Toward a Personalized Medicine Approach to the Management of Inflammatory Bowel Disease

  • The American Journal of Gastroenterology (2014) 109, 9941004 (2014)
  • doi:10.1038/ajg.2014.110
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The medical management of inflammatory bowel disease (IBD) is evolving toward a personalized medicine-based model. Modern therapeutic algorithms that feature use of tumor necrosis factor (TNF) antagonists in combination with immunosuppressive are highly effective when initiated in high-risk patients early in the course of disease. Defined targets that guide intensification of therapy are critical interventions. In this model, therapy is optimized through appropriate pretreatment testing, therapeutic drug monitoring, and patient-based monitoring strategies. This review discusses the current application of personalized medicine to the management of IBD.

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  1. 1.

    , , et al. Right medication, right dose, right patient, right time, and right route: how do we select the right patient-controlled analgesia (PCA) device? Pain Manag Nurs 2007;8:140–145.

  2. 2.

    , , et al. Treat to target: a proposed new paradigm for the management of Crohn's disease. Clin Gastroenterol Hepatol 2013 (e-pub ahead of print).

  3. 3.

    , , et al. posaconazole therapeutic drug monitoring in the real-life setting: a single-center experience and review of the literature. Pharmacotherapy 2013;33:1117–1125.

  4. 4.

    , , et al. Personalized cancer medicine: molecular diagnostics, predictive biomarkers, and drug resistance. Clin Pharmacol Ther 2013;93:252–259.

  5. 5.

    , , . Pharmacogenomics in the treatment of inflammatory bowel disease. Pharmacogenomics 2010;11:421–437.

  6. 6.

    , , et al. Genetic variants within the MAP kinase signalling network and anti-TNF treatment response in rheumatoid arthritis patients. Ann Rheum Dis 2011;70:98–103.

  7. 7.

    , , et al. Polymorphisms in apoptosis genes predict response to infliximab therapy in luminal and fistulizing Crohn's disease. Aliment Pharmacol Ther 2005;22:613–626.

  8. 8.

    , , et al. A positive response to infliximab in Crohn disease: association with a higher systemic inflammation before treatment but not with -308 TNF gene polymorphism. Scand J Gastroenterol 2002;37:818–824.

  9. 9.

    , , et al. Response to infliximab treatment in Crohn's disease is not associated with mutations in the CARD15 (NOD2) gene: an analysis in 534 patients from two multicenter, prospective GCP-level trials. Pharmacogenetics 2002;12:509–515.

  10. 10.

    , , et al. Pharmacogenetic investigation of the TNF/TNF-receptor system in patients with chronic active Crohn's disease treated with infliximab. Pharmacogenomics J 2002;2:127–136.

  11. 11.

    , , et al. Association of the tumour necrosis factor-308 variant with differential response to anti-TNF agents in the treatment of rheumatoid arthritis. Hum Mol Genet 2008;17:3532–3538.

  12. 12.

    , , et al. Tumour necrosis factor alpha -308G->A polymorphism is not associated with response to TNFalpha blockers in Caucasian patients with rheumatoid arthritis: systematic review and meta-analysis. Ann Rheum Dis 2010;69:1022–1028.

  13. 13.

    , , et al. Tumour necrosis factor-alpha receptor 1 and 2 polymorphisms in inflammatory bowel disease and their association with response to infliximab. Aliment Pharmacol Ther 2004;20:303–310.

  14. 14.

    , , et al. ANCA pattern and LTA haplotype relationship to clinical responses to anti-TNF antibody treatment in Crohn's disease. Gastroenterology 2001;120:1347–1355.

  15. 15.

    , , et al. IBD5 polymorphisms in inflammatory bowel disease: association with response to infliximab. World J Gastroenterol 2005;11:1187–1192.

  16. 16.

    , , et al. NOD2/CARD15 does not influence response to infliximab in Crohn's disease. Gastroenterology 2002;123:106–111.

  17. 17.

    , , et al. Predictive model for the outcome of infliximab therapy in Crohn's disease based on apoptotic pharmacogenetic index and clinical predictors. Inflamm Bowel Dis 2007;13:372–379.

  18. 18.

    , , et al. Disease activity, ANCA, and IL23R genotype status determine early response to infliximab in patients with ulcerative colitis. Am J Gastroenterol 2010;105:1811–1819.

  19. 19.

    , , et al. Genome-wide association identifies multiple ulcerative colitis susceptibility loci. Nat Genet 2010;42:332–337.

  20. 20.

    , , et al. Genome wide association (GWA) predictors of anti-TNFalpha therapeutic responsiveness in pediatric inflammatory bowel disease. Inflamm Bowel Dis 2010;16:1357–1366.

  21. 21.

    , . Glucocorticoid receptor gene polymorphisms and glucocorticoid resistance in inflammatory bowel disease: a meta-analysis. Dig Dis Sci 2012;57:3065–3075.

  22. 22.

    , , et al. Infliximab, azathioprine, or combination therapy for Crohn's disease. N Engl J Med 2010;362:1383–1395.

  23. 23.

    , , et al. Early combined immunosuppression or conventional management in patients with newly diagnosed Crohn's disease: an open randomised trial. Lancet 2008;371:660–667.

  24. 24.

    , . The thiopurine S-methyltransferase gene locus — implications for clinical pharmacogenomics. Pharmacogenomics 2002;3:89–98.

  25. 25.

    , , et al. Human thiopurine methyltransferase pharmacogenetics: gene sequence polymorphisms. Clin Pharmacol Ther 1997;62:60–73.

  26. 26.

    , , et al. Thiopurine S-methyltransferase deficiency: two nucleotide transitions define the most prevalent mutant allele associated with loss of catalytic activity in Caucasians. Am J Hum Genet 1996;58:694–702.

  27. 27.

    , , et al. Characterisation of novel defective thiopurine S-methyltransferase allelic variants. Biochem Pharmacol 2008;76:404–415.

  28. 28.

    , , et al. Functional characterization of 23 allelic variants of thiopurine S-methyltransferase gene (TPMT*2 - *24). Pharmacogenet Genomics 2008;18:887–893.

  29. 29.

    , , et al. Characterization of a novel sequence variant, TPMT*28, in the human thiopurine methyltransferase gene. Pharmacogenet Genomics 2010;20:700–707.

  30. 30.

    , , et al. TPMT*26 (208F—>L), a novel mutation detected in a Chinese. Br J Clin Pharmacol 2009;68:120–123.

  31. 31.

    , , et al. Detection of one single mutation predicts thiopurine S-methyltransferase activity in a population of Saami in northern Norway. Clin Pharmacol Ther 2001;70:183–188.

  32. 32.

    , , et al. Molecular diagnosis of thiopurine S-methyltransferase deficiency: genetic basis for azathioprine and mercaptopurine intolerance. Ann Intern Med 1997;126:608–614.

  33. 33.

    , , et al. Highly multiplexed genotyping of thiopurine s-methyltransferase variants using MALD-TOF mass spectrometry: reliable genotyping in different ethnic groups. Clin Chem 2008;54:1637–1647.

  34. 34.

    , , et al. Comprehensive analysis of thiopurine S-methyltransferase phenotype-genotype correlation in a large population of German-Caucasians and identification of novel TPMT variants. Pharmacogenetics 2004;14:407–417.

  35. 35.

    , , et al. Systematic review of thiopurine methyltransferase genotype and enzymatic testing strategies. Ther Drug Monit 2011;33:192–199.

  36. 36.

    , , et al. A comparison of molecular and enzyme-based assays for the detection of thiopurine methyltransferase mutations. Br J Haematol 2000;110:599–604.

  37. 37.

    , , et al. Aplastic anemia secondary to azathioprine in systemic lupus erythematosus: report of a case with normal thiopurine S-methyltransferase enzyme activity and review of the literature. Lupus 2013;22:1526–1528.

  38. 38.

    , , et al. Genotypic analysis of thiopurine S-methyltransferase in patients with Crohn's disease and severe myelosuppression during azathioprine therapy. Gastroenterology 2000;118:1025–1030.

  39. 39.

    , . Initiating azathioprine for Crohn's disease. Clin Gastroenterol Hepatol 2012;10:460–465.

  40. 40.

    . Clinical use and practical application of TPMT enzyme and 6-mercaptopurine metabolite monitoring in IBD. Rev Gastroenterol Disord 2003;3 (Suppl 1): S30–S38.

  41. 41.

    , , et al. Lack of effect of intravenous administration on time to respond to azathioprine for steroid-treated Crohn's disease. North American Azathioprine Study Group. Gastroenterology 1999;117:527–535.

  42. 42.

    , , . The utility of thiopurine methyltransferase enzyme testing in inflammatory bowel disease. Can J Gastroenterol 2013;27:39–43.

  43. 43.

    , , et al. Avoiding adverse drug reactions by pharmacogenetic testing: a systematic review of the economic evidence in the case of TPMT and AZA-induced side effects. Int J Technol Assess Health Care 2008;24:294–302.

  44. 44.

    , , et al. Pharmacoeconomic analyses of azathioprine, methotrexate and prospective pharmacogenetic testing for the management of inflammatory bowel disease. Pharmacoeconomics 2006;24:767–781.

  45. 45.

    , , et al. Clinical Pharmacogenetics Implementation Consortium guidelines for thiopurine methyltransferase genotype and thiopurine dosing. Clin Pharmacol Ther 2011;89:387–391.

  46. 46.

    , , et al. Are patients with intermediate TPMT activity at increased risk of myelosuppression when taking thiopurine medications? Pharmacogenomics 2010;11:177–188.

  47. 47.

    , , et al. Assessment of thiopurine S-methyltransferase activity in patients prescribed thiopurines: a systematic review. Ann Intern Med 2011;154:814–823.

  48. 48.

    , , . Response to biologic therapy in Crohn's disease is improved with early treatment: an analysis of health claims data. Inflamm Bowel Dis 2012;18:2225–2231.

  49. 49.

    , , et al. Penetrating or stricturing diseases are the major determinants of time to first and repeat resection surgery in Crohn's disease. Digestion 2013;87:212–221.

  50. 50.

    , , et al. Perianal disease combined with NOD2 genotype predicts need for IBD-related surgery in Crohn's disease patients from a population-based cohort. J Clin Gastroenterol 2013;47:242–245.

  51. 51.

    , , . Review article: Altering the natural history of Crohn's disease—evidence for and against current therapies. Aliment Pharmacol Ther 2007;25:3–12.

  52. 52.

    , , et al. Validation of endoscopic activity scores in patients with Crohn's disease based on a post-hoc analysis of data from SONIC. Gastroenterology 2013;145:978–986. e5.

  53. 53.

    , , et al. Development and validation of a new, simplified endoscopic activity score for Crohn's disease: the SES-CD. Gastrointest Endosc 2004;60:505–512.

  54. 54.

    , , et al. Genetic risk profiling and prediction of disease course in Crohn's disease patients. Clin Gastroenterol Hepatol 2009;7:972–980 e2.

  55. 55.

    , , et al. Distinct and overlapping genetic loci in Crohn's disease and ulcerative colitis: correlations with pathogenesis. Inflamm Bowel Dis 2011;17:1936–1942.

  56. 56.

    , , et al. Serological antibodies in inflammatory bowel disease: a systematic review. Inflamm Bowel Dis 2012;18:1340–1355.

  57. 57.

    , , et al. Predicting outcome in severe ulcerative colitis. Gut 1996;38:905–910.

  58. 58.

    , , et al. Severe pediatric ulcerative colitis: a prospective multicenter study of outcomes and predictors of response. Gastroenterology 2010;138:2282–2291.

  59. 59.

    , , et al. Development, validation, and evaluation of a pediatric ulcerative colitis activity index: a prospective multicenter study. Gastroenterology 2007;133:423–432.

  60. 60.

    , , et al. Prognosis of severe attacks in ulcerative colitis: effect of intensive medical treatment. Dig Liver Dis 2004;36:461–466.

  61. 61.

    , , et al. Predicting the outcome of corticoid therapy for acute ulcerative colitis. Results of a prospective, randomized, double-blind clinical trial. J Clin Gastroenterol 1987;9:50–54.

  62. 62.

    , , et al. Severe ulcerative colitis: prospective study of parameters determining outcome. J Gastroenterol Hepatol 2004;19:1247–1252.

  63. 63.

    , , et al. Steroid-refractory ulcerative colitis: predictive factors of response to cyclosporine and validation in an independent cohort. Inflamm Bowel Dis 2008;14:347–352.

  64. 64.

    , . Intensive intravenous regimen for severe attacks of ulcerative colitis. Lancet 1974;1:1067–1070.

  65. 65.

    , , et al. Predicting the outcome of severe ulcerative colitis: development of a novel risk score to aid early selection of patients for second-line medical therapy or surgery. Aliment Pharmacol Ther 2004;19:1079–1087.

  66. 66.

    , , et al. Fecal calprotectin predicts the clinical course of acute severe ulcerative colitis. Am J Gastroenterol 2009;104:673–678.

  67. 67.

    , , et al. Colonoscopy of acute colitis. A safe and reliable tool for assessment of severity. Dig Dis Sci 1994;39:1550–1557.

  68. 68.

    , , et al. Novel endoscopic activity index is useful for choosing treatment in severe active ulcerative colitis patients. J Gastroenterol 2010;45:936–943.

  69. 69.

    , , et al. Adalimumab induction therapy for Crohn disease previously treated with infliximab: a randomized trial. Ann Intern Med 2007;146:829–838.

  70. 70.

    , , et al. Effect of once- or twice-daily MMX mesalamine (SPD476) for the induction of remission of mild to moderately active ulcerative colitis. Clin Gastroenterol Hepatol 2007;5:95–102.

  71. 71.

    , , . Clinical pharmacokinetics and pharmacodynamics of mycophenolate in patients with autoimmune disease. Clin Pharmacokinet 2013;52:303–331.

  72. 72.

    , , et al. How are azathioprine and 6-mercaptopurine dosed by gastroenterologists? Results of a survey of clinical practice. Inflamm Bowel Dis 2008;14:514–518.

  73. 73.

    , , et al. Pharmacogenomics and metabolite measurement for 6-mercaptopurine therapy in inflammatory bowel disease. Gastroenterology 2000;118:705–713.

  74. 74.

    , , et al. Thiopurine metabolite monitoring in paediatric inflammatory bowel disease. Aliment Pharmacol Ther 2007;25:941–947.

  75. 75.

    , , et al. 6-thioguanine nucleotide-adapted azathioprine therapy does not lead to higher remission rates than standard therapy in chronic active Crohn disease: results from a randomized, controlled, open trial. Clin Chem 2007;53:1306–1314.

  76. 76.

    , , et al. Association of 6-thioguanine nucleotide levels and inflammatory bowel disease activity: a meta-analysis. Gastroenterology 2006;130:1047–1053.

  77. 77.

    , , et al. T1192 A randomized trial of metabolite-adjusted versus weight-based dosing of azathioprine (AZA) in Crohn's disease (CD) [Clinicaltrials. Gov Identifier Nct00113503]. Gastroenterology 2009;136.

  78. 78.

    , , et al. 6-Mercaptopurine metabolism in Crohn's disease: correlation with efficacy and toxicity. Gut 1996;39:401–406.

  79. 79.

    , , et al. 6-MP metabolite profiles provide a biochemical explanation for 6-MP resistance in patients with inflammatory bowel disease. Gastroenterology 2002;122:904–915.

  80. 80.

    , , et al. Thiopurine S-methyltransferase polymorphisms and thiopurine toxicity in treatment of inflammatory bowel disease. World J Gastroenterol 2010;16:3187–3195.

  81. 81.

    , , et al. Incidence, risk factors and clinical course of thiopurine-induced liver injury in patients with inflammatory bowel disease. Aliment Pharmacol Ther 2005;22:775–782.

  82. 82.

    , , et al. Hepatotoxicity associated with 6-methyl mercaptopurine formation during azathioprine and 6-mercaptopurine therapy does not occur on the short-term during 6-thioguanine therapy in IBD treatment. J Crohns Colitis 2012;6:95–101.

  83. 83.

    , , et al. Pharmacokinetics, dose adjustments, and 6-mercaptopurine/methotrexate drug interactions in two patients with thiopurine methyltransferase deficiency. Acta Paediatr 1998;87:108–111.

  84. 84.

    , , et al. Scheduled maintenance treatment with infliximab is superior to episodic treatment for the healing of mucosal ulceration associated with Crohn's disease. Gastrointest Endosc 2006;63:433–442; quiz 464.

  85. 85.

    , , et al. Adalimumab for maintenance of clinical response and remission in patients with Crohn's disease: the CHARM trial. Gastroenterology 2007;132:52–65.

  86. 86.

    , , et al. Certolizumab pegol for the treatment of Crohn's disease. N Engl J Med 2007;357:228–238.

  87. 87.

    , . Loss of response and requirement of infliximab dose intensification in Crohn's disease: a review. Am J Gastroenterol 2009;104:760–767.

  88. 88.

    , , et al. Clinical and biological consequences of immunization to infliximab in pediatric Crohn's disease. Clin Immunol 2006;118:11–19.

  89. 89.

    , , et al. Maximizing the effect of biologics in inflammatory bowel disease. Minerva Gastroenterol Dietol 2012;58:101–122.

  90. 90.

    , , et al. Infliximab dose intensification in Crohn's disease. Inflamm Bowel Dis 2007;13:1093–1099.

  91. 91.

    , , et al. Maintenance infliximab for Crohn's disease: the ACCENT I randomised trial. Lancet 2002;359:1541–1549.

  92. 92.

    , , et al. Maintenance infliximab does not result in increased abscess development in fistulizing Crohn's disease: results from the ACCENT II study. Aliment Pharmacol Ther 2006;23:1127–1136.

  93. 93.

    , , et al. Comparison of scheduled and episodic treatment strategies of infliximab in Crohn's disease. Gastroenterology 2004;126:402–413.

  94. 94.

    FDA. FDA Approves Adalimumab for Crohn's Diseases. 2007 [19 February 2013]; Available from: .

  95. 95.

    FDA. FDA approves Humira to treat ulcerative colitis. 2012 [cited 19 February 2013]; Available from: .

  96. 96.

    , , et al. Influence of immunogenicity on the long-term efficacy of infliximab in Crohn's disease. N Engl J Med 2003;348:601–608.

  97. 97.

    , , et al. Intravenous hydrocortisone premedication reduces antibodies to infliximab in Crohn's disease: a randomized controlled trial. Gastroenterology 2003;124:917–924.

  98. 98.

    , , et al. Incidence and importance of antibody responses to infliximab after maintenance or episodic treatment in Crohn's disease. Clin Gastroenterol Hepatol 2004;2:542–553.

  99. 99.

    , , et al. Effectiveness of concomitant immunosuppressive therapy in suppressing the formation of antibodies to infliximab in Crohn's disease. Gut 2007;56:1226–1231.

  100. 100.

    , , et al. Antibody response to infliximab and its impact on pharmacokinetics can be transient. Am J Gastroenterol 2013;108:962–971.

  101. 101.

    , , . Meta-analysis: efficacy and safety of combination therapy of infliximab and immunosuppressives for Crohn's disease. Eur J Gastroenterol Hepatol 2011;23:1100–1110.

  102. 102.

    , , et al. A pooled analysis of infections, malignancy, and mortality in infliximab- and immunomodulator-treated adult patients with inflammatory bowel disease. Am J Gastroenterol 2012;107:1051–1063.

  103. 103.

    , , et al. Risk of lymphoma associated with combination anti-tumor necrosis factor and immunomodulator therapy for the treatment of Crohn's disease: a meta-analysis. Clin Gastroenterol Hepatol 2009;7:874–881.

  104. 104.

    , , et al. Influence of trough serum levels and immunogenicity on long-term outcome of adalimumab therapy in Crohn's disease. Gastroenterology 2009;137:1628–1640.

  105. 105.

    , , et al. Adalimumab for maintenance treatment of Crohn's disease: results of the CLASSIC II trial. Gut 2007;56:1232–1239.

  106. 106.

    , , et al. Clinical response to adalimumab: relationship to anti-adalimumab antibodies and serum adalimumab concentrations in rheumatoid arthritis. Ann Rheum Dis 2007;66:921–926.

  107. 107.

    , , et al. Immunogenicity negatively influences the outcome of adalimumab treatment in Crohn's disease. Aliment Pharmacol Ther 2008;28:1122–1126.

  108. 108.

    , , et al. Influence of immunogenicity on the long-term efficacy of infliximab in Crohn's disease. N Engl J Med 2003;348:601–608.

  109. 109.

    , , . Therapeutic drug monitoring of tumor necrosis factor antagonists in inflammatory bowel disease. Clin Gastroenterol Hepatol 2012;10:1079–1087; quiz e85–6.

  110. 110.

    , , et al. An enzyme-linked immunosorbent assay for therapeutic drug monitoring of infliximab. Ther Drug Monit 2006;28:169–174.

  111. 111.

    , , et al. Development and validation of a homogeneous mobility shift assay for the measurement of infliximab and antibodies-to-infliximab levels in patient serum. J Immunol Methods 2012;382:177–188.

  112. 112.

    , , et al. Individualized monitoring of drug bioavailability and immunogenicity in rheumatoid arthritis patients treated with the tumor necrosis factor alpha inhibitor infliximab. Arthritis Rheum 2006;54:3782–3789.

  113. 113.

    , , et al. Utility of measuring serum concentrations of anti-TNF agents and anti-drug antibodies in inflammatory bowel disease. Curr Drug Metab 2011;12:594–598.

  114. 114.

    , , et al. Clinical utility of measuring infliximab and human anti-chimeric antibody concentrations in patients with inflammatory bowel disease. Am J Gastroenterol 2010;105:1133–1139.

  115. 115.

    , , et al. The immunogenicity to the first anti-TNF therapy determines the outcome of switching to a second anti-TNF therapy in spondyloarthritis patients. Arthritis Res Ther 2013;15:R79.

  116. 116.

    , , et al. A test-based strategy is more cost effective than empiric dose-escalation for patients with Crohn's disease who lose responsiveness to infliximab. Clin Gastroenterol Hepatol 2013;11:654–666.

  117. 117.

    , , et al. Individualised therapy is more cost-effective than dose intensification in patients with Crohn's disease who lose response to anti-TNF treatment: a randomised, controlled trial. Gut 2013 advance online publication, 22 July 2013 (e-pub ahead of print).

  118. 118.

    , , et al. A test-based strategy is more cost effective than empiric dose escalation for patients with Crohn's disease who lose responsiveness to infliximab. Clin Gastroenterol Hepatol 2013;11:654–666.

  119. 119.

    , , et al. Fecal loss of infliximab as a cause of lack of response in severe inflammatory bowel disease. In: European Crohn's and Colitis Organization (ECCO) meeting. Vienna, Austria 2013, p. P500.

  120. 120.

    , , et al. Meta-analysis of tight control strategies in rheumatoid arthritis: protocolized treatment has additional value with respect to the clinical outcome. Rheumatology (Oxford) 2010;49:2154–2164.

  121. 121.

    , , et al. Evolving definitions of remission in Crohn's disease. Inflamm Bowel Dis 2013;19:1645–1653.

  122. 122.

    , , et al. Adalimumab induces deep remission in patients with Crohn's disease. Clin Gastroenterol Hepatol 2013;12:414–422.

  123. 123.

    , , et al. Results of the 2nd part Scientific Workshop of the ECCO. II: Measures and markers of prediction to achieve, detect, and monitor intestinal healing in inflammatory bowel disease. J Crohns Colitis 2011;5:484–498.

  124. 124.

    , , . Outpatients with inflammatory bowel disease (IBD) strongly prefer annual telephone calls from an IBD nurse instead of outpatient visits. Gastroenterol Nurs 2013;36:92–96.

  125. 125.

    , , et al. eHealth: individualisation of infliximab treatment and disease course via a self-managed web-based solution in Crohn's disease. Aliment Pharmacol Ther 2012;36:840–849.

  126. 126.

    , , et al. E-health empowers patients with ulcerative colitis: a randomised controlled trial of the web-guided ‘Constant-care’ approach. Gut 2010;59:1652–1661.

  127. 127.

    , , et al. Guided self-management and patient-directed follow-up of ulcerative colitis: a randomised trial. Lancet 2001;358:976–981.

  128. 128.

    . Optimizing the therapeutic potential of azathioprine/6-mercaptopurine in the treatment of inflammatory bowel disease. J Clin Gastroenterol 2003;36:379–981.

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Author information


  1. Department of Medicine, Division of Gastroenterology, Western University, London, Ontario, Canada

    • Mahmoud H Mosli
    • , Reena Khanna
    • , Bandar Al-Judaibi
    •  & Brian G Feagan
  2. Robarts Clinical Trials, Robarts Research Institute, London, Ontario, Canada

    • Mahmoud H Mosli
    • , William J Sandborn
    • , Reena Khanna
    •  & Brian G Feagan
  3. Department of Medicine, Division of Gastroenterology, King Abdulaziz University, Jeddah, Saudi Arabia

    • Mahmoud H Mosli
  4. Division of Gastroenterology, University of California San Diego, La Jolla, California, USA

    • William J Sandborn
  5. Department of Medicine, Division of Clinical Pharmacology, Western University, London, Ontario, Canada

    • Richard B Kim
  6. Department of Medicine, Division of Gastroenterology, King Khalid University Hospital, King Saud University, Riyadh, Saudi Arabia

    • Bandar Al-Judaibi


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Competing interests

Guarantor of the article: Brian G. Feagan, MD.

Specific author contributions: M.H.M.: contributed to the paper's concept and intellectual content, performed the literature review, drafted, critiqued, and revised the article; B.J., R.B.K., R.K., W.J.S., and B.G.F.: contributed to the paper's concept and intellectual content, critiqued, and revised the article.

Financial support: None.

Potential competing interests: Reena Khanna has received speaker's fees from Takeda. Professor Sandborn has received consulting fees from AbbVie, ActoGeniX NV, AGI Therapeutics, Alaven Pharmaceuticals, Alba Therapeutics, Albireo, Alfa Wasserman, Amgen, AM-Pharma BV, Anaphore, Astellas Pharma, Athersys, Atlantic Healthcare, Axcan Pharma, BioBalance, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Celek Pharmaceuticals, Cellerix SL, Centocor, Cerimon Pharmaceuticals, ChemoCentryx, CoMentis, Cosmo Technologies, Coronado Biosciences, Cytokine Pharmasciences, Eagle Pharmaceuticals, Eisai Medical Research, ELAN, EnGene, Eli Lilly, Enteromedics, Exagen Diagnostics, Ferring, Flexion Therapeutics, Funxional Therapeutics, Genzyme, Genentech, Gilead Sciences, Given Imaging, GlaxoSmithKline, Human Genome Sciences, Ironwood Pharmaceuticals, KaloBios Pharmaceuticals, Lexicon Pharmaceuticals, Lycera, Merck Research Laboratories, MerckSerono, Millennium, Nisshin Kyorin Pharmaceuticals, Novo Nordisk, NPS Pharmaceuticals, Optimer Pharmaceuticals, Orexigen Therapeutics, PDL Biopharma, Pfizer, Procter and Gamble, Prometheus Laboratories, ProtAb Limited, Purgenesis Technologies, Receptos, Relypsa Inc, Salient Pharmaceuticals, Salix Pharmaceuticals, Santarus, ScheringPlough, Shire Pharmaceuticals, Sigmoid Pharma, Sirtris Pharmaceuticals, SLA Pharma (UK), Targacept, Teva Pharmaceuticals, Therakos, Tillotts Pharma AG, TxCell SA, UCB Pharma, Viamet Pharmaceuticals, Vascular Biogenics, Warner Chilcott and Wyeth. He has received lecture fees from AbbVie, Bristol-Myers Squibb, and Janssen. He has received research support from AbbVie, Bristol-Myers Squibb, Genentech, GlaxoSmithKline, Janssen Biotech, Millennium Pharmaceuticals, Novartis, Pfizer, Procter & Gamble, Shire Pharmaceuticals, and UCB Pharma. Brian G. Feagan has received payment for development of educational presentations, including service on the speakers' bureau for Abbott/AbbVie, JnJ/Janssen, Takeda, Warner-Chilcott, UCB Pharma. He has received travel/accommodation compensation from Abbott/AbbVie, Actogenix, Albireo Pharma, Amgen, Astra Zeneca, Avaxia Biologics Inc., Axcan, Baxter Healthcare Corp., Boehringer-Ingelheim, Bristol-Myers Squibb, Calypso Biotech, Celgene, Elan/Biogen, EnGene, Ferring Pharma, Roche/Genentech, GiCare Pharma, Gilead, Given Imaging Inc., GSK, Ironwood Pharma, Janssen Biotech (Centocor), JnJ/Janssen, Kyowa Kakko Kirin Co Ltd., Lexicon, Lilly, Merck, Millennium, Nektar, Novonordisk, Prometheus Therapeutics and Diagnostics, Pfizer, Receptos, Salix Pharma, Serono, Shire, Sigmoid Pharma, Synergy Pharma Inc., Takeda, Teva Pharma, Tillotts, UCB Pharma, Vertex Pharma, Warner-Chilcott, Wyeth, Zealand, and Zyngenia. He has received compensation for his membership on the scientific advisory boards of Abbott/AbbVie, Amgen, Astra Zeneca, Avaxia Biologics Inc., Bristol-Myers Squibb, Celgene, Centocor Inc., Elan/Biogen, Ferring, JnJ/Janssen, Merck, Novartis, Novonordisk, Pfizer, Prometheus Laboratories, Salix Pharma, Takeda, Teva, Tillotts Pharma AG, and UCB Pharma. The remaining authors declare no conflict of interest.

Corresponding author

Correspondence to Brian G Feagan.