Article information
Resumen
La información nueva que ha sido comunicada en la DDW (Digestive Disease Week) nos permite especular sobre el futuro en la enfermedad inflamatoria intestinal (EII). La manipulación de la dieta y del microbioma probablemente tendrá un papel cada vez mayor en el tratamiento de las EII, y a más largo plazo en la prevención. En el tratamiento con biológicos, éstos se utilizarán cada vez antes y cada vez más, aunque la nueva información sobre niveles, cicatrización mucosa y los nuevos estudios comparativos permitirán utilizarlos de forma cada vez más precisa y personalizada. Además de infliximab, adalimumab, natalizumab y certolizumab se utilizarán otros biológicos, entre los cuales los primeros serán el ustekinumab, el golimumab y el vedolizumab. En el futuro próximo, la colitis ulcerosa será tratada tan frecuentemente con biológicos como la enfermedad de Crohn. Se desarrollarán nuevos modelos de atención que incluirán una participación cada vez mayor del paciente y de los enfermeros. La capacidad de predicción de los nuevos modelos de diagnóstico y pronóstico permitirá una mejor individualización de las decisiones.
Palabras clave:
Enfermedad inflamatoria intestinal
Colitis ulcerosa
Enfermedad de Crohn
Azatioprina
Infliximab
Adalimumab
Vedolizumab
Golimumab
Dieta
Microbiota
Abstract
The new information presented in Digestive Disease Week has allowed us to speculate on the future of inflammatory bowel disease. Manipulation of diet and the microbioma will probably play an increasingly important role in the treatment of this disease and, in the long term, in its prevention. Biological agents will probably be used earlier and more widely; new information on levels of biological agents, mucosal healing and new comparative studies will also allow these agents to be used in a more precise and personalized way. In addition to infliximab, adalimumab, natalizumab and certolizumab, other biological agents will be employed; among the first of these to be used will be ustekinumab, golimumab and vedolizumab. In the near future, biological agents will be used as frequently in ulcerative colitis as in Crohn's disease. New healthcare models will be developed that will progressively include greater participation among patients and nurses. The ability to predict new diagnostic and prognostic models will allow decisions to be more individualized.
Keywords:
Inflammatory bowel disease
Ulcerative colitis
Azathioprine
Infliximab
Adalimumab
Vedolizumab
Golimumab
Diet
Microbiota
Full text is only aviable in PDF
Bibliografía
[1.]
J. Wagensberg.
Más árboles que ramas: 1116 aforismos para navegar por la realidad.
Tusquets Editores, (2012),
[2.]
S. Devkota, Y. Wang, M.W. Musch, V. Leone, H. Fehlner-Peach, A. Nadimpalli, et al.
Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10–/– mice.
Nature, 5 (2012), pp. 104-108
[3.]
C.H. Bernstein, F. Shanahan.
Disorders of a modern lifestyle: reconciling the modern epidemiology of inflammatory bowel diseases.
Gut, 57 (2008), pp. 1185-1191
[4.]
J.K. Kou, B. Abraham, H. El-Serag.
Dietary intake and risk of developing inflammatory bowel disease: a systematic review of the literature.
Am J Gastroenterol, 106 (2011), pp. 563-573
[5.]
E. Cabré, M.A. Gassull.
Nutrition in inflammatory bowel disease: impact on disease and therapy.
Curr Opin Gastroenterol, 17 (2001), pp. 342-349
[6.]
A. Spor, O. Koren, R. Ley.
Unravelling the effects of the environment and host genotype on the gut microbiome.
Nat Rev Microbiology, 9 (2011), pp. 279-290
[7.]
B. Begue, J. Verdier, F. Rieux-Laucat, O. Goulet, A. Morali, D. Canioni, et al.
Defective IL 10 signaling defining a subgroup of patients with inflammatory bowel disease.
Am J Gastroenterol, 106 (2011), pp. 1544-1555
[8.]
L.R. Ferguson.
Potential value of nutrigenomics in Crohn's disease.
Nat Rev Gastroenterol Hepatol, 9 (2012), pp. 260-270
[9.]
T. Sonnweber, C. Ress, M. Nairz, I. Theuri, A. Schroll, A.T. Murphy, et al.
High-fat diet causes iron deficiency via hepcidin-independent reduction of duodenal iron absorption.
J Nut Biochemistry, (2012),
[10.]
The Human Microbiome Project Consortium.
Structure, function and diversity of the healthy human microbiome.
Nature, 486 (2012), pp. 207-214
[11.]
F. Guarner.
Microbiota intestinal y enfermedades inflamatorias del intestino.
Gastroentero Hepatol, 34 (2011), pp. 147-154
[12.]
H. Chung, S.J. Pamp, J.A. Hill, N.K. Suran, S.M. Edelman, E.B. Troy, et al.
Gut immune maturation depends on colonization with a host-specifi microbiota.
Cell, 149 (2012), pp. 1578-1593
[13.]
I. Cho, M.J. Blaser.
The human microbiome: at the interface of health and disease.
Nat Rev Genetics, 13 (2012), pp. 260-270
[14.]
W.S. Garrett, G.M. Lord, S. Punit, G. Lugo-Villarino, S. Mazmanian, S. Ito, et al.
Communicable ulcerative colitis induced by T-bet deficiency in the innate immune system.
Cell, 131 (2007), pp. 33-45
[15.]
S.Y. Shaw, J.F. Blanchard, C.H. Bernstein.
Association between the use of antibiotics in the first year of life and pediatric inflammatory bowel disease.
Am J Gastroenterol, 105 (2010), pp. 2687-2692
[16.]
P. Dewint, B.E. Hansen, E. Verhe, B. Oldenburg, D.W. Hommes, M.J. Pierick, et al.
Adding ciprofloxacin to adalimumab results in higher fistula clorure rate in perianal fistulizing Crohn's disease.
Gastroenterology, 142 (2012), pp. S1160
[17.]
X. Qiu, J. Audet, G. Wong, S. Pillet, A. Bello, T. Cabral, et al.
Successful treatment of ebola virus-infected cynomolgus macaques with monoclonal antibodies.
Sci Transl Med, 4 (2012),
[18.]
A.N. Ananthakrishnan, D.G. Binion.
Improved efficacy of biological maintenance therapy in “Early”compared with “Late”Crohn's Disease: strike while the iron is hot with anti-TNF agents?.
Am J Gastroenterol, 105 (2010), pp. 1583-1585
[19.]
J.D. Isaacs.
The changing face of rheumatoid arthritis: sustained remission for all?.
Nat Rev Immunology, 10 (2010), pp. 605-611
[20.]
G. D’Haens, F. Baert, G. Van Asche, P. Caenepeel, P. Vergauwe, H. Tuynman, et al.
Early combined immunosuppression on conventional management in patients with newly diagnosed Crohn's disease: an open ranomised trial.
Lancet, 371 (2008), pp. 660-667
[21.]
P. Schmiedlin-Ren, L.J. Reingold, A.C. Rittershauss, J.S. Brudi, J. Adler, B.J. McKenna, et al.
AntiTNF therapy alters the natural history of experimental Crohn's disease when begun early, but not late, in the disease course.
Gastroenterology, 142 (2012), pp. S191-S192
[22.]
P. Rutgeerts, S. Vermeire, G. Van Assche.
Biological therapies for inflammatory bowel diseases.
Gastroenterology, 136 (2009), pp. 1182-1197
[23.]
J. Cosnes, A. Bourrier, D. Laharie, Y. Bouhnik, S. Nahon, J. Bonnet, et al.
Accelerated step-care therapy with early azathioprine (AZA) vs. conventional step-care therapy in Crohn's disease. A randomized study.
Gastroenterology, 142 (2012),
[24.]
M. Sans, A. López San-Román, M. Esteve, F. Bermejo, V. García-Sánchez, Y. Torres, et al.
Early use of azathioprine has a steroid sparing effect on recently diagnosed Crohn's disease patients.
Gastroenterology, 140 (2011), pp. S109
[25.]
C.A. Jackson, J. Clatworthy, A. Robinson, R. Horne.
Factors associated with non-adherence to oral medication for inflammatory bowel disease: a systematic review.
Am J Gastroenterol, 105 (2010), pp. 525-539
[26.]
M.E. Porter, E. Olmsted Teisberg.
Redifining health care: creating value-based competition on results.
Harvard Business Review Press, (2006),
[27.]
E. Louis, J.Y. Mary, G. Vernier-Massouille, J.C. Grimaud, Y. Bouhnik, D. Laharie, et al.
Maintenance of remission among patients with Crohn's disease on antimetabolite therapy after infliximab therapy is stopped.
Gastroenterology, 142 (2012), pp. 63-70
[28.]
J.P. Gisbert, J. Panés.
Loss of response and requirement of infliximab dose intensification in Crohn's disease: a review.
Am J Gastroenterol, 104 (2009), pp. 760-767
[29.]
M. Chaparro, I. Guerra, P. Muñoz-Linares, J.P. Gisbert.
Systematic review: antibodies and anti-TNF levels in inflammatory bowel disease.
Aliment Pharmacol Ther, (2012),
[30.]
N. Vande Casteele, G. Compernolle, V. Ballet, G. Van Assche, A. Gils, S. Vermeire, et al.
Results on the optimisation phase of the prospective controlled trough level adapted infliximab treatment (TAXIT) trial.
Gastroenterology, 142 (2012), pp. S211-S212
[31.]
D. Ginard, S. Khorrami, I. Marín-Jiménez, M. Chaparro, M. Aguas, F. Muñoz, et al.
Effectiveness and safety of ustekinumab as rescue therapy in multi-drug resistant Crohn's disease.
Gastroenterology, 142 (2012), pp. S355
[32.]
W.J. Sandborn, B.G. Feagan, R.N. Fedorak, E. Scherl, M.R. Fleisher, S. Katz, et al.
A randomized trial of ustekinumab, a human interleukin-12/23 monoclonal antibody, in patients with moderate-to-severe Crohn's disease.
Gastroenterology, 135 (2008), pp. 1130-1141
[33.]
W.J. Sandborn, C. Gasink, L.L. Gao, M. Blank, J. Johanns, C. Guzzo, et al.
A multicenter, randomized, double-blind, placebo-controlled phase2b study of ustekinumab, a human monoclonal antibody to IL-12/23p40, in patients with moderately to severely active Crohn's disease: results through week 22 From the Certifi Trial.
Gastroenterology, 140 (2011), pp. S109
[34.]
W.J. Sandborn, B.G. Feagan, C.W. Marano, R. Strauss, J. Johanns, H. Zhang, et al.
943d a phase 2/3 randomized, placebo-controlled, double-blind study to evaluate the safety and efficacy of subcutaneous golimumab induction therapy in patients with moderately to severely active ulcerative colitis: PURSUIT SC.
Gastroenterology, 142 (2012), pp. S161
[35.]
I. Ordas, D.R. Mould, B.G. Feagan, W.J. Sandborn.
Anti-TNF monoclonal antibodies in inflammatory bowel disease: pharmacokinetics- based dosing paradigms.
Clin Pharmacol Ther, 91 (2012), pp. 635-646
[36.]
B. Feagan, P. Rutgeerts, B.E. Sands, W.J. Sandborn, J.F. Colombel, S. Hanauer, et al.
Induction therapy for ulcerative colitis: results of GEMINI I, a randomized, placebo-controlled, doubleblind, multicenter phase 3 trial.
Gastroenterology, 142 (2012), pp. S160-S161
[37.]
O. Dewit, X. Hebuterne, J.-L. Dupas, S.M. Howaldt, J. Bures, S. Schreiber, et al.
Results of a phase II, randomized, doublé-blind, controlled trial of the efficacy of active therapeutic immunization with TNF-kinoid in patients with moderate to severe Crohn's disease with secondary resistance to TNF antagonist.
Gastroenterology, 142 (2012), pp. S567-S568
[38.]
S.H. Odes, H. Vardi, D. Greenberg, M. Friger, R.W. Stockbrugger, C. O’Morain, et al.
Cost-effectiveness of episodic or maintenance infliximab treatment versus standard treatment in a community-based incidence cohort of adult ulcerative colitis patients with 10-years follow-up.
Gastroenterology, 142 (2012), pp. S256
[39.]
M.E. Van der Valk, M.J.J. Mangen, G. Dijkstra, A.A. Van Bodegraven, H. Fidder, D.J. De Jong, et al.
AntiTNF therapy is a major cost-driver in inflammatory bowel disease: results from the COIN study.
Gastroenterology, 142 (2012), pp. S263
[40.]
R. Gosciny, A. Uderzo.
Astèrix et Cleopathre.
Hachette, (1999),
[41.]
European Strategy, and Policy Analysis System (ESPAS).
Citizens in an interconnected and polycentric world Global Trends. 2030.
Institute for Security Studies, (2012),
[42.]
J.B. Essers, S. Ripke, B. Neale, R.J. Xavier, M. Vu, M. Dubinsky, et al.
Genetics, serologies, and smoking predict highly morbid Crohn's disease in erronously diagnosed UC patients.
Gastroenterology, 142 (2012), pp. S39-S40
[43.]
F.D. Van Schalk, B. Oldenburg, A. Hart, P.D. Siersema, M.G. Van Oijen, H.D. Bueno-De-Mesquita.
Serological markers can predict inflammatory bowel disease years before the diagnosis: results from a nested case-control study within a european cohort study.
Gastroenterology, 142 (2012), pp. S39
Copyright © 2012. Elsevier España, S.L.. Todos los derechos reservados
