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JAMA. 2011;305:160–6.",{"doi":387},"10.1001\u002Fjama.2010.1983",false,{"id":390,"createTime":391,"updateTime":392,"relativeEntities":393,"slug":394,"properties":395,"entityType":124,"verifyStatus":125,"verifyTime":408,"verifyNote":126,"syncStatus":21,"languages":22,"translateLanguages":409,"viewCount":23,"primaryUrl":411,"fullTextUrl":22,"authors":412,"publicationType":164,"publisherRelationship":441,"citationCount":22,"citationInfo":22,"publishDate":469,"publishYear":470,"citationAnalyzeStatus":21,"lastCitationAnalyze":22,"indexDatabases":22,"openAccess":22,"references":22,"isForceReanalyzing":388},"a8e5544f-d20b-452c-9b31-ffab4c9a45da","2023-12-27T23:12:57.309+00:00","2025-01-14T23:57:03.202+00:00",[],"Maneuvering-Clinical-Pathways-for-Crohn-s-Disease",{"references":396,"abstract":398,"title":401,"doi":404,"keywords":406},{"VOID":397},"•• Lichtenstein GR, Loftus EV, Isaacs KL, Regueiro MD, Gerson LB, Sands BE. ACG Clinical Guideline: management of Crohn’s disease in adults. Am J Gastroenterol. 2018;113(4):481–517 This clinical guideline describes current recommendations for management of Crohn’s disease in adults in the USA.\nNguyen GC, Loftus EV Jr, Hirano I, Falck-Ytter Y, Singh S, Sultan S, et al. American Gastroenterological Association Institute Guideline on the management of Crohn’s disease after surgical resection. Gastroenterology. 2017;152(1):271–5.\nGionchetti P, Dignass A, Danese S, Magro Dias FJ, Rogler G, Lakatos PL, et al. 3rd European evidence-based consensus on the diagnosis and management of Crohn’s disease 2016: part 2: surgical management and special situations. J Crohns Colitis 2017;11(2):135–149.\nGomollon F, Dignass A, Annese V, Tilg H, Van Assche G, Lindsay JO, et al. 3rd European evidence-based consensus on the diagnosis and management of Crohn’s disease 2016: part 1: diagnosis and medical management. J Crohns Colitis 2017;11(1):3–25.\nYarur AJ, Strobel SG, Deshpande AR, Abreu MT. Predictors of aggressive inflammatory bowel disease. Gastroenterol Hepatol (N Y). 2011;7(10):652–9.\nKlein A, Eliakim R. Non steroidal anti-inflammatory drugs and inflammatory bowel disease. Pharmaceuticals (Basel). 2010;3(4):1084–92.\nChoung RS, Princen F, Stockfisch TP, Torres J, Maue AC, Porter CK, et al. Serologic microbial associated markers can predict Crohn’s disease behaviour years before disease diagnosis. Aliment Pharmacol Ther. 2016;43(12):1300–10.\nDubinsky MC, Kugathasan S, Mei L, Picornell Y, Nebel J, Wrobel I, et al. Increased immune reactivity predicts aggressive complicating Crohn’s disease in children. Clin Gastroenterol Hepatol. 2008;6(10):1105–11.\nPanaccione R, Colombel JF, Louis E, Peyrin-Biroulet L, Sandborn WJ. Evolving definitions of remission in Crohn’s disease. Inflamm Bowel Dis. 2013;19(8):1645–53.\nFreeman HJ. Use of the Crohn’s disease activity index in clinical trials of biological agents. World J Gastroenterol. 2008;14(26):4127–30.\nD’Inca R, Caccaro R. Measuring disease activity in Crohn’s disease: what is currently available to the clinician. Clin Exp Gastroenterol. 2014;7:151–61.\n• Rutgeerts P, Gasink C, Chan D, Lang Y, Pollack P, Colombel JF, et al. Efficacy of ustekinumab for inducing endoscopic healing in patients with Crohn’s disease. Gastroenterology. 2018;155(4):1045–58 This endoscopic substudy of Crohn’s disease patients who participated in one of the three pivotal clnical trials with ustekinumab showed benefit in endoscopic improvement in as early as 8 weeks in patients with moderate to severe Crohn’s disease.\nOrlando A, Guglielmi FW, Cottone M, Orlando E, Romano C, Sinagra E. Clinical implications of mucosal healing in the management of patients with inflammatory bowel disease. Dig Liver Dis. 2013;45(12):986–91.\nColombel JF, Louis E, Peyrin-Biroulet L, Sandborn WJ, Panaccione R. Deep remission: a new concept? Dig Dis. 2012;30(Suppl 3):107–11.\nMosli MH, Zou G, Garg SK, Feagan SG, MacDonald JK, Chande N, et al. C-reactive protein, fecal calprotectin, and stool lactoferrin for detection of endoscopic activity in symptomatic inflammatory bowel disease patients: a systematic review and meta-analysis. Am J Gastroenterol. 2015;110(6):802–19 quiz 20.\nSandborn WJ, Feagan BG, Lichtenstein GR. Medical management of mild to moderate Crohn’s disease: evidence-based treatment algorithms for induction and maintenance of remission. Aliment Pharmacol Ther. 2007;26(7):987–1003.\nHazlewood GS, Rezaie A, Borman M, Panaccione R, Ghosh S, Seow CH, et al. Comparative effectiveness of immunosuppressants and biologics for inducing and maintaining remission in Crohn’s disease: a network meta-analysis. Gastroenterology. 2015;148(2):344–54 e5 quiz e14-5.\nBenchimol EI, Seow CH, Steinhart AH, Griffiths AM. Traditional corticosteroids for induction of remission in Crohn’s disease. Cochrane Database Syst Rev. 2008;2:CD006792.\nJohnson CM, Dassopoulos T. Update on the use of thiopurines and methotrexate in inflammatory bowel disease. Curr Gastroenterol Rep. 2018;20(11):53.\nAdegbola SO, Sahnan K, Warusavitarne J, Hart A, Tozer P. Anti-TNF therapy in Crohn’s disease. Int J Mol Sci. 2018;19(8).\nFeuerstein JD, Nguyen GC, Kupfer SS, Falck-Ytter Y, Singh S, American Gastroenterological Association Institute clinical guidelines C. American Gastroenterological Association Institute Guideline on therapeutic drug monitoring in inflammatory bowel disease. Gastroenterology. 2017;153(3):827–34.\nDrobne D, Kurent T, Golob S, Svegl P, Rajar P, Terzic S, et al. Success and safety of high infliximab trough levels in inflammatory bowel disease. Scand J Gastroenterol. 2018;53(8):940–6.\nBodini G, Giannini EG, Savarino V, Del Nero L, Pellegatta G, De Maria C, et al. Adalimumab trough serum levels and anti-adalimumab antibodies in the long-term clinical outcome of patients with Crohn’s disease. Scand J Gastroenterol. 2016;51(9):1081–6.\nStrik AS, van den Brink GR, Ponsioen C, Mathot R, Lowenberg M, D’Haens GR. Suppression of anti-drug antibodies to infliximab or adalimumab with the addition of an immunomodulator in patients with inflammatory bowel disease. Aliment Pharmacol Ther. 2017;45(8):1128–34.\nUngar B, Kopylov U, Engel T, Yavzori M, Fudim E, Picard O, et al. Addition of an immunomodulator can reverse antibody formation and loss of response in patients treated with adalimumab. Aliment Pharmacol Ther. 2017;45(2):276–82.\nVaughn BP, Martinez-Vazquez M, Patwardhan VR, Moss AC, Sandborn WJ, Cheifetz AS. Proactive therapeutic concentration monitoring of infliximab may improve outcomes for patients with inflammatory bowel disease: results from a pilot observational study. Inflamm Bowel Dis. 2014;20(11):1996–2003.\n• Vande Casteele N, Ferrante M, Van Assche G, Ballet V, Compernolle G, Van Steen K, et al. Trough concentrations of infliximab guide dosing for patients with inflammatory bowel disease. Gastroenterology. 2015;148(7):1320–9 e3 This study showed that optimizing initial trough concentration of infliximab increased the number of patients in clinical remission.\nColombel JF, Panaccione R, Bossuyt P, Lukas M, Baert F, Vanasek T, et al. Effect of tight control management on Crohn’s disease (CALM): a multicentre, randomised, controlled phase 3 trial. Lancet. 2018;390(10114):2779–89.\n• Jorgensen KK, Olsen IC, Goll GL, Lorentzen M, Bolstad N, Haavardsholm EA, et al. Switching from originator infliximab to biosimilar CT-P13 compared with maintained treatment with originator infliximab (NOR-SWITCH): a 52-week, randomised, double-blind, non-inferiority trial. Lancet. 2017;389(10086):2304–16 This study showed that patients with inflammatory diseases who were stable on originator infliximab could be switched to the biosimilar CT-P13 with no loss of efficacy or increase in immunogenicity when compared to those who stayed on the originator drug.\nRaffals LE, Nguyen GC, Rubin DT. Switching between biologics and biosimilars in inflammatory bowel disease. Clin Gastroenterol Hepatol. 2018.\nReinisch W, Jahnsen J, Schreiber S, Danese S, Panes J, Balsa A, et al. Evaluation of the cross-reactivity of antidrug antibodies to CT-P13 and infliximab reference product (Remicade): an analysis using immunoassays tagged with both agents. BioDrugs. 2017;31(3):223–37.\nKawamoto E, Nakahashi S, Okamoto T, Imai H, Shimaoka M. Anti-integrin therapy for multiple sclerosis. Autoimmune Dis. 2012;2012:357101.\nNelson SM, Nguyen TM, McDonald JW, MacDonald JK. Natalizumab for induction of remission in Crohn’s disease. Cochrane Database Syst Rev. 2018;(8):CD006097.\nWarnke C, Menge T, Hartung HP, Racke MK, Cravens PD, Bennett JL, et al. Natalizumab and progressive multifocal leukoencephalopathy: what are the causal factors and can it be avoided? Arch Neurol. 2010;67(8):923–30.\n•• Sandborn WJ, Feagan BG, Rutgeerts P, Hanauer S, Colombel JF, Sands BE, et al. Vedolizumab as induction and maintenance therapy for Crohn’s disease. N Engl J Med. 2013;369(8):711–21 This study showed vedolizumab as an effective induction and maintenance agent in patients who had no response or unacceptable side effects from glucocorticoids, immunosupressants, or anti-TNFα agents.\nScribano ML. Vedolizumab for inflammatory bowel disease: from randomized controlled trials to real-life evidence. World J Gastroenterol. 2018;24(23):2457–67.\nSands BE, Van Assche G, Tudor D, Akhundova-Unadkat G, Curtis RI, Tan T. Vedolizumab in combination with corticosteroids for induction therapy in Crohn’s disease: a post hoc analysis of GEMINI 2 and 3. Inflamm Bowel Dis. 2019.\nWilliet N, Boschetti G, Fovet M, Di Bernado T, Claudez P, Del Tedesco E, et al. Association between low trough levels of vedolizumab during induction therapy for inflammatory bowel diseases and need for additional doses within 6 months. Clin Gastroenterol Hepatol. 2017;15(11):1750–7 e3.\nYacoub W, Williet N, Pouillon L, Di-Bernado T, De Carvalho Bittencourt M, Nancey S, et al. Early vedolizumab trough levels predict mucosal healing in inflammatory bowel disease: a multicentre prospective observational study. Aliment Pharmacol Ther. 2018;47(7):906–12.\n• Vermeire S, Loftus EV Jr, Colombel JF, Feagan BG, Sandborn WJ, Sands BE, et al. Long-term efficacy of vedolizumab for Crohn’s disease. J Crohns Colitis. 2017;11(4):412–24 This study showed that most patients with clinical response to vedolizumab at 6 weeks continue to have clinical response at 2 years.\nAl-Bawardy B, Ramos GP, Willrich MAV, Jenkins SM, Park SH, Aniwan S, et al. Vedolizumab drug level correlation with clinical remission, biomarker normalization, and mucosal healing in inflammatory bowel disease. Inflamm Bowel Dis. 2018.\n•• Feagan BG, Sandborn WJ, Gasink C, Jacobstein D, Lang Y, Friedman JR, et al. Ustekinumab as induction and maintenance therapy for Crohn’s disease. N Engl J Med. 2016;375(20):1946–60 This clinical trial showed ustekinumab as an effective induction and maintenance agent for patients who previously failed anti-TNFα therapy or immunomodulators\u002Fglucocorticoids.\nBattat R, Kopylov U, Bessissow T, Bitton A, Cohen A, Jain A, et al. Association between ustekinumab trough concentrations and clinical, biomarker, and endoscopic outcomes in patients with Crohn’s disease. Clin Gastroenterol Hepatol. 2017;15(9):1427–34 e2.\nPapp K, Gottlieb AB, Naldi L, Pariser D, Ho V, Goyal K, et al. Safety surveillance for ustekinumab and other psoriasis treatments from the Psoriasis Longitudinal Assessment and Registry (PSOLAR). J Drugs Dermatol. 2015;14(7):706–14.\nDotan I, Ron Y, Yanai H, Becker S, Fishman S, Yahav L, et al. Patient factors that increase infliximab clearance and shorten half-life in inflammatory bowel disease: a population pharmacokinetic study. Inflamm Bowel Dis. 2014;20(12):2247–59.\nJuncadella AC, Alame AM, Sands LR, Deshpande AR. Perianal Crohn’s disease: a review. Postgrad Med. 2015;127(3):266–72.\nHukkinen M, Pakarinen MP, Piekkala M, Koivusalo A, Rintala R, Kolho KL. Treatment of complex perianal fistulas with seton and infliximab in adolescents with Crohn’s disease. J Crohns Colitis. 2014;8(8):756–62.\nPark EJ, Song KH, Baik SH, Park JJ, Kang J, Lee KY, et al. The efficacy of infliximab combined with surgical treatment of fistulizing perianal Crohn’s disease: comparative analysis according to fistula subtypes. Asian J Surg. 2018;41(5):438–47.\nYarur AJ, Kanagala V, Stein DJ, Czul F, Quintero MA, Agrawal D, et al. Higher infliximab trough levels are associated with perianal fistula healing in patients with Crohn’s disease. Aliment Pharmacol Ther. 2017;45(7):933–40.\nJi CC, Takano S. Clinical efficacy of adalimumab versus infliximab and the factors associated with recurrence or aggravation during treatment of anal fistulas in Crohn’s disease. Intest Res. 2017;15(2):182–6.\nCastano-Milla C, Chaparro M, Saro C, Barreiro-de Acosta M, Garcia-Albert AM, Bujanda L, et al. Effectiveness of adalimumab in perianal fistulas in Crohn’s disease patients naive to anti-TNF therapy. J Clin Gastroenterol. 2015;49(1):34–40.\nFu YM, Chen M, Liao AJ. A meta-analysis of adalimumab for fistula in Crohn’s disease. Gastroenterol Res Pract. 2017;2017:1745692.\nWest RL, van der Woude CJ, Hansen BE, Felt-Bersma RJ, van Tilburg AJ, Drapers JA, et al. Clinical and endosonographic effect of ciprofloxacin on the treatment of perianal fistulae in Crohn’s disease with infliximab: a double-blind placebo-controlled study. Aliment Pharmacol Ther. 2004;20(11–12):1329–36.\nDewint P, Hansen BE, Verhey E, Oldenburg B, Hommes DW, Pierik M, et al. Adalimumab combined with ciprofloxacin is superior to adalimumab monotherapy in perianal fistula closure in Crohn’s disease: a randomised, double-blind, placebo controlled trial (ADAFI). Gut. 2014;63(2):292–9.\nGold SL, Cohen-Mekelburg S, Schneider Y, Steinlauf A. Perianal fistulas in patients with Crohn’s disease, part 1: current medical management. Gastroenterol Hepatol (N Y). 2018;14(8):470–81.\nFeagan BG, Schwartz D, Danese S, Rubin DT, Lissoos TW, Xu J, et al. Efficacy of vedolizumab in fistulising Crohn’s disease: exploratory analyses of data from GEMINI 2. J Crohns Colitis. 2018;12(5):621–6.\nSingh S, Garg SK, Pardi DS, Wang Z, Murad MH, Loftus EV Jr. Comparative efficacy of pharmacologic interventions in preventing relapse of Crohn’s disease after surgery: a systematic review and network meta-analysis. Gastroenterology. 2015;148(1):64–76 e2 quiz e14.\nYamada A, Komaki Y, Patel N, Komaki F, Pekow J, Dalal S, et al. The use of vedolizumab in preventing postoperative recurrence of Crohn’s disease. Inflamm Bowel Dis. 2018;24(3):502–9.\nHiraoka S, Takashima S, Kondo Y, Inokuchi T, Sugihara Y, Takahara M, et al. Efficacy of restarting anti-tumor necrosis factor alpha agents after surgery in patients with Crohn’s disease. Intest Res. 2018;16(1):75–82.\nRutgeerts P, Geboes K, Vantrappen G, Beyls J, Kerremans R, Hiele M. Predictability of the postoperative course of Crohn’s disease. Gastroenterology. 1990;99(4):956–63.\nCohen-Mekelburg S, Schneider Y, Gold S, Scherl E, Steinlauf A. Risk stratification for prevention of recurrence of postoperative Crohn’s disease. Gastroenterol Hepatol (N Y). 2017;13(11):651–8.\nCatalan-Serra I, Brenna O. Immunotherapy in inflammatory bowel disease: novel and emerging treatments. Hum Vaccin Immunother. 2018:1–15.\nWhite JR, Phillips F, Monaghan T, Fateen W, Samuel S, Ghosh S, et al. Review article: novel oral-targeted therapies in inflammatory bowel disease. Aliment Pharmacol Ther. 2018;47(12):1610–22.",{"EN":399,"VI":400},"Crohn’s disease management has changed significantly with increasing use of biologics. We review the recent literature on the clinical management of Crohn’s disease and new approaches in selecting and optimizing therapy. Recent studies have addressed the efficacy of proactive anti-TNFα trough level monitoring, the efficacy of biosimilars, and the efficacy and immunogenicity of newer biologics including anti-integrin therapy and anti-IL12\u002F23 therapy. Optimizing anti-TNFα therapy according to trough concentrations correlates with improved remission rates. Patients can be switched from the reference drug to a biosimilar, or vice versa, without a measurable change in efficacy, safety, or immunogenicity. Immunomodulators are effective in decreasing immunogenicity and boosting anti-TNFα drug level. The anti-integrin and anti-IL12\u002F23 therapies are effective as induction and maintenance therapy with low immunogenicity and excellent safety profiles. Patients at high risk for post-operative recurrence should be started on a biologic therapy within 4 weeks post-op. Multiple biologic therapies are currently available for treatment of Crohn’s disease including anti-TNFα therapy, anti-integrin therapy, and anti-IL12\u002F23 therapy. The choice of first-line therapy should be based on individual risk-benefit analysis, route of administration, and patient preference. Patient with inadequate response should have their trough level checked and therapy optimized. Therapeutic prophylaxis for post-operative recurrence should be based on patient’s risk factors for recurrence.","Quản lý bệnh Crohn đã thay đổi đáng kể với sự gia tăng việc sử dụng các loại thuốc sinh học. Chúng tôi xem xét tài liệu gần đây về quản lý lâm sàng bệnh Crohn và các phương pháp mới trong việc lựa chọn và tối ưu hóa liệu pháp. Các nghiên cứu gần đây đã đề cập đến tính hiệu quả của việc theo dõi nồng độ trong máu kháng TNFα, tính hiệu quả của các loại thuốc sinh học tương tự, và tính hiệu quả cũng như tính miễn dịch của những loại thuốc sinh học mới hơn bao gồm liệu pháp kháng tích cực và liệu pháp kháng IL12\u002F23. Tối ưu hóa liệu pháp kháng TNFα theo nồng độ trong máu có liên quan đến tỷ lệ thuyên giảm cao hơn. Bệnh nhân có thể được chuyển từ thuốc tham chiếu sang thuốc sinh học tương tự, hoặc ngược lại, mà không có sự thay đổi đáng kể về tính hiệu quả, độ an toàn hay tính miễn dịch. Các thuốc điều chỉnh miễn dịch có hiệu quả trong việc giảm tính miễn dịch và làm tăng nồng độ thuốc kháng TNFα. Các liệu pháp kháng tích cực và kháng IL12\u002F23 có hiệu quả như liệu pháp khởi đầu và duy trì với tính miễn dịch thấp và hồ sơ an toàn rất tốt. Bệnh nhân có nguy cơ cao tái phát sau phẫu thuật nên bắt đầu liệu pháp sinh học trong vòng 4 tuần sau phẫu thuật. Nhiều liệu pháp sinh học hiện có để điều trị bệnh Crohn bao gồm liệu pháp kháng TNFα, liệu pháp kháng tích cực và liệu pháp kháng IL12\u002F23. Việc lựa chọn liệu pháp điều trị ban đầu nên dựa trên phân tích rủi ro-lợi ích cá nhân, đường dùng thuốc và sở thích của bệnh nhân. Bệnh nhân có phản ứng không đủ cần được kiểm tra nồng độ thuốc của họ và tối ưu hóa liệu pháp. Dự phòng liệu pháp cho sự tái phát sau phẫu thuật nên dựa trên các yếu tố rủi ro của bệnh nhân về sự tái phát.",{"EN":402,"VI":403},"Maneuvering Clinical Pathways for Crohn’s Disease","Chiến lược Lâm sàng cho Bệnh Crohn",{"VOID":405},"10.1007\u002Fs11894-019-0687-4",{"VI":407},"Bệnh Crohn, thuốc sinh học, TNFα, tái phát, tối ưu hóa liệu pháp","2025-01-14T07:49:14.713+00:00",[410],"VI","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11894-019-0687-4",[413,429],{"id":414,"sortIndex":23,"researcher":22,"roles":415,"affiliations":417,"properties":426},"a4960465-142c-4b18-9e1f-87c83c9e67f4",[416],"AUTHOR",[418],{"id":22,"sortIndex":23,"affiliation":419,"properties":22},{"id":420,"createTime":421,"updateTime":421,"relativeEntities":422,"slug":22,"properties":423,"entityType":51,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23},"80091d09-f9e8-4b03-bfe1-4ad63675a15d","2023-12-27T23:12:57.331+00:00",[],{"title":424},{"VI":425},"Section of Gastroenterology, Hepatology and Nutrition, Inflammatory Bowel Disease Center, University of Chicago Medicine, Chicago, USA",{"title":427},{"VI":428},"Thomas X. Lu",{"id":430,"sortIndex":79,"researcher":22,"roles":431,"affiliations":432,"properties":438},"7e739c98-0e10-48c4-aea5-cb61cad77aa9",[416],[433],{"id":22,"sortIndex":23,"affiliation":434,"properties":22},{"id":420,"createTime":421,"updateTime":421,"relativeEntities":435,"slug":22,"properties":436,"entityType":51,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23},[],{"title":437},{"VI":425},{"title":439},{"VI":440},"Russell D. Cohen",{"url":411,"publisher":442,"properties":464},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":443,"slug":10,"properties":444,"entityType":20,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23,"subjectFields":449,"manageAffiliations":450,"indexDatabases":451,"url":22,"thumbnailPath":22,"statistic":459,"gsStatistic":22,"type":100,"analyzePriority":22},[],{"issn":445,"eissn":446,"title":447,"url":448},{"VOID":13},{"VOID":15},{"EN":17},{"VOID":19},[],[],[452],{"id":56,"indexDatabase":453,"url":69,"indexYears":70,"academicFieldIds":458,"indexDatabaseRanking":74},{"id":58,"createTime":59,"updateTime":60,"relativeEntities":454,"label":455,"description":456,"key":66,"publicationTags":457,"standard":22},[],{"EN":63,"VI":63},{"EN":63,"VI":65},[68],[72,73],{"impactFactor":23,"impactFactorByYear":460,"i10Index":23,"i10IndexLast5Year":23,"totalPublication":77,"totalPublicationByYear":461,"totalCitation":23,"totalCitationByYear":462,"totalCitationPerPublication":23,"totalCitationPerPublicationByYear":463,"hindexLast5Year":23,"hindex":23},{},{"1996":79,"1999":80,"2000":81,"2001":82,"2002":83,"2003":84,"2004":85,"2005":86,"2006":87,"2007":83,"2008":88,"2009":81,"2010":89,"2011":90,"2012":91,"2013":81,"2014":92,"2015":93,"2016":87,"2017":94,"2018":90,"2019":92,"2020":95,"2021":96,"2022":97,"2023":82,"2024":52},{},{},{"volume":465,"pages":467},{"VOID":466},"21",{"VOID":468},"1-9","2019-04-23",2019,{"id":472,"createTime":473,"updateTime":474,"relativeEntities":475,"slug":476,"properties":477,"entityType":124,"verifyStatus":125,"verifyTime":474,"verifyNote":126,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23,"primaryUrl":486,"fullTextUrl":22,"authors":487,"publicationType":164,"publisherRelationship":515,"citationCount":22,"citationInfo":22,"publishDate":543,"publishYear":544,"citationAnalyzeStatus":21,"lastCitationAnalyze":22,"indexDatabases":22,"openAccess":22,"references":22,"isForceReanalyzing":388},"46db5197-f828-45d1-945a-1be769b07832","2024-01-19T19:30:39.010+00:00","2025-01-02T23:52:10.149+00:00",[],"Advances-in-Biliary-Access",{"references":478,"abstract":480,"title":482,"doi":484},{"VOID":479},"Enochsson L, Swahn F, Arnelo U, Nilsson M, Lohr M, Persson G. Nationwide, population-based data from 11,074 ERCP procedures from the Swedish Registry for Gallstone Surgery and ERCP. Gastrointest Endosc. 2010;72(6):1175–84, 84 e1–3.\nPeng C, Nietert PJ, Cotton PB, Lackland DT, Romagnuolo J. Predicting native papilla biliary cannulation success using a multinational Endoscopic Retrograde Cholangiopancreatography (ERCP) Quality Network. BMC Gastroenterol. 2013;13:147.\nWilliams EJ, Ogollah R, Thomas P, Logan RF, Martin D, Wilkinson ML, et al. What predicts failed cannulation and therapy at ERCP? Results of a large-scale multicenter analysis. Endoscopy. 2012;44(7):674–83.\nLiao WC, Angsuwatcharakon P, Isayama H, Dhir V, Devereaux B, Khor CJ, et al. International consensus recommendations for difficult biliary access. Gastrointest Endosc. 2017;85(2):295–304.\nAngsuwatcharakon P, Rerknimitr R, Ridtitid W, Ponauthai Y, Kullavanijaya P. Success rate and cannulation time between precut sphincterotomy and double-guidewire technique in truly difficult biliary cannulation. J Gastroenterol Hepatol. 2012;27(2):356–61.\nHarewood GC, Baron TH. An assessment of the learning curve for precut biliary sphincterotomy. Am J Gastroenterol. 2002;97(7):1708–12.\nYoo YW, Cha SW, Lee WC, Kim SH, Kim A, Cho YD. Double guidewire technique vs transpancreatic precut sphincterotomy in difficult biliary cannulation. World J Gastroenterol. 2013;19(1):108–14.\nIto K, Fujita N, Noda Y, Kobayashi G, Obana T, Horaguchi J, et al. Can pancreatic duct stenting prevent post-ERCP pancreatitis in patients who undergo pancreatic duct guidewire placement for achieving selective biliary cannulation? A prospective randomized controlled trial. J Gastroenterol. 2010;45(11):1183–91.\nTse F, Yuan Y, Moayyedi P, Leontiadis GI, Barkun AN. Double-guidewire technique in difficult biliary cannulation for the prevention of post-ERCP pancreatitis: a systematic review and meta-analysis. Endoscopy. 2017;49(1):15–26.\nCha SW, Leung WD, Lehman GA, Watkins JL, McHenry L, Fogel EL, et al. Does leaving a main pancreatic duct stent in place reduce the incidence of precut biliary sphincterotomy-associated pancreatitis? A randomized, prospective study. Gastrointest Endosc. 2013;77(2):209–16.\nMavrogiannis C, Liatsos C, Romanos A, Petoumenos C, Nakos A, Karvountzis G. Needle-knife fistulotomy versus needle-knife precut papillotomy for the treatment of common bile duct stones. Gastrointest Endosc. 1999;50(3):334–9.\nTestoni PA, Mariani A, Aabakken L, Arvanitakis M, Bories E, Costamagna G, et al. Papillary cannulation and sphincterotomy techniques at ERCP: European Society of Gastrointestinal Endoscopy (ESGE) Clinical Guideline. Endoscopy. 2016;48(7):657–83.\nNavaneethan U, Konjeti R, Venkatesh PG, Sanaka MR, Parsi MA. Early precut sphincterotomy and the risk of endoscopic retrograde cholangiopancreatography related complications: an updated meta-analysis. World J Gastrointest Endosc. 2014;6(5):200–8.\nTang Z, Yang Y, Yang Z, Meng W, Li X. Early precut sphincterotomy does not increase the risk of adverse events for patients with difficult biliary access: a systematic review of randomized clinical trials with meta-analysis and trial sequential analysis. Medicine (Baltimore). 2018;97(36):e12213.\nPecsi D, Farkas N, Hegyi P, Varju P, Szakacs Z, Fabian A, et al. Transpancreatic sphincterotomy is effective and safe in expert hands on the short term. Dig Dis Sci. 2019;64(9):2429–44.\nDhir V, Bhandari S, Bapat M, Maydeo A. Comparison of EUS-guided rendezvous and precut papillotomy techniques for biliary access (with videos). Gastrointest Endosc. 2012;75(2):354–9.\nLee A, Aditi A, Bhat YM, Binmoeller KF, Hamerski C, Sendino O, et al. Endoscopic ultrasound-guided biliary access versus precut papillotomy in patients with failed biliary cannulation: a retrospective study. Endoscopy. 2017;49(2):146–53.\nIwashita T, Yasuda I, Mukai T, Iwata K, Ando N, Doi S, et al. EUS-guided rendezvous for difficult biliary cannulation using a standardized algorithm: a multicenter prospective pilot study (with videos). Gastrointest Endosc. 2016;83(2):394–400.\nNakai Y, Isayama H, Matsubara S, Kogure H, Mizuno S, Hamada T, et al. A novel “hitch-and-ride” deep biliary cannulation method during rendezvous endoscopic ultrasound-guided ERCP technique. Endoscopy. 2017;49(10):983–8.\nShah JN, Marson F, Weilert F, Bhat YM, Nguyen-Tang T, Shaw RE, et al. Single-operator, single-session EUS-guided anterograde cholangiopancreatography in failed ERCP or inaccessible papilla. Gastrointest Endosc. 2012;75(1):56–64.\nDhir V, Bhandari S, Bapat M, Joshi N, Vivekanandarajah S, Maydeo A. Comparison of transhepatic and extrahepatic routes for EUS-guided rendezvous procedure for distal CBD obstruction. United European Gastroenterol J. 2013;1(2):103–8.\nIwashita T, Doi S, Yasuda I. Endoscopic ultrasound-guided biliary drainage: a review. Clin J Gastroenterol. 2014;7(2):94–102.\nIwashita T, Yasuda I, Mukai T, Iwata K, Doi S, Uemura S, et al. Endoscopic ultrasound-guided antegrade biliary stenting for unresectable malignant biliary obstruction in patients with surgically altered anatomy: single-center prospective pilot study. Dig Endosc. 2017;29(3):362–8.\nWeilert F, Binmoeller KF, Marson F, Bhat Y, Shah JN. Endoscopic ultrasound-guided anterograde treatment of biliary stones following gastric bypass. Endoscopy. 2011;43(12):1105–8.\nKawakubo K, Isayama H, Kato H, Itoi T, Kawakami H, Hanada K, et al. Multicenter retrospective study of endoscopic ultrasound-guided biliary drainage for malignant biliary obstruction in Japan. J Hepatobiliary Pancreat Sci. 2014;21(5):328–34.\nKhashab MA, Messallam AA, Penas I, Nakai Y, Modayil RJ, De la Serna C, et al. International multicenter comparative trial of transluminal EUS-guided biliary drainage via hepatogastrostomy vs. choledochoduodenostomy approaches. Endosc Int Open. 2016;4(2):E175–81.\nPark DH, Jang JW, Lee SS, Seo DW, Lee SK, Kim MH. EUS-guided biliary drainage with transluminal stenting after failed ERCP: predictors of adverse events and long-term results. Gastrointest Endosc. 2011;74(6):1276–84.\nNennstiel S, Weber A, Frick G, Haller B, Meining A, Schmid RM, et al. Drainage-related complications in percutaneous transhepatic biliary drainage: an analysis over 10 years. J Clin Gastroenterol. 2015;49(9):764–70.\nArtifon EL, Aparicio D, Paione JB, Lo SK, Bordini A, Rabello C, et al. Biliary drainage in patients with unresectable, malignant obstruction where ERCP fails: endoscopic ultrasonography-guided choledochoduodenostomy versus percutaneous drainage. J Clin Gastroenterol. 2012;46(9):768–74.\nBaniya R, Upadhaya S, Madala S, Subedi SC, Shaik Mohammed T, Bachuwa G. Endoscopic ultrasound-guided biliary drainage versus percutaneous transhepatic biliary drainage after failed endoscopic retrograde cholangiopancreatography: a meta-analysis. Clin Exp Gastroenterol. 2017;10:67–74.\n•• Sharaiha RZ, Khan MA, Kamal F, Tyberg A, Tombazzi CR, Ali B, et al. Efficacy and safety of EUS-guided biliary drainage in comparison with percutaneous biliary drainage when ERCP fails: a systematic review and meta-analysis. Gastrointest Endosc. 2017;85(5):904–14 Meta-analysis of nine studies showing that EUS-biliary drainage was associated with better clinical success, fewer post-procedure adverse events, and lower rate of reintervention compared to percutaneous biliary drainage.\n•• Bang JY, Navaneethan U, Hasan M, Hawes R, Varadarajulu S. Stent placement by EUS or ERCP for primary biliary decompression in pancreatic cancer: a randomized trial (with videos). Gastrointest Endosc. 2018;88(1):9–17 Results of a randomized controlled trial revealed similar rates of adverse events and treatment outcomes for primary treatment for distal biliary obstruction in pancreatic cancer with EUS or ERCP-based biliary drainage.\nPaik WH, Lee TH, Park DH, Choi JH, Kim SO, Jang S, et al. EUS-guided biliary drainage versus ERCP for the primary palliation of malignant biliary obstruction: a multicenter randomized clinical trial. Am J Gastroenterol. 2018;113(7):987–97.\nPark JK, Woo YS, Noh DH, Yang JI, Bae SY, Yun HS, et al. Efficacy of EUS-guided and ERCP-guided biliary drainage for malignant biliary obstruction: prospective randomized controlled study. Gastrointest Endosc. 2018;88(2):277–82.\nAnderloni A, Fugazza A, Troncone E, Auriemma F, Carrara S, Semeraro R, et al. Single-stage EUS-guided choledochoduodenostomy using a lumen-apposing metal stent for malignant distal biliary obstruction. Gastrointest Endosc. 2019;89(1):69–76.\nHan SY, Kim SO, So H, Shin E, Kim DU, Park DH. EUS-guided biliary drainage versus ERCP for first-line palliation of malignant distal biliary obstruction: a systematic review and meta-analysis. Sci Rep. 2019;9(1):16551.\nHathorn KE, Bazarbashi AN, Sack JS, McCarty TR, Wang TJ, Chan WW, et al. EUS-guided biliary drainage is equivalent to ERCP for primary treatment of malignant distal biliary obstruction: a systematic review and meta-analysis. Endosc Int Open. 2019;7(11):E1432–E41.\nJin Z, Wei Y, Lin H, Yang J, Jin H, Shen S, et al. Endoscopic ultrasound-guided versus endoscopic retrograde cholangiopancreatography-guided biliary drainage for primary treatment of distal malignant biliary obstruction: a systematic review and meta-analysis. Dig Endosc. 2020;32(1):16–26.\n• El Chafic AH, Shah JN, Hamerski C, Binmoeller KF, Irani S, James TW, et al. EUS-guided choledochoduodenostomy for distal malignant biliary obstruction using electrocautery-enhanced lumen-apposing metal stents: first US, multicenter experience. Dig Dis Sci. 2019;64(11):3321–7 Results of first and only US, multicenter study showed high technical and clinical success rates, with a low rate of adverse events of EUS-biliary drainage using electrocautery enhanced lumen apposing metal stent.\nRyou M, Benias PC, Kumbhari V. Initial clinical experience of a steerable access device for EUS-guided biliary drainage. Gastrointest Endosc. 2020;91(1):178–84.\nAngrisani L, Santonicola A, Iovino P, Vitiello A, Higa K, Himpens J, et al. IFSO worldwide survey 2016: primary, endoluminal, and revisional procedures. Obes Surg. 2018;28(12):3783–94.\nKedia P, Sharaiha RZ, Kumta NA, Kahaleh M. Internal EUS-directed transgastric ERCP (EDGE): game over. Gastroenterology. 2014;147(3):566–8.\nBukhari M, Kowalski T, Nieto J, Kunda R, Ahuja NK, Irani S, et al. An international, multicenter, comparative trial of EUS-guided gastrogastrostomy-assisted ERCP versus enteroscopy-assisted ERCP in patients with Roux-en-Y gastric bypass anatomy. Gastrointest Endosc. 2018;88(3):486–94.\n• Kedia P, Tarnasky PR, Nieto J, Steele SL, Siddiqui A, Xu MM, et al. EUS-directed transgastric ERCP (EDGE) versus laparoscopy-assisted ERCP (LA-ERCP) for Roux-en-Y gastric bypass (RYGB) anatomy: a multicenter early comparative experience of clinical outcomes. J Clin Gastroenterol. 2019;53(4):304–8 Results of a multicenter study revealed that the EDGE procedure has similar technical success and adverse events compared with LA-ERCP with the benefit of significantly shorter procedure times and hospital stay.\nNgamruengphong S, Nieto J, Kunda R, Kumbhari V, Chen YI, Bukhari M, et al. Endoscopic ultrasound-guided creation of a transgastric fistula for the management of hepatobiliary disease in patients with Roux-en-Y gastric bypass. Endoscopy. 2017;49(6):549–52.\nJames HJ, James TW, Wheeler SB, Spencer JC, Baron TH. Cost-effectiveness of endoscopic ultrasound-directed transgastric ERCP compared with device-assisted and laparoscopic-assisted ERCP in patients with Roux-en-Y anatomy. Endoscopy. 2019;51(11):1051–8.\nAdler DG, Lieb JG 2nd, Cohen J, Pike IM, Park WG, Rizk MK, et al. Quality indicators for ERCP. Gastrointest Endosc. 2015;81(1):54–66.",{"EN":481},"Bile duct cannulation using conventional techniques fails in up to 16% of endoscopic retrograde cholangiopancreatography (ERCP) procedures. Advanced techniques to gain biliary access include ERCP-based maneuvers, and newer endoscopic ultrasound (EUS)–guided interventions. In this article, we review the evidence supporting the use of various ERCP and EUS techniques for biliary access, as well as studies comparing these different techniques. In comparative studies, biliary access after failed conventional cannulation was more successful with EUS-rendezvous compared to precut papillotomy. EUS-guided drainage compares favorably with percutaneous drainage with respect to clinical success, safety profile, and cost-efficiency. Recent randomized trials comparing EUS to ERCP drainage in malignant obstruction have found similar success rates between these techniques. EUS-guided techniques compare favorably to ERCP-based methods for biliary access and drainage. The advent of newer technologies to facilitate interventional EUS may further change current treatment approaches.",{"EN":483},"Advances in Biliary Access",{"VOID":485},"10.1007\u002Fs11894-020-00800-3","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11894-020-00800-3",[488,503],{"id":489,"sortIndex":23,"researcher":22,"roles":490,"affiliations":491,"properties":500},"faa674cd-b3df-4d11-b093-7deea0b828f2",[416],[492],{"id":22,"sortIndex":23,"affiliation":493,"properties":22},{"id":494,"createTime":495,"updateTime":495,"relativeEntities":496,"slug":22,"properties":497,"entityType":51,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23},"4fdc9a9b-c40d-4699-ae7f-b843b8987031","2024-01-19T19:30:39.033+00:00",[],{"title":498},{"VI":499},"Department of Gastroenterology, Ochsner Health – New Orleans, New Orleans, USA",{"title":501},{"VI":502},"Abdul H. El Chafic",{"id":504,"sortIndex":79,"researcher":22,"roles":505,"affiliations":506,"properties":512},"560d44e5-56c6-4e68-88e0-d113af7ef2d1",[416],[507],{"id":22,"sortIndex":23,"affiliation":508,"properties":22},{"id":494,"createTime":495,"updateTime":495,"relativeEntities":509,"slug":22,"properties":510,"entityType":51,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23},[],{"title":511},{"VI":499},{"title":513},{"VI":514},"Janak N. Shah",{"url":486,"publisher":516,"properties":538},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":517,"slug":10,"properties":518,"entityType":20,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23,"subjectFields":523,"manageAffiliations":524,"indexDatabases":525,"url":22,"thumbnailPath":22,"statistic":533,"gsStatistic":22,"type":100,"analyzePriority":22},[],{"issn":519,"eissn":520,"title":521,"url":522},{"VOID":13},{"VOID":15},{"EN":17},{"VOID":19},[],[],[526],{"id":56,"indexDatabase":527,"url":69,"indexYears":70,"academicFieldIds":532,"indexDatabaseRanking":74},{"id":58,"createTime":59,"updateTime":60,"relativeEntities":528,"label":529,"description":530,"key":66,"publicationTags":531,"standard":22},[],{"EN":63,"VI":63},{"EN":63,"VI":65},[68],[72,73],{"impactFactor":23,"impactFactorByYear":534,"i10Index":23,"i10IndexLast5Year":23,"totalPublication":77,"totalPublicationByYear":535,"totalCitation":23,"totalCitationByYear":536,"totalCitationPerPublication":23,"totalCitationPerPublicationByYear":537,"hindexLast5Year":23,"hindex":23},{},{"1996":79,"1999":80,"2000":81,"2001":82,"2002":83,"2003":84,"2004":85,"2005":86,"2006":87,"2007":83,"2008":88,"2009":81,"2010":89,"2011":90,"2012":91,"2013":81,"2014":92,"2015":93,"2016":87,"2017":94,"2018":90,"2019":92,"2020":95,"2021":96,"2022":97,"2023":82,"2024":52},{},{},{"volume":539,"pages":541},{"VOID":540},"22",{"VOID":542},"1-8","2020-12-04",2020,{"id":546,"createTime":547,"updateTime":548,"relativeEntities":549,"slug":550,"properties":551,"entityType":124,"verifyStatus":125,"verifyTime":548,"verifyNote":126,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23,"primaryUrl":560,"fullTextUrl":22,"authors":561,"publicationType":164,"publisherRelationship":590,"citationCount":22,"citationInfo":22,"publishDate":618,"publishYear":619,"citationAnalyzeStatus":21,"lastCitationAnalyze":22,"indexDatabases":22,"openAccess":22,"references":22,"isForceReanalyzing":388},"65d483ee-cfed-49da-b414-d02ab8cdbdc1","2023-11-24T10:31:38.263+00:00","2025-02-24T23:50:08.198+00:00",[],"Diagnosis-and-Management-of-Pouchitis-and-Ileoanal-Pouch-Dysfunction",{"references":552,"abstract":554,"title":556,"doi":558},{"VOID":553},"Fazio VW, Ziv Y, Church JM, et al.: Ileal pouch-anal anastomosis: complications and function in 1005 patients. Ann Surg 1995, 222:120–127.\nSandborn WJ: Pouchitis following ileal pouch-anal anastomosis: definition, pathogenesis, and treatment. Gastroenterology 1994, 107:1856–1860.\nCoffey JC, Winter DC, Neary P, et al.: Quality of life after ileal pouch-anal anastomosis: an evaluation of diet and other factors using the Cleveland Global Quality of Life instrument. Dis Colon Rectum 2002, 45:30–38.\nStocchi L, Pemberton JH: Pouch and pouchitis. Gastroenterol Clin North Am 2001, 30:223–241.\nHurst RD, Molinari M, Chung TP, et al.: Prospective study of the incidence, timing and treatment of pouchitis in 104 consecutive patients after restorative proctocolectomy. Arch Surg 1996, 131:497–500; discussion 501–502.\nOhge H, Furne JK, Springfield J, et al.: Association between fecal hydrogen sulfide production and pouchitis. Dis Colon Rectum 2005, 48:469–475.\nGosselink MP, Schouten WR, van Lieshout LM, et al.: Eradication of pathogenic bacteria and restoration of normal pouch flora: comparison of metronidazole and ciprofloxacin in the treatment of pouchitis. Dis Colon Rectum 2004, 47:1519–1525.\nOhge H, Furne JK, Springfield J, et al.: Association between fecal hydrogen sulfide production and pouchitis. Dis Colon Rectum 2005, 48:469–475.\nFalk A, Olsson C, Ahrne S, et al.: Ileal pelvic pouch microbiota from two former ulcerative colitis patients, analysed by DNA-based methods, were unstable over time and showed the presence of Clostridium perfringens. Scand J Gastroenterol 2007, 42:973–985.\n•• Komanduri S, Gillevet PM, Sikaroodi M, et al.: Dysbiosis in pouchitis: evidence of unique microfloral patterns in pouch inflammation. Clin Gastroenterol Hepatol 2007, 5:352–360. This article describes a comprehensive study of microbiota using 16sRNA-based molecular microbiology in pouchitis patients.\nMcLaughlin SD, Walker AW, Churcher C, et al.: The bacteriology of pouchitis: a molecular phylogenetic analysis using 16 S rRNA gene cloning and sequencing [abstract]. Available at http:\u002F\u002Fwww.broadmedical.org\u002Fabout\u002Fannual_meetings\u002F2010\u002FAbstract-McLaughlin.html. Accessed August 2010.\nOttesen EA, Hong JW, Quake SR, et al.: Microfluidic digital PCR enables multigene analysis of individual environmental bacteria. Science 2006, 314:1464–1467.\nLiu WT, Zhu L: Environmental microbiology-on-a-chip and its future impacts. Trends Biotechnol 2005, 23:174–179.\nMarcy Y, Ouverney C, Bik EM, et al.: Dissecting biological “dark matter” with single-cell genetic analysis of rare and uncultivated TM7 microbes from the human mouth. Proc Natl Acad Sci U S A 2007, 104:11889–11894.\n•• Turroni S, Vitali B, Candela M, et al.: Antibiotics and probiotics in chronic pouchitis: a comparative proteomic approach. World J Gastroenterol 2010, 16:30–41. This article describes the first study to investigate the role of proteomics in chronic pouchitis.\nKroesen AJ, Leistenschneider P, Lehmann K, et al.: Increased bacterial permeation in long-lasting ileoanal pouches. Inflamm Bowel Dis 2006, 12:736–744.\nDeSilva HJ, Jones M, Prince C, et al.: Lymphocyte and macrophage subpopulations in pelvic ileal reservoirs. Gut 1991, 32:1160–1165.\nHirata I, Berrebi G, Austin LL, et al.: Immunohistological characterization of intraepithelial and lamina propria lymphocytes in control ileum and colon and inflammatory bowel disease. Dig Dis Sci 1986, 31:593–603.\n• Navaneethan U, Shen B: Secondary pouchitis: those with identifiable etiopathogenetic or triggering factors. Am J Gastroenterol 2010, 105:51–64. This article presents a comprehensive review of the various causes of secondary pouchitis.\nCasadesus D, Tani T, Wakai T, et al.: Possible role of human cytomegalovirus in pouchitis after proctocolectomy with ileal pouch-anal anastomosis in patients with ulcerative colitis. World J Gastroenterol 2007, 13:1085–1089.\n•• Shen B, Jiang ZD, Fazio VW, et al.: Clostridium difficile infection in patients with ileal pouch-anal anastomosis. Clin Gastroenterol Hepatol 2008, 6:782–788. This article describes a very important study showing that C. difficile infection not only can occur in patients without a colon, but also can be common.\nShen B, Remzi FH, Nutter B, et al.: Association between Immune-associated disorders and adverse outcomes of Ileal pouch-anal anastomosis. Am J Gastroenterol 2009, 104:655–664.\n• Shen B, Plesec TP, Remer E, et al.: Asymmetric endoscopic inflammation of the ileal pouch: a sign of ischemic pouchitis? Inflamm Bowel Dis 2010, 16:836–846. This article provides a description of ischemic pouchitis as a new disease entity.\nShen B, Bennett AE, Fazio VW, et al.: Collagenous pouchitis. Dig Liver Dis 2006, 38:704–709.\nShen B, Fazio VW, Bennett AE, et al.: Effect of withdrawal of non-steroidal anti-inflammatory drug use in patients with the ileal pouch. Dig Dis Sci 2007, 52:3321–3328.\nSandborn WJ: Pouchitis: risk factors, frequency, natural history, classification and public health perspective. In Trends in Inflammatory Bowel Disease 1996. Edited by McLeod RS, Martin F, Sutherland LR, et al. Lancaster, UK: Kluwer Academic Publishers; 1997:51–63.\nShen L, Lian L, Goldblum JR, Remzi FH: Development of de novo celiac disease after restorative proctocolectomy and ileal pouch-anal anastomosis. Inflamm Bowel Dis 2009, 15:1131–1132.\n• Navaneethan U, Shen B: Pros and cons of antibiotic therapy for pouchitis. Expert Rev Gastroenterol Hepatol 2009, 3:547–359. This article provides a comprehensive review of risks and benefits of antibiotic use in pouchitis.\nHeuschen UA, Allemeyer EH, Hinz G, et al.: Diagnosing pouchitis: comparative validation of two scoring systems in routine follow-up. Dis Colon Rectum 2002, 45:776–786.\nShen B, Pardi DS, Bennett AE, et al.: The efficacy and tolerability of AST-120 (spherical carbon adsorbent) in active pouchitis. Am J Gastroenterol 2009, 104:1468–1474.\n•• Pardi DS, D’Haens G, Shen B, et al.: Clinical guidelines for the management of pouchitis. Inflamm Bowel Dis 2009, 15:1424–1431. The authors present the only available guidelines on management of pouchitis.\nShen B, Achkar J-P, Lashner BA, et al.: Endoscopic and histologic evaluations together with symptom assessment are required to diagnose pouchitis. Gastroenterology 2001, 121:261–267.\nShen B, Achkar JP, Connor JT, et al.: Modified pouchitis disease activity index: a simplified approach to the diagnosis of pouchitis. Dis Colon Rectum 2003, 46:748–753.\nSandborn WJ, Tremaine WJ, Batts KP, et al.: Pouchitis after ileal pouch-anal anastomosis: a Pouchitis Disease Activity Index. Mayo Clin Proc 1994, 69:409–415.\nMoskowitz RL, Shepherd NA, Nicholls RJ: An assessment of inflammation in the reservoir after restorative proctocolectomy with ileoanal ileal reservoir. Int J Colorectal Dis 1986, 1:167–174.\nShen B, Shermock KM, Fazio VW, et al.: A cost-effectiveness analysis of diagnostic strategies for symptomatic patients with ileal pouch-anal anastomosis. Am J Gastroenterol 2003, 98:2460–2467.\nLohmuller JL, Pemberton HJ, Dozois RR, et al.: Pouchitis and extraintestinal manifestations of inflammatory bowel disease after ileal pouch-anal anastomosis. Ann Surg 1990, 211:622–629.\nWolf JM, Achkar JP, Lashner BA, et al.: Afferent limb ulcers predict Crohn’s disease in patients with ileal pouch-anal anastomosis. Gastroenterology 2004, 126:1686–1691.\nApel R, Cohen Z, Andrews CW Jr, et al.: Prospective evaluation of early morphological changes in pelvic ileal pouches. Gastroenterology 1994, 107:435–443.\nVeress B, Reinholt FP, Lindquist K, et al.: Long-term histomorphological surveillance of the pelvic ileal pouch: dysplasia develops in a subgroup of patients. Gastroenterology 1995, 109:1090–1097.\nPardi DS, Sandborn WJ: Systematic review: the management of pouchitis. Aliment Pharmacol Ther 2006, 23:1087–1096.\nNavaneethan U, Shen B: Laboratory tests for patients with ileal pouch-anal anastomosis: clinical utility in predicting, diagnosing, and monitoring pouch disorders. Am J Gastroenterol 2009, 104:2606–2615.\nKuisma J, Nuutinen H, Luukkonen P, et al.: Long term metabolic consequences of ileal pouch–anal anastomosis for ulcerative colitis. Am J Gastroenterol 2001, 96:3110–3116.\nM’koma AE: Serum biochemical evaluation of patients with functional pouches ten to 20 years after restorative proctocolectomy. Int J Colorectal Dis 2006, 21:711–720.\nLu H, Lian L, Navaneethan U, Shen B: Clinical utility of C-reactive protein in patients with ileal pouch anal anastomosis. Inflamm Bowel Dis 2010 (Epub ahead of print).\nWalkowiak J, Banasiewicz T, Krokowicz P, et al.: Fecal pyruvate kinase (M2-PK): a new predictor for inflammation and severity of pouchitis. Scand J Gastroenterol 2005, 40:1493–1494.\nJohnson MW, Maestranzi S, Duffy AM, et al.: Fecal calprotectin: a noninvasive diagnostic tool and marker of severity in pouchitis. Eur J Gastroenterol Hepatol 2008, 20:174–179.\nParsi M, Shen B, Achkar J, et al.: Fecal lactoferrin for diagnosis of symptomatic patients with ileal pouch-anal anastomosis. Gastroenterology 2004, 126:1280–1286.\nLim M, Gonsalves S, Thekkinkattil D, et al.: The assessment of a rapid noninvasive immunochromatographic assay test for fecal lactoferrin in patients with suspected inflammation of the ileal pouch. Dis Colon Rectum 2008, 51:96–99.\nMelmed GY, Fleshner PR, Bardakcioglu O, et al.: Family history and serology predict Crohn’s disease after ileal pouch-anal anastomosis for ulcerative colitis. Dis Colon Rectum 2008, 51:100–108.\nTang L, Boone J, Moore L, et al.: Clinical significance of stool ASCA in disorders of the ileal pouch [abstract]. Inflamm Bowel Dis 2008, 12: S2.\nShen B: Campylobacter infection in patients with ileal pouches. Am J Gastroenterol 2010, 105:472–473.\n• McLaughlin SD, Clark SK, Shafi S, et al.: Fecal coliform testing to identify effective antibiotic therapies for patients with antibiotic-resistant pouchitis. Clin Gastroenterol Hepatol 2009, 7:545–548. This article describes the first study to report the use of fecal coliform testing for treating patients with antibiotic-resistant pouchitis.\nSeggerman RE, Chen MY, Waters GS, Ott DJ: Radiology of ileal pouch-anal anastomosis surgery. AJR Am J Roentgenol 2003, 180:999–1002.\nShen B, Fazio VW, Remzi FH, et al.: Comprehensive evaluation of inflammatory and noninflammatory sequelae of ileal pouch-anal anastomoses. Am J Gastroenterol 2005, 100:93–101.\nShepherd NA, Hulten L, Tytgat GN, et al.: Workshop: pouchitis. Int J Colorectal Dis 1989, 4:205–229.\nSagar PM, Pemberton JH: Ileo-anal pouch function and dysfunction. Dig Dis 1997, 15:172–188.\nMadden MV, McIntyre AS, Nicholls RJ: Double-blind crossover trial of metronidazole versus placebo in chronic unremitting pouchitis. Dig Dis Sci 1994, 39:1193–1196.\nShen B, Achkar JP, Lashner BA, et al.: A randomized clinical trial of ciprofloxacin and metronidazole to treat acute pouchitis. Inflamm Bowel Dis 2001, 7:301–305.\nPepin J, Saheb N, Coulombe MA, et al.: Emergence of fluoroquinolones as the predominant risk factor for Clostridium difficile–associated diarrhea: a cohort study during an epidemic in Quebec. Clin Infect Dis 2005, 41:1254–1260.\nIsaacs KL, Sandler RS, Abreu M, et al.: Rifaximin for the treatment of active pouchitis: A randomized, double-blind, placebo-controlled pilot study. Inflamm Bowel Dis 2007, 13:1250–1255.\nShen B, Remzi FH, Lopez AR, Queener E: Rifaximin for maintenance therapy in antibiotic-dependent pouchitis. BMC Gastroenterol 2008, 8:26.\nShen B, Fazio V, Remzi F, et al.: Combined ciprofloxacin and tinidazole therapy in the treatment of chronic refractory pouchitis. Dis Col Rectum 2007, 50:498–508.\n• Ha CY, Bauer JJ, Lazarev M, et al.: Early institution of tinidazole may prevent pouchitis following ileal-pouch anal anastomosis (IPAA) surgery in ulcerative colitis (UC) patients [abstract]. Gastroenterology 2010, 138:S69. The authors describe a randomized, controlled trial of tinidazole in preventing pouchitis after IPAA surgery.\nGionchetti P, Rizzello F, Helwig U, et al.: Prophylaxis of pouchitis onset with probiotic therapy: a double-blind, placebo-controlled trial. Gastroenterology 2003, 124:1202–1209.\nGionchetti P, Rizzello F, Venturi A, et al.: Oral bacteriotherapy as maintenance treatment in patients with chronic pouchitis: a double-blind, placebo-controlled trial. Gastroenterology 2000, 119:305–309.\nElahi B, Nikfar S, Derakhshani S, et al.: On the benefit of probiotics in the management of pouchitis in patients underwent ileal pouch anal anastomosis: a meta-analysis of controlled clinical trials. Dig Dis Sci 2008, 53:1278–1284.\nShen B, Remzi FH, Lavery IC, et al.: Administration of adalimumab in the treatment of Crohn’s disease of the ileal pouch. Aliment Pharmacol Ther 2009, 29:519–526.\nWischmeyer P, Pemberton JH, Phillips SF: Chronic pouchitis after ileal pouch-anal anastomosis: responses to butyrate and glutamine suppositories in a pilot study. Mayo Clin Proc 1993, 68:978–981.\nTremaine WJ, Sandborn WJ, Wolff BG, et al.: Bismuth carbomer foam enemas for active chronic pouchitis: a randomized, double-blind, placebo-controlled trial. Aliment Pharmacol Ther 1997, 11:1041–106.",{"EN":555},"Restorative proctocolectomy with ileal pouch-anal anastomosis (IPAA) has become the surgical treatment of choice for patients with medically refractory ulcerative colitis (UC) or UC with dysplasia and for the majority of patients with familial adenomatous polyposis. However, UC patients with IPAA are susceptible to inflammatory and noninflammatory sequelae, such as pouchitis, Crohn’s disease of the pouch, cuffitis, and irritable pouch syndrome, in addition to common surgery-associated complications, which adversely affect the surgical outcome and compromise health-related quality of life. Pouchitis is the most frequent long-term complication of IPAA in patients with UC, with a cumulative prevalence of up to 50%. Pouchitis may be classified based on the etiology into idiopathic and secondary types, and the management is often different. Pouchoscopy is the most important tool for the diagnosis and differential diagnosis in patients with pouch dysfunction. Antibiotic therapy is the mainstay of treatment for active pouchitis. Some patients may develop dependency on antibiotics, requiring long-term maintenance therapy. Although management of antibiotic-dependent or antibiotic-refractory pouchitis has been challenging, secondary etiology for pouchitis should be evaluated and modified, if possible.",{"EN":557},"Diagnosis and Management of Pouchitis and Ileoanal Pouch Dysfunction",{"VOID":559},"10.1007\u002Fs11894-010-0143-y","http:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs11894-010-0143-y",[562,578],{"id":563,"sortIndex":23,"researcher":22,"roles":564,"affiliations":565,"properties":575},"a0502a0b-bb2f-4c17-adad-2f6aa6546ef0",[416],[566],{"id":22,"sortIndex":23,"affiliation":567,"properties":22},{"id":568,"createTime":569,"updateTime":569,"relativeEntities":570,"slug":571,"properties":572,"entityType":51,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23},"7105ebda-6d73-4cb2-bb66-8a1b386e16db","2023-11-24T10:31:38.281+00:00",[],"The-Pouchitis-Clinic-Digestive-Disease-Institute-The-Cleveland-Clinic-Foundation-Cleveland-USA",{"title":573},{"VI":574},"The Pouchitis Clinic, Digestive Disease Institute, The Cleveland Clinic Foundation, Cleveland, USA",{"title":576},{"VI":577},"Udayakumar Navaneethan",{"id":579,"sortIndex":79,"researcher":22,"roles":580,"affiliations":581,"properties":587},"cb121403-f674-49b3-b6fe-011663d0ede7",[416],[582],{"id":22,"sortIndex":23,"affiliation":583,"properties":22},{"id":568,"createTime":569,"updateTime":569,"relativeEntities":584,"slug":571,"properties":585,"entityType":51,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23},[],{"title":586},{"VI":574},{"title":588},{"VI":589},"Bo Shen",{"url":560,"publisher":591,"properties":613},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":592,"slug":10,"properties":593,"entityType":20,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23,"subjectFields":598,"manageAffiliations":599,"indexDatabases":600,"url":22,"thumbnailPath":22,"statistic":608,"gsStatistic":22,"type":100,"analyzePriority":22},[],{"issn":594,"eissn":595,"title":596,"url":597},{"VOID":13},{"VOID":15},{"EN":17},{"VOID":19},[],[],[601],{"id":56,"indexDatabase":602,"url":69,"indexYears":70,"academicFieldIds":607,"indexDatabaseRanking":74},{"id":58,"createTime":59,"updateTime":60,"relativeEntities":603,"label":604,"description":605,"key":66,"publicationTags":606,"standard":22},[],{"EN":63,"VI":63},{"EN":63,"VI":65},[68],[72,73],{"impactFactor":23,"impactFactorByYear":609,"i10Index":23,"i10IndexLast5Year":23,"totalPublication":77,"totalPublicationByYear":610,"totalCitation":23,"totalCitationByYear":611,"totalCitationPerPublication":23,"totalCitationPerPublicationByYear":612,"hindexLast5Year":23,"hindex":23},{},{"1996":79,"1999":80,"2000":81,"2001":82,"2002":83,"2003":84,"2004":85,"2005":86,"2006":87,"2007":83,"2008":88,"2009":81,"2010":89,"2011":90,"2012":91,"2013":81,"2014":92,"2015":93,"2016":87,"2017":94,"2018":90,"2019":92,"2020":95,"2021":96,"2022":97,"2023":82,"2024":52},{},{},{"volume":614,"pages":616},{"VOID":615},"12",{"VOID":617},"485-494","2010-10-02",2010,{"id":621,"createTime":622,"updateTime":622,"relativeEntities":623,"slug":22,"properties":624,"entityType":124,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23,"primaryUrl":633,"fullTextUrl":22,"authors":634,"publicationType":164,"publisherRelationship":696,"citationCount":22,"citationInfo":22,"publishDate":724,"publishYear":725,"citationAnalyzeStatus":21,"lastCitationAnalyze":22,"indexDatabases":22,"openAccess":22,"references":22,"isForceReanalyzing":388},"2690564c-f13d-4715-bcaa-4bc3ae8da2b2","2023-12-24T23:49:03.145+00:00",[],{"references":625,"abstract":627,"title":629,"doi":631},{"VOID":626},"• Kaitlin JP, Schultz K. Cystic fibrosis: overview of gastrointestinal disease. UpToDate. May 2011, version 19.2. This paper from Kaitlin and Schultz provides an in depth overview of gastrointestinal complications as they relate to increasing morbidity in patients with cystic fibrosis. Topic review includes intestinal abnormalities (such as gastroesophageal reflux disease, meconium ileus, distal intestinal obstruction syndrome, intussusception, small intestine bacterial overgrowth, constipation, and rectal prolapse), pancreatic insufficiency, and hepatobiliary disease.\nBrodzicki J, Trawinska M, Korzon M. Frequency, consequences and pharmacological treatment of gastroesophageal reflux in children with cystic fibrosis. Med Sci Monit. 2002;8:529–37.\nMilla PJ. Cystic fibrosis: present and future. Digestion. Eur J Gastroenterol Hepatol. 1996;59:579–88.\nRozmanic V, Tjesic-Drinkovic D, Banac S, et al. Gastroesophageal reflux and gastric hyperacidity in cystic fibrosis patients. Pedijatrija danas. 2010;6:45–52.\nGregory PC. Gastrointestinal pH, motility\u002Ftransit and permeability in cystic fibrosis. J Pediatr Gastroenterol Nutr. 1996;23:513–23.\nMalfroot A, Dab I. New insights on gastro-oesophageal reflux in cystic fibrosis by longitudinal follow up. Arch Dis Child. 1991;66:1339–45.\nGustafsson PM, Fransson SG, Kuellman M, et al. Gastro-oesophageal reflux and severity of pulmonary disease in cystic fibrosis. Scan J Gastroenterol. 1991;26:449–56.\n• Blondeau K, Pauwels A, Dupont LJ, et al. Characteristics of gastroesophageal reflux and potential risk of gastric content aspiration in children with cystic fibrosis. J Pediatr Gastroenterol Nutr. 2010;50(2):161–6. Blondeau et al. use combined esophageal pH monitoring and multichannel intraluminal impedance to assess the characteristics of GER (acidic, weakly acidic, and weakly alkaline) in children with cystic fibrosis. In this study, Blondeau and colleagues find that GER is a primary phenomenon in cystic fibrosis patients and not secondary to cough.\nCucchiara S, Raia V, Minella R, et al. Ultrasound measurement of gastric emptying time in patients with cystic fibrosis and effect of ranitidine on delayed gastric emptying. J Pediatr. 1996;128:485–8.\nButton BM, Heine RG, Catto-Smith AG, et al. Postural drainage and gastro-oesophageal reflux in infants with cystic fibrosis. Arch Dis Child. 1997;76:148–50.\nDab I, Malfroot A. Gastroesophageal reflux: a primary defect in cystic fibrosis? Scan J Gastroenterol. 1988;143:125–31.\nFathi H, Moon I, Donaldson J. Cough in adult cystic fibrosis: diagnosis and response to fundoplication. Cough. 2009;5:1–6.\nLedson MJ, Tran J, Walshaw MJ. Prevalence and mechanisms of gastro-oesophageal reflux in adult cystic fibrosis patients. J R Soc Med. 1996;91:7–9.\nCucchiara S, Santamaria F, Andreotti MR. Mechanisms of gastro-oesophageal reflux in cystic fibrosis. Arch Dis Child. 1991;66:617–22.\n• Button BM, Roberts S, Kotsimbos TC, et al. Gastroesophageal reflux (symptomatic and silent): a potentially significant problem in patients with cystic fibrosis before and after lung transplantation. J Heart Lung Trans. 2005;24:1522–9. Using esophageal pH monitoring with a dual pH probe, Button et al. found that GER (both the symptomatic and the silent) is significant in CF patients and contributes to declining lung function through microaspiration and reflux bronchospasm. The authors also show that pre-existing GER is exacerbated following lung replacement.\nBontempo I, Piretta L, Corazziari E, et al. Effects of intraluminal acidification on oesophageal motor activity. Gut. 1994;35:884–90.\nHodson ME, Geddes DM, editors. Cystic fibrosis. London: Chapman & Hall; 1995.\nLedson MJ, Wilson GE, Tran J, et al. Tracheal microaspiration in adult cystic fibrosis. J R Soc Med. 1998;91:10–2.\nGilljam J, Chaparro C, Tullise E, et al. GI complications after lung transplantation in patients with cystic fibrosis. Chest. 2003;1:37–41.\nYoung LR, Hadjiliadis D, Davis RD, et al. Lung transplantation exacerbates gastroesophageal reflux disease. Chest. 2003;5:1689–93.\nEggermont E. Gastrointestinal manifestations in cystic fibrosis. Eur J Gastroenterol Hepatol. 1996;8:731–8.\n• Blondeau K, Mertens V, Vanaudenaerde BA, et al. Gastro-oesophageal reflux and gastric aspiration in lung transplant patients with or without chronic rejection. Eur Respir J. 2008;31:707–13. Blondeau and colleagues are the first to report the use of combined esophageal pH monitoring and multichannel intraluminal impedance to characterize the frequency and type (acid and non-acid) of GER in patients with cystic fibrosis. Also, in this study, Blondeau and colleagues found that treatment with PPI did not reduce the levels of pepsin and bile in bronchoalveolar lavage fluid.\nPalmer SM, Miralles AP, Howell DN, et al. Gastroesophageal reflux as a reversible cause of allograft dysfunction after lung trasnplantation. Chest. 2000;118:1214–7.\nVerleden GM, Dupont LJ, Van Raemdonck DE. Is it bronchiolitis obliterans syndrome or is it chronic rejection: a reappraisal? Eur Respir J. 2005;25:221–4.\nVerlden GM, Bankier A, Boehler A. Bronchiolitis obliterans syndrome after lung transplantation: diagnosis and treatment. Eur Respir Mon. 2004;29:1–25.\nNavarro J, Rainisio M, Harms HK, et al. Factors associated with poor pulmonary function: cross-sectional analysis of data from the ERCF. Eur Respir J. 2001;18:298–305.\nScott RB, O’Loughlin EV, Gall DG. Gastroesophageal reflux in patients with cystic fibrosis. J Pediatr. 1985;106:223–7.\nWinnans CS, Harris LD. Quantitation of lower esophageal sphincter competence. Gastroenterology. 1967;52:773–8.\nWoodley FW, Hayes J, Mousa H. Acid gastroesophageal reflux in symptomatic infants is primarily a function of classic 2-phase and pH-only acid reflux event types. J Pediatr Gastroenterol Nutr. 2009;48:550–8.\nWoodley FW, Mousa H. “pH-Only” acid reflux events in infants during later phases of the feeding cycle are less acidic and cleared more efficiently than classic 2-phase acid reflux events. J Pediatr Gastroenterol Nutr. 2009;48:41–7.\nWoodley FW, Machado R, Kaul A, et al. Using combined multichannel intraluminal impedance and esophageal pH monitoring to assess gastroesophageal reflux in children with cystic fibrosis. Manuscript in preparation. 2012.\nVan der Lef HPJ, Arets HGM, Froeling SP. Gastric acid inhibition for fat malabsorption or gastroesophageal reflux disease in cystic fibrosis: Longitudinal effect on bacterial colonization and pulmonary function. J Pediatr. 2009;155:629–33.\nNussbaum E, Maggi JC, Mathis R, et al. Association of lipid-laden alveolar macrophages and gastroesophageal reflux in children. J Pediatr. 1987;110:190–4.\nKajetanowicz A, Stinson D, Laybolt KS, et al. Lipid-laden macrophages in the tracheal aspirate of ventilated neonates receiving Intralipid: a pilot study. Pediatr Pulmonol. 1999;28(2):101–8.\nPrakash UB, Rosenow EC. Pulmonary complications from ophthalmic preparations. Mayo Clin Proc. 1990;65(4):521–9.\nRamsey BW, Farrell PM, Pencharz P. Nutritional assessment and management in cystic fibrosis: a consensus report. Am J Clin Nutr. 1992;55:108–16.\nButton BM, Heine RG, Catto-Smith AG. Postural drainage in cystic fibrosis: is there a link with gastro-oesophageal reflux? J Paediatr Child Health. 1998;34:330–4.\nDoumit M, Krishman U, Jaffe A, et al. Acid and non-acid reflux during physiotherapy in young children with cystic fibrosis. Pediatr Pumonol. 2012;47:119–24.",{"EN":628},"Cystic fibrosis (CF) is an inherited disease that affects both the lungs and the digestive system in children and adults. Thick mucus fills the gut and blocks lumens of the pancreas and hepatobiliary systems, creating insufficient pancreas function and liver disease. Chronic gastrointestinal (GI) complications, including intestinal obstruction, occur in neonates, and poor digestion and gastroesophageal reflux disease (GERD) in children. Although GI symptoms tend to improve with age, CF and associated GERD eventually create respiratory insufficiency; the only available treatment option at this stage is a bilateral lung transplant, which carries considerable morbidity and mortality. While GERD may reoccur as a complication of lung transplantation, GERD symptoms are often reduced following a fundoplication.",{"EN":630},"Gastroesophageal Reflux in Cystic Fibrosis: Current Understandings of Mechanisms and Management",{"VOID":632},"10.1007\u002Fs11894-012-0261-9","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11894-012-0261-9",[635,670],{"id":636,"sortIndex":23,"researcher":22,"roles":637,"affiliations":638,"properties":667},"c5b8cc27-b597-499e-9da4-f251356cb5d3",[416],[639,647,657],{"id":22,"sortIndex":23,"affiliation":640,"properties":22},{"id":641,"createTime":642,"updateTime":642,"relativeEntities":643,"slug":22,"properties":644,"entityType":51,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23},"ddec9bb1-b8e5-4cc9-858f-292f5169c5bf","2023-12-24T23:49:03.191+00:00",[],{"title":645},{"VI":646},"Center for Advanced Research in Neuromuscular Gastrointestinal Disorders, The Ohio State University, Nationwide Children’s Hospital, Columbus, USA",{"id":648,"sortIndex":79,"affiliation":649,"properties":656},"4b64333a-c4f6-4043-8996-ac88341f1795",{"id":650,"createTime":651,"updateTime":651,"relativeEntities":652,"slug":22,"properties":653,"entityType":51,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23},"0da566bf-abd7-4b12-ac8a-199adbdc3413","2023-12-24T23:49:03.196+00:00",[],{"title":654},{"VI":655},"Fellowship in the Advanced Training in Gastrointestinal Motility and Functional Disorders, The Ohio State University, Nationwide Children’s Hospital, Columbus, USA",{},{"id":658,"sortIndex":196,"affiliation":659,"properties":666},"26852a29-8a6c-40d2-9a38-71041d7bb83a",{"id":660,"createTime":661,"updateTime":661,"relativeEntities":662,"slug":22,"properties":663,"entityType":51,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23},"12e7dbd5-bfa9-469f-b4a2-8008e7f2308d","2023-12-24T23:49:03.177+00:00",[],{"title":664},{"VI":665},"Division of Pediatric Gastroenterology, The Ohio State University College of Medicine, Nationwide Children’s Hospital, Columbus, USA",{},{"title":668},{"VI":669},"Hayat M. Mousa",{"id":671,"sortIndex":79,"researcher":22,"roles":672,"affiliations":673,"properties":693},"06dcc5ab-9bc0-4db6-b636-d19c76155eeb",[416],[674,681,688],{"id":675,"sortIndex":196,"affiliation":676,"properties":680},"e028f192-140a-4b76-9383-3beb2d4c00c9",{"id":660,"createTime":661,"updateTime":661,"relativeEntities":677,"slug":22,"properties":678,"entityType":51,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23},[],{"title":679},{"VI":665},{},{"id":682,"sortIndex":79,"affiliation":683,"properties":687},"18ecacf0-75b4-47ce-9137-c735c74c394a",{"id":650,"createTime":651,"updateTime":651,"relativeEntities":684,"slug":22,"properties":685,"entityType":51,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23},[],{"title":686},{"VI":655},{},{"id":22,"sortIndex":23,"affiliation":689,"properties":22},{"id":641,"createTime":642,"updateTime":642,"relativeEntities":690,"slug":22,"properties":691,"entityType":51,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23},[],{"title":692},{"VI":646},{"title":694},{"VI":695},"Frederick W. 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Science 2003, 299:1033–1036.",{"EN":736},"Indigenous intestinal microbes have co-evolved with the intestinal immune system to form a symbiotic ecosystem. In the postnatal period, intestinal microbes provide the developing gut with stimuli that are necessary for healthy maturation of the intestinal immune system. Cross talk between the host and commensal microbes is an essential component of gut homeostasis mechanisms also in later life. During recent years, innovative research has shed light on the molecular mechanisms of these interactions.",{"EN":738},"Commensal bacteria and epithelial cross talk in the developing intestine",{"VOID":740},"10.1007\u002Fs11894-007-0047-7","2025-01-25T23:47:50.971+00:00","Author affiliation is blank","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11894-007-0047-7",[745,760],{"id":746,"sortIndex":79,"researcher":22,"roles":747,"affiliations":748,"properties":757},"d6e6806e-41e6-416c-93c8-d00ed8e52b8b",[416],[749],{"id":22,"sortIndex":23,"affiliation":750,"properties":22},{"id":751,"createTime":752,"updateTime":752,"relativeEntities":753,"slug":22,"properties":754,"entityType":51,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23},"47a9366d-ffad-4ddc-88d8-0d76302c4221","2023-12-25T07:25:04.813+00:00",[],{"title":755},{"VI":756},"Mucosal Immunology Laboratory, Massachusetts General Hospital, Charlestown, USA",{"title":758},{"VI":759},"W. Allan Walker",{"id":761,"sortIndex":23,"researcher":22,"roles":762,"affiliations":763,"properties":764},"899db7a2-3028-4b12-98f6-b9c816c647d4",[416],[],{"title":765},{"VI":766},"Samuli Rautava",{"url":743,"publisher":768,"properties":790},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":769,"slug":10,"properties":770,"entityType":20,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23,"subjectFields":775,"manageAffiliations":776,"indexDatabases":777,"url":22,"thumbnailPath":22,"statistic":785,"gsStatistic":22,"type":100,"analyzePriority":22},[],{"issn":771,"eissn":772,"title":773,"url":774},{"VOID":13},{"VOID":15},{"EN":17},{"VOID":19},[],[],[778],{"id":56,"indexDatabase":779,"url":69,"indexYears":70,"academicFieldIds":784,"indexDatabaseRanking":74},{"id":58,"createTime":59,"updateTime":60,"relativeEntities":780,"label":781,"description":782,"key":66,"publicationTags":783,"standard":22},[],{"EN":63,"VI":63},{"EN":63,"VI":65},[68],[72,73],{"impactFactor":23,"impactFactorByYear":786,"i10Index":23,"i10IndexLast5Year":23,"totalPublication":77,"totalPublicationByYear":787,"totalCitation":23,"totalCitationByYear":788,"totalCitationPerPublication":23,"totalCitationPerPublicationByYear":789,"hindexLast5Year":23,"hindex":23},{},{"1996":79,"1999":80,"2000":81,"2001":82,"2002":83,"2003":84,"2004":85,"2005":86,"2006":87,"2007":83,"2008":88,"2009":81,"2010":89,"2011":90,"2012":91,"2013":81,"2014":92,"2015":93,"2016":87,"2017":94,"2018":90,"2019":92,"2020":95,"2021":96,"2022":97,"2023":82,"2024":52},{},{},{"volume":791,"pages":793},{"VOID":792},"9",{"VOID":794},"385-392","2007-10-03",2007,{"id":798,"createTime":799,"updateTime":800,"relativeEntities":801,"slug":802,"properties":803,"entityType":124,"verifyStatus":125,"verifyTime":800,"verifyNote":126,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23,"primaryUrl":812,"fullTextUrl":22,"authors":813,"publicationType":164,"publisherRelationship":867,"citationCount":22,"citationInfo":22,"publishDate":894,"publishYear":895,"citationAnalyzeStatus":21,"lastCitationAnalyze":22,"indexDatabases":22,"openAccess":22,"references":22,"isForceReanalyzing":388},"5d9833d2-a8e5-411d-a0e5-6cb8f0b3b9be","2023-12-05T06:45:36.699+00:00","2025-01-23T23:46:10.304+00:00",[],"Radiation-Enteritis",{"references":804,"abstract":806,"title":808,"doi":810},{"VOID":805},"Walsh D. 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Small bowel exclusion from the pelvis by a polyglycolic acid mesh sling. J Surg Oncol. 1984;26:107–12.\nRodier JF, Janser JC, Rodier D, et al. Prevention of radiation enteritis by an absorbable polyglycolic acid mesh sling. A 60-case multicentric study. Cancer. 1991;68:2545–9.\nBeitler A, Rodriguez-Bigas MA, Weber TK, Lee RJ, Cuenca R, Petrelli NJ. Complications of absorbable pelvic mesh slings following surgery for rectal carcinoma. Dis Colon Rectum. 1997;40:1336–41.\nHoffman JP, Sigurdson ER, Eisenberg BL. Use of saline-filled tissue expanders to protect the small bowel from radiation. Oncology. 1998;12:51–4. discussion 4, 60, 2, passim.\nSugarbaker PH. Intrapelvic prosthesis to prevent injury of the small intestine with high dosage pelvic irradiation. Surg Gynecol Obstet. 1983;157:269–71.\nFreund H, Gunderson L, Krause R, Fischer JE. Prevention of radiation enteritis after abdominoperineal resection and radiotherapy. 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Dig Liver Dis Off J Ital Soc Gastroenterol Ital Assoc Study Liver. 2013;45:110–4.\nOnodera H, Nagayama S, Mori A, Fujimoto A, Tachibana T, Yonenaga Y. Reappraisal of surgical treatment for radiation enteritis. World J Surg. 2005;29:459–63.\nSpyropoulos BG, Misiakos EP, Fotiadis C, Stoidis CN. Antioxidant properties of probiotics and their protective effects in the pathogenesis of radiation-induced enteritis and colitis. Dig Dis Sci. 2011;56:285–94.\nHan W, Mercenier A, Ait-Belgnaoui A, et al. Improvement of an experimental colitis in rats by lactic acid bacteria producing superoxide dismutase. Inflamm Bowel Dis. 2006;12:1044–52.\nCarroll IM, Andrus JM, Bruno-Barcena JM, Klaenhammer TR, Hassan HM, Threadgill DS. Anti-inflammatory properties of Lactobacillus gasseri expressing manganese superoxide dismutase using the interleukin 10-deficient mouse model of colitis. Am Jo Physiol Gastrointest Liver Physiol. 2007;293:G729–38.\nKullisaar T, Zilmer M, Mikelsaar M, et al. 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Results of a double-blind, randomized study to evaluate the efficacy and safety of Antibiophilus in patients with radiation-induced diarrhoea. Eur J Gastroenterol Hepatol. 2001;13:391–6.\nFloch MH, Walker WA, Guandalini S, et al. Recommendations for probiotic use–2008. J Clin Gastroenterol. 2008;42 Suppl 2:S104–8.\nHille A, Christiansen H, Pradier O, et al. Effect of pentoxifylline and tocopherol on radiation proctitis\u002Fenteritis. Strahlenther Onkol Organ Deutsch Rontgengesellschaft. 2005;181:606–14.\nGothard L, Cornes P, Brooker S, et al. Phase II study of vitamin E and pentoxifylline in patients with late side effects of pelvic radiotherapy. Radiother Oncol J Eur Soc Ther Radiol Oncol. 2005;75:334–41.\nDelanian S, Lefaix JL. Current management for late normal tissue injury: radiation-induced fibrosis and necrosis. Semin Radiat Oncol. 2007;17:99–107.\nHamama S, Gilbert-Sirieix M, Vozenin MC, Delanian S. 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Radiogr Rev Publ Radiol Soc N Am Inc. 2010;30:235–52.",{"EN":807},"Radiation enteritis continues to be a major health concern in recipients of radiation therapy. The incidence of radiation enteritis is expected to continue to rise during the coming years paralleling the unprecedented use of radiotherapy in pelvic cancers. Radiation enteritis can present as either an acute or chronic syndrome. The acute form presents within hours to days of radiation exposure and typically resolves within few weeks. The chronic form may present as early as 2 months or as long as 30 years after exposure. Risk factors can be divided into patient and treatment-related factors. Chronic radiation enteritis is characterized by progressive obliterative endarteritis with exaggerated submucosal fibrosis and can manifest by stricturing, formation of fistulae, local abscesses, perforation, and bleeding. In the right clinical context, diagnosis can be confirmed by cross-sectional imaging, flexible or video capsule endoscopy. Present treatment strategies are directed primarily towards symptom relief and management of emerging complications. Recently, however, there has been a shift towards rational drug design based on improved understanding of the molecular basis of disease in an effort to limit the fibrotic process and prevent organ damage.",{"EN":809},"Radiation Enteritis",{"VOID":811},"10.1007\u002Fs11894-014-0383-3","http:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs11894-014-0383-3",[814,843,855],{"id":815,"sortIndex":196,"researcher":22,"roles":816,"affiliations":817,"properties":840},"9ad3067f-a436-43c6-8b15-ef026f0be644",[416],[818,828],{"id":22,"sortIndex":23,"affiliation":819,"properties":22},{"id":820,"createTime":821,"updateTime":822,"relativeEntities":823,"slug":824,"properties":825,"entityType":51,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23},"8c112a95-9e95-4cb7-afe1-29e4b20d5120","2023-12-05T06:45:36.711+00:00","2024-12-28T03:29:35.562+00:00",[],"Division-of-Gastroenterology-Department-of-Internal-Medicine-American-University-of-Beirut-Medical-Center-Beirut-Lebanon",{"title":826},{"VI":827},"Division of Gastroenterology, Department of Internal Medicine, American University of Beirut Medical Center, Beirut, Lebanon",{"id":829,"sortIndex":79,"affiliation":830,"properties":839},"62999070-0889-41d5-98d0-af13f09ee28f",{"id":831,"createTime":832,"updateTime":833,"relativeEntities":834,"slug":835,"properties":836,"entityType":51,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23},"ce529c7e-ebeb-4fd9-9261-8f1564ec65bb","2023-12-05T06:45:36.727+00:00","2025-02-03T20:35:36.836+00:00",[],"Division-of-Gastroenterology-American-University-of-Beirut-Medical-Center-Beirut-Lebanon",{"title":837},{"VI":838},"Division of Gastroenterology, American University of Beirut Medical Center, Beirut, Lebanon",{},{"title":841},{"VI":842},"Ala I. 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Available at www.unos.org.\nUnited Network for Organ Sharing: Policy 3.6. Allocation of livers. Available at http:\u002F\u002Fwww.unos.org\u002FPoliciesandBylaws2\u002Fpolicies\u002Fpdfs\u002Fpolicy_8.pdf. Accessed November 19, 2008.\nFreeman RB Jr, Edwards EB: Liver transplant waiting time does not correlate with waiting list mortality: implications for liver allocation policy. Liver Transpl 2000, 6:543–552.\nInstitute of Medicine: Analysis of waiting times. In Committee on Organ Transplantation. Assessing current policies and the potential impact of the DHHS final rule. Washington, DC: National Academy Press; 1999:57–78.\nMalinchoc M, Kamath PS, Gordon FD, et al.: A model to predict poor survival in patients undergoing transjugular intrahepatic portosystemic shunts. Hepatology 2000, 31:864–871.\nKamath PS, Wiesner RH, Malinchoc M, et al.: A model to predict survival in patients with end-stage liver disease. Hepatology 2001, 33:464–470.\nWiesner RH, Edwards E, Freeman R, et al.: Model for endstage liver disease (MELD) and allocation of donor livers. Gastroenterology 2003, 124:91–96.\nFink MA, Angus PW, Gow PJ, et al.: Liver transplant recipient selection: MELD versus clinical judgement. Liver Transpl 2005, 11:621–626.\nWiesner R, Lake JR, Freeman RB, Gish RG: Model for end-stage liver disease (MELD) exception guidelines. Liver Transpl 2006, 12(Suppl):S85–S87.\nGonwa TA, McBride MA, Anderson K, et al.: Continued influence of preoperative renal function on outcome of orthotopic liver transplant (OLTX) in the US: Where will MELD lead us? Am J Transplant 2006, 6:2651–2659.\nMachicao VI, Srinivas TR, Hemming AW, et al.: Impact of implementation of the MELD scoring system on the prevalence and incidence of chronic renal disease following liver transplantation. Liver Transpl 2006, 12:754–761.\nGonwa TA, Jennings L, Mai ML, et al.: Estimation of glomerular filtration rates before and after orthotopic liver transplantation: evaluation of current equations. Liver Transpl 2004, 10:301–309.\nCholongitas E, Shusang V, Marelli L, et al.: Review article: renal function assessment in cirrhosis—difficulties and alternative measurements. Aliment Pharmacol Ther 2007, 26:969–978.\nNair S, Verma S, Thuluvath PJ: Pretransplant renal function predicts survival in patients undergoing orthotopic liver transplantation. Hepatology 2002, 35:1179–1185.\nMenon KVN, Nyberg SL. Harmsen WS, et al.: MELD and other factors associated with survival after liver transplantation. Am J Transplant 2004, 4:819–825.\nGonwa TA, Mai ML, Klintmalm GB: Chronic renal failure after transplantation of a nonrenal organ [letter]. N Engl J Med 2003, 349:2563–2565.\nNair SP, Krishnan M, Scheel P, Thuluvath PJ: Renal allograft survival in patients who had simultaneous liver and kidney transplantation compared with those who had kidney transplantation alone. Transplant Proc 2001, 33:1139–1140.\nAfonso RC, Hidalgo R, Zurstrassen MP, et al.: Impact of renal failure on liver transplantation survival. Transplant Proc 2008, 40:808–810.\nRichardson D: Dialysis in non-renal organ (liver) transplantation. Nephron 2001, 88:296–306.\nOjo AO, Held PJ, Port FK, et al.: Chronic renal failure after transplantation of a nonrenal organ. N Engl J Med 2003, 349:931–940.\nVelidedeoglu E, Bloom RD, Crawford MD, et al.: Early kidney dysfunction post liver transplantation predicts late chronic kidney disease. Transplantation 2004, 77:553–556.\nDellon ES, Galanko JA, Medapalli RK, Russo MW: Impact of dialysis and older age on survival after liver transplantation. Am J Transplant 2006, 6:2183–2190.\nKasiske BL, Snyder JJ, Matas AJ, et al.: Preemptive kidney transplantation: the advantage and the advantaged. J Am Soc Nephrol 2002, 13:1358–1364.\nDanovitch GM, Cohen DJ, Weir MR, et al.: Current status of kidney and pancreas transplantation in the United States, 1994–2003. Am J Transplant 2005, 5:904–915.\nLafayette RA, Pare G, Schmidt CH, et al.: Pretransplant renal dysfunction predicts poorer outcome in liver transplantation. Clin Nephrol 1997, 48:159–164.\nGonwa TA, Klintmalm GB, Levy M, et al.: Impact of pretransplant renal function on survival after liver transplantation. Transplantation 1995, 59:361–365.\nMargreiter R, Kramar R, Huber C, et al.: Combined liver and kidney transplantation [case report]. Lancet 1984, 1(8385):1077–1078.\nPomfret EA, Fryer JP, Sima CS, et al.: Liver and intestine transplantation in the United States, 1996–2005. Am J Transplant 2007, 7:1376–1389.\nLocke JE, Warren DS, Singer AL, et al.: Declining outcomes in simultaneous liver-kidney transplantation in the MELD era: ineffective usage of renal allografts. Transplantation 2008, 85:935–942.\nFong TL, Bunnapradist S, Jordan SC, et al.: Analysis of the United Network for Organ Sharing database comparing renal allografts and patient survival in combined liver-kidney transplantation with the collateral allografts in kidney alone of kidney-pancreas transplantation. Transplantation 2003, 76:348–353.\nSimpson N, Cho YW, Cicciarelli JC, et al.: Comparison of renal allograft outcomes in combined liver-kidney transplantation versus subsequent kidney transplantation in liver transplant recipients: analysis of UNOS database. Transplantation 2006, 82:1298–1303.\nRuiz R, Kunitake H, Wilkinson AH, et al.: Long-term analysis of combined liver-kidney transplantation at a single center. Arch Surg 2006, 141:735–741.\nRuiz R, Barri YM, Jennings LW, et al.: Hepatorenal syndrome: a proposal for kidney after liver transplantation (KALT). Liver Transpl 2007, 13:838–847.\nCampbell MS, Kotlyar DS, Brensinger CM, et al.: Renal function after orthotopic liver transplantation is predicted by duration of pretransplantation creatinine elevation. Liver Transpl 2005, 11:1048–1055.\nPichler R, Dittrich MO, Anderson AE, et al.: Prediction of benefit from simultaneous liver-kidney transplantation versus liver-alone transplantation: potential role for native kidney biopsy. J Am Soc Nephrol 2006, 17:2919–2927.\nCoppo R, D’Amico G: Factors predicting progression of IgA nephropathies. J Nephrol 2005, 18:503–512.\nDavis CL, Gonwa TA, Wilkinson AH: Pathophysiology of renal disease associated with liver disorders: implications for liver transplantation. Part I. Liver Transpl 2002, 8:91–109.\nDavis CL, Gonwa TA, Wilkinson AH: Identification of patients best suited for combined liver-kidney transplantation: part II. Liver Transpl 2002, 8:193–211.\nDavis CL, Feng S, Sung R, et al.: Simultaneous liver-kidney transplantation: evaluation to decision making. Am J Transplant 2007, 7:1702–1709.",{"EN":950},"Model for End-Stage Liver Disease (MELD) allocation has improved the process for ranking patients on the liver transplant list. One unintended consequence has been an increase in the number of simultaneous liver-kidney (SLK) transplants. Some have argued that the system unfairly advantages patients with kidney disease and that some kidneys are being prematurely placed in SLK transplantation. This review summarizes the MELD score, assessment of kidney function in cirrhosis, the impact of kidney function in liver disease, and changes in kidney function status in liver transplant recipients in the MELD era. Finally, recommendations regarding who should receive SLK transplants are reviewed.",{"EN":952},"The impact of MELD allocation on simultaneous liver-kidney transplantation",{"VOID":954},"10.1007\u002Fs11894-009-0012-8","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11894-009-0012-8",[957,964],{"id":958,"sortIndex":23,"researcher":22,"roles":959,"affiliations":960,"properties":961},"4069d19f-d33a-44e4-a40c-de312a331884",[416],[],{"title":962},{"VI":963},"Julie A. Thompson",{"id":965,"sortIndex":79,"researcher":22,"roles":966,"affiliations":967,"properties":976},"17d23b7e-29ea-4848-8f68-ed18b2fe7e63",[416],[968],{"id":22,"sortIndex":23,"affiliation":969,"properties":22},{"id":970,"createTime":971,"updateTime":971,"relativeEntities":972,"slug":22,"properties":973,"entityType":51,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23},"d5b66998-6408-4830-9b40-43b7053c243d","2024-02-14T02:38:55.582+00:00",[],{"title":974},{"VI":975},"Division of Gastroenterology & Hepatology, Minneapolis, USA",{"title":977},{"VI":978},"John R. Lake",{"url":955,"publisher":980,"properties":1002},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":981,"slug":10,"properties":982,"entityType":20,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23,"subjectFields":987,"manageAffiliations":988,"indexDatabases":989,"url":22,"thumbnailPath":22,"statistic":997,"gsStatistic":22,"type":100,"analyzePriority":22},[],{"issn":983,"eissn":984,"title":985,"url":986},{"VOID":13},{"VOID":15},{"EN":17},{"VOID":19},[],[],[990],{"id":56,"indexDatabase":991,"url":69,"indexYears":70,"academicFieldIds":996,"indexDatabaseRanking":74},{"id":58,"createTime":59,"updateTime":60,"relativeEntities":992,"label":993,"description":994,"key":66,"publicationTags":995,"standard":22},[],{"EN":63,"VI":63},{"EN":63,"VI":65},[68],[72,73],{"impactFactor":23,"impactFactorByYear":998,"i10Index":23,"i10IndexLast5Year":23,"totalPublication":77,"totalPublicationByYear":999,"totalCitation":23,"totalCitationByYear":1000,"totalCitationPerPublication":23,"totalCitationPerPublicationByYear":1001,"hindexLast5Year":23,"hindex":23},{},{"1996":79,"1999":80,"2000":81,"2001":82,"2002":83,"2003":84,"2004":85,"2005":86,"2006":87,"2007":83,"2008":88,"2009":81,"2010":89,"2011":90,"2012":91,"2013":81,"2014":92,"2015":93,"2016":87,"2017":94,"2018":90,"2019":92,"2020":95,"2021":96,"2022":97,"2023":82,"2024":52},{},{},{"volume":1003,"pages":1005},{"VOID":1004},"11",{"VOID":1006},"76-82","2009-01-17",2009,{"id":1010,"createTime":1011,"updateTime":1012,"relativeEntities":1013,"slug":1014,"properties":1015,"entityType":124,"verifyStatus":125,"verifyTime":1012,"verifyNote":126,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23,"primaryUrl":1024,"fullTextUrl":22,"authors":1025,"publicationType":164,"publisherRelationship":1043,"citationCount":22,"citationInfo":22,"publishDate":1070,"publishYear":939,"citationAnalyzeStatus":21,"lastCitationAnalyze":22,"indexDatabases":22,"openAccess":22,"references":22,"isForceReanalyzing":388},"eda295e6-8ecd-4716-9295-98d56980c035","2024-02-02T10:38:15.391+00:00","2024-12-30T23:44:12.376+00:00",[],"Advances-in-therapeutic-approaches-to-ulcerative-colitis-and-crohn-s-disease",{"references":1016,"abstract":1018,"title":1020,"doi":1022},{"VOID":1017},"Bebb JR, Scott BB: Systematic review: How effective are the usual treatments for ulcerative colitis? Aliment Pharmacol Ther 2004, 20:143–149.\nBebb JR, Scott BB: Systematic review: How effective are the usual treatments for Crohn’s disease? Aliment Pharmacol Ther 2004, 20:151–159.\nHanauer SB, Stromberg U: Oral Pentasa in the treatment of active Crohn’s disease: a meta-analysis of double-blind, placebo-controlled trials. Clin Gastroenterol Hepatol 2004, 2:379–388. This paper changed the perception of mesalamine as therapy for mild to moderate ileal Crohn’s disease (results in text).\nFeagan BG: 5-ASA therapy for active Crohn’s disease: old friends, old data, and a new conclusion. Clin Gastroenterol Hepatol 2004, 2:376–378.\nHanauer SB: The case for using 5-aminosalicylates in Crohn’s disease: pro. Inflamm Bowel Dis 2005, 11:609–612.\nHanauer SB, Sandborn WJ, Katz S, et al.: Efficacy and safety of mesalazine 4.8g\u002Fday (800mg tablet) compared with 2.4g\u002Fday (400mg tablet) in treating moderately active ulcerative colitis: ASCEND II study. Gut 2005, 54(Suppl II):A3.\nHanauer SB, Sandborn W, Kornbluth A, et al.: Delayed-release mesalamine 4.8g\u002Fday (800mg tablet) versus 2.4g\u002Fday (400mg tablet) for treatment of moderately active ulcerative colitis: combined analysis of two randomised, double-blind, controlled trials. Gastroenterology 2005, 128(Suppl 2):A-74.\nKane S, Huo D, Aikens J, Hanauer S: Medication nonadherence and the outcomes of patients with quiescent ulcerative colitis. Am J Med 2003, 114:39–43.\nMarteau PR, Probert C, Lindgren S, et al.: Combined oral and enema treatment with Pentasa (mesalazine) is superior to oral therapy alone in patients with extensive mild\u002Fmoderate active colitis: a randomised, double-blind, placebo controlled study. Gut 2005, 54:960–965. This report confirmed that combined oral and topical therapy, rather than oral mesalamine alone, is more effective for inducing remission for active ulcerative colitis.\nTravis SPL: Transatlantic divide: first line therapy for acute colitis. Pract Gastroenterol 2005, 29:66–70.\nRousseaux C, Lefebvre B, Dubuquoy L, et al.: Intestinal antiinflammatory effect of 5-aminosalicylic acid is dependent on peroxisome proliferator-activated receptor-gamma. J Exp Med 2005, 201:1205–1215.\nVan Staa TP, Card TR, Leufkens HG, Logan RF: 5-aminosalicylate use and colorectal cancer risk in inflammatorybowel disease: a large epidemiological study. Gut 2005 Jun 30, [Epub ahead of print]. This article provides good evidence for chemopreventive role of 5-ASA. Regular users of mesalamine (6-12 prescriptions before cancer diagnosed) had an OR of 1.13 (0.49-2.59); for 13 to 30 prior prescriptions it was 0.30 (0.11-0.83), and for more than 30 prior prescriptions it was 0.31 (0.11-0.84).\nFrieri G, Mariateresa P, Brigida G, et al.: Long-term oral plus topical mesalazine in frequently relapsing ulcerative colitis. Dig Liver Dis 2005, 37:92–96.\nPrantera C, Viscido A, Biancone L, et al.: A new oral delivery system for 5-ASA: preliminary clinical findings for MMx. Inflamm Bowel Dis 2005, 11:421–427.\nLichtenstein GR, Cohen RD, Feagan BG, et al.: Safety of in fliximab and other Crohn’s disease therapies: updated Treat registry data with over 10 000 patient-years of follow-up. Gastroenterology 2005, 128(Suppl 2):A-580.\nCreed TJ, Dayan CM, Probert CSJ, Hearing SD: Basiliximab for steroid-resistant ulcerative colitis. Gut 2004, 53(Suppl III):A97.\nFranchimont D: Overview of the actions of glucocorticoids on the immune response: a good model to characterize new pathways of immunosuppression for new treatment strategies. Ann N Y Acad Sci 2004, 1024:124–137.\nLowenberg M, Verhaar A, vand den Blink B, et al.: Essential role for c-Raf in steroid-insensitive Crohn’s disease. Gastroenterology 2005, 128(Suppl 2):A-505.\nTiede I, Fritz G, Strand S, et al.: CD28-dependent Rac 1 activation is the molecular target of azathioprine in primary human CD4+ T lymphocytes. J Clin Invest 2003, 111:1143–1145.\nAberra FN, Lichtenstein GR: Review article: Monitoring of immunomodulators in inflammatory bowel disease. Aliment Pharmacol Ther 2005, 21:307–319.\nNeurath MF, Kiesslich R, Tiechgräber U, et al.: Analysis of 6-thioguanosine di-(TGDP) and triphosphate (TGTP) levels as a novel method for clinical monitoring of azathioprine therapy in Crohn’s disease. Gastroenterology 2005, 128(Suppl 2):A-12.\nHanauer SB, Korelitz BI, Rutgeerts P, et al.: Post-operative maintenance of Crohn’s disease remission with 6-mercaptopurine, mesalamine or placebo: a 2 year trial. Gastroenterology 2004, 127:723–729.\nArdizzone S, Maconi G, Sampietro GM, et al.: Azathioprine and mesalamine for prevention of relapse after conservative surgery for Crohn’s disease. Gastroenterology 2004, 127:730–737.\nCosnes J, Nion-Larmurier I, Beaugere L, et al.: Impact of the increasing use of immunosuppressants in Crohn’s disease on the need for intestinal surgery. Gut 2005, 54:237–241.\nDejaco C, Angelberger S, Waldhoer T, et al.: Pregnancy and birth outcome under thiopurine therapy for inflammatory bowel disease. Gastroenterology 2005, 128(Suppl. 2):A-12.\nSiegel CA, Sands BE: Review article: Practical management of inflammatory bowel disease patients taking immunomodulators. Aliment Pharmacol Ther 2005, 22:1–16.\nCummings JRF, Herrlinger KR, Travis SP, et al.: Oral methotrexate in ulcerative colitis. Aliment Pharmacol Ther 2005, 21:385–389.\nVan Assche G, D’Haens G, Noman M, et al.: Randomized, double-blind comparison of 4mg\u002Fkg versus 2mg\u002Fkg intravenous cyclosporine in severe ulcerative colitis. Gastroenterology 2003, 125:1025–1031.\nJärnerot G, Hertervig E, Friis-Liby I, et al.: In fliximab as rescue therapy in severe to moderately severe ulcerative colitis: a randomized, placebo-controlled study. Gastroenterology 2005, 128:1805–11. Small but pivotal trial showing efficacy of IFX for in-patients with severe, active ulcerative colitis refractory to intravenous steroids (results and comparison with ACT trials in text).\nCampbell S, Travis SPL, Jewell DP: Ciclosporin use in acute ulcerative colitis: a long-term experience. Eur J Gastroenterol Hepatol 2005, 17:79–84.\nBaumgart DC, Pintoffl JP, Sturm A, et al.: Tacrolimus (FK506) rescue therapy is safe and effective in patients with severe and refractory inflammatory bowel disease: a long term follow up. Gastroenterology 2005, 128(Suppl 2):A-198.\nRutgeerts P, Feagan BG, Olson A, et al.: A randomised placebocontrolled trial of infliximab therapy for active ulcerative colitis: Act 1 trial. Gastroenterology 2005, 128(Suppl 2):A-105.\nSandborn WJ, Rachmilewitz D, Hanauer SB, P, et al.: In fliximab induction and maintenance therapy for active ulcerative colitis: the Act 2 trial. Gastroenterology 2005, 128(Suppl 2):A-104.\nTargan SR, Hanauer SB, Van Deventer SJ, et al.: A short-term study of chimeric monoclonal antibody cA2 to tumor necrosis factor alpha for Crohn’s disease. Crohn’s Disease cA2 Study Group. N Engl J Med 1997, 337:1029–1035.\nHommes DW, Baert F, Van Assche G, et al.: Management of recent onset Crohn’s disease: a controlled randomized trial comparing step-up and top-down therapy. Gastroenterology 2005, in press.\nLémman M, Mary J-Y, Duclos B, et al.: Infliximab as a bridge therapy in steroid-dependent Crohn’s disease patients treated with azathioprine. A randomized, double-blind, placebo-controlled trial. Gastroenterology 2005, in press.\nNoman M, Vermeire S, Van Assche G, et al.: The effectiveness of immunosuppression to suppress formation of antibodies to infliximab in Crohn’s disease. Gut 2004, 53(Suppl. VI):A-47.Z.\nGhosh S: Anti-TNF therapy in Crohn’s disease. Novartis Found Symp 2004, 263:193–205, discussion 205–218.\nRampton DS: Preventing TB in patients with Crohn’s disease needing in fliximab or other anti-TNF therapy. Gut 2005, 54:1360–1362.\nShih CE, Bayless TM, Harris ML: Maintenance of longterm response to in fliximab over 1 to 5 years in Crohn’s disease including shortening doing intervals or increasing dosage. Gastroenterology 2004, 126(Suppl 2):A-631.\nWilliams JB, Cross RK, Thameen D, et al.: Long-term in fliximab maintenance infusion regimens and rates of hospital lisation, surgery and disability in Crohn’s disease patients. Gastroenterology 2005, 128(Suppl 2):A-589.\nRutgeerts P, Feagan BG, Lichtenstein GR, et al.: Comparison of scheduled and episodic treatment strategies of infliximab in Crohn’s disease. Gastroenterology 2004, 126:402–413. Further analysis of ACCENT trial showing that episodic therapy is associated with shorter response, less mucosal healing, and higher rates of hospitalization and abdominal surgery.\nLichtenstein GR, Yan S, Bala M, et al.: In fliximab maintenance treatment reduces hospitalizations, surgeries and procedures in fistulizing Crohn’s disease. Gastroenterology 2005, 128:862–869.\nJewell DP, Satsangi J, Lobo A, et al.: In fliximab use in Crohn’s disease: impact on health care resources in the UK. Eur J Gastroenterol Hepatol 2005, 17:1047–1052.\nNesbitt AM, Henry AJ: High affinity and potency of the pegylated FAB’ fragment CDP870: a direct comparison with other anti-TNF agents. Gut 2004, 53(Suppl VI):A-47.\nPRECiSE. UCB announce that CIMZIA TM demonstrates significant positive results in its two pivotal phase III Crohn’s disease trials. Internet press release 26 July 2005. Accessible at: http:\u002F\u002Fir.ucb-group.com\u002Fphoenix.zhtml?c=137495&p=irolnewsArticle& ID=735014&highlight=\nMacIntosh DG, Lukas M, Sandborn W, et al.: A randomised, double-blind, placebo-controlled trial of the clinical assessment of adalimumab safety and efficacy studied as an induction therapy in Crohn’s disease. Gut 2004, 53(Suppl VI):A-47.\nSandborn W, Hanauer S, Lukas M, et al.: Induction and maintenance of clinical remission and response in subjects with Crohn’s disease treated during a 6-month open-label period with fully human anti-TNF alpha monoclonal antibody adalimumab (Humira). Gastroenterology 2005, 128(Suppl 2):A-111.\nPapadakis KA, Shaye OA, Vasiliauskas EA, et al.: Safety and efficacy of adalimumab (D2E7) in Crohn’s disease patients with an attenuated response to in fliximab. Am J Gastroenterol 2005, 100:75–79.\nRutgeerts P, Reinisch W, Colombel J-F, et al.: Preliminary results of a phase I\u002FII study of HuZAF, an anti-IFNg monoclonal antibody in patients with moderate to severe active Crohn’s disease. Gastroenterology 2002, 122 Suppl 4:A-61.\nVan Assche G, Pearce T: Fontolizumab (Huzaf), a humanized anti-IFN-gamma antibody, has clinical activity and excellent tolerability in moderate to severe Crohn’s disease. Gut 2004, 53(Suppl VI):A48.\nDe Villiers W, Katz S, Salzberg BA, et al.: Chronic dosing of fontolizumab (Huzaf), a humanised anti-IFN-gamma antibody in patients with moderate to severe Crohn’s disease. Gastroenterology 2005, 128(Suppl 2):A-111.\nTargan SR, Salzberg BA, Mayer L, et al.: A phase I-II study: multiple dose levels of visilizumab are well tolerated and produce rapid and sustained improvement in ulcerative colitis patients refractory to treatment with intravenous steroids (IVSR-UC). Gastroenterology 2005, 128(Suppl 2):A-75.\nHommes DW, Plevy S, Salzberg BA, et al.: Epstein-Barr virus (EBV) replication in severe active, steroid-resistant ulcerative colitis patients treated with visilizumab, an anti-CD3 antibody. Gastroenterology 2005, 128(Suppl. 2):A-75.\nMannon PJ, Fuss I, Mayer L, et al.: Anti-interleukin-12 antibody for active Crohn’s disease. N Engl J Med 2004, 351:2069–2079.\nIto H, Takazoe M, Fukuda Y, et al.: A pilot randomised trial of a human anti-interleukin-6 receptor monoclonal antibody in active Crohn’s disease. Gastroenterology 2004, 126:989–996.\nFeagan BG, Greenberg GR, Wild G, et al.: Treatment of ulcerative colitis with a humanized antibody to the alpha4beta7 integrin. N Engl J Med 2005, 352:2499–2507.\nRutgeerts P, Enns R, Colombel JF, et al.: 6-month steroid-sparing results of natalizumab in a controlled study of patients with Crohn’s disease. Gut 2004, 53(Suppl. VI):A-48.\nVan Assche G, Van Ranst M, Sciot R, et al.: Progressive multifocal leukoencephalopathy after natalizumab therapy for Crohn’s disease. N Engl J Med 2005, 353:362–368.\nChey WY, Volfova M, Konecny M, et al.: Two phase 3 studies of alicaforsen (ISIS2302), an anti-sense oligonulceotide to human ICAM-1, in the treatment of moderate to severe Crohn’s disease. Gastroenterology 2005, 128(Suppl. 2):A-112.\nVan Deventer SJ, Volfova M, Flisiak R, et al.: A phase 2 doseranging, double blind, placebo-controlled study of alicaforsen enema in subjects with acute exacerbation of mild to moderate left-sided ulcerative colitis. Gastroenterology 2005, 128(Suppl. 2):A-74.\nMiner PB, Nichols T, Schwartz H, et al.: A phase 2 trial to assess the safety and efficacy of two dose formulations of alicaforsen enema compared with mesalamine enema for acute ulcerative colitis. Gastroenterology 2005, 128(Suppl. 2):A-74.\nBraat H, Rottiers P, Huyghebaert N, et al.: Interleukin-10 producing Lactococcus lactis for the treatment of Crohn’s disease. Gastroenterology 2005, 128(Suppl. 2):A-104.\nHerrlinger KR, Witthoeft T, Raedler A, et al.: Randomised, doubleblind, double-dummy, controlled trial of subcutaneous recombinant human interleukin-11 vs prednisolone in active Crohn’s disease. Gut 2004, 53(Suppl. VI):A-49.\nMahmood A, Melley L, Fitzgerald A, et al.: Phase I\u002FII trial of trefoil factor family 3 (TFF-3) enema therapy with oral mesalazine for mild to moderate left-sided colitis. Gastroenterology 2005, 128(Suppl. 2):A-581.\nKorzenik JR, Dieckgraefe B, Valentine JF, et al.: Sargramostim for active Crohn’s disease. N Engl J Med 2005, 352:2193–2201.\nValentine J, Stone C, Korzenik J, et al.: Repeated cycles of sargramostim for active Crohn’s disease: update from an open label trial (n.o.v.e.l. 5). Gastroenterology 2005, 128(Suppl. 2):A-111.\nBuchman AL, Katz S, Barish C, et al.: Semapimod treatment of Crohn’s disease. Gastroenterology 2004, 126 Suppl 2:A-464.\nTravis SPL, Yap LM, Hawkey CJ, et al.: RDP58—a novel and potentially effective oral therapy for ulcerative colitis (UC): results of parallel prospective, multicenter, blinded, placebocontrolled trials. 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Gastroenterology 2005, 128(Suppl. 2):A-326.",{"EN":1019},"Advances (from 2004 to 2006) in the use of conventional agents include the molecular mechanisms of action, which have implications for monitoring (azathioprine and thioguanosine triphosphate) and chemoprevention (mesalamine and peroxisome proliferator activated receptor [PPAR]γ). Advances in biotherapy include new data on monoclonal antibodies (infliximab in ulcerative colitis, adalimumab, certolizumab pegol, fontolizumab, selective anti-adhesion molecules, and others), antisense oligonucleotides, the development of small molecules, and cell-gene therapy (including helminth ova, leukocytapheresis, stem cell transplantation, and probiotic intestinal mucosal delivery systems). However, management of inflammatory bowel disease is about more than drug therapy, dose, and timing. The goals remain induction of remission, limitation of side effects, modification of the pattern of disease, and avoidance of complications. With the cost and complexity of biotherapy, inflammatory bowel disease is emerging as a specific subspecialty.",{"EN":1021},"Advances in therapeutic approaches to ulcerative colitis and crohn’s disease",{"VOID":1023},"10.1007\u002Fs11894-005-0079-9","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11894-005-0079-9",[1026],{"id":1027,"sortIndex":23,"researcher":22,"roles":1028,"affiliations":1029,"properties":1040},"96069c3b-b448-435d-a71e-a98cf3335fbb",[416],[1030],{"id":22,"sortIndex":23,"affiliation":1031,"properties":22},{"id":1032,"createTime":1033,"updateTime":1034,"relativeEntities":1035,"slug":1036,"properties":1037,"entityType":51,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23},"2392ce8c-4f18-4b2b-87b5-9f9810f68dd1","2024-01-20T23:37:09.074+00:00","2024-09-19T03:04:42.225+00:00",[],"Gastroenterology-Unit-John-Radcliffe-Hospital-Oxford-UK",{"title":1038},{"VI":1039},"Gastroenterology Unit, John Radcliffe Hospital, Oxford, UK",{"title":1041},{"VI":1042},"Simon Travis",{"url":1024,"publisher":1044,"properties":1066},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1045,"slug":10,"properties":1046,"entityType":20,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"syncStatus":21,"languages":22,"translateLanguages":22,"viewCount":23,"subjectFields":1051,"manageAffiliations":1052,"indexDatabases":1053,"url":22,"thumbnailPath":22,"statistic":1061,"gsStatistic":22,"type":100,"analyzePriority":22},[],{"issn":1047,"eissn":1048,"title":1049,"url":1050},{"VOID":13},{"VOID":15},{"EN":17},{"VOID":19},[],[],[1054],{"id":56,"indexDatabase":1055,"url":69,"indexYears":70,"academicFieldIds":1060,"indexDatabaseRanking":74},{"id":58,"createTime":59,"updateTime":60,"relativeEntities":1056,"label":1057,"description":1058,"key":66,"publicationTags":1059,"standard":22},[],{"EN":63,"VI":63},{"EN":63,"VI":65},[68],[72,73],{"impactFactor":23,"impactFactorByYear":1062,"i10Index":23,"i10IndexLast5Year":23,"totalPublication":77,"totalPublicationByYear":1063,"totalCitation":23,"totalCitationByYear":1064,"totalCitationPerPublication":23,"totalCitationPerPublicationByYear":1065,"hindexLast5Year":23,"hindex":23},{},{"1996":79,"1999":80,"2000":81,"2001":82,"2002":83,"2003":84,"2004":85,"2005":86,"2006":87,"2007":83,"2008":88,"2009":81,"2010":89,"2011":90,"2012":91,"2013":81,"2014":92,"2015":93,"2016":87,"2017":94,"2018":90,"2019":92,"2020":95,"2021":96,"2022":97,"2023":82,"2024":52},{},{},{"volume":1067,"pages":1068},{"VOID":935},{"VOID":1069},"475-484","2005-11-01"]