High Degree of Practice Variability in Colonic Dysplasia Surveillance for Patients With Inflammatory Bowel Disease.
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ABSTRACT:
SUBMITTER: Lewis JD
PROVIDER: S-EPMC9340525 | biostudies-literature | 2022 Aug
REPOSITORIES: biostudies-literature
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High Degree of Practice Variability in Colonic Dysplasia Surveillance for Patients With Inflammatory Bowel Disease.
Lewis James D JD Cross Raymond K RK Long Millie M Singh Siddharth S Herfarth Hans H Weiss Alexandra A Buchner Anna A
Inflammatory bowel diseases 20220801 8
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Project description:BackgroundThe development of chromoendoscopy (CE) and high definition endoscopy (HDE) has improved detection of subtle colonic dysplasia in patients with inflammatory bowel diseases (IBDs). The role of random biopsies for dysplasia surveillance is unclear.MethodsWe reviewed patients with IBD who underwent a CE or HDE colonoscopy and had colonic dysplasia detected. Detection of dysplasia was classified as either visible or random and graded as low grade dysplasia (LGD), high grade dysplasia (HGD), or indefinite for dysplasia. Multivariable regression adjusted for relevant confounders examined the predictors of dysplasia detectable on random biopsies alone.ResultsThe study included 300 patients (203 ulcerative colitis, 97 Crohn's disease with colonic involvement) contributing 442 colonoscopies; the mean disease duration was 24.5 years; 7.2% had primary sclerosing cholangitis (PSC). Three hundred sixty-two colonoscopies (82%) had only visible dysplasia, 52 (12%) had only random dysplasia, and 28 (6%) had both visible and random dysplasia. Longer disease duration (odds ratio, 1.04; 95% CI, 1.01-1.07), active inflammation (odds ratio, 2.89; 95% CI, 1.26-6.67), and concomitant PSC (odds ratio, 3.66; 95% CI, 1.21-11.08) were associated with detecting dysplasia on random biopsies compared with visible lesions. Patients with random dysplasia (21%) or both random and visible dysplasia (21%) were more likely to undergo surgical resection compared with those with only visible dysplasia (5%; P < 0.001) and have subsequent development of colorectal cancer (15%, 7%, 1%, respectively; P < 0.0001).ConclusionNearly one fifth of dysplasia detected in patients with IBD was found on random biopsies. Patients with high risk characteristics may benefit from continuing the practice of random biopsies during surveillance examinations.
| S-EPMC8128394 | biostudies-literature
Project description:BackgroundIn inflammatory bowel disease (IBD), many scenarios call for fecal diversion, leaving behind defunctionalized bowel. The theoretical risk of colorectal cancer (CRC) in this segment is frequently cited as a reason for resection. To date, no studies have characterized the incidence of neoplasia in the diverted colorectal segments of IBD patients.MethodsA retrospective cohort analysis was conducted for IBD patients identified through a tertiary care center pathology database. Patients that had undergone colorectal diversion and were diverted for ≥ 1 year were included. Incidence of diverted dysplasia/CRC was calculated for Crohn's disease (CD) and ulcerative colitis (UC) with respect to diverted patient-years (dpy) and patient-years of disease (pyd).ResultsIn total, 154 patients comprising 754 dpy and 1984 pyd were analyzed. Only 2 cases of diverted colorectal dysplasia (CD 1, UC 1) and 1 case of diverted CRC (UC) were observed. In the UC cohort (n = 75), the rate of diversion-associated CRC was 4.5 cases/1000 dpy (95% CI 0.11-25/1000) or 1.5 cases/1000 pyd (95% CI 0.04-8.2/1000). In the CD cohort (n = 79), no patients developed CRC, although a dysplasia rate of 1.9 cases/1000 dpy (95% CI 0.05-11/1000) or 0.77 cases/1000 pyd (95% CI 0.02-4.3/1000) was observed. All patients developing neoplasia had disease duration > 10 years and microscopic inflammation.ConclusionsDiverted dysplasia occurred infrequently with rates overlapping those reported in registries for IBD-based rectal cancers. Neoplasia was undetected in patients with < 10 pyd, regardless of diversion duration, suggesting low yield for endoscopic surveillance before this time.
| S-EPMC5974732 | biostudies-literature
Project description:Background and aimsThe long-term risk of high-grade dysplasia [HGD] and colorectal cancer [CRC] following low-grade dysplasia [LGD] in inflammatory bowel disease [IBD] patients is relatively unknown. We aimed to determine the long-term cumulative incidence of advanced neoplasia [HGD and/or CRC], and to identify risk factors for advanced neoplasia in a nationwide IBD cohort with a history of LGD.MethodsThis is a nationwide cohort study using data from the Dutch National Pathology Registry [PALGA] to identify all IBD patients with LGD between 1991 and 2010 in the Netherlands. Follow-up data were collected until January 2016. We determined the cumulative incidence of advanced neoplasia and identified risk factors via multivariable Cox regression analysis.ResultsWe identified 4284 patients with colonic LGD with a median follow-up of 6.4 years after initial LGD diagnosis. The cumulative incidence of subsequent advanced neoplasia was 3.6, 8.5, 14.4 and 21.7%, after 1, 5, 10 and 15 years, respectively. The median time to develop advanced neoplasia after LGD was 3.6 years. Older age [≥ 55 years] at moment of LGD (hazard ratio [HR] 1.73, 95% confidence interval [CI] 1.44-2.06), male sex [HR 1.33, 95% CI 1.10-1.60], and follow-up at an academic [vs non-academic] medical centre [HR 1.37, 95% CI 1.07-1.76] were independent risk factors for advanced neoplasia following LGD.ConclusionsIn a large nationwide cohort with long-term follow-up of IBD patients with LGD, the cumulative incidence of advanced neoplasia was 21.7% after 15 years. Older age at LGD [≥55 years], male sex and follow-up by a tertiary IBD referral centre were independent risk factors for advanced neoplasia development after initial LGD.
| S-EPMC6903794 | biostudies-literature
Project description:BackgroundInflammatory bowel disease (IBD) incidence has been increased in Iran as a developing country. Surveillance is a standard method for accessing valid data about disease epidemiology to make relevant decisions for disease control, prevention, and management. We designed Isfahan IBD Surveillance Project (IISP) to make a surveillance system in this area.MethodsThe project is designed in 3 phases. At the first phase, a model of step-wise approach (core, expanded core, and optional variables) for IBD surveillance was designed and implemented among IBD patients registered at a major referral gastrointestinal diseases clinic in Isfahan. Data bank program and its software were designed with suitable and multifunctional features. A total of 352 IBD cases were registered to data bank and analyzed as a pilot study of IISP.ResultsA total of 352 IBD patients, including 245 ulcerative colitis (UC), 80 Crohn's disease (CD), and 27 indeterminate colitis, were registered to the data bank. Bloody stool and abdominal cramp were the most common presentation symptom among UC and CD, respectively. Extensive pancolitis was the most prevalent phenotype (40%) of UC. Over two-thirds of our IBD patients were in remission states. Biologic agents had been prescribed in about 10% of patients during disease. Primary sclerosing cholangitis was detected in about 7% and 10% of CD and UC patients, respectively.ConclusionsValid data from a standard surveillance system are a relevant, trustworthy tool for making decision by health policy-makers. Integrated comprehensive interventional programs for disease control and management is the second phase of IISP.
| S-EPMC6852201 | biostudies-literature
Project description:Interventions: This is a back-to-back crossover tandem colonoscopy study comparing the Endocuff device and standard care (high definition white light endoscopy with chromoendoscopy) compared with standard care alone for dysplasia surveillance in patients with inflammatory bowel disease. The Endocuff device is a small cap that attaches to the end of a standard colonoscope. Small, soft, finger-like projections extend from this cap on withdrawal of the colonoscope with the aim of flattening mucosal folds, anchoring the colonoscope and thus improving rate of dysplasia detection. The colonoscopies will be performed by endoscopists with training and experience in performing dye-spray chromoendoscopy, interventional endoscopy and who have had previous experience using the Endocuff device. All patients will receive two passes with the colonoscopy (one standard, and one with Endocuff) during the same anaesthetic, on the same day. Approximate length of each procedure will be about 15-20 minutes with a few minutes between crossover. This will occur at an endoscopy suite within Eastern Health. Follow-up will be via phone call at days 1, 7 and 21 post-procedure.
Primary outcome(s): Dysplastic lesion miss rate: as defined as the number of lesions detected on the second colonoscopy which was missed during the first colonoscopy (regardless of Endocuff use or standard colonoscopy)[During colonoscopy];Dysplasia detection rate: as defined as the number of participants with one or more dysplastic lesions (adenomas with low-grade dyspalasia, adenomas with high-grade dysplasia, carcinoma insitu, invasive carcinoma)[During colonoscopy and confirmation with histology after colonoscopy]
Study Design: Purpose: Prevention; Allocation: Randomised controlled trial; Masking: Open (masking not used);Assignment: Crossover;Type of endpoint: Safety/efficacy
| 2466130 | ecrin-mdr-crc
Project description:Inflammatory Bowel Disease (IBD) is characterized by chronic inflammation of the gastrointestinal tract that associates with, among others, increased risk of colorectal cancer. There is a growing evidence that miRNAs have important roles in pathological processes, such as inflammation or carcinogenesis. Understanding the molecular mechanisms such as alterations in microRNAome upon chronic intestinal inflammation is critical for understanding the exact pathomechanism of IBD. Hence, we conducted a genome wide microRNAome analysis by applying miRNA-Seq in a rat model of experimental colitis, validated the data by QPCR, examined the expression of a selection of precursor and mature miRNAs, performed in depth biological interpretation using Ingenuity Pathway Analysis and tested the obtained results on samples derived from human patients. We identified specific, interdependent expression pattern of activator/repressor transcription factors, miRNAs and their direct targets in the inflamed colon samples. Particularly, decreased expression of the miR-200 family members (miR-200a/b/c,-141, and -429) and miR-27b correlates with the reduced level of their enhancers (HNF1B, E2F1), elevated expression of their repressors (ZEB2, NFKB1) and increased expression of their target genes (ZEB2, RUNX1). Moreover, the marked upregulation of six miR-27b target genes (IFI16, GCA, CYP1B1, RUNX1, MEF2C and MMP13) in the inflamed colon tissues is a possible direct consequence of the lack of repression due to the downregulated miRNA-27b expression. Our data indicate that changes in microRNAome are associated with the pathophysiology of IBD, consequently, microRNAs offer potential targets for the diagnosis, prognosis and treatment of IBD.
| S-EPMC9513375 | biostudies-literature
Project description:Inflammatory bowel disease (IBD) is an immunoinflammatory illness of the gut initiated by an immune response to bacteria in the microflora. The resulting immunopathogenesis leads to lesions in epithelial lining of the colon through which bacteria may infiltrate the tissue causing recurring bouts of diarrhea, rectal bleeding, and malnutrition. In healthy individuals such immunopathogenesis is avoided by the presence of regulatory cells that inhibit the inflammatory pathway. Highly relevant to the search for treatment strategies is the identification of components of the inflammatory pathway that allow regulatory mechanisms to be overridden and immunopathogenesis to proceed. In vitro techniques have identified cellular interactions involved in inflammation-regulation crosstalk. However, tracing immunological mechanisms discovered at the cellular level confidently back to an in vivo context of multiple, simultaneous interactions has met limited success. To explore the impact of specific interactions, we have constructed a system of 29 ordinary differential equations representing different phenotypes of T-cells, macrophages, dendritic cells, and epithelial cells as they move and interact with bacteria in the lumen, lamina propria, and lymphoid tissue of the colon. Simulations revealed the positive inflammatory feedback loop formed by inflammatory M1 macrophage activation of T-cells as a driving force underlying the immunopathology of IBD. Furthermore, strategies that remove M1 from the site of infection, by either (i) increasing its potential to switch to a regulatory M2 phenotype or (ii) increasing the rate of reversion (for M1 and M2 alike) to a resting state, cease immunopathogenesis even as bacteria are eliminated by other inflammatory cells. Based on these results, we identify macrophages and their mechanisms of plasticity as key targets for mucosal inflammation intervention strategies. In addition, we propose that the primary mechanism behind the association of PPARgamma mutation with IBD is its ability to mediate the M1 to M2 switch.
| S-EPMC2878745 | biostudies-literature
Project description:Intestinal mesenchymal cells play essential roles in epithelial homeostasis, matrix remodeling, immunity, and inflammation. But the extent of heterogeneity within the colonic mesenchyme in these processes remains unknown. Using unbiased single-cell profiling of over 16,500 colonic mesenchymal cells, we reveal four subsets of fibroblasts expressing divergent transcriptional regulators and functional pathways, in addition to pericytes and myofibroblasts. We identified a niche population located in proximity to epithelial crypts expressing SOX6, F3 (CD142), and WNT genes essential for colonic epithelial stem cell function. In colitis, we observed dysregulation of this niche and emergence of an activated mesenchymal population. This subset expressed TNF superfamily member 14 (TNFSF14), fibroblastic reticular cell-associated genes, IL-33, and Lysyl oxidases. Further, it induced factors that impaired epithelial proliferation and maturation and contributed to oxidative stress and disease severity in vivo. Our work defines how the colonic mesenchyme remodels to fuel inflammation and barrier dysfunction in IBD.
| S-EPMC6176871 | biostudies-literature
Project description:Background & aimsLittle is known about the clinical significance of indefinite dysplasia (IND) in patients with inflammatory bowel diseases (IBD) undergoing colonoscopic surveillance for colorectal neoplasia.MethodsWe conducted a retrospective cohort analysis of 492 patients with colonic IBD for 8 or more years or concomitant primary sclerosing cholangitis, with no history of advanced colorectal neoplasia (high-grade dysplasia or colorectal cancer) or colectomy, undergoing colorectal neoplasia surveillance at a tertiary IBD referral center from 2001 through 2017. Subjects received consistent histopathologic grading of dysplasia. We collected data on time to development of (advanced) colorectal neoplasia or colectomy using Kaplan Meier methods. We identified factors independently associated with (advanced) colorectal neoplasia with multivariable Cox regression analysis.ResultsAfter 2149 person-years of follow-up, 53 patients (10.8%) received a diagnosis of IND without prior or synchronous low-grade dysplasia (LGD). Compared to patients without dysplasia, patients with IND had a significantly higher risk of advanced colorectal neoplasia (adjusted hazard ratio, 6.85; 95% CI, 1.78-26.4) and colorectal neoplasia (adjusted hazard ratio, 3.25; 95% CI, 1.50-7.05), but not colectomy (P = .78). Compared to IND, LGD was associated with a significantly higher risk of advanced colorectal neoplasia (P = .05). Following a diagnosis of no dysplasia, IND only, or LGD, the incidence rates of advanced colorectal neoplasia were 0.4% per patient-year, 3.1% per patient-year, and 8.4% per patient-year, respectively.ConclusionsIn a retrospective analysis of patients with IBD undergoing colorectal neoplasia surveillance with consistent histopathologic grading of dysplasia, IND was independently associated with a significant increase in risk of advanced colorectal neoplasia. These findings require validation and if confirmed, a reappraisal of the colorectal neoplasia surveillance guidelines.
| S-EPMC7354098 | biostudies-literature
Project description:Microarrays were used to analyze the gene expression in endoscopic-derived intestinal mucosal biopsies from patients with inflammatory bowel disease (IBD) and controls Mucosal biopsies were obtained at endoscopy from the colon of 97 ulcerative colitis (UC), 8 Crohn's disease (CD) patients and 11 controls. The biopsies were taken at the most affected sites but at a distance of ulcerations. Disease activity was endoscopically assessed. Total RNA extracted from mucosal biopsies was used to analyze mRNA expression via Affymetrix Human Gene 1.0 ST arrays
2015-05-27 | E-GEOD-59071 | biostudies-arrayexpress