The gut microbiota of patients with Inflammatory Bowel Disease (IBD) may have a role in disease aetiology and course [1]. Patients with IBD often have dysbiotic microbiota, with lower microbial diversity and cell counts, with both absolute and relative abundance of commensal microorganisms [2, 3]. Conversely, during remission following anti-inflammatory therapy, the gut microbiota has been observed to shift to a more eubiosis-like composition [3–6]. Furthermore, lower proportions of taxa with pro-inflammatory properties and mucus-degrading bacteria, as well as higher proportions of short-chain fatty acid-producing bacteria, have been associated with a higher likelihood of favourable outcomes with medical treatment [3, 5, 6]. In this study, Caenepeel and colleagues monitored changes in intestinal microbiota and stool features in order to develop and validate a predictive model to assist clinicians in determining a patient-specific therapeutic strategy.
At present, disease activity in Inflammatory Bowel Disease (IBD) is primarily monitored using faecal calprotectin, serum C-reactive protein (CRP) and endoscopic examination [1]. Whilst these are powerful tools, all three approaches have notable limitations. Faecal calprotectin testing requires a patient either to provide a stool sample whilst attending clinic or to return with a sample at a later date. Serum CRP requires a blood sample to be taken by a healthcare professional and endoscopy is invasive. Interleukin (IL)-6, whilst not routinely used in clinical settings to monitor disease activity, is known to play a role in IBD pathogenesis by increasing T-cell resistance against apoptosis, resulting in chronic inflammation [2].
Inflammatory Bowel Diseases (IBD), comprising the two most common subtypes of Crohn's Disease (CD) and Ulcerative Colitis (UC), are chronic inflammatory conditions of the gastrointestinal tract. Tumour necrosis factor (TNF) inhibitors, particularly infliximab, have been pivotal in the management of moderate to severe IBD. While effective, intravenous administration of infliximab typically involves regular visits to hospital-based infusion centres. Particularly from a patient convenience point of view, many individuals would prefer to administer medication at home without the need to attend infusion centres and without the need for intravenous administration. The development of a subcutaneous (SC) formulation of infliximab (CT-P13) aims to enhance patient convenience and adherence by allowing self-administration at home [1–3] . In the LIBERTY trials, Hanauer and colleagues sought to examine the efficacy and safety of CT-P13 SC as maintenance therapy in IBD, in two randomised, placebo-controlled phase 3 trials.
A biomarker-stratified comparison of top-down versus accelerated step-up treatment strategies for patients with newly diagnosed Crohn’s disease (PROFILE): a multicentre, open-label randomised controlled trial
There is debate on the optimal management of newly diagnosed active Crohn’s Disease (CD). The most commonly used treatment strategy around the world is a “step-up” treatment approach. This involves initial use of steroids at diagnosis to induce remission, followed by introduction of immunomodulators such as azathioprine to maintain that remission. Subsequently, if this treatment fails to control inflammation, patients are escalated to advanced therapies such as anti-TNF biological agents. When performed rapidly, this can be referred to as “accelerated step-up” treatment, and indeed in many countries this accelerated step-up approach is considered standard of care (conventional) treatment. An alternative treatment strategy is a more “top-down” approach , where there is early introduction of an advanced therapy, typically an anti-TNF agent.
Safety and efficacy of autologous haematopoietic stem-cell transplantation with low-dose cyclophosphamide mobilisation and reduced intensity conditioning versus standard of care in refractory Crohn's disease (ASTIClite): an open-label, multicentre, randomised controlled trial
A large number of patients living with Inflammatory Bowel Disease (IBD), including Crohn’s Disease (CD), show persistent disease activity and bowel damage despite medical or surgical therapy [1]. Haematopoietic stem-cell transplantation (HSCT) is a procedure able to “reset” the immune system by replacing autoreactive lymphocytes. A total of 232 patients (data from case series, observational studies and one clinical trial) had previously undergone HSCT for CD. Although there were promising clinical results, there were also some significant associated risks, including life-threatening side effects and mortality [2]. In a previous randomised controlled trial, called ASTIC, HSCT did not demonstrate superiority over standard therapy when an extremely high bar was set for the primary endpoint, i.e. induction of sustained disease remission in CD (defined as medication-free clinical remission for 3 months without any evidence of disease activity at endoscopy or imaging). Apart from the lack of efficacy demonstrated for the primary endpoint, the HSCT arm was also hampered by a significant burden of side effects [3].
Ulcerative Colitis (UC) is characterised by episodes of recurrent inflammation affecting the colonic mucosa. Accurate assessment of disease activity and prediction of clinical outcomes are crucial for effective management. Traditionally, histological examination has been the gold standard for evaluating mucosal inflammation, but it is time-consuming and subject to inter-observer variability. Recent advances in artificial intelligence (AI) may offer a potential solution. Iacucci and colleagues explored the application of machine learning in diagnosing histological remission and predicting clinical outcomes in UC patients.
Patients with colonic inflammatory bowel disease (IBD) face an elevated risk of colorectal cancer (CRC) compared to the general population.[1, 2] Colonoscopic surveillance has been shown to be associated with a reduction in CRC and CRC-related mortality in these patients.[3] Current guidelines recommend initiating surveillance 8-10 years after disease onset, with follow-ups every 1-5 years based on individual risk factors.[4–6] These factors include disease duration, severity, associated primary sclerosing cholangitis (PSC), family history of CRC, and other risks. The risk factors for CRC in IBD patients are dynamic, comprising both modifiable (inflammation, dysplasia detection, disease extent) and non-modifiable (age, family history, PSC) elements that change over time and with treatment, exerting varying influences, including protective effects, on the risk of developing CRC.[7]
