Philippe Marteau’s research while affiliated with Sorbonne University and other places

Background and aims Achieving deep remission, encompassing clinical, endoscopic, and biological remission, is the goal in managing Crohn’s disease (CD). The role of histological remission remains unclear. This study aimed to examine the impact of histological inflammation on clinical relapse risk in CD and explore the relationship between histology, endoscopic scores, and biomarkers. Methods Patients from the prospective STORI cohort underwent ileocolonoscopy with CDEIS calculation and 2 biopsies from the most inflamed or previously inflamed areas. Histological scores (Robarts, Geboes, modified Geboes, Nancy, and IBD-DCA) were determined by two independent pathologists in a central reading process. Histological remission was defined by specific score thresholds. Clinical relapse, defined by CDAI >250 or a CDAI increase of 70 points over two weeks, was monitored for at least one year. Results Out of 115 patients included in STORI, 160 biopsies (44 ileal and 116 colonic) from 76 patients were analyzed. Histological remission rates were 46% (Nancy), 55% (Robarts), 61% (Geboes), and 41% (IBD-DCA). During follow-up, 35 patients (46%) experienced a clinical relapse: 37% with histological remission and 56% without, based on the Nancy score. Among the mucosal healing (MH) subgroup (45 patients), 34% with histological remission and 44% without relapsed (p=0.18). Histological scores did not predict clinical relapse. Only faecal calprotectin (FC) was a significant predictor in multivariate analysis (p=0.029). Conclusion Despite correlations with endoscopy and biomarkers, histological scores did not predict clinical relapse in CD patients in remission. Thus, these scores are not recommended for clinical practice to assess relapse risk in CD.

Background Deep remission has become the target in the management of Crohn’s disease (CD). The role of histology in the management of CD has not yet been established. The aim of this work was to study the impact of histological inflammation on the risk of clinical relapse in patients with CD in clinical and endoscopic remission and to study the correlation between histology and endoscopic scores and biomarkers. Methods All patients included in STORI (1) were eligible for inclusion. Fecal calproptectin and colonoscopy with CDEIS calculation were performed at inclusion. Two biopsies, taken either from the most inflammed macroscopic area or from an area with previous inflammation in case of mucosal healing (MH) were prospectively performed. MH was defined by the absence of ulcers. Different histological scores were calculated by 2 independent pathologists: Robart, Geboes, modified Geboes, Nancy, and DCA-IBD scores. Histological remission was defined by Nancy=0 ; Geboes ≤2 ; modified Geboes of grade 0 ; Robarts ≤3, IBD-DCA of C≤1 and A=0. Clinical relapse was prospectively evaluated in the STORI trial as CDAI>250 or CDAI between 150 and 250 with an increase of 70 points during 2 successive weeks compared to the inclusion visit. (1) Louis E et al .Gastroenterology 2012 Results Eighty biopsies (22 ileal and 58 colonic) were available from 76/115 patients included in STORI. Among the 45 patients with MH, 30 had colonic biopsies, 11 had ileal biopsies and 4 had biopsies in both locations. Among colonic biopsies 68% had histological remission according to Nancy and modified Geboes scores, 65% according to DCA-IBD and Geboes scores and 71% according to Robarts score. Among ileal biopsies 53% had histological remission according to Nancy score, 47% according to Modified Geboes, Geboes and DCA-IBD scores, and 67% according to the Robarts score. Thirty-five patients (46%) experienced a clinical relapse during the follow-up including 16/45 (36%) and 19/31 (61%) in the group with MH and without MH respectively. Histological characteristics and histological scores were not predictive of clinical relapse. In the total cohort (n=76), the CDEIS score was correlated to Nancy (p<0,001, r=0,43), Geboes (p<0,001, r=0,47) and Robarts (p<0,001, r=0,45) scores. Fecal calprotectin was correlated to Nancy (p<0,001, r=0,48), Geboes (p<0,001, r=0,45) and Robarts (p<0,001, r=0,46) scores. The histological scores of Nancy, Robarts and Geboes were highly correlated (p<0,0001 ; r > 0,9). Conclusion Although correlated with endoscopy and biomarkers, histology was not predictive of clinical relapse in CD patients in clinical and endoscopic remission. These findings do not support the use of histology to predict clinical relapse in CD in clinical practice.

Background Whether healthcare workers with inflammatory bowel disease (IBD) are at increased risk of Novel coronavirus disease (COVID-19) due to occupational exposure is unknown. Aim To assess the risk of COVID-19 in healthcare workers with IBD. Methods A case control study enrolled 326 healthcare workers with IBD from 17 GETAID centres and matched non-healthcare workers with IBD controls (1:1) for gender, age, disease subtype and year of diagnosis. The study period was year 2020 during the COVID-19 outbreak. Results In total, 59 COVID-19 were recorded among cases (n = 32) and controls (n = 27), including 2 severe COVID-19 (requiring hospitalization, mechanic ventilation) but no death. No difference was observed between healthcare workers and controls regarding the overall incidence rates of COVID-19 4.9 ± 2.2 vs. 3.8 ± 1.9 per 100 patient-semesters, p = 0.34) and the overall incidence rates of severe COVID-19 (0.6 ± 7.8 vs. 0.3 ± 5.5 per 100 patient-semesters, p = 0.42). In multivariate analysis in the entire study population, COVID-19 was associated with patients with body mass index > 30 kg/m² (HR = 2.48, 95%CI[1.13-5.44], p = 0.02). Conclusion Healthcare workers with IBD do not have an increased risk of COVID-19 compared with other patients with IBD.

Due to the potential role of the gut microbiota and bile acids in the pathogenesis of both inflammatory bowel disease (IBD) and sporadic colorectal cancer, we aimed to determine whether these factors were associated with colorectal cancer in IBD patients. 215 IBD patients and 51 non-IBD control subjects were enrolled from 10 French IBD centers between September 2011 and July 2018. Fecal samples were processed for bacterial 16S rRNA gene sequencing and bile acid profiling. Demographic, clinical, endoscopic, and histological outcomes were recorded. Characteristics of IBD patients included: median age: 41.6 (IQR 22); disease duration 13.2 (13.1); 47% female; 21.9% primary sclerosing cholangitis; 109 patients with Crohn’s disease (CD); 106 patients with ulcerative colitis (UC). The prevalence of cancer was 2.8% (6/215: 1 CD; 5 UC), high-grade dysplasia 3.7% (8/215) and low-grade dysplasia 7.9% (17/215). Lachnospira was decreased in IBD patients with cancer, while Agathobacter was decreased and Escherichia-Shigella increased in UC patients with any neoplasia. Bile acids were not associated with cancer or neoplasia. Unsupervised clustering identified three gut microbiota clusters in IBD patients associated with bile acid composition and clinical features, including a higher risk of neoplasia in UC in two clusters when compared to the third (relative risk (RR) 4.07 (95% CI 1.6–10.3, P < .01) and 3.56 (95% CI 1.4–9.2, P < .01)). In this multicentre observational study, a limited number of taxa were associated with neoplasia and exploratory microbiota clusters co-associated with clinical features, including neoplasia risk in UC. Given the very small number of cancers, the robustness of these findings will require assessment and validation in future studies.

Background: Bubbles often mask the mucosa during capsule endoscopy (CE). Clinical scores assessing the cleanliness and the amount of bubbles in the small bowel (SB) are poorly reproducible unlike machine learning (ML) solutions. We aimed to measure the amount of bubbles with ML algorithms in SB CE recordings, and compare two polyethylene glycol (PEG)-based preparations, with and without simethicone, in patients with obscure gastro-intestinal bleeding (OGIB). Patients & methods: All consecutive outpatients with OGIB from a tertiary care center received a PEG-based preparation, without or with simethicone, in two different periods. The primary outcome was a difference in the proportions (%) of frames with abundant bubbles (>10%) along the full-length video sequences between the two periods. SB CE recordings were analyzed by a validated computed algorithm based on a grey-level of co-occurrence matrix (GLCM), to assess the abundance of bubbles in each frame. Results: In total, 105 third generation SB CE recordings were analyzed (48 without simethicone and 57 with simethicone-added preparations). A significant association was shown between the use of a simethicone-added preparation and a lower abundance of bubbles along the SB (p = 0.04). A significantly lower proportion of "abundant in bubbles" frames was observed in the fourth quartile (30.5% vs. 20.6%, p = 0.02). There was no significant impact of the use of simethicone in terms of diagnostic yield, SB transit time and completion rate. Conclusion: An accurate and reproducible computed algorithm demonstrated significant decrease in the abundance of bubbles along SB CE recordings, with a marked effect in the last quartile, in patients for whom simethicone had been added in PEG-based preparations, compared to those without simethicone.

Resumen La gastroenteropatía exudativa es una pérdida anormal de proteínas plasmáticas (en particular albúmina) a través del tracto digestivo. Puede sospecharse en presencia de hipoalbuminemia complicada en ocasiones por edemas o incluso anasarca y sin proteinuria. Los diagnósticos difíciles pueden establecerse mediante la demostración de un aumento de la excreción fecal de alfa-1-antitripsina. Las causas son múltiples (enteritis y colitis de cualquier etiología, enfermedades sistémicas, tumores, etc.). La búsqueda de estas causas consiste en utilizar la exploración física (signos asociados y características del paciente) y las pruebas complementarias (en particular, el hemograma completo, las endoscopias y la tomografía computarizada) para identificar un obstáculo linfático, ulceraciones de la mucosa digestiva o un aumento de la permeabilidad intestinal sin ninguna lesión evidente. El mejor tratamiento es el de la causa. El tratamiento sintomático se basa en la administración de albúmina, a veces en una dieta baja en grasas y en la anticoagulación.

Riassunto Una gastroenteropatia essudativa è una perdita anomala di proteine plasmatiche (soprattutto albumina) attraverso il tratto digestivo. Si può sospettare in presenza di ipoalbuminemia eventualmente complicata da edema o anche anasarca e senza proteinuria. Le diagnosi difficili possono essere fatte mettendo in evidenza un aumento della clearance fecale dell’alfa-1-antitripsina. Le cause sono numerose (enteriti e coliti di ogni origine, malattie sistemiche, tumori, ecc.). La loro ricerca consiste, attraverso la clinica (segni associati e stato di salute) e gli esami complementari (soprattutto emocromo con formula leucocitaria, endoscopia e tomografia computerizzata), nell’identificare un ostacolo linfatico, delle ulcerazioni della mucosa digestiva o un aumento della permeabilità intestinale senza lesioni evidenti. Il miglior trattamento è quello della causa. Il trattamento sintomatico si basa sulla somministrazione di albumina, a volte su una dieta povera di grassi e sull’anticoagulazione.