Personalizing Therapy for Inflammatory Bowel Diseases
Personalizing Therapy for Inflammatory Bowel Diseases
Several questions remain unanswered in our goal to develop a personalized approach to the management of IBD. Clinical risk factors, complemented in some situations by serology and genetics have allowed us to predict likelihood of complications in CD. However, the effectiveness of early intervention in those who have not yet developed complicated disease but are 'predicted to be likely to do so' remains to be established. Indeed whether such early intervention can truly prevent the development of internal penetrating disease or strictures in CD has not been demonstrating either through clinical trials or through follow-up of prospective patient cohorts. In addition to continued randomized controlled trials of novel therapies, it is important to also conduct high-quality comparative effectiveness studies and trials comparing various therapeutic algorithms. Indeed, two such recent trials, the SONIC trial and the top-down/step-up trial, while examining already widely available therapies, have significantly informed about the practice regarding the use of these agents. We also lack the ability currently to tailor an individual's treatment based on the likely dominant mechanism in driving their inflammatory process. This becomes particularly relevant with the availability of a spectrum of agents targeting different inflammatory pathways: anti-TNF biologics, anti-integrin therapy, anti-IL-12/23 antibodies, chemokine antagonists, janus kinase inhibitors and others. Furthermore, whether some individuals remain uniquely susceptible to the effect of environmental factors also has not been explored, but indeed this is likely to be the case as data on the role of the external environment suggest heterogeneity in its effect with conflicting results.
Gaps in Research
Several questions remain unanswered in our goal to develop a personalized approach to the management of IBD. Clinical risk factors, complemented in some situations by serology and genetics have allowed us to predict likelihood of complications in CD. However, the effectiveness of early intervention in those who have not yet developed complicated disease but are 'predicted to be likely to do so' remains to be established. Indeed whether such early intervention can truly prevent the development of internal penetrating disease or strictures in CD has not been demonstrating either through clinical trials or through follow-up of prospective patient cohorts. In addition to continued randomized controlled trials of novel therapies, it is important to also conduct high-quality comparative effectiveness studies and trials comparing various therapeutic algorithms. Indeed, two such recent trials, the SONIC trial and the top-down/step-up trial, while examining already widely available therapies, have significantly informed about the practice regarding the use of these agents. We also lack the ability currently to tailor an individual's treatment based on the likely dominant mechanism in driving their inflammatory process. This becomes particularly relevant with the availability of a spectrum of agents targeting different inflammatory pathways: anti-TNF biologics, anti-integrin therapy, anti-IL-12/23 antibodies, chemokine antagonists, janus kinase inhibitors and others. Furthermore, whether some individuals remain uniquely susceptible to the effect of environmental factors also has not been explored, but indeed this is likely to be the case as data on the role of the external environment suggest heterogeneity in its effect with conflicting results.
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