scholarly journals OP14 Adenomas in patients with inflammatory bowel disease: Increased risk of advanced neoplasia

2012 ◽  
Vol 6 ◽  
pp. S7
Author(s):  
F. van Schaik ◽  
E. Mooiweer ◽  
M. van der Have ◽  
T. Belderbos ◽  
F. ten Kate ◽  
...  
2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S307-S308
Author(s):  
M De Jong ◽  
S Vos ◽  
I Nagtegaal ◽  
Y van Herwaarden ◽  
L Derikx ◽  
...  

Abstract Background The presence of serrated lesions (SLs) is an established risk factor for colorectal neoplasia development in the general population. However, the impact of SLs on the colorectal neoplasia risk in inflammatory bowel disease (IBD) patients is unknown. In addition, SLs might have been misclassified in IBD patients in the past, in part due to revisions of classification systems. Presently, SLs are categorised as hyperplastic lesions, sessile SLs, and traditional serrated adenomas. We aimed (1) to compare the colorectal neoplasia risk in IBD patients with SLs vs. IBD patients without SLs, and 2) to study the subclassification of SLs in IBD patients before and after histopathological review by two expert gastrointestinal pathologists. Methods We identified all IBD patients with colonic SLs from 1996 to 2019 in a tertiary referral centre using the local histopathology database. Patients with neoplasia prior to SL diagnosis were excluded. Clinical data from patients’ charts were retrieved until June 2019. A subgroup of 135 SLs was reviewed by two pathologists. The log-rank analysis was used to compare the cumulative (advanced) neoplasia incidence in IBD patients with SL vs. IBD patients without SL undergoing surveillance in the same time period. Patients were censored at the end of surveillance or at colectomy. Results We identified 376 SLs in 204 IBD patients (61.9% ulcerative colitis (UC)). In the original reports, 91.9% was classified as a hyperplastic lesion. After histopathological review, 120/136 (88%) of the SLs were confirmed (16 were no SL). Of the 120 confirmed SLs, 62.2% was classified as a sessile SL, 37.8% as a hyperplastic lesion, and 0.8% as a traditional serrated adenoma. The mean time from IBD diagnosis to the first serrated lesion was 14.3 ( ± 12.3) years. A total of 41/204 (20.0%) of patients developed neoplasia (3 CRC, 3 HGD, and 35 LGD; including 2 HGD and 17 LGD at the moment of serrated lesion detection). In the 304 patients without SL (52.6% UC), 63 developed neoplasia (20.7%; 8 CRC, 5 HGD and 50 LGD). Patients who received follow-up colonoscopies after SL (n = 127) had an increased cumulative risk of neoplasia (p < 0.01), but no increased risk of advanced neoplasia (p = 0.50) compared with the group of IBD patients without SL (Figure 1). Conclusion The presence of SLs in IBD patients was associated with a relatively high risk of synchronous colorectal neoplasia as well as an increased risk of subsequent neoplasia, although not with an increased risk of advanced neoplasia. Histopathological review confirmed the SL diagnosis in the majority of lesions, although a large proportion of the hyperplastic lesions was reclassified as a sessile SL.


2013 ◽  
Vol 19 (2) ◽  
pp. 342-349 ◽  
Author(s):  
Fiona D.M. van Schaik ◽  
Erik Mooiweer ◽  
Mike van der Have ◽  
Tim D.G. Belderbos ◽  
Fiebo J.W. ten Kate ◽  
...  

2019 ◽  
Vol 156 (6) ◽  
pp. S-859
Author(s):  
Michiel E. de Jong ◽  
Heleen Kanne ◽  
Loes Nissen ◽  
Iris D. Nagtegaal ◽  
Joost Drenth ◽  
...  

2019 ◽  
Vol 13 (Supplement_1) ◽  
pp. S073-S074
Author(s):  
M de Jong ◽  
H Kanne ◽  
L Nissen ◽  
I Nagtegaal ◽  
J Drenth ◽  
...  

2012 ◽  
Vol 142 (5) ◽  
pp. S-638
Author(s):  
Erik Mooiweer ◽  
Fiona D. van Schaik ◽  
Mike V. Have ◽  
Tim D. Belderbos ◽  
Fiebo J. ten Kate ◽  
...  

2020 ◽  
Vol 8 (Suppl 3) ◽  
pp. A38-A38
Author(s):  
Shilpa Ravindran ◽  
Heba Sidahmed ◽  
Harshitha Manjunath ◽  
Rebecca Mathew ◽  
Tanwir Habib ◽  
...  

BackgroundPatients with inflammatory bowel disease (IBD) have increased risk of developing colorectal cancer (CRC), depending on the duration and severity of the disease. The evolutionary process in IBD is driven by chronic inflammation leading to epithelial-to-mesenchymal transition (EMT) events in colonic fibrotic areas. EMT plays a determinant role in tumor formation and progression, through the acquisition of ‘stemness’ properties and the generation of neoplastic cells. The aim of this study is to monitor EMT/cancer initiating tracts in IBD in association with the deep characterization of inflammation in order to assess the mechanisms of IBD severity and progression towards malignancy.Methods10 pediatric and 20 adult IBD patients, admitted at Sidra Medicine (SM) and Hamad Medical Corporation (HMC) respectively, have been enrolled in this study, from whom gut tissue biopsies (from both left and right side) were collected. Retrospectively collected tissues (N=10) from patients with malignancy and history of IBD were included in the study. DNA and RNA were extracted from fresh small size (2–4 mm in diameter) gut tissues using the BioMasher II (Kimble) and All Prep DNA/RNA kits (Qiagen). MicroRNA (miRNA; N=700) and gene expression (N=800) profiling have been performed (cCounter platform; Nanostring) as well as the methylation profiling microarray (Infinium Methylation Epic Bead Chip kit, Illumina) to interrogate up to 850,000 methylation sites across the genome.ResultsDifferential miRNA profile (N=27 miRNA; p<0.05) was found by the comparison of tissues from pediatric and adult patients. These miRNAs regulate: i. oxidative stress damage (e.g., miR 99b), ii. hypoxia induced autophagy; iii. genes associated with the susceptibility to IBD (ATG16L1, NOD2, IRGM), iv. immune responses, such as TH17 T cell subset (miR 29). N=6 miRNAs (miR135b, 10a196b, 125b, let7c, 375) linked with the regulation of Wnt/b-catenin, EM-transaction, autophagy, oxidative stress and play role also in cell proliferation and mobilization and colorectal cancer development were differentially expressed (p<0.05) in tissues from left and right sides of gut. Gene expression signature, including genes associated with inflammation, stemness and fibrosis, has also been performed for the IBD tissues mentioned above. Methylation sites at single nucleotide resolution have been analyzed.ConclusionsAlthough the results warrant further investigation, differential genomic profiling suggestive of altered pathways involved in oxidative stress, EMT, and of the possible stemness signature was found. The integration of data from multiple platforms will provide insights of the overall molecular determinants in IBD patients along with the evolution of the disease.Ethics ApprovalThis study was approved by Sidra Medicine and Hamad Medical Corporation Ethics Boards; approval number 180402817 and MRC-02-18-096, respectively.


2021 ◽  
Vol 14 ◽  
pp. 175628482110202
Author(s):  
Kanika Sehgal ◽  
Devvrat Yadav ◽  
Sahil Khanna

Inflammatory bowel disease (IBD) is a chronic disease of the intestinal tract that commonly presents with diarrhea. Clostridioides difficile infection (CDI) is one of the most common complications associated with IBD that lead to flare-ups of underlying IBD. The pathophysiology of CDI includes perturbations of the gut microbiota, which makes IBD a risk factor due to the gut microbial alterations that occur in IBD, predisposing patients CDI even in the absence of antibiotics. Superimposed CDI not only worsens IBD symptoms but also leads to adverse outcomes, including treatment failure and an increased risk of hospitalization, surgery, and mortality. Due to the overlapping symptoms and concerns with false-positive molecular tests for CDI, diagnosing CDI in patients with IBD remains a clinical challenge. It is crucial to have a high index of suspicion for CDI in patients who seem to be experiencing an exacerbation of IBD symptoms. Vancomycin and fidaxomicin are the first-line treatments for the management of CDI in IBD. Microbiota restoration therapies effectively prevent recurrent CDI in IBD patients. Immunosuppression for IBD in IBD patients with CDI should be managed individually, based on a thorough clinical assessment and after weighing the pros and cons of escalation of therapy. This review summarizes the epidemiology, pathophysiology, the diagnosis of CDI in IBD, and outlines the principles of management of both CDI and IBD in IBD patients with CDI.


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