in adult life. It highlights the urgency for discovering novel approaches to prevention focusing on maternal and child health. Diabetes risk through epigenetic changes can be transmitted inter-generationally thus creating a vicious cycle that will continue to feed the diabetes epidemic. History provides important lessons and there are lessons to learn from major catastrophic events such as the Dutch Winter Hunger and Chinese famines. The Chinese famine may have been the trigger for what may be viewed as a diabetes “avalanche” many decades later. The drivers of the epidemic are indeed genes and environment but they are now joined by deleterious early life events. Looking to the future there is the potential scenario of future new “hot spots” for type 2 diabetes in regions e.g., the Horn of Africa, now experiencing droughts and famine. This is likely to occur should improved economic and living conditions occur over the next few decades. Type 2 diabetes will remain one of the greatest challenges to human health for many years to come.",{"EN":1925},"Diabetes and its drivers: the largest epidemic in human history?",{"VOID":1927},"Benedictow OJ. The black death, 1346–1353: the complete history. Woodbridge: The Boydell Press; 2004.\nInternational Diabetes Federation. IDF Diabetes. 7th ed. Brussels: International Diabetes Federation; 2015. http:\u002F\u002Fwww.diabetesatlas.org.\nInternational Diabetes Federation. IDF Diabetes. 1st ed. Brussels: International Diabetes Federation; 2000. http:\u002F\u002Fwww.diabetesatlas.org.\nWild S, Roglic G, Green A, Sicree R, King H. Global prevalence of diabetes – Estimates for the year 2000 and projections for 2030. Diabetes Care. 2004;27:1047–53.\nWest KM. Standardization of definition, classification, and reporting in diabetes-related epidemiologic studies. Diabetes Care. 1979;2:65–76.\nZimmet P, Alberti KG, Magliano DJ, Bennett PH. Diabetes mellitus statistics on prevalence and mortality: facts and fallacies. Nature Rev Endocrinol. 2016. doi:10.1038\u002Fnrendo.2016.105. Published online: 08 July 2016.\nHouechanou YCN, Lacroix P, Mizehoun GC, Preux PM, Marin B, Houinato DS. Magnitude of cardiovascular risk factors in rural and urban areas in Benin. Findings from a nationwide steps survey. PLoS ONE. 2015;10:1–13. doi:10.1371\u002Fjournal.pone.0126441. e0126441.\nFajans SS, Conn JW. The early recognition of diabetes mellitus. Ann NY Acad Sci. 1959;82:208–18.\nChristensen JO, Sandbaek A, Lauritzen T, Borch-Johnsen K. Population-based stepwise screening for unrecognized type 2 diabetes in general practice is ineffective despite reliable algorithms. Diabetologia. 2004;47:1566–73.\nDavies J, Yudkin JS, Atun R. Liberating data: the crucial weapon in the fight against NCDs. Lancet Diabetes Endocrinol. 2016;4:197–98.\nGBD 2013 Mortality and Causes of Death Collaborators. Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet. 2015;385:117–71.\nZimmet P. Epidemiology of diabetes and its macrovascular manifestations in pacific populations: the medical effects of social progress. Diabetes Care. 1979;2:144–53.\nDowse GK, Gareeboo H, Zimmet PZ, et al. High prevalence of NIDDM impaired glucose tolerance in Indian, creole, and Chinese Mauritians. Diabetes. 1990;39:390–6.\nPrior IAM, Rose BS, Davidson F. Metabolic Maladies in New Zealand Maoris. Brit Med J. 1964;1:1065–9.\nBennett PH, Burch TA, Miller M. Diabetes Mellitus in American (PIMA) Indians. Lancet. 1971;298:125–8.\nWise PH, Edwards FM, Thomas DW, Elliott RB, Hatcher L, Craig R. Hyperglycaemia in the Urbanized Aboriginal. The Davenport Study. Med J Aust. 1970;2:1001–6.\nZimmet P, Taft P, Guinea A, Guthrie W, Thoma K. The high prevalence of diabetes mellitus on a central pacific island. Diabetologia. 1977;13:111–5.\nSoderberg S, Zimmet P, Tuomilehto J, et al. Increasing prevalence of type 2 diabetes mellitus in all ethnic groups in Mauritius. Diabetic Med. 2005;22:61–8.\nMagliano DJ, Soderberg S, Zimmet PZ, et al. Explaining the increase of diabetes prevalence and plasma glucose in Mauritius. Diabetes Care. 2012;35:87–91.\nRamachandran A, Mary S, Yamuna A, Murugesan N, Snehalatha C. High prevalence of diabetes and cardiovascular risk factors associated with urbanization in India. Diabetes Care. 2008;31:893–8.\nYang WY, Lu JM, Weng JP, et al. Prevalence of diabetes among Men and women in China. N Engl J Med. 2010;362:1090–101.\nSatman I, Yilmaz T, Sengul A, et al. Population-based study of diabetes and risk characteristics in Turkey. Results of the Turkish Epidemiology Study (TURDEP). Diabetes Care. 2002;25:1551–6.\nGuest CS, O’Dea K. Diabetes in Aborigines and other Australian populations. Aust J Public Health. 1992;16:340–9.\nHoy WE. Kidney disease in Aboriginal Australians: a perspective from the Northern Territory. Clin Kidney J. 2014;7:524–30.\nMathers M. Dialysis in Central Australia. Current Issues in Indigenous Affairs U3A Hawthorn. 2012. p. 1–7.\nRowley KG, O’Dea K. Diabetes in Australian Aboriginal and Torres Strait Islander peoples. PNG Med J. 2001;44:164–70.\nDunstan DW, Zimmet PZ, Welborn TA, et al. The rising prevalence of diabetes and impaired glucose tolerance. The Australian diabetes, obesity and lifestyle study. Diabetes Care. 2002;25:829–34.\nCameron AJ, Welborn TA, Zimmet PZ, et al. Overweight and obesity in Australia: the 1999–2000 Australian Diabetes, Obesity and Lifestyle Study (AusDiab). Med J Aust. 2003;178:427–32.\nHuang ES, Basu A, O’Grady M, Capretta JC. Projecting the future diabetes population size and related costs for the U.S. Diabetes Care. 2009;32:2225–9.\nKhambalia A, Phongsavan P, Smith BJ, et al. Prevalence and risk factors of diabetes and impaired fasting glucose in Nauru. BMC Public Health. 2011;11:719.\nFranco M, Bilal U, Ordunez P, et al. Population-wide weight loss and regain in relation to diabetes burden and cardiovascular mortality in Cuba 1980–2010: repeated cross sectional surveys and ecological comparison of secular trends. BMJ. 2013;346:f1515.\nKing H, Finch C, Collins A, et al. Glucose tolerance in Papua New Guinea: ethnic differences, association with environmental and behavioural factors and the possible emergence of glucose intolerance in a highland community. Med J Aust. 1989;51:204–10.\nO’Dea K. Marked improvement in carbohydrate and lipid metabolism in diabetic Australian aborigines after temporary reversion to traditional lifestyle. Diabetes. 1984;33:596–603.\nTuomilehto J, Lindstrom J, Eriksson JG, et al. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. N Engl J Med. 2001;344:1343–50.\nKoestler A. The call girls. London and Sydney: Pan Books; 1976.\nBarker DJP. Maternal nutrition, fetal nutrition, and disease in later life. Nutrition. 1997;13:807–13.\nRavelli ACJ, van der Meulen JHP, Michels RPJ, et al. Glucose tolerance in adults after prenatal exposure to famine. Lancet. 1998;351:173–7.\nDiKotter F. Mao’s great famine. The history of China’s most devastating catastrophe. 1958–1962. USA: Bloomsberg Publishing; 2010.\nLi YP, He YN, Qi L, et al. Exposure to the Chinese famine in early life and the risk of hyperglycemia and type 2 diabetes in adulthood. Diabetes Care. 2010;59:2400–6.\nXu Y, Wang L, He J, 2010 China Noncommunicable Disease Surveillance Group, et al. Prevalence and control of diabetes in Chinese adults. JAMA. 2013;310:948–59.\nSoh SE, Tint MT, Gluckman PD, et al. Cohort profile: Growing Up in Singapore Towards healthy Outcomes (GUSTO) birth cohort study. Int J Epidemiol. 2014;43:1401–9.\nGluckman P, Hanson M. MisMatch. Why our world no longer fits our bodies. Oxford: Oxford University Press; 2008.\nLumey LH, Khalangot MD, Vaiseman AM. Association between type 2 diabetes and prenatal exposure to the Ukraine famine of 1932–33: a retrospective cohort study. Lancet Diabetes Endocrinol. 2015;3:787–94.\nKing H, Keuky L, Seng S, Khun T, Roglic G, Pinget M. Diabetes and associated disorders in Cambodia: two epidemiological surveys. Lancet. 2005;366:1633–9.\nZimmet PZ, Magliano DJ, Herman WH, Shaw JE. Diabetes: a 21st century challenge. Lancet Diabetes Endocrinol. 2014;2:56–64.\nZhang P, Zhang XZ, Brown J, et al. Global healthcare expenditure on diabetes for 2010 and 2030. Diab Res Clin Pract. 2010;87:293–301.",{"VOID":1929},"10.1186\u002Fs40842-016-0039-3","http:\u002F\u002Fclindiabetesendo.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs40842-016-0039-3",[1932],{"id":1933,"sortIndex":32,"researcher":28,"roles":1934,"affiliations":1935,"properties":1944,"displayName":1946,"givenName":28,"familyName":28},"3d23e9e0-4769-4f70-9861-d64bdbaef764",[934],[1936],{"id":1937,"sortIndex":32,"affiliation":1938,"properties":28},"d67ee741-907e-4b74-a7e2-5c48d1ca20d0",{"id":1937,"createTime":28,"updateTime":28,"relativeEntities":1939,"slug":28,"properties":1940,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1943,"statistic":28},[],{"title":1941},{"VI":1942},"Monash University & Baker IDI Heart and Diabetes Institute, Melbourne, Australia",[],{"title":1945},{"VI":1946},"Paul Z. Zimmet",{"url":1930,"publisher":1948,"properties":1967},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1949,"slug":872,"properties":1950,"entityType":25,"verifyStatus":878,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1953,"manageAffiliations":1954,"indexDatabases":1955,"url":892,"thumbnailPath":28,"statistic":1962,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":1951,"title":1952},{"VOID":875},{"EN":877},[],[],[1956],{"id":883,"indexDatabase":1957,"url":889,"indexYears":890,"academicFieldIds":28,"indexDatabaseRanking":891},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":1958,"label":1959,"description":1960,"key":781,"publicationTags":1961,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],{"impactFactor":32,"impactFactorByYear":1963,"i10Index":205,"i10IndexLast5Year":48,"totalPublication":895,"totalPublicationByYear":1964,"totalCitation":897,"totalCitationByYear":1965,"totalCitationPerPublication":900,"totalCitationPerPublicationByYear":1966,"hindexLast5Year":205,"hindex":205},{"2016":109,"2017":105,"2018":223,"2019":346,"2020":228,"2021":820,"2022":347,"2023":167},{"2015":146,"2016":47,"2017":47,"2018":199,"2019":205,"2020":129,"2021":128,"2022":145,"2023":46,"2024":49},{"2015":131,"2016":278,"2017":139,"2018":122,"2019":899,"2020":200,"2021":357,"2022":42},{"2015":902,"2016":903,"2017":904,"2018":363,"2019":905,"2020":906,"2021":346,"2022":169},{"pages":1968,"volume":1969},{"VOID":1217},{"VOID":1970},"3","2017-01-18",2017,[891],{"id":1975,"createTime":1976,"updateTime":1977,"relativeEntities":1978,"slug":1979,"properties":1980,"entityType":926,"verifyStatus":26,"verifyTime":1977,"verifyNote":928,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1989,"fullTextUrl":28,"authors":1990,"publicationType":1090,"publisherRelationship":2155,"citationCount":28,"citationInfo":28,"publishDate":2179,"publishYear":2180,"citationAnalyzeStatus":878,"lastCitationAnalyze":28,"indexDatabases":2181,"openAccess":28,"references":28,"isForceReanalyzing":1119},"16f7fce7-2e2d-46ea-9ea4-fca3a6e0aae1","2023-12-18T11:27:12.307+00:00","2025-01-20T06:53:54.495+00:00",[],"Hyperinsulinemic-hypoglycemia-in-adolescents-case-report-and-systematic-review",{"abstract":1981,"title":1983,"references":1985,"doi":1987},{"EN":1982},"Hyperinsulinemic hypoglycemia is the most common cause of severe and persistent hypoglycemia in neonates and children. It is a heterogeneous condition with dysregulated insulin secretion, which persists in the presence of low blood glucose levels. We report a case of a 15 year-old male with hyperinsulinemic hypoglycemia, who underwent a subtotal pancreatectomy after inadequate response to medical therapy. Pathological examination was positive for nesidioblastosis (diffuse β-cell hyperplasia by H-E and immunohistochemical techniques). The patient’s blood glucose levels normalized after surgery and he remains asymptomatic after 1 year of follow-up. The systematic review allowed us to identify 41 adolescents from a total of 205 cases reported in 22 manuscripts, from a total of 454 found in the original search done in PubMed and Lilacs. Although very well reported in children, hyperinsulinemic hypoglycemia can occur in adolescents or young adults, as it happens in our reported case. These patients can be seen, treated and reported by pediatricians or adult teams either way due to the wide age range used to define adolescence. Most of them do not respond to medical treatment, and subtotal distal pancreatectomy has become the elected procedure with excellent long-term response in the vast majority.",{"EN":1984},"Hyperinsulinemic hypoglycemia in adolescents: case report and systematic review",{"VOID":1986},"Shah P, Rahman SA, Demirbulek H, Güemes M, Hussain K. Hyperinsulinaemic hypoglycaemia in children and adults. Lancet Diabetes Endocrinol. 2016;5:729–74.\nRahman SA, Nessa A, Hussain K. Molecular mechanisms of congenital hyperinsulinism. J Mol Endocrinol. 2015;54:R119–29.\nShin JJ, Gorden P, Libutti SK. Insulinoma: pathophysiology, localization and management. Future Oncol. 2010;6:229–37.\nSempoux C, Capito C, Bellanné-Chantelot C, et al. Morphological Mosaicism of the pancreatic islets: a novel anatomopathological form of persistent hyperinsulinemic hypoglycemia of infancy. J Clin Endocrinol Metab. 2011;96:3785–93.\nVerkarre V, Fournet JC, de Lonlay P, et al. Paternal mutation of the sulfonylurea receptor (SUR1) gene and maternal loss of 11p15 imprinted genes lead to persistent hyperinsulinism in focal adenomatous hyperplasia. J Clin Invest. 1998;102:1286–91.\nCryer PE, Axelrod L, Grossman AB, et al. Evaluation and management of adult hypoglycemic disorders: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2009;94:709–28.\nGuerrero-Fernández J, González Casado L, Espinoza Colindres L, Gracia BR. Hiperinsulinismo congénito revisión de 22 casos. An Pediatr (Barc). 2006;65:22–31.\nParashar K, Upadhyay V, Corkery JJ. Partial or near-total pancreatectomy for nesidioblastosis? Eur J Pediatr Surg. 1995;5:146–8.\nElsaied A, El-Ghazaly M, Esharkawy A. Near-total pancreatectomy for persistant hyperinsulinemic hypoglycemia of infancy (nesidioblastosis): Mansoura experience. Annals of Pediatric Surgery. 2012;8:49–53.\nMoazam F, Rodgers BM, Talbert JL, Rosenbloom AL. Near-total pancreatectomy in persistent infantile hypoglycemia. Arch Surg. 1982;117:1151–4.\nKramer JL, Bell MJ, DeSchryver K, Bower RJ, Ternberg JL, White NH. Clinical and histologic indications for extensive pancreatic resection in nesidioblastosis. Am J Surg. 1982;143:116–9.\nHarness JK, Geelhoed GW, Thompson NW, Nishiyama RH, Fajans SS, Kraft RO, et al. Nesidioblastosis in adults. Surg Dilemma Arch Surg. 1981;116:575–80.\nDunger DB, Burns C, Ghale GK, Muller DP, Spitz L. Grant DB pancreatic exocrine and endocrine function after subtotal pancreatectomy for nesidioblastosis. J Pediatr Surg. 1988;23:112–5.\nPedrazzoli S, Pasquali C, Alfano D'AA. Surgical treatment of insulinoma. Br J Surg. 1994;81:672–6.\nRother KI, Carney JA, Couce M, Charlesworth J, Butler PC. Islet amyloid polypeptide in pancreatic tissue of children with persistent hyperinsulinemic hypoglycemia caused by primary islet hyperplasia and nesidioblastosis. J Clin Endocrinol Metab. 1995;80:1956–9.\nLeibowitz G, Glaser B, Higazi AA, Salameh M, Cerasi E, Landau H. Hyperinsulinemic hypoglycemia of infancy (nesidioblastosis) in clinical remission: high incidence of diabetes mellitus and persistent beta-cell dysfunction at long-term follow-up. J Clin Endocrinol Metab. 1995;80:386–92.\nFuller PJ, Ehrlich AR, Susil B, Zeimer H. Insulin gene expression in adult-onset nesidioblastosis. Clin Endocrinol. 1997;47:245–50.\nDacou-Voutetakis C, Psychou F, Maniati-Christidis M. Persistent hyperinsulinemic hypoglycemia of infancy: long-term results. J Pediatr Endocrinol Metab. 1998;11:131–41.\nUeda Y, Kurihara K, Kondoh T, Okanoue T, Chiba T. Islet-cell hyperplasia causing hyperinsulinemic hypoglycemia in an adult. J Gastroenterol. 1998;33:125–8.\nVan der Wal BC, de Krijger RR, de Herder WW, Kwekkeboom DJ, van der Ham F, Bonjer HJ, et al. Adult hyperinsulinemic hypoglycemia not caused by an insulinoma: a report of two cases. Virchows Arch. 2000;436:481–6.\nService FJ, Natt N, Thompson GB, Grant CS, van Heerden JA, Andrews JC, et al. Noninsulinoma pancreatogenous hypoglycemia: a novel syndrome of hyperinsulinemic hypoglycemia in adults independent of mutations in Kir6.2 and SUR1 genes. J Clin Endocrinol Metab. 1999;84:1582–9.\nThompson GB, Service FJ, Andrews JC, Lloyd RV, Natt N, van Heerden JA, et al. Noninsulinoma pancreatogenous hypoglycemia syndrome: an update in 10 surgically treated patients. Surgery. 2000;128:937–44 discussion 944-5.\nWitteles RM, Straus FH II, Sugg SL, Koka MR, Costa EA. Kaplan EL adult-onset nesidioblastosis causing hypoglycemia: an important clinical entity and continuing treatment dilemma. Arch Surg. 2001;136(6):656–63.\nMartinez-Ibanez V, Gussinyer M, Toran N, Lloret J, Abad P, Carrascosa A, Boix-Ochoa J. Pancreatectomy extension in persistent hyperinsulinaemic hypoglycaemia: a new strategy. Eur J Pediatr Surg. 2002;12:262–6.\nBin-Abbas BS, Al-Ashwal AA. Diabetes in anonpancreatectomized child with nesidioblastosis. Diabetes Care. 2004;27:626–7. https:\u002F\u002Fdoi.org\u002F10.2337\u002Fdiacare.27.2.626.\nAnlauf M, Wieben D, Perren A, Sipos B, Komminoth P, Raffel A, et al. Persistent hyperinsulinemic hypoglycemia in 15 adults with diffuse nesidioblastosis: diagnostic criteria, incidence, and characterization of beta-cell changes. Am J Surg Pathol. 2005;29:524–33.\nRaffel A, Krausch M, Anlauf M, Wieben D, Braunstein S, Klöppel G, et al. Diffuse nesidioblastosis as a cause of hyperinsulinemic hypoglycemia in adults: a diagnostic and therapeutic challenge. Surgery. 2007;141:179–84 discussion 185-6.\nKovács E, Németh H, Pásztor E, Pfliegler G. Hyperinsulinemic hypoglycemia in adults. Case reports and a short review. Orv Hetil. 2008;149:1659–64.\nRestrepo K, Garavito G, Rojas L, Romero A, Neira F, Oliveros R, et al. Nesidioblastosis del adulto coexistente con insulinota. Rev Colomb C Ancerol. 2009;13:49–60.\nSoares F, Providência R, Pontes M. 2013 Nesidioblastosis: an undescribed cause of transient loss of conscience in young adults. Europace. 2013;15:1506.\nDe Jesús J, Fung L, Garcia F, Núñez M. Nesidioblastosis en adolescentes: a propósito de un caso. Rev Venez Endocrinol Metab. 2015;13:48–53.\nCastillo-López MG, Fernandez MF, Sforza N, Barbás N, Mendez J, Pattin F, Mendez G, Ogresta F, Gondolesi I, Barros Schelotto P, Musso C, Gondolesi GE. Hyperinsulinemic hypoglycemia in an adolescent: case report and systematic review. Manuscript submitted for publication.\nSandler R, Horwitz DL, Rubenstein AH, Kuzuya H. Hypoglycemia and endogenous hyperinsulinism complicating diabetes mellitus. Am J Med. 1975;59:730–6.\nTucker ON, Crotty PL, Conlon KC. The management of insulinoma. Br J Surg. 2006;93:264–75.\nFerrario C, Stoll D, Boubaker A, Matter M, Yan P, Puder JJ. Diffuse nesidioblastosis with hypoglycemiamimicking an insulinoma: a case report. J Med Case Rep. 2012;6:2–6.\nChrist E, Wild D, Antwi K, Waser B, Fani M, Schwanda S, et al. Preoperative localization of adult nesidioblastosis using 68Ga-DOTA-exendin-4-PET\u002FCT. Endocrine. 2015;50(821):821–3.\nChrist E, Wild D, Ederer S, Behe M, Nicolas G, Caplin ME, et al. Glucagon-like peptide-1 receptor imaging for the localisation of insulinomas: a prospective multicentre imaging study. Lancet Diabetes Endocrinol. 2013;1:115–22.\nHardy OT, Hernandez-Pampaloni M, Saffer JR, Suchi M, Ruchelli E, Zhuang H, et al. Diagnosis and localization of focal congenital hyperinsulinism by 18F-Fluorodopa PET scan. J Pediatr. 2006;150:140–5.\nStanley C. Perspective on the genetics and diagnosis of congenital Hyperinsulinism disorders. J Clin Endocrinol Metab. 2016;101:815–26.\nShah P, Rahman SA, Demirbilek H, Guemes M, Hussain K. Hyperinsulinemic hypoglycemia in children and adults. Lancet Diabetes Endocrinol. 2017;5:729–42.\nRibeiro MJ, De Lonlay P, Delzescaux T, Boddaert N, Jaubert F, Bourgeois S, et al. Characterization of hyperinsulinism in infancy assessed with PET and 18F-fluoro-L-DOPA. J Nucl Med. 2005;46:560–6.\nZani A, Nah SA, Ron O, Totonelli G, Ismail D, Smith VV, et al. The predictive value of preoperative fluorine-18-L-3,4-dihydroxyphenylalanine positron emission tomography-computed tomography scans in children with congenital hyperinsulinism of infancy. J Pediatr Surg. 2011;46:204–8.\nRibeiro MJ, Boddaert N, Bellanné-Chantelot C, Bourgeois S, Valayannopoulos V, Delzescaux T, et al. The added value of [18F]fluoro-L-DOPA PET in the diagnosis of hyperinsulinism of infancy: a retrospective study involving 49 children. Eur J Nucl Med Mol Imaging. 2007;34:2120–8.\nHardy OT, Hernandez-Pampaloni M, Saffer JR, Scheuermann JS, Ernst LM, Freifelder R, et al. Accuracy of [18F] fluorodopa positron emission tomography for diagnosing and localizing focal congenital hyperinsulinism. J Clin Endocrinol Metab. 2007;92:4706–11.\nMohnike W, Barthlen W, Mohnike K, Blankenstein O. Positron emission tomography\u002Fcomputed tomography diagnostics by means of fluorine-18-L-dihydroxyphenylalanine in congenital hyperinsulinism. Semin Pediatr Surg. 2011;20:23–7.\nTreglia G, Mirk P, Giordano A, Rufini V. Diagnostic performance of fluorine-18-dihydroxyphenylalanine positron emission tomography in diagnosing and localizing the focal form of congenital hyperinsulinism: a meta-analysis. Pediatr Radiol. 2012;42:1372–9.\nDoi S, Yamada T, Kito Y, Obara S, Fujii Y, Nishimura T, Kato T, et al. Adult-Onset Focal Nesidioblastosis With Nodular Formation Mimicking Insulinoma. J Endocr Soc. 2021;6(1):bvab185. https:\u002F\u002Fdoi.org\u002F10.1210\u002Fjendso\u002Fbvab185.",{"VOID":1988},"10.1186\u002Fs40842-022-00138-x","https:\u002F\u002Fclindiabetesendo.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs40842-022-00138-x",[1991,2006,2021,2034,2049,2062,2077,2092,2107,2120,2133],{"id":1992,"sortIndex":32,"researcher":28,"roles":1993,"affiliations":1994,"properties":2003,"displayName":2005,"givenName":28,"familyName":28},"d1603b78-909f-4c2f-93cd-f41139373a2c",[934],[1995],{"id":1996,"sortIndex":32,"affiliation":1997,"properties":28},"8b14b944-4069-4ca1-8e30-5d144e43b2a7",{"id":1996,"createTime":28,"updateTime":28,"relativeEntities":1998,"slug":28,"properties":1999,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2002,"statistic":28},[],{"title":2000},{"VI":2001},"Diabetes Metabolic department, Hospital Universitario Fundación Favaloro, Buenos Aires, Argentina",[],{"title":2004},{"VI":2005},"M. 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Gondolesi",{"url":1989,"publisher":2156,"properties":2175},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":2157,"slug":872,"properties":2158,"entityType":25,"verifyStatus":878,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":2161,"manageAffiliations":2162,"indexDatabases":2163,"url":892,"thumbnailPath":28,"statistic":2170,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":2159,"title":2160},{"VOID":875},{"EN":877},[],[],[2164],{"id":883,"indexDatabase":2165,"url":889,"indexYears":890,"academicFieldIds":28,"indexDatabaseRanking":891},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":2166,"label":2167,"description":2168,"key":781,"publicationTags":2169,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],{"impactFactor":32,"impactFactorByYear":2171,"i10Index":205,"i10IndexLast5Year":48,"totalPublication":895,"totalPublicationByYear":2172,"totalCitation":897,"totalCitationByYear":2173,"totalCitationPerPublication":900,"totalCitationPerPublicationByYear":2174,"hindexLast5Year":205,"hindex":205},{"2016":109,"2017":105,"2018":223,"2019":346,"2020":228,"2021":820,"2022":347,"2023":167},{"2015":146,"2016":47,"2017":47,"2018":199,"2019":205,"2020":129,"2021":128,"2022":145,"2023":46,"2024":49},{"2015":131,"2016":278,"2017":139,"2018":122,"2019":899,"2020":200,"2021":357,"2022":42},{"2015":902,"2016":903,"2017":904,"2018":363,"2019":905,"2020":906,"2021":346,"2022":169},{"pages":2176,"volume":2177},{"VOID":1597},{"VOID":2178},"8","2022-03-15",2022,[891],{"id":2183,"createTime":2184,"updateTime":2185,"relativeEntities":2186,"slug":2187,"properties":2188,"entityType":926,"verifyStatus":26,"verifyTime":2185,"verifyNote":928,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":2197,"fullTextUrl":28,"authors":2198,"publicationType":1090,"publisherRelationship":2214,"citationCount":28,"citationInfo":28,"publishDate":2238,"publishYear":1515,"citationAnalyzeStatus":878,"lastCitationAnalyze":28,"indexDatabases":2239,"openAccess":28,"references":28,"isForceReanalyzing":1119},"17968fa4-34e9-4f43-9aa4-fd05fb070810","2024-02-11T01:25:05.843+00:00","2025-01-13T13:08:30.295+00:00",[],"SHBG-and-total-testosterone-levels-in-men-with-adult-onset-hypogonadism-what-are-we-overlooking-",{"abstract":2189,"title":2191,"references":2193,"doi":2195},{"EN":2190},"Adult onset male hypogonadism (AOH) is a common clinical condition whose diagnosis and management are controversial, and is often characterized by a low level of SHBG, but our understanding of why testosterone levels are low when SHBG is low is incomplete. This retrospective chart review was performed to compare the relationship between SHBG and testosterone in the plasma of men presenting for evaluation of AOH with a cohort of men treated chronically with transdermal testosterone. The level of SHBG was \u003C 30 nmol\u002FL in 73% of men who presented for evaluation of AOH, and was inversely proportional to BMI in both the untreated and the testosterone-treated men. As in previous populations, the level of SHBG was highly positively correlated (r = 0.71, p \u003C 0.01) with the total testosterone level in untreated men presenting for evaluation of AOH, but no relationship was found between the level of SHBG and total testosterone among men who were being treated with a transdermal testosterone preparation. These findings further support the idea that SHBG regulates testicular negative feedback either directly or by modulating the entry of testosterone or estradiol into cells in the hypothalamus and\u002For pituitary to control gonadotropin synthesis and secretion which explains in part the low testosterone levels in men with AOH. Not applicable",{"EN":2192},"SHBG and total testosterone levels in men with adult onset hypogonadism: what are we overlooking?",{"VOID":2194},"Khera M, Broderick GA, Carson CC 3rd, Dobs AS, Faraday MM, Goldstein I, et al. Adult-onset hypogonadism. Mayo ClinProc. 2016;91(7):908–26. .\nRastrelli G, Carter EL, Ahern T, Finn JD, Antonio L, O’Neill TW, et al. Development of and recovery from secondary hypogonadism in aging men: prospective results from the EMAS. J ClinEndocrinolMetab. 2015;100(8):3172–82.\nYeap BB, Grossmann M, McLachlan RI, Handelsman DJ, Wittert GA, Conway AJ, et al. Endocrine Society of Australia position statement on male hypogonadism (part 2): treatment and therapeutic considerations. Med J Aust. 2016;205(5):228–31.\nHammond GL. Plasma steroid-binding proteins: primary gatekeepers of steroid hormone action. J Endocrinol. 2016;230(1):R13-25. .\nGoldman AL, Bhasin S, Wu FCW, Krishna M, Matsumoto AM, Jasuja R. A reappraisal of testosterone’s binding in circulation: physiological and clinical implications. Endocr Rev. 2017;38(4):302–24. .\nAvvakumov GV, Grishkovskaya I, Muller YA, Hammond GL. Resolution of the human sex hormone-binding globulin dimer interface and evidence for two steroid-binding sites per homodimer. J BiolChem. 2001;276(37):34453–7.\nZakharov MN, Bhasin S, Travison TG, Xue R, Ulloor J, Vasan RS, et al. A multi-step, dynamic allosteric model of testosterone’s binding to sex hormone binding globulin. Mol Cell Endocrinol. 2015;399:190–200. .\nVermeulen A, Kaufman JM, Giagulli VA. Influence of some biological indexes on sex hormone-binding globulin and androgen levels in aging or obese males. J ClinEndocrinolMetab. 1996;81(5):1821–6.\nWinters SJ, Kelley DE, Goodpaster B. The analog free testosterone assay: are the results in men clinically useful? ClinChem. 1998;44(10):2178–82.\nZhao Y, Nichols JE, Bulun SE, Mendelson CR, Simpson ER. Aromatase P450 gene expression in human adipose tissue Role of a Jak\u002FSTAT pathway in regulation of the adipose-specific promoter. J BiolChem. 1995;270(27):16449–57.\nSchneider G, Kirschner MA, Berkowitz R, Ertel NH. Increased estrogen production in obese men. J ClinEndocrinolMetab. 1979;48(4):633–8.\nKley HK, Edelmann P, Krüskemper HL. Relationship of plasma sex hormones to different parameters of obesity in male subjects. Metabolism. 1980;29(11):1041–5.\nGiagulli VA, Kaufman JM, Vermeulen A. Pathogenesis of the decreased androgen levels in obese men. J ClinEndocrinolMetab. 1994;79(4):997–1000.\nDhindsa S, Furlanetto R, Vora M, Ghanim H, Chaudhuri A, Dandona P. Low estradiol concentrations in men with subnormal testosterone concentrations and type 2 diabetes. Diabetes Care. 2011;34(8):1854–9. .\nTajar A, Huhtaniemi IT, O’Neill TW, Finn JD, Pye SR, Lee DM, et al. Characteristics of androgen deficiency in late-onset hypogonadism: results from the European Male Aging Study (EMAS). J ClinEndocrinolMetabol. 2012;97(5):1508–16.\nVeldhuis J, Yang R, Roelfsema F, Takahashi P. Proinflammatory cytokine infusion attenuates LH’s feedforward on testosterone secretion: modulation by age. J ClinEndocrinolMetab. 2016;101(2):539–49.\nRoseweir AK, Millar RP. The role of kisspeptin in the control of gonadotrophin secretion. Hum Reprod Update. 2009;15(2):203–12. .\nFarooqi IS, Jebb SA, Langmack G, Lawrence E, Cheetham CH, Prentice AM, et al. Effects of recombinant leptin therapy in a child with congenital leptin deficiency. N Engl J Med. 1999;341(12):879–84.\nChan JL, Heist K, DePaoli AM, Veldhuis JD, Mantzoros CS. The role of falling leptin levels in the neuroendocrine and metabolic adaptation to short-term starvation in healthy men. J Clin Invest. 2003;111(9):1409–21.\nRosner W. The functions of corticosteroid-binding globulin and sex hormone-binding globulin: recent advances. Endocr Rev. 1990;11(1):80–91. .\nde Ronde W, van der Schouw YT, Muller M, Grobbee DE, Gooren LJ, Pols HA, et al. Associations of sex-hormone-binding globulin (SHBG) with non-SHBG-bound levels of testosterone and estradiol in independently living men. J ClinEndocrinolMetab. 2005;90(1):157–62.\nde Ronde W, van der Schouw YT, Pierik FH, Pols HA, Muller M, Grobbee DE, et al. Serum levels of sex hormone-binding globulin (SHBG) are not associated with lower levels of non-SHBG-bound testosterone in male newborns and healthy adult men. ClinEndocrinol. 2005;62(4):498–503.\nAydın B, Winters SJ. Sex hormone-binding globulin in children and adolescents. J Clin Res PediatrEndocrinol. 2016;8(1):1–12.\nKeelan JA, Mattes E, Tan H, Dinan A, Newnham JP, Whitehouse AJ, et al. Androgen concentrations in umbilical cord blood and their association with maternal, fetal and obstetric factors. PLoS ONE. 2012;7(8):e42827.\nPasquali R, Macor C, Vicennati V, Novo F, De lasio R, Mesini P, et al. Effects of acute hyperinsulinemia on testosterone serum concentrations in adult obese and normal-weight men. Metabolism. 1997;46(5):526–269. .\nSalter CA, Mulhall JP. Guideline of guidelines: testosterone therapy for testosterone deficiency. BJU Int. 2019;124(5):722–9. .\nKidd GS, Glass AR, Vigersky RA. The hypothalamic-pituitary-testicular axis in thyrotoxicosis. J ClinEndocrinolMetab. 1979;48(5):798–802. .\nHudson RW, Edwards AL. Testicular function in hyperthyroidism. J Androl. 1992;13(2):117–24.\nRuder H, Corvol P, Mahoudeau JA, Ross GT, Lipsett MB. Effects of induced hyperthyroidism on steroid metabolism in man. J ClinEndocrinolMetab. 1971;33(3):382–7.\nSelva DM, Hammond GL. Thyroid hormones act indirectly to increase sex hormone-binding globulin production by liver via hepatocyte nuclear factor-4alpha. J MolEndocrinol. 2009;43(1):19–27. .\nJanne M, Hammond GL. Hepatocyte nuclear factor-4 controls transcription from a TATA-less human sex hormone-binding globulin gene promoter. J BiolChem. 1998;273(51):34105–14.\nGlinoer D, de Nayer P, Bourdoux P, Lemone M, Robyn C, van Steirteghem A, et al. Regulation of maternal thyroid during pregnancy. J ClinEndocrinolMetab. 1990;71(2):276–87.\nAin KB, Mori Y, Refetoff S. Reduced clearance rate of thyroxine-binding globulin (TBG) with increased sialylation: a mechanism for estrogen-induced elevation of serum TBG concentration. J ClinEndocrinolMetab. 1987;65(4):689–96.\nSherins RJ, Loriaux DL. Studies of the role of sex steroids in the feedback control of FSH concentrations in men. J ClinEndocrinolMetab. 1973;36(5):886–93.\nSanten RJ. Is aromatization of testosterone to estradiol required for inhibition of luteinizing hormone secretion in men? J ClinInvestig. 1975;56(6):1555–63.\nWinters SJ, Janick JJ, Loriaux DL, Sherins RJ. Studies on the role of sex steroids in the feedback control of gonadotropin concentrations in men. II. Use of the estrogen antagonist, clomiphene citrate. J ClinEndocrinolMetab. 1979;48(2):222–7.\nWinters SJ, Troen P. Evidence for a role of endogenous estrogen in the hypothalamic control of gonadotropin secretion in men. J ClinEndocrinolMetab. 1985;61(5):842–5.\nHayes FJ, Seminara SB, Decruz S, Boepple PA, Crowley WF Jr. Aromatase inhibition in the human male reveals a hypothalamic site of estrogen feedback. J ClinEndocrinolMetab. 2000;85(9):3027–35.\nMarynick SP, Loriaux DL, Sherins RJ, Pita JC Jr, Lipsett MB. Evidence that testosterone can suppress pituitary gonadotropin secretion independently of peripheral aromatization. J ClinEndocrinolMetab. 1979;49(3):396–8.\nMorishima A, Grumbach MM, Simpson ER, Fisher C, Qin K. Aromatase deficiency in male and female siblings caused by a novel mutation and the physiological role of estrogens. J ClinEndocrinolMetab. 1995;80(12):3689–98.\nKeevil BG, Adaway J. Assessment of free testosterone concentration. J Steroid BiochemMolBiol. 2019;190:207–11.\nHandelsman DJ. Free testosterone: pumping up the tires or ending the free ride? Endocr Rev. 2017;38(4):297–301.\nKushnir MM, Rockwood AL, Yue B, Meikle AW. High sensitivity measurement of estrone and estradiol in serum and plasma using LC-MS\u002FMS. Methods MolBiol. 2010;603:219–28.\nDunn JF, Nisula BC, Rodbard D. Transport of steroid hormones: binding of 21 endogenous steroids to both testosterone-binding globulin and corticosteroid-binding globulin in human plasma. J ClinEndocrinolMetab. 1981;53(1):58–68.\nGrossmann M. Hypogonadism and male obesity: focus on unresolved questions. ClinEndocrinol. 2018;89(1):11–21.\nJarecki P, Herman WA, Pawliczak E, Lacka K. Can low SHBG serum concentration be a good early marker of male hypogonadism in metabolic syndrome? Diabetes MetabSyndrObes. 2019;12:2181–91.",{"VOID":2196},"10.1186\u002Fs40842-020-00106-3","https:\u002F\u002Fclindiabetesendo.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs40842-020-00106-3",[2199],{"id":2200,"sortIndex":32,"researcher":28,"roles":2201,"affiliations":2202,"properties":2211,"displayName":2213,"givenName":28,"familyName":28},"16f59011-0c2e-414b-a297-bb60a25d6cea",[934],[2203],{"id":2204,"sortIndex":32,"affiliation":2205,"properties":28},"88530fc1-eea8-4293-8144-ea906dc8c3f6",{"id":2204,"createTime":28,"updateTime":28,"relativeEntities":2206,"slug":28,"properties":2207,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2210,"statistic":28},[],{"title":2208},{"VI":2209},"Division of Endocrinology, Metabolism and Diabetes, University of Louisville, Louisville, USA",[],{"title":2212},{"VI":2213},"Stephen J. 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