Персонализированная терапия воспалительных заболеваний кишечника
Персонализированная терапия воспалительных заболеваний кишечника
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Аннотация
Персонализированная медицина представляет собой совокупность основанных на индивидуальных особенностях пациента методов профилактики, диагностики и лечения болезней. К ним относят генетические, эпигенетические, транскриптомные, протеомные, метаболомные и метагеномные маркеры, а также совокупность фенотипических признаков организма пациента в целом и его отдельных тканей или клеток.
В статье показана актуальность применения генетических и микробиологических исследований, мониторинга концентрации в крови генно-инженерных биологических препаратов и уровня антител к ним в качестве предикторов эффективности терапии у каждого из больных воспалительными заболеваниями кишечника (ВЗК). Обсужден также ряд персональных данных для повышения качества прогнозирования исходов ВЗК у каждого пациента и более точного подбора схемы лечения.
Ключевые слова: болезнь Крона, воспалительные заболевания кишечника, генно-инженерные биологические препараты, персонализированная медицина, трансплантация фекальной микрофлоры, язвенный колит.
For example, treatment of inflammatory bowel diseases (IBD) can most clearly show the importance of applying personalized approaches. Currently in the treatment of patients with IBD paid great attention to genetic studies, monitoring of the concentration of the biological drugs and the level of antibodies to them, the role of microbiota as a predictor of effectiveness of therapy of IBD. Used clinical, laboratory, instrumental methods, as well as new biomarkers to assess the forecasting efficiency of conservative therapy in IBD patient. In the future treatment of patients with IBD will include a number of personalized data in order to better predict outcomes of the disease in each patient and more accurately select the appropriate treatment regimen.
Keywords: Crohn's disease, inflammatory bowel disease, genetically engineered biological preparations, personalized medicine, transplantation of fecal microflora, ulcerative colitis.
В статье показана актуальность применения генетических и микробиологических исследований, мониторинга концентрации в крови генно-инженерных биологических препаратов и уровня антител к ним в качестве предикторов эффективности терапии у каждого из больных воспалительными заболеваниями кишечника (ВЗК). Обсужден также ряд персональных данных для повышения качества прогнозирования исходов ВЗК у каждого пациента и более точного подбора схемы лечения.
Ключевые слова: болезнь Крона, воспалительные заболевания кишечника, генно-инженерные биологические препараты, персонализированная медицина, трансплантация фекальной микрофлоры, язвенный колит.
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For example, treatment of inflammatory bowel diseases (IBD) can most clearly show the importance of applying personalized approaches. Currently in the treatment of patients with IBD paid great attention to genetic studies, monitoring of the concentration of the biological drugs and the level of antibodies to them, the role of microbiota as a predictor of effectiveness of therapy of IBD. Used clinical, laboratory, instrumental methods, as well as new biomarkers to assess the forecasting efficiency of conservative therapy in IBD patient. In the future treatment of patients with IBD will include a number of personalized data in order to better predict outcomes of the disease in each patient and more accurately select the appropriate treatment regimen.
Keywords: Crohn's disease, inflammatory bowel disease, genetically engineered biological preparations, personalized medicine, transplantation of fecal microflora, ulcerative colitis.
Список литературы
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6. Adler J, Rangwalla SC, Dwamena BA, Higgins PD. The prognostic power of the NOD2 genotype for complicated Crohn’s disease: a meta-analysis. Am J Gastroenterol. 2011;106(4):699-712.
7. Ananthakrishnan AN, Huang H, Nguyen DD, Sauk J, Yajnik V, Xavier RJ. Differential effect of genetic burden on disease phenotypes in Crohn’s disease and ulcerative colitis: analysis of a North American cohort.
Am J Gastroenterol. 2014;109(3):395-400.
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9. Sherlock ME, Walters T, Tabbers MM, et al. Infliximab-induced psoriasis and psoriasiform skin lesions in pediatric Crohn disease and a potential association with IL-23 receptor polymorphisms. J Pediatr Gastroenterol Nutr. 2013;56(5):512-8.
10. Frank DN, Robertson CE, Hamm CM, et al. Disease phenotype and genotype are associated with shifts in intestinal-associated microbiota in inflammatory bowel diseases. Inflamm Bowel Dis. 2011;17(1):179-84.
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12. Steenholdt C, Bendtzen K, Brynskov J, Thomsen OØ, Munck LK, Christensen LA, Pedersen G, Kjeldsen J, Ainsworth MA. Changes in serum through levels of infliximab during treatment intensification but not in anti-infliximab antibody detection are associated with clinical outcomes after therapeutic failure in Crohn’s disease. J Crohns Colitis. 2015;9:238-45.
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Inflamm Bowel Dis. 2014;20:1714-21.
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19. Schwab M, Schaeffeler E, Marx C, Zanger U, Aulitzky W, Eichelbaum M. Shortcoming in the diagnosis of TPMT deficiency in a patient with Crohn’s disease using phenotyping only. Gastroenterology. 2001;121(2):498-9.
20. Gardiner SJ, Gearry RB, Begg EJ, Zhang M, Barclay ML. Thiopurine dose in intermediate and normal metabolizers of thiopurinemethyltransferase may differ three-fold. Clin Gastroenterol Hepatol. 2008; 6(6):654-60.
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23. Sparrow MP, Hande SA, Friedman S, et al. Allopurinol safely and effectively optimizes tioguanine metabolites in inflammatory bowel disease patients not responding to azathioprine and mercaptopurine. Aliment Pharmacol Ther. 2005;22(5):441-6.
24. Yarur AJ, Kubiliun MJ, Czul F, et al. Concentrations of 6-thioguanine nucleotide correlate with trough levels of infliximab in patients with inflammatory bowel disease on combination therapy. Clin Gastroenterol Hepatol. 2015;13(6):1118-24.e3.
25. Hendler SA, Cohen BL, Colombel JF, Sands BE, Mayer L, Agarwal S. Highdose infliximab therapy in Crohn’s disease: clinical experience, safety, and efficacy. J Crohns Colitis. 2015;9(3):266-75.
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28. Hiroz P, Vavricka SR, Fournier N, Safroneeva E, Pittet V, Rogler G, Schoepfer AM. Analysis of TNF-antagonist switch over time and associated risk factors in the Swiss Inflammatory Bowel Disease Cohort. Scand J Gastroenterol. 2014;49(10):1207-18.
29. Billiert T, Rutgeerts P, et al. Targeting TNF-a for the treatment of inflammatory bowel disease. Expert Opin Biol Ther. 2014;14(1):75-101.
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32. Chiu YL, Rubin DT, Vermeire S, et al. Serum adalimumab concentration and clinical remission in patients with Crohn’s disease. Inflamm Bowel Dis. 2013;19(6):1112-22.
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34. Hoekman DR, Lowenberg M, Mathot RA, et al. Non-trough IFX concentrations reliably predict trough level and accelerate dose-adjustment in Crohn’s disease. Gastroenterology. 2015;148(4):S107.
35. Papamichael K, Vande Casteele N, Billiet T, et al. Early therapeutic drug monitoring for prediction of short-term mucosal healing in patients with ulcerative colitis treated with infliximab. Gastroenterology. 2015;148(4):S848.
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2. Ripke S, Weersma RK, et al; International IBD Genetics Consortium (IIBDGC). Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease. Nature. 2012;491(7422):119-24.
3. Jostins L, Lees CW, Barrett JC, Parkes M, Satsangi J. New IBD genetics: common pathways with other diseases. Gut. 2011;60(12):1739-53.
4. Lichtenstein GR, Targan SR, Dubinsky MC, et al. Combination of genetic and quantitative serological immune markers are associated with complicated Crohn’s disease behavior. Inflamm Bowel Dis. 2011;17(12):2488-96.
5. Cleynen I, Gonzblez JR, Figueroa C, et al. Genetic factors conferring an increased susceptibility to develop Crohn’s disease also influence disease phenotype: results from the IBDchip European Project. Gut. 2013;62(11):1556-65.
6. Adler J, Rangwalla SC, Dwamena BA, Higgins PD. The prognostic power of the NOD2 genotype for complicated Crohn’s disease: a meta-analysis. Am J Gastroenterol. 2011;106(4):699-712.
7. Ananthakrishnan AN, Huang H, Nguyen DD, Sauk J, Yajnik V, Xavier RJ. Differential effect of genetic burden on disease phenotypes in Crohn’s disease and ulcerative colitis: analysis of a North American cohort.
Am J Gastroenterol. 2014;109(3):395-400.
8. Waterman M, Knight J, Dinani A, et al. Predictors of outcome in ulcerative colitis. Inflamm Bowel Dis. 2015;21(9):2097-105.
9. Sherlock ME, Walters T, Tabbers MM, et al. Infliximab-induced psoriasis and psoriasiform skin lesions in pediatric Crohn disease and a potential association with IL-23 receptor polymorphisms. J Pediatr Gastroenterol Nutr. 2013;56(5):512-8.
10. Frank DN, Robertson CE, Hamm CM, et al. Disease phenotype and genotype are associated with shifts in intestinal-associated microbiota in inflammatory bowel diseases. Inflamm Bowel Dis. 2011;17(1):179-84.
11. Steenholdt C, Brynskov J, Thomsen OØ, Munck LK, Christensen LA, Pedersen G, Kjeldsen J, Ainsworth MA. Implications of infliximab treatment failure and influence of personalized treatment on patient-reported health-related quality of life and productivity outcomes in Crohn’s disease. J Crohns Colitis. 2015;9:1032-42.
12. Steenholdt C, Bendtzen K, Brynskov J, Thomsen OØ, Munck LK, Christensen LA, Pedersen G, Kjeldsen J, Ainsworth MA. Changes in serum through levels of infliximab during treatment intensification but not in anti-infliximab antibody detection are associated with clinical outcomes after therapeutic failure in Crohn’s disease. J Crohns Colitis. 2015;9:238-45.
13. Frederiksen MT, Ainsworth MA, Brynskov J, Thomsen OØ, Bendtzen K, Steenholdt C. Antibodies against infliximab (IFX) are associated with de novo development of antibodies to adalimumab (ADL) and therapeutic failure in IFX-to-ADL switchers with inflammatory bowel disease.
Inflamm Bowel Dis. 2014;20:1714-21.
14. Steenholdt C, Frederiksen MT, Bendtzen K, Ainsworth MA, Thomsen OØ, Brynskov J. Time course and clinical implications of development of antibodies against adalimumab in patients with inflammatory bowel disease. J Clin Gastroenterol. 2016;50:483-9. doi: 10.1097/mcg. 0000000000000375
15. Feagan BG, Rutgeerts P, Sands BE, et al. Vedolizumab as induction and maintenance therapy for ulcerative colitis. N Engl J Med. 2013;369:699-710.
16. Ford LT, Berg JD. Thiopurine S-methyltransferase (TPMT) assessment prior to starting thiopurine drug treatment; a pharmacogenomic test whose time has come. J Clin Pathol. 2010;63(4):288-95.
17. Morales A, Salguti S, Miao С, et al. Relationship between 6-mercaptopurine dose and 6-thioguanine nucleotide levels in patients with inflammatory bowel disease. Inflamm Bowel Dis. 2007;13:380-5.
18. Winter JW, Gaffney D, Shapiro D, et al. Assessment of thiopurinemethyltransferase enzyme activity is superior to genotype in predicting myelosuppression following azathioprine therapy in patients with inflammatory bowel disease. Aliment Pharmacol Ther. 2007;25(9):1069-77.
19. Schwab M, Schaeffeler E, Marx C, Zanger U, Aulitzky W, Eichelbaum M. Shortcoming in the diagnosis of TPMT deficiency in a patient with Crohn’s disease using phenotyping only. Gastroenterology. 2001;121(2):498-9.
20. Gardiner SJ, Gearry RB, Begg EJ, Zhang M, Barclay ML. Thiopurine dose in intermediate and normal metabolizers of thiopurinemethyltransferase may differ three-fold. Clin Gastroenterol Hepatol. 2008; 6(6):654-60.
21. Osterman MT, Kundu R, Lichtenstein GR, Lewis JD. Association of 6-thioguanine nucleotide levels and inflammatory bowel disease activity: a meta-analysis. Gastroenterology. 2006;130(4):1047-53.
22. Yarur AJ, Abreu MT, Deshpande AR, Kerman DH, Sussman DA. Therapeutic drug monitoring in patients with inflammatory bowel disease. World J Gastroenterol. 2014;20(13):3475-84.
23. Sparrow MP, Hande SA, Friedman S, et al. Allopurinol safely and effectively optimizes tioguanine metabolites in inflammatory bowel disease patients not responding to azathioprine and mercaptopurine. Aliment Pharmacol Ther. 2005;22(5):441-6.
24. Yarur AJ, Kubiliun MJ, Czul F, et al. Concentrations of 6-thioguanine nucleotide correlate with trough levels of infliximab in patients with inflammatory bowel disease on combination therapy. Clin Gastroenterol Hepatol. 2015;13(6):1118-24.e3.
25. Hendler SA, Cohen BL, Colombel JF, Sands BE, Mayer L, Agarwal S. Highdose infliximab therapy in Crohn’s disease: clinical experience, safety, and efficacy. J Crohns Colitis. 2015;9(3):266-75.
26. 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(5):483-93.
27. Taxonera C, Olivares D, Mendoza JL, Díaz-Rubio M, Rey E. Need for infliximab dose intensification in Crohn’s disease and ulcerative colitis. World J Gastroenterol. 2014 July 21;20(27):9170-7.
28. Hiroz P, Vavricka SR, Fournier N, Safroneeva E, Pittet V, Rogler G, Schoepfer AM. Analysis of TNF-antagonist switch over time and associated risk factors in the Swiss Inflammatory Bowel Disease Cohort. Scand J Gastroenterol. 2014;49(10):1207-18.
29. Billiert T, Rutgeerts P, et al. Targeting TNF-a for the treatment of inflammatory bowel disease. Expert Opin Biol Ther. 2014;14(1):75-101.
30. 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(9):736-43.
31. Yarur AJ, Jain A, Hauenstein SI, et al. Higher adalimumab levels are associated with histologic and endoscopic remission in patients with Crohn’s disease and ulcerative colitis. Inflamm Bowel Dis. 2016;22(2):409-15.
32. Chiu YL, Rubin DT, Vermeire S, et al. Serum adalimumab concentration and clinical remission in patients with Crohn’s disease. Inflamm Bowel Dis. 2013;19(6):1112-22.
33. Vande Casteele N, Mould DR, Gils A, et al. Adequate trough concentrations and sustained TNF suppression early on during induction therapy with adalimumab predict remission in anti-TNF naïve Crohn’s disease patients. Gastroenterology. 2015;148(4):S854-5.
34. Hoekman DR, Lowenberg M, Mathot RA, et al. Non-trough IFX concentrations reliably predict trough level and accelerate dose-adjustment in Crohn’s disease. Gastroenterology. 2015;148(4):S107.
35. Papamichael K, Vande Casteele N, Billiet T, et al. Early therapeutic drug monitoring for prediction of short-term mucosal healing in patients with ulcerative colitis treated with infliximab. Gastroenterology. 2015;148(4):S848.
36. Imaeda H, Takahashi K, Fujimoto T, et al. Clinical utility of newly developed immunoassays for serum concentrations of adalimumab and anti-adalimumab antibodies in patients with Crohn’s disease. J Gastroenterol. 2014;49(1):100-9.
37. 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.
38. Vaughn BP, Martinez-Vazquez M, Patwardhan VR, Moss AC, Sandborn WJ, Singh N, Rosenthal CJ, Melmed GY, et al. Early infliximab trough levels are associated with persistent remission in pediatric patients with inflammatory bowel disease. Inflamm Bowel Dis. 2014;20(10):1708-13.
39. Colombel JF, Feagan BG, Sandborn WJ, van Assche G, Robinson AM. Therapeutic drug monitoring of biologics for inflammatory bowel disease. Inflamm Bowel Dis. 2012;18(2):349-58.
40. Kingsley MJ, Abreu MT. A Personalized Approach to Managing Inflammatory Bowel Disease. Gastroenterol Hepatol. 2016;12(5):308-15.
41. Vande Casteele N, Gils A, Singh S, et al. Antibody response to infliximab and its impact on pharmacokinetics can be transient. Am J Gastroenterol. 2013;108(6):962-71.
42. Knyazev OV, Parfenov AI, Ruchkina IN, Konoplyannikov AG, Sagynbaeva VE, Ivkina TI. New opportunities to overcome the secondary ineffectiveness of anticytokine therapy in patients with inflammatory bowel diseases. Terapevticheskii Arkhiv = Therapeutic Arкhiv. 2013;85(2):57-60 (In Russ.)
43. Ben-Horin S, Waterman M, Kopylov U, et al. Addition of an immunomodulator to infliximab therapy eliminates antidrug antibodies in serum and restores clinical response of patients with inflammatory bowel disease. Clin Gastroenterol Hepatol. 2013;11(4):444-7.
44. Vermeire S, Gabriels F, Ballet V, et al. The effect of dose escalation on trough levels in patients who lost response to infliximab. Gut. 2010;59(S3):A81.
45. Yarur AJ, Jain A, Sussman DA, et al. The association of tissue anti-TNF drug levels with serological and endoscopic disease activity in inflammatory bowel disease: the ATLAS study. Gut. 2016;65(2): 249-55.
46. Kelly OB, O’Donnell S, Stempak JM, et al. Dose optimization of infliximab using therapeutic drug monitoring is more effective than dose optimization based on clinical assessment alone in patients with active inflammatory bowel disease. Gastroenterology. 2015;148(4):S856.
47. Golovenko AO, Khalif IL, Golovenko OV, Veselov VV. Predictors of the effectiveness of infliximab in patients with severe attack of ulcerative colitis. Rossiiskii zhurnal gastroenterologii, gepatologii, koloproktologii = Russian Journal of Gastroenterology, Hepatology, Coloproctology. 2013; (3):65-73 (In Russ.)
48. Monterubbianesi R, Aratari A, Armuzzi A, et al. Infliximab three-dose induction regimen in severe corticosteroid-refractory ulcerative colitis: early and late outcome and predictors of colectomy. J Crohns Colitis. 2014 Aug;8(8):852-8.
49. Solberg IC, Høivik ML, Cvancarova M, Moum B; IBSEN Study Group. Risk matrix model for prediction of colectomy in a population-based study of ulcerative colitis patients (the IBSEN study). Scand J Gastroenterol. 2015;50(12):1456-62. doi: 10.3109/00365521.2015. 1064991. Epub 2015 Jul 3.
50. Solberg IC, Cvancarova M, Vatn MH, Moum B; IBSEN Study Group. Risk matrix for prediction of advanced disease in a population-based study of patients with Crohn's Disease (the IBSEN Study). Inflamm Bowel Dis. 2014 Jan;20(1):60-8. doi: 10.1097/01.MIB.0000436956. 78220.67
51. Golovenko AO, Khalif IL, Golovenko OV. Prevention of postoperative relapse of Crohn's disease. Koloproktologiya = Coloproctology. 2012;(4):40-8 (In Russ.)
52. Choung RS, Stockfisch TP, Princen F, et al. Longitudinal status of serological markers predict Crohn’s disease phenotype before diagnosis: a “PREDICTS” study. Gastroenterology. 2015;148(4):S22.
53. Dubinsky MC, Kugathasan S, Mei L, et al; Western Regional Pediatric IBD Research Alliance; Pediatric IBD Collaborative Research Group; Wisconsin Pediatric IBD Alliance. Increased immune reactivity predicts aggressive complicating Crohn’s disease in children. Clin Gastroenterol Hepatol. 2008;6(10):1105-11.
54. Hamilton AL, Kamm MA, Selvaraj F, et al. Serological antibodies for the prediction of post-operative recurrent Crohn’s disease results from the POCER study. Gastroenterology. 2015;148(4):S116.
55. Gazouli M, Anagnostopoulos AK, Papadopoulou A, et al. Serum protein profile of Crohn’s disease treated with infliximab. J Crohns Colitis. 2013;7(10):e461-e470.
56. Wang W, Chen L, Zhou R, et al. Increased proportions of Bifidobacterium and the Lactobacillus group and loss of butyrate-producing bacteria in inflammatory bowel disease. J Clin Microbiol. 2014;52(2):398-406.
57. Machiels K, Joossens M, Sabino J, et al. A decrease of the butyrate-producing species Roseburiahominis and Faecalibacteriumprausnitzii defines dysbiosis in patients with ulcerative colitis. Gut. 2014;63(8):1275-83.
58. Wills ES, Jonkers DM, Savelkoul PH, Masclee AA, Pierik MJ, Pen-
ders J. Fecal microbial composition of ulcerative colitis and Crohn’s disease patients in remission and subsequent exacerbation. PLoS One. 2014;9(3):e90981.
59. Michail S, Durbin M, Turner D, et al. Alterations in the gut microbiome of children with severe ulcerative colitis. Inflamm Bowel Dis. 2012;18(10):1799-808.
60. Rajca S, Grondin V, Louis E, et al. Alterations in the intestinal microbiome (dysbiosis) as a predictor of relapse after infliximab withdrawal in Crohn’s disease. Inflamm Bowel Dis. 2014;20(6):978-86.
61. Moayyedi P, Surette MG, Kim PT, et al. Fecal microbiota transplantation induces remission in patients with active ulcerative colitis in a randomized controlled trial. Gastroenterology. 2015;149(1):102-9.e6.
62. Rossen NG, Fuentes S, van der Spek MJ, et al. Findings from a randomized controlled trial of fecal transplantation for patients with ulcerative colitis. Gastroenterology. 2015;149(1):110-18.e4.
63. Grinspan AM, Kelly CR. Fecal microbiota transplantation for ulcerative colitis: not just yet. Gastroenterology. 2015;149(1):15-8.
64. Marthn R, Chain F, Miquel S, et al. The commensal bacterium Faecalibacteriumprausnitzii is protective in DNBS-induced chronic moderate and severe colitis models. Inflamm Bowel Dis. 2014;20(3):417-430.
2. Ripke S, Weersma RK, et al; International IBD Genetics Consortium (IIBDGC). Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease. Nature. 2012;491(7422):119-24.
3. Jostins L, Lees CW, Barrett JC, Parkes M, Satsangi J. New IBD genetics: common pathways with other diseases. Gut. 2011;60(12):1739-53.
4. Lichtenstein GR, Targan SR, Dubinsky MC, et al. Combination of genetic and quantitative serological immune markers are associated with complicated Crohn’s disease behavior. Inflamm Bowel Dis. 2011;17(12):2488-96.
5. Cleynen I, Gonzblez JR, Figueroa C, et al. Genetic factors conferring an increased susceptibility to develop Crohn’s disease also influence disease phenotype: results from the IBDchip European Project. Gut. 2013;62(11):1556-65.
6. Adler J, Rangwalla SC, Dwamena BA, Higgins PD. The prognostic power of the NOD2 genotype for complicated Crohn’s disease: a meta-analysis. Am J Gastroenterol. 2011;106(4):699-712.
7. Ananthakrishnan AN, Huang H, Nguyen DD, Sauk J, Yajnik V, Xavier RJ. Differential effect of genetic burden on disease phenotypes in Crohn’s disease and ulcerative colitis: analysis of a North American cohort.
Am J Gastroenterol. 2014;109(3):395-400.
8. Waterman M, Knight J, Dinani A, et al. Predictors of outcome in ulcerative colitis. Inflamm Bowel Dis. 2015;21(9):2097-105.
9. Sherlock ME, Walters T, Tabbers MM, et al. Infliximab-induced psoriasis and psoriasiform skin lesions in pediatric Crohn disease and a potential association with IL-23 receptor polymorphisms. J Pediatr Gastroenterol Nutr. 2013;56(5):512-8.
10. Frank DN, Robertson CE, Hamm CM, et al. Disease phenotype and genotype are associated with shifts in intestinal-associated microbiota in inflammatory bowel diseases. Inflamm Bowel Dis. 2011;17(1):179-84.
11. Steenholdt C, Brynskov J, Thomsen OØ, Munck LK, Christensen LA, Pedersen G, Kjeldsen J, Ainsworth MA. Implications of infliximab treatment failure and influence of personalized treatment on patient-reported health-related quality of life and productivity outcomes in Crohn’s disease. J Crohns Colitis. 2015;9:1032-42.
12. Steenholdt C, Bendtzen K, Brynskov J, Thomsen OØ, Munck LK, Christensen LA, Pedersen G, Kjeldsen J, Ainsworth MA. Changes in serum through levels of infliximab during treatment intensification but not in anti-infliximab antibody detection are associated with clinical outcomes after therapeutic failure in Crohn’s disease. J Crohns Colitis. 2015;9:238-45.
13. Frederiksen MT, Ainsworth MA, Brynskov J, Thomsen OØ, Bendtzen K, Steenholdt C. Antibodies against infliximab (IFX) are associated with de novo development of antibodies to adalimumab (ADL) and therapeutic failure in IFX-to-ADL switchers with inflammatory bowel disease.
Inflamm Bowel Dis. 2014;20:1714-21.
14. Steenholdt C, Frederiksen MT, Bendtzen K, Ainsworth MA, Thom-
sen OØ, Brynskov J. Time course and clinical implications of development of antibodies against adalimumab in patients with inflammatory bowel disease. J Clin Gastroenterol. 2016;50:483-9. doi: 10.1097/mcg. 0000000000000375
15. Feagan BG, Rutgeerts P, Sands BE, et al. Vedolizumab as induction and maintenance therapy for ulcerative colitis. N Engl J Med. 2013;369:699-710.
16. Ford LT, Berg JD. Thiopurine S-methyltransferase (TPMT) assessment prior to starting thiopurine drug treatment; a pharmacogenomic test whose time has come. J Clin Pathol. 2010;63(4):288-95.
17. Morales A, Salguti S, Miao С, et al. Relationship between 6-mercaptopurine dose and 6-thioguanine nucleotide levels in patients with inflammatory bowel disease. Inflamm Bowel Dis. 2007;13:380-5.
18. Winter JW, Gaffney D, Shapiro D, et al. Assessment of thiopurinemethyltransferase enzyme activity is superior to genotype in predicting myelosuppression following azathioprine therapy in patients with inflammatory bowel disease. Aliment Pharmacol Ther. 2007;25(9):1069-77.
19. Schwab M, Schaeffeler E, Marx C, Zanger U, Aulitzky W, Eichelbaum M. Shortcoming in the diagnosis of TPMT deficiency in a patient with Crohn’s disease using phenotyping only. Gastroenterology. 2001;121(2):498-9.
20. Gardiner SJ, Gearry RB, Begg EJ, Zhang M, Barclay ML. Thiopurine dose in intermediate and normal metabolizers of thiopurinemethyltransferase may differ three-fold. Clin Gastroenterol Hepatol. 2008; 6(6):654-60.
21. Osterman MT, Kundu R, Lichtenstein GR, Lewis JD. Association of 6-thioguanine nucleotide levels and inflammatory bowel disease activity: a meta-analysis. Gastroenterology. 2006;130(4):1047-53.
22. Yarur AJ, Abreu MT, Deshpande AR, Kerman DH, Sussman DA. Therapeutic drug monitoring in patients with inflammatory bowel disease. World J Gastroenterol. 2014;20(13):3475-84.
23. Sparrow MP, Hande SA, Friedman S, et al. Allopurinol safely and effectively optimizes tioguanine metabolites in inflammatory bowel disease patients not responding to azathioprine and mercaptopurine. Aliment Pharmacol Ther. 2005;22(5):441-6.
24. Yarur AJ, Kubiliun MJ, Czul F, et al. Concentrations of 6-thioguanine nucleotide correlate with trough levels of infliximab in patients with inflammatory bowel disease on combination therapy. Clin Gastroenterol Hepatol. 2015;13(6):1118-24.e3.
25. Hendler SA, Cohen BL, Colombel JF, Sands BE, Mayer L, Agarwal S. Highdose infliximab therapy in Crohn’s disease: clinical experience, safety, and efficacy. J Crohns Colitis. 2015;9(3):266-75.
26. 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(5):483-93.
27. Taxonera C, Olivares D, Mendoza JL, Díaz-Rubio M, Rey E. Need for infliximab dose intensification in Crohn’s disease and ulcerative colitis. World J Gastroenterol. 2014 July 21;20(27):9170-7.
28. Hiroz P, Vavricka SR, Fournier N, Safroneeva E, Pittet V, Rogler G, Schoepfer AM. Analysis of TNF-antagonist switch over time and associated risk factors in the Swiss Inflammatory Bowel Disease Cohort. Scand J Gastroenterol. 2014;49(10):1207-18.
29. Billiert T, Rutgeerts P, et al. Targeting TNF-a for the treatment of inflammatory bowel disease. Expert Opin Biol Ther. 2014;14(1):75-101.
30. 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(9):736-43.
31. Yarur AJ, Jain A, Hauenstein SI, et al. Higher adalimumab levels are associated with histologic and endoscopic remission in patients with Crohn’s disease and ulcerative colitis. Inflamm Bowel Dis. 2016;22(2):409-15.
32. Chiu YL, Rubin DT, Vermeire S, et al. Serum adalimumab concentration and clinical remission in patients with Crohn’s disease. Inflamm Bowel Dis. 2013;19(6):1112-22.
33. Vande Casteele N, Mould DR, Gils A, et al. Adequate trough concentrations and sustained TNF suppression early on during induction therapy with adalimumab predict remission in anti-TNF naïve Crohn’s disease patients. Gastroenterology. 2015;148(4):S854-5.
34. Hoekman DR, Lowenberg M, Mathot RA, et al. Non-trough IFX concentrations reliably predict trough level and accelerate dose-adjustment in Crohn’s disease. Gastroenterology. 2015;148(4):S107.
35. Papamichael K, Vande Casteele N, Billiet T, et al. Early therapeutic drug monitoring for prediction of short-term mucosal healing in patients with ulcerative colitis treated with infliximab. Gastroenterology. 2015;148(4):S848.
36. Imaeda H, Takahashi K, Fujimoto T, et al. Clinical utility of newly developed immunoassays for serum concentrations of adalimumab and anti-adalimumab antibodies in patients with Crohn’s disease. J Gastroenterol. 2014;49(1):100-9.
37. 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.
38. Vaughn BP, Martinez-Vazquez M, Patwardhan VR, Moss AC, Sandborn WJ, Singh N, Rosenthal CJ, Melmed GY, et al. Early infliximab trough levels are associated with persistent remission in pediatric patients with inflammatory bowel disease. Inflamm Bowel Dis. 2014;20(10):1708-13.
39. Colombel JF, Feagan BG, Sandborn WJ, van Assche G, Robinson AM. Therapeutic drug monitoring of biologics for inflammatory bowel disease. Inflamm Bowel Dis. 2012;18(2):349-58.
40. Kingsley MJ, Abreu MT. A Personalized Approach to Managing Inflammatory Bowel Disease. Gastroenterol Hepatol. 2016;12(5):308-15.
41. Vande Casteele N, Gils A, Singh S, et al. Antibody response to infliximab and its impact on pharmacokinetics can be transient. Am J Gastroenterol. 2013;108(6):962-71.
42. Князев О.В., Парфенов А.И., Ручкина И.Н., Коноплянников А.Г., Сагынбаева В.Э., Ивкина Т.И. Новые возможности преодоления вторичной неэффективности антицитокиновой терапии у больных воспалительными заболеваниями кишечника. Терапевтический архив. 2013;85(2):57-60 [Knyazev OV, Parfenov AI, Ruchkina IN, Konoplyannikov AG, Sagynbaeva VE, Ivkina TI. New opportunities to overcome the secondary ineffectiveness of anticytokine therapy in patients with inflammatory bowel diseases. Terapevticheskii Arkhiv = Therapeutic Arкhiv. 2013;85(2):57-60 (In Russ.)].
43. Ben-Horin S, Waterman M, Kopylov U, et al. Addition of an immunomodulator to infliximab therapy eliminates antidrug antibodies in serum and restores clinical response of patients with inflammatory bowel disease. Clin Gastroenterol Hepatol. 2013;11(4):444-7.
44. Vermeire S, Gabriels F, Ballet V, et al. The effect of dose escalation on trough levels in patients who lost response to infliximab. Gut. 2010;59(S3):A81.
45. Yarur AJ, Jain A, Sussman DA, et al. The association of tissue anti-TNF drug levels with serological and endoscopic disease activity in inflammatory bowel disease: the ATLAS study. Gut. 2016;65(2): 249-55.
46. Kelly OB, O’Donnell S, Stempak JM, et al. Dose optimization of infliximab using therapeutic drug monitoring is more effective than dose optimization based on clinical assessment alone in patients with active inflammatory bowel disease. Gastroenterology. 2015;148(4):S856.
47. Головенко А.О., Халиф И.Л., Головенко О.В., Веселов В.В. Предикторы эффективности инфликсимаба у больных с тяжелой атакой язвенного колита. Российский журнал гастроэнтерологии, гепатологии, колопроктологии. 2013;(3):65-73 [Golovenko AO, Khalif IL, Golovenko OV, Veselov VV. Predictors of the effectiveness of infliximab in patients with severe attack of ulcerative colitis. Rossiiskii zhurnal gastroenterologii, gepatologii, koloproktologii = Russian Journal of Gastroenterology, Hepatology, Coloproctology. 2013; (3):65-73 (In Russ.)].
48. Monterubbianesi R, Aratari A, Armuzzi A, et al. Infliximab three-dose induction regimen in severe corticosteroid-refractory ulcerative colitis: early and late outcome and predictors of colectomy. J Crohns Colitis. 2014 Aug;8(8):852-8.
49. Solberg IC, Høivik ML, Cvancarova M, Moum B; IBSEN Study Group. Risk matrix model for prediction of colectomy in a population-based study of ulcerative colitis patients (the IBSEN study). Scand J Gastroenterol. 2015;50(12):1456-62. doi: 10.3109/00365521.2015. 1064991. Epub 2015 Jul 3.
50. Solberg IC, Cvancarova M, Vatn MH, Moum B; IBSEN Study Group. Risk matrix for prediction of advanced disease in a population-based study of patients with Crohn's Disease (the IBSEN Study). Inflamm Bowel Dis. 2014 Jan;20(1):60-8. doi: 10.1097/01.MIB.0000436956. 78220.67
51. Головенко АО, Халиф ИЛ, Головенко ОВ. Профилактика послеоперационных рецидивов болезни Крона. Колопроктология. 2012;(4):40-8 [Golovenko AO, Khalif IL, Golovenko OV. Prevention of postoperative relapse of Crohn's disease. Koloproktologiya = Coloproctology. 2012;(4):40-8 (In Russ.)].
52. Choung RS, Stockfisch TP, Princen F, et al. Longitudinal status of serological markers predict Crohn’s disease phenotype before diagnosis: a “PREDICTS” study. Gastroenterology. 2015;148(4):S22.
53. Dubinsky MC, Kugathasan S, Mei L, et al; Western Regional Pediatric IBD Research Alliance; Pediatric IBD Collaborative Research Group; Wisconsin Pediatric IBD Alliance. Increased immune reactivity predicts aggressive complicating Crohn’s disease in children. Clin Gastroenterol Hepatol. 2008;6(10):1105-11.
54. Hamilton AL, Kamm MA, Selvaraj F, et al. Serological antibodies for the prediction of post-operative recurrent Crohn’s disease results from the POCER study. Gastroenterology. 2015;148(4):S116.
55. Gazouli M, Anagnostopoulos AK, Papadopoulou A, et al. Serum protein profile of Crohn’s disease treated with infliximab. J Crohns Colitis. 2013;7(10):e461-e470.
56. Wang W, Chen L, Zhou R, et al. Increased proportions of Bifidobacterium and the Lactobacillus group and loss of butyrate-producing bacteria in inflammatory bowel disease. J Clin Microbiol. 2014;52(2):398-406.
57. Machiels K, Joossens M, Sabino J, et al. A decrease of the butyrate-producing species Roseburiahominis and Faecalibacteriumprausnitzii defines dysbiosis in patients with ulcerative colitis. Gut. 2014;63(8):1275-83.
58. Wills ES, Jonkers DM, Savelkoul PH, Masclee AA, Pierik MJ, Pen-
ders J. Fecal microbial composition of ulcerative colitis and Crohn’s disease patients in remission and subsequent exacerbation. PLoS One. 2014;9(3):e90981.
59. Michail S, Durbin M, Turner D, et al. Alterations in the gut microbiome of children with severe ulcerative colitis. Inflamm Bowel Dis. 2012;18(10):1799-808.
60. Rajca S, Grondin V, Louis E, et al. Alterations in the intestinal microbiome (dysbiosis) as a predictor of relapse after infliximab withdrawal in Crohn’s disease. Inflamm Bowel Dis. 2014;20(6):978-86.
61. Moayyedi P, Surette MG, Kim PT, et al. Fecal microbiota transplantation induces remission in patients with active ulcerative colitis in a randomized controlled trial. Gastroenterology. 2015;149(1):102-9.e6.
62. Rossen NG, Fuentes S, van der Spek MJ, et al. Findings from a randomized controlled trial of fecal transplantation for patients with ulcerative colitis. Gastroenterology. 2015;149(1):110-18.e4.
63. Grinspan AM, Kelly CR. Fecal microbiota transplantation for ulcerative colitis: not just yet. Gastroenterology. 2015;149(1):15-8.
64. Marthn R, Chain F, Miquel S, et al. The commensal bacterium Faecalibacteriumprausnitzii is protective in DNBS-induced chronic moderate and severe colitis models. Inflamm Bowel Dis. 2014;20(3):417-430.
________________________________________________
2. Ripke S, Weersma RK, et al; International IBD Genetics Consortium (IIBDGC). Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease. Nature. 2012;491(7422):119-24.
3. Jostins L, Lees CW, Barrett JC, Parkes M, Satsangi J. New IBD genetics: common pathways with other diseases. Gut. 2011;60(12):1739-53.
4. Lichtenstein GR, Targan SR, Dubinsky MC, et al. Combination of genetic and quantitative serological immune markers are associated with complicated Crohn’s disease behavior. Inflamm Bowel Dis. 2011;17(12):2488-96.
5. Cleynen I, Gonzblez JR, Figueroa C, et al. Genetic factors conferring an increased susceptibility to develop Crohn’s disease also influence disease phenotype: results from the IBDchip European Project. Gut. 2013;62(11):1556-65.
6. Adler J, Rangwalla SC, Dwamena BA, Higgins PD. The prognostic power of the NOD2 genotype for complicated Crohn’s disease: a meta-analysis. Am J Gastroenterol. 2011;106(4):699-712.
7. Ananthakrishnan AN, Huang H, Nguyen DD, Sauk J, Yajnik V, Xavier RJ. Differential effect of genetic burden on disease phenotypes in Crohn’s disease and ulcerative colitis: analysis of a North American cohort.
Am J Gastroenterol. 2014;109(3):395-400.
8. Waterman M, Knight J, Dinani A, et al. Predictors of outcome in ulcerative colitis. Inflamm Bowel Dis. 2015;21(9):2097-105.
9. Sherlock ME, Walters T, Tabbers MM, et al. Infliximab-induced psoriasis and psoriasiform skin lesions in pediatric Crohn disease and a potential association with IL-23 receptor polymorphisms. J Pediatr Gastroenterol Nutr. 2013;56(5):512-8.
10. Frank DN, Robertson CE, Hamm CM, et al. Disease phenotype and genotype are associated with shifts in intestinal-associated microbiota in inflammatory bowel diseases. Inflamm Bowel Dis. 2011;17(1):179-84.
11. Steenholdt C, Brynskov J, Thomsen OØ, Munck LK, Christensen LA, Pedersen G, Kjeldsen J, Ainsworth MA. Implications of infliximab treatment failure and influence of personalized treatment on patient-reported health-related quality of life and productivity outcomes in Crohn’s disease. J Crohns Colitis. 2015;9:1032-42.
12. Steenholdt C, Bendtzen K, Brynskov J, Thomsen OØ, Munck LK, Christensen LA, Pedersen G, Kjeldsen J, Ainsworth MA. Changes in serum through levels of infliximab during treatment intensification but not in anti-infliximab antibody detection are associated with clinical outcomes after therapeutic failure in Crohn’s disease. J Crohns Colitis. 2015;9:238-45.
13. Frederiksen MT, Ainsworth MA, Brynskov J, Thomsen OØ, Bendtzen K, Steenholdt C. Antibodies against infliximab (IFX) are associated with de novo development of antibodies to adalimumab (ADL) and therapeutic failure in IFX-to-ADL switchers with inflammatory bowel disease.
Inflamm Bowel Dis. 2014;20:1714-21.
14. Steenholdt C, Frederiksen MT, Bendtzen K, Ainsworth MA, Thomsen OØ, Brynskov J. Time course and clinical implications of development of antibodies against adalimumab in patients with inflammatory bowel disease. J Clin Gastroenterol. 2016;50:483-9. doi: 10.1097/mcg. 0000000000000375
15. Feagan BG, Rutgeerts P, Sands BE, et al. Vedolizumab as induction and maintenance therapy for ulcerative colitis. N Engl J Med. 2013;369:699-710.
16. Ford LT, Berg JD. Thiopurine S-methyltransferase (TPMT) assessment prior to starting thiopurine drug treatment; a pharmacogenomic test whose time has come. J Clin Pathol. 2010;63(4):288-95.
17. Morales A, Salguti S, Miao С, et al. Relationship between 6-mercaptopurine dose and 6-thioguanine nucleotide levels in patients with inflammatory bowel disease. Inflamm Bowel Dis. 2007;13:380-5.
18. Winter JW, Gaffney D, Shapiro D, et al. Assessment of thiopurinemethyltransferase enzyme activity is superior to genotype in predicting myelosuppression following azathioprine therapy in patients with inflammatory bowel disease. Aliment Pharmacol Ther. 2007;25(9):1069-77.
19. Schwab M, Schaeffeler E, Marx C, Zanger U, Aulitzky W, Eichelbaum M. Shortcoming in the diagnosis of TPMT deficiency in a patient with Crohn’s disease using phenotyping only. Gastroenterology. 2001;121(2):498-9.
20. Gardiner SJ, Gearry RB, Begg EJ, Zhang M, Barclay ML. Thiopurine dose in intermediate and normal metabolizers of thiopurinemethyltransferase may differ three-fold. Clin Gastroenterol Hepatol. 2008; 6(6):654-60.
21. Osterman MT, Kundu R, Lichtenstein GR, Lewis JD. Association of 6-thioguanine nucleotide levels and inflammatory bowel disease activity: a meta-analysis. Gastroenterology. 2006;130(4):1047-53.
22. Yarur AJ, Abreu MT, Deshpande AR, Kerman DH, Sussman DA. Therapeutic drug monitoring in patients with inflammatory bowel disease. World J Gastroenterol. 2014;20(13):3475-84.
23. Sparrow MP, Hande SA, Friedman S, et al. Allopurinol safely and effectively optimizes tioguanine metabolites in inflammatory bowel disease patients not responding to azathioprine and mercaptopurine. Aliment Pharmacol Ther. 2005;22(5):441-6.
24. Yarur AJ, Kubiliun MJ, Czul F, et al. Concentrations of 6-thioguanine nucleotide correlate with trough levels of infliximab in patients with inflammatory bowel disease on combination therapy. Clin Gastroenterol Hepatol. 2015;13(6):1118-24.e3.
25. Hendler SA, Cohen BL, Colombel JF, Sands BE, Mayer L, Agarwal S. Highdose infliximab therapy in Crohn’s disease: clinical experience, safety, and efficacy. J Crohns Colitis. 2015;9(3):266-75.
26. 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(5):483-93.
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Авторы
А.И. Парфенов, О.В. Князев, А.В. Каграманова, Н.А. Фадеева
ГБУЗ «Московский клинический научно-практический центр им. А.С. Логинова Департамента здравоохранения Москвы», Москва, Россия
S.A. Loginov Moscow Clinical Research and Practical Center, Moscow Healthcare Department, Moscow, Russia
ГБУЗ «Московский клинический научно-практический центр им. А.С. Логинова Департамента здравоохранения Москвы», Москва, Россия
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S.A. Loginov Moscow Clinical Research and Practical Center, Moscow Healthcare Department, Moscow, Russia
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