“That Was Me” A Patient's Perspective on Flat Lesion in Inflammatory Bowel Disease

The Detection of Flat and Depressed Colorectal Lesions: Which Endoscopic Imaging Approach?

High Resolution Colonoscopy With Chromoscopy Versus Standard Colonoscopy for the Detection of Colonic Neoplasia: A Randomized Study

4485 Incidence of depressed colorectal neoplasia in southern brazil.

The Commensal Microbiota and Enteropathogens in the Pathogenesis of Inflammatory Bowel Diseases

IntroductionPatients with inflammatory bowel disease (IBD) have an increased risk of colorectal cancer. In 2009 the British Society of Gastroenterology updated guidelines recommending chromoendoscopy with targeted biopsies of suspicious areas,...

Background It is uncertain if sessile serrated lesions (SSLs) in patients with inflammatory bowel disease (IBD) represent coincidental sporadic lesions or a distinct biological entity. Molecular studies suggest SSLs in IBD are more frequently KRAS mutated, contrasting with the BRAF driven pathway typical of sporadic SSLs.¹,² More recent data supports a distinct clinicopathologic and molecular profile,3 the understanding of which is critical for optimising surveillance strategies. Methods Colonic serrated lesions from St. Mark’s Hospital pathology database (2014–2022) were reviewed and classified as SSL or dysplastic SSL (SSL-D) and stratified by disease background: IBD, serrated polyposis syndrome (SPS) or sporadic. Cases with overlapping conditions or indeterminate features were excluded. Lesion size, location, patient demographics and IBD subtype and extent were compared. Ethical approval was obtained for this study. Results IBD group: 224 SSLs were identified (200 SSL, 24 SSL-D; dysplasia rate 10.7%). 132 out of 157 patients had ulcerative colitis. No significant differences were seen in lesion location, size or IBD related factors between SSL and SSL-D (Table 1). Median cumulative inflammatory burden for SSL-D was 3.58. SSL-Ds did not show a significant right-sided predominance. SSL-Ds were more frequent in older patients (median 69 vs 60 yrs, p = 0.006). Sporadic group: 5304 SSLs (5030 SSL, 274 SSL-D; dysplasia rate 5.2%) were identified. SSL-Ds were predominantly right-sided and more frequent in older patients (median 68 vs 61 yrs; p < 0.001). SPS group: 4554 SSLs (3662 SSL, 82 SSL-D; dysplasia rate 2.2%) were identified. SSL-Ds were also mainly right-sided and more frequent in older patients (median 64 vs 41 yrs; p < 0.001). The proportion of low to high grade dysplasia was similar across groups (p = 0.32), but dysplasia rates were significantly higher in IBD (p < 0.000001). SSL-Ds occured throughout the IBD colon, lacking the right-sided predominance seen in sporadic or SPS cases (IBD p = 0.3; Sporadic p = <0.001; SPS p = 0.007). Demographically, groups were similar with no significant age difference (p = 0.058). Conclusion SSLs in IBD show a significantly higher dysplasia rate than those in SPS or sporadic cases, despite similar demographic and morphologic features. SSL-Ds in IBD were more likely to be found throughout the colon compared with the typical right sided dominance seen in SPS and sporadic cases. Traditional risk factors for advanced neoplasia, including disease duration and extent, did not distinguish dysplastic from non-dysplastic SSLs in IBD, although small numbers of SSL-D may underestimate significant findings. Further clinical and molecular investigation is needed to clarify the unexpectedly high dysplasia rate in IBD associated SSLs.

Patient-reported outcomes are essential in determining the broad impact of inflammatory bowel disease (IBD) and treatments from the patient's perspective. The primary study objectives were to compare the gastrointestinal symptoms and worry of pediatric patients with IBD with matched healthy controls and to compare Crohn's disease and ulcerative colitis with each other using the Pediatric Quality of Life Inventory (PedsQL) Gastrointestinal Symptoms and Gastrointestinal Worry Scales. PedsQL Gastrointestinal Symptoms and Worry Scales were completed in a 9-site study by 256 pediatric patients with IBD and 259 parents of patients (263 families; Crohn's disease [n = 195], ulcerative colitis [n = 68]). Ten Gastrointestinal Symptoms Scales measuring stomach pain, stomach discomfort when eating, food and drink limits, trouble swallowing, heartburn and reflux, nausea and vomiting, gas and bloating, constipation, blood in poop, and diarrhea were administered along with 2 Gastrointestinal Worry Scales. A matched group of 384 healthy children families completed the PedsQL in an Internet survey. PedsQL Gastrointestinal Symptoms and Worry Scales distinguished between pediatric patients with IBD in comparison with healthy controls (P < 0.001), with larger effect sizes for symptoms indicative of IBD, supporting known-groups validity and clinical interpretability including minimal important difference scores. Patients with Crohn's disease or ulcerative colitis did not demonstrate significantly different gastrointestinal symptoms or worry in comparison with each other. The PedsQL Gastrointestinal Symptoms and Worry Scales may be used as common metrics across pediatric patients with IBD, including Crohn's disease and ulcerative colitis separately to measure gastrointestinal-specific symptoms in clinical research and practice.

INTRODUCTION: Hepatocellular Carcinoma (HCC) commonly occurs in patients with Cirrhosis and Hepatitis B. Inflammatory Bowel Disease (IBD) is well known to be associated with intestinal malignancy like colon cancer and extra intestinal malignancy such as Cholangiocarcinoma. There are few case reports showing increased risk of HCC among patients with IBD, but larger studies are lacking so we aim to study association between HCC and IBD in a nationwide database. METHODS: We performed data analysis on Nationwide readmissions Database (NRD) from year 2010 through 2014. We compared hospitalized adult patients with IBD and HCC with patients with IBD alone. Patients with liver disease and primary sclerosing cholangitis were excluded from analysis. Univariate analysis was done for categorical data using chi-square or fisher's exact test while continuous data were analyzed using t-test. Multivariate logistic regression analysis was performed to look for factors associated with HCC in patients with IBD and factors associated with mortality. RESULTS: There were total of 939224 weighted admissions with IBD and 350(180 Ulcerative Colitis, 170 Crohn's Disease) admissions with both IBD + HCC. In Univariate Analysis, male gender, age more than 50, higher CCI (Charlson's Comorbidity Index) were significantly more in IBD+HCC group. Mean total Charges (58177 USD vs 44201 USD, P &lt; 0.001) and in hospital mortality (3.2% vs 1.4%, P &lt; 0.0001) were significantly higher in IBD + HCC group (Table 1). Multivariate analysis showed that significantly more patients with IBD + HCC group were male (Odds Ratio (OR) 2.9, P &lt; 0.0001) but significantly less patients in IBD + HCC group were having diabetes (OR 0.51, P 0.0002). Among IBD patients, male gender (OR 1.15, P 0.001), age more than 50 (OR 11, P 0.0001), renal failure (OR 3.3, P 0.001) and higher CCI (OR 3.1, P 0.0001) were associated with higher in hospital mortality in multivariate analysis. CONCLUSION: HCC does co-exist in about 0.04% patients with IBD. There is no clear pathophysiology of developing HCC among patients with IBD. One theory is development of HCC due to IBD itself altering gut microbiome and causing passage of harmful bacteria to portal circulation which causes abnormal expression of cell adhesion molecules in liver causing immune mediated damage to liver. Another mechanism is development of HCC due to immunomodulating effect of medications like Azathioprine in treatment of IBD. There is need of more research to find factors associated HCC development among IBD patients.

Background Therapeutic drug monitoring and pharmacokinetic modeling, implemented in the treatment of patients with inflammatory bowel disease (IBD), improve drug efficacy and reduce side effects. Recently, Ustekinumab (UST) levels associated with therapeutic targets have been established, principally during induction, highlighting the need for appropriate optimization of this phase to improve response to UST treatment. Objectives To evaluate the effectiveness of proactive dose optimization of UST using pharmacokinetic modeling during induction (target concentration at week 8) in the treatment of IBD with UST. Methods A prospective comparative study was conducted on IBD patients initiating UST treatment, divided into two groups: standard induction protocol (initial intravenous UST dose adjusted to weight) or optimized induction protocol (following the initial weight-adjusted intravenous UST dose, UST levels were measured at 4 weeks and, using a pharmacokinetic model—including weight, height, and serum albumin levels—induction dosing was adjusted). UST plasma concentration was measured by FIA at 4 weeks in the optimized group and at 8 weeks from treatment initiation in all patients. Data on IBD and the clinical status of patients at UST treatment initiation were reviewed. Results A total of 88 patients were included: 72 in the standard protocol group (male 52.8%; Crohn's disease 59.2%; prior biologic use 95.8%; fecal calprotectin &amp;gt;150 g/kg 61.5%) and 16 in the optimized group (male 56.3%; Crohn's disease 68.8%; prior biologic use 93.88%; fecal calprotectin &amp;gt;150 g/kg 68.8%), with no significant differences in baseline characteristics between groups. The mean UST concentration at the end of induction (8 weeks) was significantly higher in patients with optimization via pharmacokinetic model compared to the standard protocol (15.4 [10.4-20.3] µg/ml vs 9.2 [7.7-10.7] µg/ml; p&amp;gt;0.0018) (Fig. A). In the optimized group, 6 patients (37.5%) received additional intravenous UST doses (3 patients received 1 dose and 3 patients received 2 doses before week 8). The percentage of patients achieving a UST concentration ≥ 6.6 µg/ml (linked to biochemical remission at weeks 12 and 24) and ≥ 9 µg/ml (associated with treatment durability ≥ 12 months) was significantly higher in the optimized group compared to those on the standard protocol (Figs. B and C). Conclusion Optimized UST treatment, through proactive dose adjustment based on pharmacokinetic modeling, achieves a target UST concentration during induction that should ensure treatment efficacy.

Covering the Cover

Purpose: Currently patients with primary sclerosing cholangitis (PSC) and inflammatory bowel disease (IBD) are advised to undergo colon cancer screening with colonoscopy on an annual basis with little evidence to support this approach. The aims of our study were 1) to determine the timing of development of colonic neoplasms in patients with PSC and IBD and 2) to describe the location and type of colonic neoplasms seen in this patient population. Methods: A computerized database was searched for patients with PSC, IBD, and colon cancer or dysplasia seen at the Mayo Clinic Rochester between 1995 and 2005. Medical charts were reviewed for the date of diagnosis of PSC, IBD, and colon neoplasms as well as the location and type of neoplasm. Results: 54 patients with PSC, IBD, and colon neoplasms were found with a mean age of 51 at diagnosis of colon neoplasm (range 45.4 to 57.5), and 70% were male. 37 patients (69%) had UC, 6 (11%) had Crohn's disease with colonic involvement, and 11 (20%) had indeterminate colitis. 38 patients had IBD diagnosed prior to PSC by a median of 10.8 years (range 5.3 to 17.9), 9 patients had PSC diagnosed prior to IBD by a median of 4 years (range 1.9 to 9.6), and 7 patients were diagnosed with PSC and IBD at the same time. Colon cancer was found by colonoscopy in 14 patients (26%), high grade dysplasia in 7 (13%), dysplasia associated lesions or mass in 3 (5.5%), and low grade dysplasia in 30 (55.5%). The occurrence of colon neoplasms within two years of diagnosis of IBD and PSC was 21.5 per 100 patient years of follow up, 20.5 per 100 patient years at 2-4 years, 19.3 per 100 patient years at 4-6 years, 16.8 per 100 patient years at 6-8 years, and the occurrence within 8 to 10 years from diagnosis of IBD and PSC was 20.4 per 100 patient years of follow up. Of the patients diagnosed with colon cancer, 2 adenocarcinomas (14%) were located in the cecum, 5 (36%) in the ascending colon, 4 (29%) in the transverse colon, and 3 (21%) in the rectosigmoid colon. According to AJCC staging system for colon cancer, 2 patients had stage I cancer, 4 had stage IIA cancer, 4 had stage IIIB cancer, 2 had stage IIIC, and 2 had stage IV cancer. Conclusion: The risk of colon neoplasms within two years of diagnosis with PSC and IBD was similar to the risk within 8 to 10 years of diagnosis with PSC and IBD. Colon cancers were found throughout the entire colon and were at a variety of stages at diagnosis. This data supports early and aggressive screening for colon cancer in this population with colonoscopy.

The aim of this survey was to find out whether the perspectives of patients with inflammatory bowel disease concerning biosimilars have changed since the publication of our last survey carried out in 2014-2015. An online survey consisting of 19 questions was made available by the European Federation of Crohn's and Ulcerative Colitis Associations between July 2018 and December 2018. Only respondents who had heard of biosimilars were asked to respond to all of the questions. In total, 1619 patients with inflammatory bowel disease responded the questionnaire. Most respondents were from Europe (79%), followed by Asia (8%), South America (7%) and Africa (5%). Some 44% of them had heard of biosimilars, and only these respondents continued to the biosimilar-specific questions. Respondents worried significantly more about biosimilars being less effective than the originator (50% in current and 39% in previous survey, p = 0.0004). However, respondents were more likely to believe that biosimilars will have an impact on the management of inflammatory bowel disease (75% in current and 62% in previous survey). Many patients with inflammatory bowel disease remain unfamiliar with biosimilars. Although patients still worry about different aspects regarding biosimilars, they also tend to be more confident that biosimilars will have an impact on the management of their disease. More patient education is still needed to raise awareness about biosimilars.

Dysplastic lesions in inflammatory bowel disease show increased positivity for the stem cell marker aldehyde dehydrogenase

Enhanced imaging technologies are of special importance in patients with inflammatory bowel diseases. Patients with long-lasting colitis face an increased cancer risk and neoplastic changes often evolve as subtle, multifocal, and flat lesions. Enhanced endoscopic imaging technologies enable better visualization of the mucosal architecture. These new available information can be used to better detect and characterize colorectal lesions. The better endoscopic judgment leads to more targeted biopsies and cancer detection can be facilitated. This new concept of “smart biopsies” is in particular important for screening purposes. Furthermore, the technique of endomicroscopy enables in vivo histology during ongoing endoscopy which can be used to improve cancer detection but also to increase our understanding of physiologic and pathophysiologic changes in IBD.

Background Inflammatory Bowel Disease patients (IBD) are in a higher risk of colorectal cancer (CRC) than the general population. Studies show that surveillance with chromoendoscopy (CE) is useful for prevention as it detects a higher number of dysplastic lesions, allowing their endoscopic resection and therefore preventing CRC. We aimed to assess our endoscopic results in IBD patients with previous diagnose of dysplasia. Methods We performed a retrospective data collection from IBD patients who have had dysplastic lesions in screening chromoendoscopy, performed in our hospital from January 2013 to June 2019. Demographic and clinical data at basal time were collected, as well as endoscopic and histological findings in basal chromoendoscopy and in the first follow-up Results 353 chromoendoscopies were performed in our Endoscopy Unit in this period and 50 patients showed dysplastic lesions. 14 (28%) of them had already had dysplasia in previous colonoscopies, which were performed with white light and aleatory biopsies. Basal characteristics are shown in the following table. In the initial chromoendoscopy, an average of 2.57 dysplastic lesions with an average size of 7.59 mm was detected. 70.8% were flat lesions (0-IIa/0-IIb Paris classification) and 53% were located distal to the splenic flexure. 85.7% were tubular adenomas low-grade dysplasia (LGD), 2 cases of high-grade dysplasia (HGD), one serrated polyp and one adenocarcinoma. Twenty-nine follow-up chromoendoscopy have been performed and new dysplasia lesions were found in 41.37% (average of 1.86 lesions, median 8 mm). 55.6% of the lesions were tubular adenomas LGD and 11.1% serrated adenomas LGD. Our analysis shows that patients with new lesions in the second chromoendoscopy had had worse bowel preparation on the first one (7.5 vs. 8.9, p = 0,006). We also found that these patients with new lesions had more flat lesions than sessile ones (70.6% Paris IIa, 23.5% IIb, 5.9% Is, p &amp;lt; 0,005). Conclusion Surveillance with chromoendoscopy in IBD patients with previous dysplastic lesions detects new dysplasia in 28% of them and LGD is the most frequent histology. In our sample, finding flat lesions or worse bowel cleaning in the first chromoendoscopy predicts having a higher number of lesions on the follow-up.