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IBDs, encompassing Crohn's disease (CD) and UC, are chronic, relapsing and remitting, inflammatory diseases of the GI tract. IBD is emerging as a globally important disease with epidemiological studies showing that there is a significant increase in IBD’s incidence in most regions of the world.1 In high-incidence areas such as North America, disease already affects around 0.6% of the population.1 As low/middle-income countries continue to become more industrialised, an increasing incidence is also expected to occur in areas of the globe where IBD was previously considered rare.2 ,3 Furthermore, as trends in life expectancy increase globally, the emergence of chronic health conditions, including IBD, will represent a growing proportion of individual and society health impact.
The recent acknowledgement that IBD is a progressive disease has changed the focus of therapeutic strategies. It is now widely accepted that treating effectively at earlier stages of disease, before bowel damage occurs, is likely to produce better outcomes, resulting in reduced rates of hospitalisation and surgery.4 Unfortunately, despite ongoing efforts to change therapeutic paradigms, combining early diagnosis with best available effective therapies, drug-free remission or absence of progression of bowel wall damage remains a challenge in many patients.5 ,6 Once the diagnosis of IBD is made, bowel damage has already occurred in a significant number of patients, and the immune dysregulation, dysbiosis and tissue injury associated with full-blown disease is set, and in many cases, irreversible.6 At present, all therapeutic interventions in IBD target well-established disease, and even the most potent agents are not able to prevent or reverse chronic damage often present at diagnosis. In order to truly change the natural history and long-term consequences of IBD, an effective intervention should ideally occur at an earlier phase, targeting the primary biological processes that drive disease …
Contributors All authors contributed to the manuscript concept and design. JT and JB drafted the manuscript. All authors critically revised the manuscript and approved the final version of the manuscript.
Disclaimer The views expressed in this article do not necessarily reflect the official policy or position of the Department of the Navy, Department of Defense, nor the US Government. This is a partial US Government work. There are no restrictions on its use.
Competing interests JT has served as a consultant for Takeda. JB and MSR have no COI to declare. MD has served as a consultant for Abbvie, Janssen, Celgene, Takeda, Ucb, Prometheus, and Genentech. JFC has served as a consultant or advisory board member for AbbVie, Amgen, Boehringer-Ingelheim, Celgene Corporation, Celltrion, Enterome, Ferring, Genentech, Janssen and Janssen, Medimmune, Merck & Co., Pfizer, Protagonist, Second Genome, Seres, Takeda, Theradiag, received research support from Abbvie, Janssen and Janssen, Genentech, Takeda, and has stock options for Intestinal Biotech Development and Genfit.
Provenance and peer review Not commissioned; externally peer reviewed.
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