Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), leading to coronavirus disease 2019 (COVID-19), spread exponentially, with the World Health Organization (WHO) declaring a pandemic on March 11 [1]. By August 15, more than 21,000,000 cases and 755,000 deaths had been reported worldwide [2]. People of any age with certain underlying medical conditions are at increased risk for severe illness from COVID-19.
ECCO COllaborative Network For Exceptionally Rare Case Reports (CONFER) is an initiative to identify, assemble and report together rare IBD cases of clinical relevance, which are otherwise seldom reported. By joining forces with the many Members and supporters of ECCO, a joint report of all similar rare cases can result in a large case series that will advance our knowledge about these uncommon patients.
One of the missions of the Clinical Research Committee of ECCO (ClinCom) is to facilitate innovative clinical research in the area of Inflammatory Bowel Diseases (IBD).
To promote international scientific collaboration among researchers from different European countries, ClinCom established the IBD National Study Group Meeting, which takes place at the annual ECCO Congress. With this great platform, ClinCom enables investigators to have their studies challenged and promoted at the same time. Before the meeting, investigators are invited to provide a study synopsis for their project, including background, design, objectives, outcome parameters, major inclusion and exclusion criteria, statistics and co-variates. Submitted projects are then reviewed by ClinCom and, if found feasible, discussed during the IBD National Study Group Meeting at the ECCO Congress.
I accepted the ECCO AOCC Travel Grant 2020 with great pleasure and in all humility. The grant enabled me to visit Helsinki University Central Hospital in Finland between January 13 and March 6, 2020. This gave me the opportunity to increase my knowledge on the management of IBD patients and to gain insight into the faecal microbiota transplant and human microbiome research programme in Finland. At the Hospital District of Helsinki and Uusimaa (HUS), I attended the IBD clinics and IBD inpatient rounds, which greatly enriched my experience. Further, I learned more about IBD endoscopy, including double-balloon enteroscopy and capsule endoscopy for Crohn’s Disease and faecal microbiota transplant (FMT). I intend to deploy this knowledge at our IBD centre to foster further professional growth.
Crohn's Disease (CD) is an idiopathic Inflammatory Bowel Disease (IBD) characterised by transmural inflammation of the affected tracts. The uncontrolled inflammation can lead to bowel damage, defined as the onset of strictures, abscesses or fistulas negatively impacting patients' quality of life and outcomes. The Lémann index (LI) is a recently validated tool that was specifically designed to assess the presence of penetrating or stenosing lesions and to quantify their severity. LI is a complex and time-consuming score which is based on imaging [magnetic resonance imaging (MRI)] and endoscopic procedures. Of note, it is mainly used in clinical trials, while its use in clinical practice is limited. Our aim was to develop a simplified LI and to compare the correlation between this simplified LI and the standard LI in assessing bowel damage.
Inflammatory Bowel Diseases (IBD) are devastating diseases induced by a breakdown of gut homeostasis, in which CD4+ effector T cells are major mediators of the inflammatory response. Interestingly, CD4+ effector T cells can convert into regulatory T cells, thereby controlling inflammation. However, the forces driving this T-cell plasticity remain largely unexplored, especially in IBD patients. In this regard, changes in the microbiota that can induce different T-cell profiles are commonly observed during IBD. The present proposal aims to elucidate how CD4+ T-cell plasticity can be modulated from a pro-inflammatory towards an anti-inflammatory profile in IBD patients. Our hypothesis is that the microbiota may modulate T cells towards an anti- or pro-inflammatory profile. To address this issue, we aim to analyse T-cell plasticity in IBD patients and mouse IBD models, and to correlate our findings with the microbiota composition. Furthermore, we will study whether antibiotics commonly used to treat IBD affect T-cell plasticity through microbiota-dependent processes.
Britta Siegmund is Medical Director of the Medical Department, Division of Gastroenterology, Infectiology and Rheumatology at the Charité - University Hospital Campus Benjamin Franklin Berlin, Germany. She has recently been accredited with the position of the new President-Elect of ECCO and we were happy to conduct an exclusive interview with her.
For the convenience of our ECCO News readers we recorded the interview and put it in an audio file. We hope you will enjoy listening to interesting facts about our President-Elect.
Glen Doherty is a consultant gastroenterologist at the Centre for Colorectal Disease at St Vincent's University Hospital and University College Dublin (UCD) as well as Research Director of the Centre for Colorectal Disease. In addition, he serves as an Executive Board member of the Irish Society of Gastroenterology (ISG). He joined GuiCom in 2016 and has been the chair for the last year.
The anti-TNF monoclonal antibody infliximab offers an effective treatment for patients with Inflammatory Bowel Disease (IBD) refractory to conventional immunomodulator therapies. Successful biologic therapy can lead to clinical and endoscopic remission as well as reduced hospitalisation and requirement for surgery [1].
Unfortunately, as a large protein and chimeric antibody, infliximab is immunogenic and this frequently leads to formation of anti-drug antibodies (ADA), with subsequent secondary loss of response (LOR), drug discontinuation and adverse reactions [2]. Identifying patients at increased risk of developing antibodies prior to treatment may establish which individuals require closer drug level monitoring, concomitant immunomodulator therapy and observation for adverse events.
Previous work by Sazonovs et al. identified the first genetic locus to be robustly associated with immunogenicity to anti-TNF therapies [3]. The HLADQA1*05 allele variant rs2097432, carried by approximately 40% of Europeans, significantly increased the rate of formation of infliximab ADA. In the study reviewed here, Wilson et al. aimed to independently identify whether presence of the variant allele was associated with increased risk of ADA formation, LOR, drug discontinuation and adverse events.
Perianal fistulising Crohn’s Disease is a challenging phenotype affecting more than 20% of patients diagnosed with Crohn’s Disease. It is associated with debilitating symptoms and significant morbidity, with subsequent reduced quality of life and increased disease-related work disability.
Currently treatment remains challenging, incorporating surgical and medical management; the latter is driven largely by biologic agents, specifically anti-tumour necrosis factor (TNF) agents such as adalimumab (ADA) and infliximab (IFX). Whilst ADA and IFX have proven efficacy in inducing and maintaining fistula healing and closure, a significant proportion of patients fail to respond or lose response over time. Increasing evidence suggests that this is in part due to sub-therapeutic drug levels, with or without the presence of antibodies to anti-TNF agents (ATA), with higher target drug levels required for fistula healing compared to mucosal healing in Crohn’s Disease. However, data evaluating the correlation between anti-TNF levels and perianal fistula outcomes, particularly with ADA, remain limited.
The aim of this study was to assess the association between anti-TNF levels and perianal fistula healing and closure with maintenance ADA and IFX therapy.
Arshdeep Singh 
Ferdinando D'Amico
Andres Machicote
Ignacio 
Charlotte Hedin 
