Abstract
Background
Non-alcoholic fatty liver disease (NAFLD) is strongly associated with cardiovascular disease in the general population. Both NAFLD and cardiovascular diseases seem more frequent ...in patients with inflammatory bowel disease (IBD).
Purpose
We aimed to assess the effect of NAFLD and associated liver fibrosis on the cardiovascular risk in people with IBD.
Method
We prospectively included IBD patients undergoing a routine screening program for NAFLD by transient elastography (TE) with associated controlled attenuation parameter (CAP). NAFLD and significant liver fibrosis were defined as CAP >275 dB/m and liver stiffness measurement (LSM) by TE ≥8 kPa, respectively. Nonalcoholic steatohepatitis (NASH) with liver fibrosis was defined as Fibroscan-aspartate aminotransferase (AST) score (FAST) >0.35. Cardiovascular risk was assessed with the atherosclerotic cardiovascular disease (ASCVD) risk estimator proposed by the American Heart Association and computed from age, sex, race, lipid pattern, blood pressure, diabetes treatment and smoking. Based on the American Heart Association guidelines, the 10-year cardiovascular risk by ASCVD was categorized as low if <5%, borderline if 5%–7.4%, intermediate if 7.5%–19.9% and high if ≥20% or if previous cardiovascular event.Predictors of intermediate-high cardiovascular risk were investigated by multivariable logistic regression analysis.
Result(s)
We included 405 patients with IBD (54% female; mean age 45+15 years; mean BMI 26+5 Kg/m2; 31% with ulcerative colitis; 7% with diabetes; 14% with hypertension). Overall, 278 (68%), 23 (6%), 47 (12%) and 57 (14%) were categorized as at low, borderline, intermediate and high ASCVD risk, respectively. NAFLD and significant liver fibrosis were found in 129 (32%) and 35 (9%) patients, respectively. NASH with fibrosis was found in 11 (3%) patients. Patients with NAFLD and with significant liver fibrosis diagnosed by TE with CAP had higher proportion of intermediate-high ASCVD risk category (see Figure). These findings were confirmed also in young IBD patients <55 years old with NAFLD. No difference in ASCVD risk was detected for FAST score. After adjusting for IBD disease activity, significant liver fibrosis and BMI, predictors of intermediate-high ASCVD risk were NAFLD (adjusted odds ratio aOR 2.97, 95% confidence interval CI 1.56–5.68), IBD duration (aOR 1.55 per 10 years, 95% CI 1.22–1.97), and ulcerative colitis (aOR 2.32, 95% CI 1.35–3.98). Only 30% of IBD patients classified as intermediate-high ASCVD risk were on statin treatment, with no difference between patients with and without NAFLD.
Image
Conclusion(s)
NAFLD increases cardiovascular risk, independently of age, IBD-related factors and BMI.
A potential deliverable of our finding is the targeted cardiovascular assessment in IBD patients with NAFLD and appropriate initiation of statin, particularly if they have longer IBD duration and ulcerative colitis.
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None
Disclosure of Interest
None Declared
Abstract
Background
The colonic stem cell niche is established by a gradient of WNT, R-spondin, BMP factors and their antagonists along the colonic epithelial vertical axis. Telocytes (TCFoxL1+) are ...mesenchymal cell forming a 3D hub underneath the epithelium, identified as an important source of niche factors. Specifically, they express non-canonical (nc) WNT factors and are the richest source of BMPs. Disruption of the BMPs gradient has been shown to be related to the development of several gastrointestinal diseases like Inflammatory Bowel Diseases (IBD). Such chronic inflammation drives the onset of Colitis-Associated Cancer (CAC) in about 60% of IBD patients. We previously showed that following a chronic inflammatory stress, 50% of the KO mouse for the BMP receptor 1a in colon telocytes (Bmpr1a△FoxL1+) presented malignant epithelial transformations. These cancer-like regions showed an aberrant epithelial b-catenin localization and an enlargement of the double positive α-SMA+/Vimentin+ mesenchymal population.
Purpose:
Loss of BMP signaling in TCFoxL1+ affects the mesenchymal-epithelial crosstalk and makes the colonic epithelium vulnerable to injuries, promoting/perpetuating inflammation fostering CAC onset.
Method
Following a DSS-based chronic inflammatory challenge in mutant and control mice, TCFoxL1+ ultrastructure was analyzed using transmission electron microscopy. Expression levels of members of the WNT-BMP axis (BMPs, WNTs and associated antagonists) were evaluated by qPCR in tumor-like areas and adjacent tissue. YAP cellular localization was evaluated by immunofluorescence in colon after chronic DSS challenge in Bmpr1a△FoxL1+ mice and controls. To differentiate cancer-associated fibroblasts (CAFs) subtypes, myCAF (myofibroblastic) and iCAF (inflammatory), in tumor-like region and adjacent tissue, we used co-staining against gp38, ICAM, Tagln and αSMA.
Result(s)
Following a chronic DSS-challenge, electron microscopy analysis demonstrated that TCFoxL1+ in the control mice exhibited a shortening and erosion in their telopodes (Tp). TCFoxL1+ in Bmpr1a△FoxL1+ mice tumor-like regions presented an expanded endoplasmic reticulum with fragmented and dilated Tp. A significant increase in BMP 4, 5 and 7 and in Wnt5 (nc) was detected in Bmpr1a△FoxL1+ mice compared to controls. Confocal analysis revealed a strong nuclear accumulation of YAP in cancer-like regions in mutant mice compared to controls. Finally, tumour-like regions presented an heterogeneous distribution of iCAF and myCAF compared to controls.
Conclusion(s)
These results exposed that the disruption of TCFoxL1+ associated BMP signaling disturbs the WNT-BMP gradient essential for the optimal maintenance of the SC niche and thus impacting epithelial regeneration when under stress. Thus, defective TCFoxL1+ assume a key role in the poor regeneration process of the epithelium which in the end promotes the development and progression of CAC.
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CIHR
Disclosure of Interest
None Declared
Abstract
Background
Colorectal cancer is the second leading cause of cancer death in Canada. A major risk factor for the development of colorectal cancer is chronic inflammation leading to ...colitis-associated cancer (CAC). We previously described a CAC mouse model in which tumors arise from DCLK1+ tuft cells following loss of the tumor suppressor adenomatous polyposis coli (APC) and induction of colitis. Interestingly, both colitis and CAC display epigenetic changes that modulate gene expression. However, the impact of DNA methylation changes on colonic tumorigenesis is not known. Thus, we hypothesize that inhibition of DNA methylation in DCLK1+ tuft cells reduces colonic tumorigenesis.
Purpose
In this study, we aim to investigate the role of DNA methylation in CAC by inhibiting DNA methylation using genetic and pharmacologic means.
Method
Using a publicly available dataset (GSE75214) of gene expression data analyzed by microarray from colonic biopsies of patients with ulcerative colitis and Crohn’s Disease with active disease, we examined the expression of DNA methyltransferases (DNMTs). Expression of DNMTs in mice with colitis was additionally examined by RT-qPCR and global DNA methylation levels measured by 5-mC ELISA. In separate experiments, Dclk1-CreERT2/Apcf/f mice were crossed to DNMT1f/f mice to knock-out the DNA methyltransferase DNMT1 in DCLK1+ tuft cells. Dclk1/Apcf/f and Dclk1/Apcf/f/DNMT1f/f mice were then administered three doses of tamoxifen followed by 2.5% dextran sodium sulfate (DSS) for five days to induce colitis. Fourteen weeks later, we assessed colonic tumor number and size. In a separate cohort of Dclk1/Apcf/f mice, we induced colitis and treated the mice with six doses of the DNA de-methylating drug 5-AZA-2’-deoxycytidine (5-AZA) or vehicle, and assessed colonic tumor number. To examine DNA methylation changes, we then treated WT mice with 5-AZA and DSS and isolated intestinal epithelial cells. From the intestinal epithelial cell, we isolated DNA and ran the Infinium MouseMethylation BeadChip Array.
Result(s)
Patients with IBD were found to have increased expression of DNMT1 compared to healthy controls. Mice treated with DSS similarly had increased DNMT1 expression, as well as, global methylation levels compared to controls. Deletion of DNMT1 in DCLK1+ cells significantly inhibited the number and size of colonic tumors. Treatment of mice with 5-AZA decreased global and gene specific DNA methylation levels, and significantly reduced both the number of mice with tumors, and the average colonic tumor number and size per mouse.
Conclusion(s)
Our findings demonstrate that colitis in both patients and mice is associated with DNA methylation. Furthermore, DNA hypomethylation by 5-AZA treatment or loss of DNMT1 reduces CAC formation suggesting that altered DNA methylation plays a critical role in colonic tumorigenesis.
Disclosure of Interest
None Declared
Abstract
NOT PUBLISHED AT AUTHOR’S REQUEST
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CIHR, Other
Please indicate your source of funding;
Government of Alberta
...Disclosure of Interest
None Declared
Abstract
Background
Inflammatory bowel diseases (IBD) are chronic inflammatory disorders of the gastrointestinal tract. Despite achieving endoscopic remission, up to 50% of IBD patients continue to ...experience chronic abdominal pain, with female patients displaying an increased prevalence. The reason underlying these differences in pain perception is unknown, but the influence of sex hormones represents an important biological source for variability in pain sensitivity. To date, few studies have examined sex differences in chronic visceral pain in IBD.
Purpose
Examine sex-specific differences in post-inflammatory chronic visceral pain in IBD.
Method
We used the post-inflammatory DSS mouse model of chronic visceral pain. Ovariectomy was performed to study the effects of estrogen deficiency; sham surgery was performed as a control. Male, cycling female and ovariectomized female mice were given 2.5% DSS for five days and allowed to recover for 5 weeks. Somatic pain was evaluated using the hot plate and von Frey hair tests. Visceral pain was evaluated using the visceral motor reflex (VMR) to colorectal distension five weeks after DSS treatment. Visceral and somatic pain testing in cycling females was performed in diestrus.
Result(s)
Male, cycling female and ovariectomized female mice given DSS initially lost weight when compared to controls (p<0.0001). Cycling females displayed significantly decreased colitis severity when compared to males Disease Activity Index at Day 12: 1.41 ± 0.41 cycling females, n=12; 4.41 ± 0.31 males, n=12; p<0.001 but increased severity compared to ovariectomized females Disease Activity Index at Day 12: 2.0 ± 0.41 ovariectomized females, n=13; 4.77 ± 0.6 cycling females, n=13, p=0.0005. Increased visceral hypersensitivity was seen in post-inflammatory cycling females compared to post-inflammatory males VMR at 60mmHg, post-inflammatory cycling females 0.10 ± 0.016, n=10; post-inflammatory males 0.07 ± 0.007, n=10; p=0.032 and post-inflammatory ovariectomized females VMR at 60mmHg, post-inflammatory sham females 0.072 ± 0.005, n=8; post-inflammatory ovariectomized females 0.047 ± 0.005, n=8; p=0.019. Thermal hyperalgesia and mechanical allodynia were similar across all groups.
Conclusion(s)
These data suggest that estrogen plays an important role in the severity of colitis severity and post-inflammatory visceral pain. Understanding sex-specific differences in post-inflammatory visceral pain in IBD may allow us to define novel therapeutic approaches for IBD patients.
Disclosure of Interest
None Declared
Abstract
Background
Canada is currently in the third epidemiological stage in the evolution of IBD: compounding prevalence. A high incidence of IBD, in conjunction with low mortality, leads to a ...steadily rising prevalence over time. By understanding historical epidemiological trends, we can forecast incidence and prevalence into the future to inform healthcare systems in Canada of the rising burden of IBD to society.
Purpose
To analyze past epidemiological trends in order to forecast the overall incidence and prevalence of IBD, Crohn’s disease (CD), and ulcerative colitis (UC) and stratified by age (<18, 18-64, 65+).
Method
Canadian population-based administrative data was acquired from: AB, BC, SK, MB, QC, and ON. Data were age and sex standardized to the matching year and provincial data aggregated into a representative sample of the Canadian population for prevalence (2002-2014) and incidence (2007-2014: 5-year washout period). Incidence and prevalence (per 100,000 persons) were calculated, with 95% confidence intervals (CI), using Canadian population estimates from Statistics Canada for IBD, CD, UC (IBD-unclassifiable+UC). Autoregressive Integrated Moving Average models were created, and rates forecasted from 2014 to 2035 with 95% prediction intervals (PI). Poisson (or negative binomial) for incidence and log binomial regression for prevalence estimated the Average Annual Percentage Change (AAPC), with 95% CIs, of the forecasted data.
Result(s)
The 2014 incidence of IBD in Canada was 28.4 per 100,000 (95%CI: 27.8, 29.0) and forecasted to significantly increase (AAPC: 0.58%; 95%CI: 0.04, 1.04) from 30.0 per 100,000 in 2023 to 32.1 (95%PI: 27.9, 36.3) in 2035. Pediatric onset IBD was 13.9 per 100,000 (95%CI: 13.0, 14.9) in 2014 and is forecasted to significantly increase to 18.0 per 100,000 (95%PI: 15.7, 20.2) in 2035 with an AAPC of 1.23% (95%CI: 0.76, 1.63). Adult and elderly onset incidence rates were forecasted to remain stable. Prevalence of IBD increased between 2002 (389 per 100,000) and 2014 (636 per 100,000) and is forecasted to continue to climb by an AAPC of 2.44% (95%CI: 2.34, 2.53). In 2023, the prevalence of IBD is 825 per 100,000. By 2035 prevalence is forecasted to climb to 1075 per 100,000 (95%PI: 1047, 1103) with 470,000 Canadians living with IBD. Prevalence across all age strata were forecasted to significantly increase. The highest AAPC was seen in the elderly (2.76%; 95%CI: 2.73, 2.79) with a prevalence of 841 per 100,000 (95%CI: 834, 849) in 2014 and forecasted to climb to 1534 per 100,000 (95%PI: 1519, 1550) in 2035.
Image
Conclusion(s)
Incidence of IBD continues to rise in Canada, driven by pediatric-onset IBD. In 2023, over 320,000 Canadians (0.83%) will be living with IBD. By 2035 prevalence will exceed 1% of the population with approximately 470,000 individuals in Canada with IBD. Future research should establish the environmental determinates of IBD that may influence temporal trends in the incidence of IBD, while healthcare systems adapt to the compounding prevalence of IBD.
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CIHR, Other
Please indicate your source of funding;
The Leona M. and Harry B. Helmsley Charitable Trust
Disclosure of Interest
S. Coward: None Declared, E. Benchimol Consultant of: Hoffman La-Roche Limited and Peabody & Arnold LLP for matters unrelated to medications used to treat inflammatory bowel disease and McKesson Canada and the Dairy Farmers of Ontario for matters unrelated to medications used to treat inflammatory bowel disease., C. Bernstein Grant / Research support from: Unrestricted educational grants from Abbvie Canada, Janssen Canada, Pfizer Canada, Bristol Myers Squibb Canada, and Takeda Canada. Has received research grants from Abbvie Canada, Amgen Canada, Pfizer Canada, and Sandoz Canada and contract grants from Janssen, Abbvie and Pfizer, Consultant of: Abbvie Canada, Amgen Canada, Bristol Myers Squibb Canada, JAMP Pharmaceuticals, Janssen Canada, Pfizer Canada, Sandoz Canada, and Takeda., Speakers bureau of: Abbvie Canada, Janssen Canada, Pfizer Canada and Takeda Canada, J. A. Avina-Zubieta: None Declared, A. Bitton: None Declared, L. Hracs: None Declared, J. Jones Consultant of: Janssen, Abbvie, Pfizer, Takeda, Speakers bureau of: Janssen, Abbvie, Pfizer, Takeda, E. Kuenzig: None Declared, L. Lu: None Declared, S. Murthy: None Declared, Z. Nugent: None Declared, A. Otley Grant / Research support from: Unrestricted educational grants from AbbVie Canada and Janssen Canada, Consultant of: Advisory boards of AbbVie Canada, Janssen Canada and Nestle, R. Panaccione Consultant of: Abbott, AbbVie, Alimentiv (formerly Robarts), Amgen, Arena Pharmaceuticals, AstraZeneca, Biogen, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Celltrion, Cosmos Pharmaceuticals, Eisai, Elan, Eli Lilly, Ferring, Galapagos, Fresenius Kabi, Genentech, Gilead Sciences, Glaxo-Smith Kline, JAMP Bio, Janssen, Merck, Mylan, Novartis, Oppilan Pharma, Organon, Pandion Pharma, Pendopharm, Pfizer, Progenity, Protagonist Therapeutics, Roche, Sandoz, Satisfai Health, Shire, Sublimity Therapeutics, Takeda Pharmaceuticals, Theravance Biopharma, Trellus, Viatris, UCB. Advisory Boards for: AbbVie, Alimentiv (formerly Robarts), Amgen, Arena Pharmaceuticals, AstraZeneca, Biogen, Boehringer Ingelheim, Bristol-Myers Squibb, Celgene, Eli Lilly, Ferring, Fresenius Kabi, Genentech, Gilead Sciences, Glaxo-Smith Kline, JAMP Bio, Janssen, Merck, Mylan, Novartis, Oppilan Pharma, Organon, Pandion Pharma, Pfizer, Progenity, Protagonist Therapeutics, Roche, Sandoz Shire, Sublimity Therapeutics, Takeda Pharmaceuticals, Speakers bureau of: AbbVie, Amgen, Arena Pharmaceuticals, Bristol-Myers Squibb, Celgene, Eli Lilly, Ferring, Fresenius Kabi, Gilead Sciences, Janssen, Merck, Organon, Pfizer, Roche, Sandoz, Shire, Takeda Pharmaceuticals, J.-N. Pena-Sanchez: None Declared, H. Singh Consultant of: Pendopharm, Amgen Canada, Bristol Myers Squibb Canada, Roche Canada, Sandoz Canada, Takeda Canada, and Guardant Health, Inc., L. Targownik Grant / Research support from: Investigator initiated funding from Janssen Canada, Consultant of: Advisory board AbbVie Canada, Takeda Canada, Merck Canada, Pfizer Canada, Janssen Canada, Roche Canada, and Sandoz Canada, J. Windsor: None Declared, G. Kaplan Grant / Research support from: Ferring, Janssen, AbbVie, GlaxoSmith Kline, Merck, and Shire, Consultant of: Gilead, Speakers bureau of: AbbVie, Janssen, Pfizer, Amgen, and Takeda
Abstract
Background
Fecal calprotectin (FC) is a sensitive marker of intestinal inflammation, and is used to both discriminate inflammatory bowel disease (IBD) from non-IBD patients and to monitor ...patients with IBD. It is unclear whether normal values established in adult patients are applicable in pediatrics.
Purpose
To evaluate FC’s ability to differentiate IBD from non-IBD pediatric patients, and to understand factors influencing FC in pediatric IBD(pIBD).
Method
Stool FC samples collected on all patients<19 years of age in British Columbia(BC) from May 2020 to August 2022 were run using a Buhlmann ELISA at BC Children’s Hospital(BCCH). The BCCH GI database identified patients with IBD. FC’s ordered by adult IBD providers and patients awaiting endoscopy were excluded. The remaining samples were analysed as non-IBD. The sensitivity(Sn), negative predictive value(NPV) and false positive(FP) of FC were evaluated; comparisons were made using the Wilcoxon rank-sum test and chi-squared.
Result(s)
3506 FC samples met inclusion criteria: 1853 IBD and 1653 non-IBD. 221 IBD samples were from prior to diagnosis, with median (IQR) FC 2615ug/g(1090-4183); median FC for non-IBD patients was 54ug/g(24-122). Using the Buhlmann "normal" cutoff of 80ug/g, the Sn was 0.991 (NPV 0.998) with a FP rate of 37%. Young patients were more likely to have FP's: <6yo's (n=305) had a FP rate of 42% vs 36% in those >6yo (n=1348)(p=0.035). With a FC cutoff of 160ug/g, Sn was 0.973 (NPV 0.996), with a FP rate of 20% (24% <6yo vs 19% >6yo, p=0.025). At a threshold of 250ug/g, Sn was 0.959 (NPV 0.994) with a FP rate of 13% (18% <6yo vs 12% >6yo, p=0.01). For patients <2yo, all 4 new IBD diagnosis had FC>1900ug/g. In the non-IBD population (n=69 samples <2yo), the FP rate was 52%, 30%, and 22% using a threshold of 80, 160, and 250ug/g, respectively.
Evaluating FC as a disease-monitoring tool in IBD (667 patients, 1632 samples) found that at 6, 12, 18, and 24+ months post diagnosis, FC decreased from 750(159-1883), 505(110-1566), 351(87-1379), to 308ug/g(85-1129), respectively. Similarly, the proportion of FC’s <250ug/g increased from 4.1% at diagnosis to 30%, 39.7%, 41.5%, 47% during the follow up period.
Patients with UC/IBD-U had higher FC’s, and were less likely to achieve FC<250ug/g. By 12 months post diagnosis, median FC of CD patients was 347ug/g(96-1150) and UC/IBD-U was 745ug/g(191-2017)(p=0.036), and at 18 months, CD 273ug/g(61-902) vs UC/IBD-U 932ug/g(144-2229)(p<0.001). At 2+yrs, median FC for CD patients was 259ug/g(76-1038) vs 387ug/g(108-1577) for UC/IC (p=0.017).
Patients cared for by an IBD specialist had better FC outcomes vs those managed by non-IBD GIs: median FC at 12 months was 246ug/g(n=79) vs 677ug/g(n=153)(p=0.002), with 51% vs 34% achieving FC<250(p=0.014). Similarly, at 2+yrs post diagnosis, median FC was 243ug/g(n=437) vs 356ug/g(n=407)(p=0.02).
Conclusion(s)
Higher FC thresholds are likely required in younger populations compared to established adult cutoffs. In this pIBD cohort, <50% achieve FC levels <250ug/g.
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None
Disclosure of Interest
None Declared
Abstract
Background
The NAIP-NLRC4 inflammasome is an important innate defence mechanism in intestinal epithelial cells (IECs) that protects the gut from invasive pathogens. NAIP-NLRC4 activation ...triggers pyroptotic cell death, releases active interleukin (IL)-18, and promotes the expulsion of infected enterocytes. Dysregulated inflammasomes result in exaggerated inflammation of the intestinal mucosa which is characterisitic of inflammatory bowel disease (IBD). There is increasing evidence that inflammasomes in IEC behave differently than in immune cells. However, a majority of inflammasome pathway characterization is studied immune cells. In addition, NAIP-NLRC4 activity in macrophages has been shown to be important for regulating the expression of nitric oxide (Nos2). The potential transcriptomic impact of NAIP-NLRC4 activity in IECs has yet to be explored.
Purpose
We will use intestinal orgnaoids to systematically characterize the NAIP-NLRC4 inflammasome pathway and identify the transcriptomic impact of NAIP-NLRC4 activity in IECs. To better define the role of NAIP-NLRC4 activity during a physiological infection, we have developed a novel ex vivo model of Shigella infection in 3D organoids.
Method
Organoids were derived from the ileal crypts of wild type (WT) and Nlrc4-/-, Casp1-/-, Pycard-/-, or Tlr5-/- mice and stimulated with Pam3CSk4, LPS, or flagellin. Inflammasome activation was assessed by Western blot (WB) and propidium iodide uptake. WT and Nlrc4-/- organoids were infected with WT or a non-invasive Shigella mutant and the inflammasome response was evaluated by WB and a colony forming unit assay. WT and Nlrc4-/- organoids were stimulated with flagellin and gene expression was assessed by RT-qPCR.
Result(s)
Basolateral organoid stimulation with bacterial ligands revealed a novel response of IECs to bacterial flagellin that results in pyroptosis and IL-18 processing. Basolateral internalization of flagellin occurred in a TLR5-independent manner. Inflammasome activation by flagellin was fully abrogated in Nlrc4-/- and Casp1-/- organoids while only IL-18 processing was affected in Pycard-/- organoids. Infection with only WT Shigella induced inflammasome activation in an NLRC4-dependent manner. Interestingly, flagellin stimulation of WT but not Nlrc4-/- organoids led to increased expression of Nos2. Furthermore, Nlrc4-/- organoids had significantly lower expression levels of cytokine genes Ccl20, Cxcl1, and Tnf following inflammasome activation.
Conclusion(s)
Our study demonstrates an integral role for epithelial NAIP-NLRC4 inflammasomes in the response to bacterial flagellin and Shigella infection. We have uncovered a novel response of IECs to basolateral flagellin stimulation and revealed that NAIP-NLRC4 is important for the transcriptional regulation of inflammatory genes. Further work will examine how NAIP-NLRC4 activation controls inflammation and epithelial integrity by analyzing the NLRC4-dependent transcriptome and the effects on cell proliferation, differentiation, and barrier integrity.
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CCC, CIHR
Disclosure of Interest
None Declared
Abstract
Background
The effectiveness of colonoscopy screening to prevent colorectal cancer (CRC) is directly linked to its procedural quality. An independent observer (Hawthorne effect) can improve ...colonoscopy procedural quality metrics, including adenoma detection rate (ADR). However, the results of studies are limited or controversial.
Purpose
We aimed to evaluate the colonoscopy quality metrics in a group of patients undergoing screening or diagnostic colonoscopies under stringent observer conditions.
Method
In a single-center, case–control study, consecutive patients undergoing routine screening or diagnostic colonoscopy were prospectively enrolled. In the case group, all procedural steps and quality metrics were observed and documented, and the procedure was video recorded by an independent research assistant. In the control group, colonoscopies were performed without independent observation. Colonoscopy quality metrics such as polyp, adenoma, serrated lesions, and advanced adenoma detection rates (PDR, ADR, SLDR, AADR), the mean number of adenomas detected per patient (MAP), and the mean number of adenomas and serrated lesions detected per patient (MASP) were compared. The probabilities of increased quality metrics were evaluated through regression analyses weighted by the inversed probability of observation during the procedure.
Result(s)
We included a total of 687 patients (327 cases and 360 controls) in the final analyses. The case group had significantly higher PDRs (62.4% vs. 53.1%) and ADRs (39.4% vs. 28.3%) compared with the control group. The SLDR was also higher in the case group than in the control group, but the difference was not significant (7.3% vs. 4.4%; P = 0.14). The AADR was not significantly increased. After adjusting for potential confounders, the ADR and SLDR were 50% (odds ratio OR 1.51; 95%CI 1.05–2.17) and more than twofold (OR 2.17; 95%CI 1.05–4.47) more likely to be higher in the case group than in the control group. The MAP and MASP were significantly increased in the case group compared with the control group (P < 0.001). The regression analyses for both metrics demonstrated the direct and significant association between the Hawthorne effect and elevated MAP/MASP.
Conclusion(s)
The presence of an independent observer documenting colonoscopy quality metrics and video recording the colonoscopy resulted in a significant increase in ADR and other quality metrics. The Hawthorne effect should be considered an alternative strategy to advanced devices to improve colonoscopy quality in routine practice.
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None
Disclosure of Interest
M. Taghiakbari: None Declared, D. Coman: None Declared, M. Takla: None Declared, A. N. Barkun: None Declared, M. Frija-Gruman: None Declared, M. Bouin: None Declared, S. Bouchard: None Declared, E. Deslandres: None Declared, S. Sidani: None Declared, D. von Renteln Grant / Research support from: ERBE, Ventage, Pendopharm, and Pentax, Consultant of: Boston Scientific and Pendopharm
