Introduction

This study looks at the profile of Crohn's patients who have been on at least 3 different advanced treatments, such as tumour necrosis factor inhibitors (TNFi), integrin blockers and IL12/23 inhibitors.

Aims & Methods

Objective: The purpose of this study was to evaluate the profile of Crohn’s disease patients who are in the 3^rd or 4^th line of an advanced treatment and to consider whether patients may be likely to switch to a different treatment.
Methodology: In both Q1 and Q3 2023, ~200 gastroenterologists from France, Italy, Germany, Spain, and the UK contributed ~1200 anonymous patient record forms for individuals receiving advanced therapy for Crohn’s Disease. All the forms were collected through the Therapy Watch IBD (UC and Crohn’s) online survey by Research Partnership. The survey has been conducted with similar numbers of gastroenterologists for 3 years at regular intervals. Informed consent from physicians was obtained. Where relevant, statistical comparisons were performed using a pairwise z-test.
In addition, Research Partnership has conducted research with 138 Crohn’s disease patients through their Living With Crohn’s EU5 survey. Quantitative online interviews were conducted with patients who were currently on an advanced treatment for Crohn’s.

Results

Of all the Crohn’s disease patient record forms collected in the Therapy Watch survey in 2023, 104 patients were on their 3^rd or 4^th line of advanced treatment.
The majority of 3^rd or 4^th line patients were on a non TNFi treatment, such as an integrin blocker or an IL12/ IL23 inhibitor. ~20% of patients were on a TNFi.
The patients were a mix of male and female, at 44% and 56% respectively, and with a wide age range (42% under 40, 30% aged 41-50 and 28% aged over 50). 42% had suffered with Crohn’s disease for over 10 years. The majority of patients had an existing co-morbidity, most commonly a CV condition or depression.
At the time of the survey, the current severity of Crohn’s was reported by physicians to be: 32% mild, 50% moderate and 18% severe. Approximately a quarter of them also were reported as having flares that are increasing in frequency.
From our Living With Crohn’s survey, out of 138 Crohn’s patients currently on an advanced therapy*, approximately a quarter stated that their flares had increased in the last 6 months, but they have not requested a different treatment from their physician. The reasons for not requesting a new treatment were mainly: patients feel they can still tolerate the symptoms that they experience and they are scared of potential side effects of a different treatment.
* Living With patients include those in any line of advanced treatment, not only 3^rd or 4^th line.

Conclusion

Our data suggests that the majority of 3^rd and 4^th line Crohn’s patients have moderate or severe disease, and therefore may be candidates for a switch to a new treatment as these become available for Crohn’s. 30% of 3^rd and 4^th line Crohn’s disease patients are classified as mild in severity, and this segment appear to have found a level of efficacy at this stage.
Our patient survey (Living With) has shown that even those patients who suffer increasing frequency of Crohn’s symptoms do not feel confident in switching to a different therapy; there is a level of fear of switching.

Introduction

Patients suffering from inflammatory bowel diseases (IBD) manifest an increased risk of developing colitis-associated colon cancer (CAC). Interleukin 22 (IL22) is a cytokine involved in the proliferation and survival of epithelial cells. However, it also correlates with the development of tumoral lesions. IL22 is secreted by different immune cell types, including iNKT cells, tissue resident cells possessing cytotoxic properties in colorectal cancer (CRC). In IBD patients, though, iNKT cells perform both pro-inflammatory or tolerogenic functions in a microbiota-dependent fashion, opening questions on their functional role in CAC development.

Aims & Methods

Immune cell composition and iNKT cell phenotype of inflamed, non-tumor and cancerous tissue lesions of CAC (n=49), IBD (n=20) and sporadic CRC (n=38) patients were analysed in samples obtained from Policlinico Hospital, Milan, and IOV-IRCCS, Padua. High-dimensional single-cell flow cytometry, metagenomics, RNAseq, spatial immunophenotyping and trascriptomic (Cosmx, Nanostring), ex vivo and in vitro experiments were performed to evaluate the phenotype and function of human iNKT cells. Metabolomics was performed to identify microbial-derived molecules involved in iNKT cells activation.Mechanisms were dissected in CAC murine models, either iNKT proficient or deficient.

Results

An increased expression of IL22 and a higher NKT22 infiltration was observed in CAC tissues, as well as an enrichment of Odoribacter, a gram-negative bacteria implicated in tryptophan metabolism. Stimulation of iNKT cells with Odoribacter-derived metabolites induced Ahr-dependent IL22 production by iNKT cells. Metabolomic analyses revealed an increased presence of tryptophan metabolites in the Odoribacter supernatant, promoting NKT22 differentiation both in vitro and in vivo models. Moreover, the administration of Odoribacter Supernatant or of the single purified metabolites were sufficient to increase tumorigenesis in CAC mouse models, but not in iNKT-deficient mice.
Spatial proteomics and trascriptomic analyses of human CAC tissues confirms the microbiota-dependent functional skewing of iNKT cells residing closely to cancer cells.

Conclusion

iNKT cells in CAC patients are the major IL22 producing cells and are induced by the recognition of microbiota-derived metabolites implicated in tryptophan metabolism and Aryl hydrocarbon receptor (AhR) stimulation. NKT22-microbiota interaction in CAC patients plays a potential crucial role in tumor development.

Introduction

Cendakimab is a recombinant, humanized, high-affinity, neutralizing monoclonal antibody that binds to interleukin 13 (IL-13) and blocks interaction with both its receptors, IL-13Rα1 and IL-13Rα2. IL-13 is a cytokine implicated in the pathogenesis of atopic dermatitis (AD) and is thought to be a key driver of the complex pathophysiology of eosinophilic esophagitis (EoE). IL-13 signals through both IL-13Rα1 and IL-13Rα2 to regulate cellular and molecular pathways across a variety of cell types. The binding of IL-13 to IL-13Rα1 promotes a Type 2 immune response and eosinophil recruitment, whereas the binding of IL-13 to IL-13Rα2 is believed to play a role in fibrosis and epithelial tissue remodeling. Several biomarkers associated with Type 2 inflammatory diseases are known to be regulated by IL-13. Eotaxin-3, a key biomarker, plays a central role in attracting eosinophils to the site of inflammation. Periostin, an extracellular matrix protein linked to activated fibroblasts, is implicated in tissue remodeling and fibrosis. Another enzyme governed by IL-13 is matrix metalloproteinase-12 (MMP-12)—this enzyme contributes to tissue remodeling and breakdown of extracellular matrix components. Here, we evaluate the pharmacodynamic effects of IL-13 inhibition with cendakimab on the key serum biomarkers eotaxin-3, periostin, and MMP-12 in patients with AD, with a focus on exploring potential implications for EoE.

Aims & Methods

In this phase 2, multicenter, global, randomized, double-blinded, placebo-controlled, parallel-group study (NCT04800315), 220 adults with moderate-to-severe AD received cendakimab 360 mg Q2W, 720 mg QW, 720 mg Q2W, or placebo for 16 weeks. Blood samples were collected, and a panel of biomarkers were assessed. The current analysis focuses on the assessment of serum levels of eotaxin-3, periostin, and MMP-12 using Proximity Extension Assay pre- and post-treatment on day 1 (baseline), at week 1 and week 2, and then biweekly until week 16. The least square mean percent change from baseline at week 16 for each treatment group was evaluated.

Results

For all 3 doses of cendakimab, there was a significant decrease from baseline in the levels of eotaxin-3, periostin, and MMP-12 as early as week 1 post-treatment and continued through week 16 of cendakimab treatment (Table). Compared with placebo, cendakimab resulted in significantly greater reductions in these biomarker levels through week 16.

Conclusion

Cendakimab decreased levels of key inflammatory and remodeling biomarkers over 16 weeks of treatment in patients with AD. These findings suggest that cendakimab modulates pathways of inflammation, fibrosis, and tissue remodeling in AD and add to the existing clinical evidence of its modulation in other Type 2 inflammatory diseases such as EoE.
​
Table. Least square mean percent change from baseline in key serum biomarker levels at week 16 in patients with AD

Treatment	Eotaxin-3 LS mean percent CFB (95%CI)	Periostin LS mean percent CFB (95%CI)	MMP-12 LS mean percent CFB (95%CI)
Cendakimab 360 mg Q2W	–51.53 (–61.98 to –38.20)*,†	–47.50 (–56.45 to –36.73)*,†	–52.00 (–58.39 to –44.63)*,†
Cendakimab 720 mg QW	–58.20 (–67.29 to –46.59)*,†	–55.76 (–63.31 to –46.67)*,†	–54.72 (–60.83 to –47.65)*,†
Cendakimab 720 mg Q2W	–67.77 (–74.75 to –58.85)*,†	–60.93 (–67.57 to –52.94)*,†	–61.07 (–66.27 to –55.06)*,†
Placebo	–5.80 (–26.63 to 20.94)	–23.92 (–37.15 to –7.90)*	–16.69 (–28.31 to –3.19)*

CFB, change from baseline; CI, confidence interval; LS, least square.
*P < 0.05 versus baseline.
^†P < 0.01 cendakimab versus placebo

Disclosure

ESD served as a consultant for Abbott, Abbvie, Adare/Ellodi, Aimmune, Akesobio, Alfasigma, ALK, Allakos, Amgen, Aqilion, Arena/Pfizer, Aslan, AstraZeneca, Avir, Biorasi, Calypso, Celgene/Receptos/ Bristol Myers Squibb, Celldex, Eli Lilly, EsoCap, Eupraxia, Dr. Falk Pharma, Ferring, GlaxoSmithKline, Gossamer Bio, Holoclara, Invea, Knightpoint, Landos, LucidDx, Morphic, Nexstone Immunology/Uniquity, Nutricia, Parexel/Calyx, Phathom, Regeneron, Revolo, Robarts/Alimentiv, Salix, Sanofi, Shire/Takeda, Target RWE, Upstream Bio, received research funding from Adare/Ellodi, Allakos, Arena/Pfizer, AstraZeneca, Eupraxia, Ferring, GSK, Meritage, Miraca, Nutricia, Celgene/Receptos/ Bristol Myers Squibb, Regeneron, Revolo, Shire/Takeda, and received educational grant from Allakos, Aqilion, Holoclara, and Invea. JL, SH, LG, CDO, and CC are employees and stockholders of Bristol Myers Squibb. JS served as consultant for Abbvie, Alamar, Aldena, Amgen, AObiome, Apollo, Arcutis, Arena, Asana, Aslan, Attovia, BioMX, Biosion, Bodewell, Boehringer-Ingelheim, Bristol Myers Squibb, Cara, Castle Biosciences, Celgene, Connect Biopharma, Corevitas, Dermavant, Eli Lilly, FIDE, Galderma, GlaxoSmithKline, Incyte, Invea, Kiniksa, Leo Pharma, Merck, My-Or Diagnostics, Nektar, Novartis, Optum, Pfizer, RAPT, Recludix, Regeneron, Sandoz, Sanofi-Genzyme, Shaperon, TARGET-RWE, Teva, Union, UpToDate, participated on a data safety monitoring board or advisory board for Biosion and Sanofi, received grants or contracts from Galderma, Incyte, Pfizer, received honoraria from Abbvie, Eli Lilly, Leo Pharma, Pfizer, Regeneron, Sanofi-Genzyme.

Introduction

Crohn’s disease (CD), a variant of inflammatory bowel disease, is a complex, debilitating, chronic and relapsing disorder of the gastrointestinal tract. If poorly controlled, patients are at risk of intestinal obstruction and infection due to the formation of strictures, fistulae and narrowing of the intestinal lumen, often requiring surgical intervention. As the precise aetiology remains unclear, current treatments for CD are limited. An altered composition of native gut microbiota may play a role in CD pathogenesis, with recent faecal microbiota transplantation (FMT) studies revealing variable therapeutic efficacy in CD management. Orally administered Emu Oil, derived from Emu adipose tissue, has demonstrated anti-inflammatory and reparative properties in models of intestinal disease.

Aims & Methods

The current study aimed to determine whether Emu Oil-modulated FMT could reduce disease severity and modulate the gut microbiota in a mouse model of trinitrobenzene sulfonic acid (TNBS)-induced Crohn’s-like colitis. Female ARC(s) mice were assigned to FMT donor (n=5/group) and recipient (n=10/group) groups. Donor mice were orally administered either Water (80μl), Olive Oil (OO) or Emu Oil (160μl) daily (days -7 to 0); fresh faeces were collected (days -1 to 3) and pooled per group. Recipient mice were administered TNBS (3mg; day 0) and donor faecal supernatant (120μl; day 3) intrarectally and euthanised on day 6. Daily bodyweight and disease activity index (DAI), colonoscopically-assessed disease severity, organ weights, intestinal permeability (fluorescein isothiocyanate [FITC]-dextran uptake), histologically-assessed colonic damage (disease severity, crypt depth), intestinal barrier function (mucin-secreting cells), acute inflammation (myeloperoxidase [MPO]) and faecal microbiome (16S rRNA amplicon sequencing) were assessed. p<0.05 was considered statistically significant.

Results

TNBS induced bodyweight loss in all groups, which normalised to day 0 values on the final day of the experimental period. Daily DAI remained elevated throughout the trial in all groups; only Emu Oil FMT normalised DAI on day 6 compared with day 0 (p<0.05). TNBS increased colonoscopically-assessed disease severity scores (p<0.05), with no significant Emu Oil nor OO FMT effect. Emu Oil FMT decreased liver weights and increased small intestinal weights relative to bodyweight, reduced histologically assessed disease severity and increased colonic mucin counts compared with Water and OO FMT (p<0.05). The most abundant genera across all groups were Muribaculaceae, Eisenbergiella and Bacteroides; while alpha and beta diversity, taxonomic profiles, FITC-dextran, crypt depth and MPO activity remained unchanged in all treatment groups (p>0.05).

Conclusion

Emu Oil-modulated FMT improved histologically-assessed indicators of intestinal disease and barrier function, compared with Water FMT and OO FMT. Interestingly, Emu Oil-modulated FMT affected liver and small intestinal organs weights, suggesting a systemic effect in this setting of disease. Importantly, key genera across taxonomic profiles were identified, however, the microbiome and remaining disease indicators were largely unchanged between treatments. Overall, Emu Oil-modulated FMT demonstrates therapeutic potential in CD management. Future studies would benefit from a deeper assessment of the gastrointestinal microbiome through long-read whole genome sequencing to further determine the role of the microbiome in EO FMT efficacy compared with conventional FMT.

Introduction

Endoscopic ultrasound (EUS) has broadened its diagnostic and therapeutic scopes, as it is able to target lesions <3mm. High-frequency radial EUS-miniprobes exhibit procedural time reduction, improving image quality and maneuverability. EndoSound Vision System (EndoSound, Oregon, USA) is a new EUS (N-EUS) portable device that fastens onto a standard gastroscope, enabling a free working channel. It is an affordable alternative to conventional-EUS devices; and a promising opportunity to shorten the difficult EUS learning curve.

Aims & Methods

We aim to determine the feasibility and effectiveness of N-EUS in terms of anatomical structures appropriate identification in comparison with conventional-EUS. This prospective study included patients ≥18 years-old undergoing EUS evaluation in June-November 2023 by eight endoscopists from different institutions from South and North America. Patients underwent two consecutive procedures: First, a conventional EUS with a linear-array echoendoscope (Pentax EG38-J1OUT, Pentax Medical, Germany). Then, a different endoscopist performed EUS using the N-EUS coupled to a video gastroscope with therapeutic access (EG29-i10, Pentax Medical, USA). A post-procedure ad-hoc survey was completed by the second endoscopist, to assess N-EUS acceptability in terms of endoscopists’ experience using this device.

Results

Thirty-one patients underwent conventional EUS and N-EUS: 16/31 performed by first-time N-EUS users, 15/31 by endoscopists with prior N-EUS exposure, with median procedural times of 30 and 15 minutes, respectively (p=.04). Main EUS indication was chronic dyspepsia (35.5%). Identified structures during N-EUS were the liver/gallbladder/common bile duct (30/31, 96.8%), full pancreas (29/31, 93.5%), kidneys/left kidney (24/31, 77%; 13/15 endoscopists with prior exposure vs 11/16 first-time N-EUS users; p<.001), left adrenal gland (20/31, 64.5%). Gallbladder (GB) was unobserved in 8 cases, 7/8 had prior cholecystectomy. Evaluation position was 54.8% supine; 3/31 switched to left lateral. All procedures were completed with 100% clinical and technical success, requiring navigation changes in 51.6%, mainly in first-time N-EUS users (p=.001). FNB tissue sampling was achieved in 100% cases. Endoscopists’ experience was predominantly described as “meeting clinical expectations”. The ad-hoc survey showed high psychometrics, with homogeneity among surveyed endoscopists, without redundancy (Cronbach’s alpha of .91), and a good construct validity (Kaiser-Meyer-Olkin Criterion of .728 and Barlett´s test p-value =.0005). When comparing both procedures, appropriate identification of GB or lack of, full pancreas, left/both kidneys and left adrenal gland was 31/31 vs 30/31, 31/31 vs 29/31, 31/31 vs 24/31 (p=.0233), and 29/31 vs 20/31 (p=.0158), respectively. Considering conventional EUS as a gold standard, the observed agreement of N-EUS to identify these structures were 96.8%, 93.5%, 77.4% and 64.5%, correspondingly. Observed agreement for kidneys and left adrenal gland increased when sub-analyzing the cases assessed by endoscopists with prior N-EUS exposure: 81.2% and 76.9%, respectively.

Conclusion

N-EUS is a safe, effective, and feasible tool for EUS evaluation, with high acceptability by endoscopists. Prior ex-vivo training may be warranted for first-time N-EUS users.

References

1. LeBlanc JK. An overview of endoscopic ultrasound equipment. Minerva Gastroenterol Dietol. 2008 Jun;54(2):177-87. PMID: 18319690 .
2. Varas Lorenzo, M.J., Abad Belando, R. and Sánchez-Vizcaíno Mengual, E. (2018), Miniprobe Endoscopic Sonography for Gastrointestinal Tract Assessment: A Case Series of 1451 Procedures. J Ultrasound Med, 37: 293-303. https://doi.org/10.1002/jum.14330
3. Deprez PH. Choice of endosonographic equipment and normal endosonographic anatomy. Best Pract Res Clin Gastroenterol. 2009;23(5):623-37. doi: 10.1016/j.bpg.2009.07.001 . PMID: 19744628 .

Disclosure

Carlos Robles-Medranda is a key opinion leader and consultant for Pentax Medical, Boston Scientific, Steris, Medtronic, Motus, Micro-tech, G-Tech Medical Supply, CREO Medical, EndoSound, and mdconsgroup. All other authors declare no conflicts of interest.

Introduction

Computer-Aided Diagnosis (CADx) systems have become available to assist endoscopists with optical polyp diagnosis. However, current CADx systems have not been trained to recognize sessile serrated lesions (SSLs) and currently classify SSLs incorrectly either as hyperplastic or adenomatous. We aimed to assess the effect of current CADx systems on diagnostic accuracy of SSL recognition among a diverse group of endoscopists.

Aims & Methods

We conducted a prospective video-based study including 17 endoscopists (gastroenterologists and surgeons, experts, and trainees). Each endoscopist reviewed the same video and image series of 115 polyps (33% SL, 33% Hyperplastic Polyps (HP), 34% tubular adenoma (TA)). Histopathological diagnosis of the polyps was used as the gold standard for comparison. Presentation of polyps (SSL, TA, HP) was randomized so that 50% of the polyps seen were presented with displaying a CADx diagnosis for the polyp and 50% were presented without displaying a CADx diagnosis.

Results

A total of 1955 optical polyp diagnoses were performed. The optical diagnostic accuracy amongst various endoscopists to recognize SSLs was: expert gastroenterologists (52.3%, 95% Confidence Interval (CI) 46.3-58.3), trainee gastroenterologists (38.2%, CI 27.2-49.1), expert surgeons (22.1%, CI 16.2-28.0) and trainee surgeons (14.9%, CI 8.4-21.5). Further details are provided in Table 1. CADx identified 52.6% of SSL as HP and 47.4% as TA. CADx identified 60.5% of HP correctly and 82.1% of TA correctly. The optical diagnostic accuracy for HP and TA improved among endoscopists when a correct CADx diagnosis was displayed to the endoscopists compared to when no CADx information was displayed (HP: 63.7% vs 38.4% / TA: 81.5% vs 70.5%; p=0.05). The optical diagnostic accuracy of the endoscopists worsened when the displayed CADx diagnosis was incorrect (HP: 24% / TA: 25%). The diagnostic accuracy of the endoscopists for SSL did not differ significantly when the CADx diagnosis, which is currently untrained to diagnose SSL and can only classify polyps as hyperplastic or adenomatous, was displayed (37.2% vs 33.1%, p=0.05).

	Sessile Serrated Lesion	Hyperplastic Polyp	Adenoma
CADx Alone	HP: 52.6 (36.8-68.5) TA: 47.4 (31.5-63.2)	Sn 60.5 (49.5-71.5) Sp 82.1 (70.0-94.1) PPV 86.8 (77.7-95.9) NPV 51.6 (39.2-64.1)	Sn 82.1 (70.0-94.1) Sp 60.5 (49.5-71.5) PPV 51.6 (39.2-64.1) NPV 86.8 (77.7-95.9)
CADx diagnosis NOT displayed All Endoscopists (n=17)	Sn 37.2 (31.9-42.4) Sp 78.6 (75.5-81.8) PPV 46.2 (40.1-52.2) NPV 71.7 (68.4-75.0)	Sn 38.4 (33.1-43.7) Sp 79.8 (76.8-82.9) PPV 48.4 (42.3-54.6) NPV 72.4 (69.2-75.7)	Sn 70.5 (65.6-75.4) Sp 64.7 (61.0-68.4) PPV 50.6 (46.1-55.2) NPV 81.0 (77.6-84.4)
CADx Displayed Correct Diagnosis All Endoscopists (n=17)	Sn 33.1 (28.0-38.3) Sp 79.4 (76.3-82.5) PPV 44.2 (38.0-50.5) NPV 70.6 (67.3-73.9)	Sn 63.7 (57.4-70.0) Sp 78.7 (74.9-82.5) PPV 60.2 (53.9-66.4) NPV 81.1 (77.4-84.8)	Sn 81.5 (76.9-86.2) Sp 86.5 (83.2-89.9) PPV 80.7 (76.0-85.3) NPV 87.2 (83.9-90.5)
CADx Displayed Incorrect Diagnosis All Endoscopists (n=17)		Sn 24.0 (15.6-32.4) Sp 77.4 (71.7-83.0) PPV 33.3 (22.4-44.2) NPV 68.3 (62.4-74.2)	Sn 25.0 (14.0-36.0) Sp 45.2 (39.1-51.4) PPV 9.8 (5.1-14.5) NPV 71.7 (64.7-78.7)
Breakdown of the performance by endoscopists category GE: Gastroenterologist Expert (n=7) GT: Gastroenterologist Trainee (n=2) SE: Surgery Expert (n=5) ST: Surgery Trainee (n=3)
Overall	GE: 52.3 (46.3-58.3) GT: 38.2 (27.2-49.1) SE: 22.1 (16.2-28.0) ST: 14.9 (8.4-21.5)	GE: 35.0 (29.2-40.7) GT: 61.8 (50.9-72.8) SE: 53.7 (46.6-60.8) ST: 42.1 (33.0-51.2)	GE: 74.7 (69.6-79.9) GT: 64.1 (53.5-74.7) SE: 66.2 (59.5-72.8) ST: 74.4 (66.4-82.3)
CADx diagnosis NOT displayed	GE: 54.1 (45.7-62.6) GT: 39.5 (23.9-55.0) SE: 23.2 (14.7-31.6) ST: 19.3 (9.1-29.5)	GE: 27.8 (20.2-35.4) GT: 57.9 (42.2-73.6) SE: 53.7 (43.7-63.7) ST: 24.6 (13.4-35.7)	GE: 72.8 (65.3-80.3) GT: 66.7 (51.9-81.5) SE: 70.4 (61.4-79.4) ST: 69.5 (57.7-81.2)
CADx Displayed Correct Diagnosis	GE: 50.4 (41.9-58.9) GT: 36.8 (21.5-52.2) SE: 21.1 (12.9-29.3) ST: 10.5 (2.6-18.5)	GE: 50.6 (40.2-60.9) GT: 84.6 (70.7-98.5) SE: 67.2 (55.9-78.4) ST: 73.2 (59.6-86.7)	GE: 85.0 (78.4-91.5) GT: 75.0 (60.0-90.0) SE: 73.4 (63.7-83.2) ST: 91.5 (83.5-99.5)
CADx Displayed Incorrect Diagnosis		GE: 25.0 (12.2-37.8) GT: 25.0 (0.5-49.5) SE: 21.4 (6.2-36.6) ST: 25.0 (3.8-46.2)	GE: 37.5 (18.1-56.9) GT: 0.0 (0.0-0.0) SE: 16.7 (0.0-33.9) ST: 27.3 (1.0-53.6)

Table 1. CADx and endoscopists performance in optical diagnosis of SSL, HP and adenomas depending on the polyp histology in percentages of correct optical diagnoses with 95% confidence intervals. For SSL, CADx is not able to provide correct diagnosis; thus is presented as CADx shown as either HP or TA)
Sn: sensitivity; Sp: specificity; PPV: positive predictive value; NPV: negative predictive value

Conclusion

Optical polyp diagnosis that includes SSL, TA, and HP recognition remains challenging. Current CADx systems when displaying correct diagnostic outputs improve diagnostic accuracy of the endoscopists. CADx systems not trained for SSL recognition do not significantly affect SSL recognition among endoscopists even if an incorrect diagnostic output (TA or HP) is displayed. Development of improved CADx systems with SSL recognition and higher diagnostic accuracy is warranted.

Disclosure

Dr Jeffrey Marks: Consultant for Boston Scientific and Steris Endoscopy

Introduction

Potential celiac disease (PCD) is a clinical condition characterized by the presence of a positive CD-specific serology and a normal intestinal architecture. Asymptomatic PCD patients are generally addressed to continue on a gluten containing diet (GCD), but long-term risks of this approach have never been explored.

Aims & Methods

In the present study we aim at investigating nutritional and autoimmune complications possibly developing overtime in a cohort of asymptomatic PCD children left on a GCD. We compared parameters of growth, nutritional status, and autoimmunity between time of diagnosis and in occasion of last medical check, after a long-term gluten containing diet.

Results

Altogether we collected data from 171 PCD children with a mean follow-up time of 3 years (range 0.35-15.3 years). During follow-up, despite patients did not reduce the amount of daily gluten intake , anti-tissue transglutaminase (anti-TG2) antibodies spontaneously and significantly decreased. Most of parameters analysed did not change over follow-up (height centile, ferritin, albumin., cholesterol, calcium, alkaline phosphatase , parathormone, vitamin D, p>0.05) or even improved (weight and BMI centile, haemoglobin, blood iron, HDL, glycaemia and HbA1C, p<0.05), always remaining in the limit of normality. Equally autoantibodies for other concomitant autoimmune disorders did not increase overtime. Similar results were obtained excluding from the analysis patients that stopped producing anti-TG2 and those with a follow up < 3 years.

Conclusion

Our pilot study provides reassuring results on the maintenance of a gluten containing diet in asymptomatic PCD children, even when a long term follow-up is considered.

Disclosure

no conflict of interest to declare