In the last decade, numerous biologics and small molecules have been tested in clinical trials for patients with Crohn’s Disease (CD), and some have already been approved and used effectively in such patients. However, there is increasing interest in the use of dietary therapies for patients with CD from both providers and patients, who often wish to start an intervention that is not associated with immunosuppression. In addition, studies in both animal models and humans have put the spotlight on different dietary components that can either provoke or suppress intestinal inflammation. As an example, specific emulsifiers that are widely used in the food industry as preservatives increase the susceptibility of mice to develop colitis [1] and also alter the faecal microbiome and metabolome in humans characterised by pro-inflammatory perturbations [2].

We are delighted to welcome Séamus and Firas and are confident that both will make a substantial contribution to the P-ECCO Committee and to the organisation as a whole.

Richard Hansen © ECCO

The risk of thrombosis in paediatric IBD has become a hot topic in recent months, prompted by the publication of two impactful papers in Journal of Crohn’s and Colitis [1, 2]. Kuenzig and colleagues presented a large Canadian population-based study which described a vastly increased thrombosis rate in children with IBD compared to the normal population: the 5-year incidence was 31.2 per 10,000 person-years among children with IBD versus 0.8 per 10,000 person-years among children without IBD (95% confidence intervals 23.7–41.0 and 0.4–1.7, respectively) [1].

Dror Shouval © ECCO

Over the past two decades, significant progress has been made in the understanding of the role of genetics in the pathogenesis of Inflammatory Bowel Disease (IBD): On the one hand, adult IBD studies have identified more than 250 single nucleotide polymorphisms that increase the risk of disease, though their individual and overall effect on the risk of developing IBD is small [1]. On the other hand, the expanding use of next-generation sequencing (NGS) platforms has resulted in the identification of more than 100 different rare monogenic disorders that directly cause IBD [2]. Given the central role of immune cells in sustaining immune tolerance in the gut, it is not surprising that in many cases monogenic disorders causing IBD result from pathogenic variants in genes involved in essential immune or epithelial pathways. Some patients with such disorders present with a clear immunodeficiency phenotype (e.g. chronic granulomatous disease, Wiskott-Aldrich syndrome), but in others IBD is the sole manifestation [3].

As the new chair of the P-ECCO Committee, it is my pleasure to introduce two newly elected members of the Committee: Richard Hansen and Dror Shouval, two wonderful paediatric gastroenterologists from Scotland and Israel, respectively. Both are very active in the paediatric IBD field and they bring a wealth of expertise and energy to our group.

In the last decade the traditional management of Inflammatory Bowel Disease (IBD), based on clinically guided treatment intensification, has been revised and the so-called treat-to-target (T2T) approach, focusing on objective and scheduled measures to monitor intestinal inflammation, has been implemented in clinical practice, both in adults and in children. The general idea behind such tight monitoring is to prevent or block intestinal damage related to persistent and uncontrolled inflammation, and to avoid long-term complications.

Anti-tumor necrosis factor alpha (TNFα) therapy is frequently used in the treatment of Crohn’s Disease (CD) and Ulcerative Colitis (UC) in both adult and paediatric patients. Nevertheless, primary or secondary treatment failure of anti-TNFα treatment is not uncommon [1]. Both primary and secondary treatment failures are attributed either to pharmacokinetic, pharmacodynamic and immunogenic factors or to adverse events in response to the specific agent [2]. In recent years, loss of response (LOR) during anti-TNFα treatment has commonly been approached through the use of therapeutic drug monitoring involving measurement of infliximab or adalimumab trough concentrations (TC) and anti-drug antibodies (ADAs). Therapeutic drug monitoring of anti-TNFα agents enables proper stratification of LOR into a specific type of LOR, with corresponding adjustment of treatment. In children, in line with findings in adults, it has consistently been shown that higher drug TC is associated with higher efficacy [3] and that LOR is most commonly attributable to either low TC or the development of anti-drug antibodies [4].

Although the relationship between IBD and nutrition is of longstanding interest, the attention paid to it has increased dramatically in recent years, with the inclusion of nutritional interventions in ECCO Guidelines on both paediatric and adult Crohn’s Disease (and of course many other IBD guidelines), bespoke publications such as the ECCO perioperative dietary therapy topical review and a flowering of clinical interest in Crohn’s Disease-specific diets.

This clinical interest in nutritional issues in IBD is also reflected in the exceptional interest in a December 2020 educational article in the UEG Journal “Mistakes in…” series, namely “Mistakes in nutrition in IBD and how to avoid them” by the ECCO Members Joe Meredith, Kostas Gerasimidis and Richard Russell (ueg.eu/a/268). Basic and translational scientific studies of the pathogenesis of IBD have increasingly evaluated the role of nutrition and particularly its interaction with the microbiome.

Since the first reports in Wuhan, China in December 2019, the new coronavirus SARS-CoV-2 has resulted in over 40 million confirmed cases of COVID-19 globally with over 1 million deaths within just 10 months. Economies have been shattered, routine healthcare has been severely disrupted, and restrictions have been imposed on travel and social and family life in a previously unthinkable manner.

Dietary advice in the management of IBD has evolved in recent years from having gastrointestinal symptom reduction as a goal to a more pathogenesis-focussed approach [1–4]. At present, dietary recommendations in adult Crohn’s Disease (CD) are limited to increasing dietary fibre by means of fruit and vegetables and decreasing processed foods [1]. The nutrition debate has long divided adult and paediatric CD care, from international guidelines all the way through to service provision arrangements, with growth failure being a common feature in paediatric CD and dietetic support being a mainstay of care in many children’s hospitals [5–7].