Targeting Disease Progression in Crohn’s Disease: Fighting an Unrelenting Enemy

In the first presentation, Prof Panaccione considered how early treatment of Crohn’s disease (CD) is key for achieving the therapeutic goals, which include symptomatic remission and mucosal healing. The latest STRIDE guidelines,1 published in 2015, endorse endoscopic remission defined as “resolution of ulceration at ileocolonoscopy”, and emphasised the need for tight monitoring of inflammation. He explored data highlighting how the ability to achieve mucosal healing decreases with increased disease duration, that benefits from mucosal healing may not be realised until the second year of treatment, and how patients who experience mucosal healing are less likely to be hospitalised and require surgery. Studies show patients do better with the ‘top-down’ approach, receiving anti-tumour necrosis factor (TNF) drugs early in the disease course, which has led to the introduction of a treatment algorithm suggesting patients with high-risk factors for poor prognosis should receive early ‘top-down’ therapy and lower-risk patients traditional ‘step-up’ therapy. The need for decisive early treatment to slow progression emphasises the importance of facilitating early diagnosis, and identifying patients for early biologic therapy. In the second presentation, Dr Iris Dotan explored data suggesting that optimal positioning for vedolizumab appears to be early in the course of disease. Furthermore, vedolizumab’s effect on clinical remission improves over time, clinical remissions have been shown to be maintained long-term, and vedolizumab reduces rates of hospitalisation. A favourable risk-benefit profile for vedolizumab has been shown for long-term use with no increase in the incidence of adverse events in the 5-year analysis. There are now 77,382 patient-years of post-marketing exposure to vedolizumab worldwide.2 The latest European Crohn’s and Colitis Organisation (ECCO) guidelines recommend the use of vedolizumab in patients with moderate to severe localised ileocaecal and colonic CD refractory to steroids and/or anti-TNF-αs.