The management of Crohn’s Disease (CD) is dependent on many factors, including disease activity, site of involvement and the need to tailor treatment for each individual patient [1]. Moreover, features such as obstruction, fistulation, strictures and abscesses can all add to the complexity of CD management. While surgery has played a large role in the management of these patients, it is by no means a cure and the risk of relapse and repeat surgeries remains high [2, 3]. Accordingly, there continues to be a large unmet need for the development of novel medications that target distinct mechanisms of action in order to provide symptomatic and endoscopic control for patients with active disease. In parallel with this need to develop new medications, there has been an increasing desire for fast-acting medications, and movement towards oral administration, which may help both to reduce costs for hospitals and patients and to enhance aspects that are important to patients, such as quality of life and work productivity [4, 5].
Submucosal injection of the RNA nucleotide GUT-1 in active ulcerative colitis patients: A randomized, double-blind, placebo-controlled phase 2a induction trial.
Atreya R, Kuhbacher T, Waldner M, et al.
J Crohns Colitis 2023. doi: 10.1093/ecco-jcc/jjad162. Online ahead of print.
Despite an increasing number of therapeutic options for Ulcerative Colitis (UC), many patients still have disease which progresses over time, and there has been renewed interest in and improved understanding of the chronic fibrosis and remodelling that occurs in UC [1–3]. In particular, there has been a growing appreciation of both the importance of the extracellular matrix (ECM) for remodelling in UC and the potential to target the ECM with new therapeutic agents [4]. One such target is carbohydrate sulphotransferase 15 (CHST15). This is a type II transmembrane Golgi protein that biosynthesises highly sulphated disaccharide units (E-units) of chondroitin sulphate, which binds to various functional proteins and pathogenic microorganisms. Targeting this molecule in mouse models has previously been shown to offer promising signals for ameliorating colitis [5]. Based on this promising pre-clinical data, blockade of CHST15 has emerged as a potentially promising therapeutic target, and such blockade can be achieved by a silencing RNA oligonucleotide molecule called GUT-1 (previously called STNM01). A prior phase I clinical trial demonstrated the safety of GUT-1 in patients with Crohn’s Disease [6]. Accordingly, Atreya and colleagues now sought to evaluate the safety, as well as the efficacy and mode of action, of GUT-1 in patients with UC as part of a phase IIa placebo-controlled, clinical trial.
The Y-ECCO Interview Corner is a chance to get to know people inside ECCO. Mark Samaan has been a fixture on the Y-ECCO Committee since 2018, and is the current Chair. He is a consultant gastroenterologist with an interest in IBD clinical trials. He has had an education in IBD spanning two continents and is a keen swimmer. We sat down to talk about his experience in IBD, and what it’s like to support a football team who famously achieve very little.
It is my pleasure to introduce the ECCO National Representatives of Portugal Helena Tavares de Sousa and Samuel Fernandes. We had an intriguing discussion on a wide range of topics such as the challenges of treating IBD in Portugal, how GEDII their national IBD group helps with clinical management but also research projects, what Portugal is doing right in producing a lot of inspiring figures in Gastroenterology that lead the European Gastroenterology Organisations like ECCO president-elect Fernando Magro, but also for their respective areas of research interest namely intestinal fibrosis for Helena and transmural inflammation for Samuel and much more!
Welcome again to a new episode of the JCC Podcast in ECCO News!
We know that there is a "window of opportunity", where starting an effective therapy can improve outcomes in Crohn´s disease. This is also the case for early introduction of anti-TNFs but, how early should we start it to change the natural history of the disease?
Robin Dart
Spyros Siakavellas