Maarten Cozijnsen
28 39. Sandborn WJ, Colombel JF, D’Haens G, et al. Association of baseline C-reactive protein and prior anti-tumor necrosis factor therapy with need for weekly dosing during maintenance therapy with adalimumab in patients with moderate to severe Crohn’s disease. Curr Med Res Opin 2013;29:483- 493. 40. Reinisch W, Wang Y, Oddens BJ, et al. C-reactive protein, an indicator for maintained response or remission to infliximab in patients with Crohn’s disease: a post-hoc analysis from ACCENT I. Aliment Pharmacol Ther 2012;35:568-576. 41. Vermeire S, Van Assche G, Rutgeerts P. C-reactive protein as a marker for inflammatory bowel disease. Inflamm Bowel Dis 2004;10:661-665. 42. Levesque BG, Greenberg GR, Zou G, et al. A prospective cohort study to determine the relationship between serum infliximab concentration and efficacy in patients with luminal Crohn’s disease. Aliment Pharmacol Ther 2014;39:1126-1135. 43. Cornillie F, Hanauer SB, Diamond RH, et al. Postinduction serum infliximab trough level and decrease of C-reactive protein level are associated with durable sustained response to infliximab: a retrospective analysis of the ACCENT I trial. Gut 2014;63:1721-1727. 44. Bortlik M, Duricova D, Malickova K, et al. Infliximab trough levels may predict sustained response to infliximab in patients with Crohn’s disease. J Crohns Colitis 2013;7:736-743. 45. Vande Casteele N, Ferrante M, Van Assche G, et al. Trough concentrations of infliximab guide dosing for patients with inflammatory bowel disease. Gastroenterology 2015;148:1320-9 e3. 46. Hofmekler T, Bertha M, McCracken C, et al. Infliximab Optimization Based on Therapeutic Drug Monitoring in Pediatric Inflammatory Bowel Disease. J Pediatr Gastroenterol Nutr 2017;64:580- 585. 47. Montero-Meléndez T, Llor X, García-Planella E, et al. Identification of Novel Predictor Classifiers for Inflammatory Bowel Disease by Gene Expression Profiling. PLoS One 2013;8. 48. Honda M, Orii F, Ayabe T, et al. Expression of glucocorticoid receptor beta in lymphocytes of patients with glucocorticoid-resistant ulcerative colitis. Gastroenterology 2000;118:859-866. 49. Fujishima S, Takeda H, Kawata S, et al. The relationship between the expression of the glucocorticoid receptor in biopsied colonic mucosa and the glucocorticoid responsiveness of ulcerative colitis patients. Clin Immunol 2009;133:208-217. 50. Gisbert JP, Nino P, Rodrigo L, et al. Thiopurine methyltransferase (TPMT) activity and adverse effects of azathioprine in inflammatory bowel disease: long-term follow-up study of 394 patients. Am J Gastroenterol 2006;101:2769-2776. 51. Urano W, Taniguchi A, Yamanaka H, et al. Polymorphisms in the methylenetetrahydrofolate reductase gene were associated with both the efficacy and the toxicity of methotrexate used for the treatment of rheumatoid arthritis, as evidenced by single locus and haplotype analyses. Pharmacogenetics 2002;12:183-190. 52. Arijs I, Quintens R, Van Lommel L, et al. Predictive value of epithelial gene expression profiles for response to infliximab in Crohn’s disease. Inflamm Bowel Dis 2010;16:2090-2098. 53. Mesko B, Poliska S, Vancsa A, et al. Peripheral blood derived gene panels predict response to infliximab in rheumatoid arthritis and Crohn’s disease. Genome Med 2013;5:59. 54. Pierik M, Vermeire S, Steen KV, 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. 55. Matsukura H, Ikeda S, Yoshimura N, et al. Genetic polymorphisms of tumour necrosis factor receptor superfamily 1A and 1B affect responses to infliximab in Japanese patients with Crohn’s disease. Aliment Pharmacol Ther 2008;27:765-770.
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