Risk Factor For Colorectal Neoplasia Research Articles

Abstract 7324: Impact of BMI on immune pathways in preinvasive colorectal lesions

Abstract Background: Obesity is a risk factor for colorectal neoplasia, possibly mediated by metabolic dysregulation or chronic inflammation. Circulating inflammatory cytokines have been associated with an increased risk of CRC, but no studies have examined the impact of BMI on immune gene expression in preinvasive lesions. Our analysis combines data from 3 retrospective epidemiologic studies among patients with colorectal adenomas or serrated polyps. Using a cross-sectional design, we investigate whether BMI categories (obese (OB), overweight (OW), normal (NL)) are associated with T-helper gene pathways. Methods: For each patient, we include demographic, clinical, and specimen (archival FFPE for RNA isolation) data. Immune gene expression data was determined using the NanoString nCounter platform on a subset of cases (n=100) balanced by study site and lesion type from our cohort (n=630). Genes were normalized using a modified RUVseq methodology. We examined 4 pathways (Th1, Th2, Th17, Treg) defined by gene lists included in the NS immune v2. panel. Differences in pathway expression by BMI categories were analyzed using our distance-based methods (Wd* multivariate analysis of variance and TW2 pairwise method) adjusted for age & sex. Using linear regression analysis, we generated coefficients (p-values) for OW and OB vs NL for genes within each pathway. Results: 86 samples passed QC. Th2 and Th1 pathways were significant for OW vs NL (p<0.05) whereas Th17 was marginally significant (<0.1). Several genes within the Th1, Th2, and Th17 pathways were enriched in OW vs. NL: e.g., IL2 (coeff. 0.77 (p=0.008), IL5 (coeff. 1.02, p=0.001), IL17F (coeff. 0.57, p=0.05), respectively. (Table) Conclusion: Enrichment of genes specific to the Th pathways in OW persons suggest that metabolic immune modulation may be important in early colorectal carcinogenesis. Differences in immune pathway and gene expression by BMI categories TW2 (p-value) Wd* (p-value) Pathways Normal (N = 22) Overweight (N = 32) Obese (N = 29) Th2 Ref. 0.017 0.15 0.038 Th1 Ref. 0.03 0.204 0.10 Th17 Ref. 0.073 0.125 0.103 MLR coefficient (p-value) Pathway Gene Overweight vs. Normal Obese vs. Normal ANOVA (p-value) Th2 IL2RA 0.34 (0.041) -0.11 (0.517) 0.010 IL4 0.58 (0.019) 0.22 (0.386) 0.052 IL5 1.02 (0.001) 0.41 (0.191) 0.004 NOTCH1 -0.05 (0.742) -0.34 (0.045) 0.078 Th1 IL12B 0.57 (0.031) 0.40 (0.136) 0.093 IL2 0.77 (0.008) 0.39 (0.179) 0.028 TBX21 0.46 (0.015) 0.19 (0.308) 0.044 Th17 IL17F 0.57 (0.050) 0.42 (0.157) 0.139 IL21 0.77 (0.004) 0.42 (0.131) 0.017 IL23R 0.29 (0.048) -0.008 (0.957) 0.047 IL6R 0.002 (0.990) 0.36 (0.039) 0.041 IRF4 -0.61 (0.007) -0.33 (0.149) 0.025 TGFB1 -0.26 (0.023) -0.19 (0.101) 0.069 Citation Format: Lauren R. Fanning, Bashir Hamidi, Ivan Korostenskij, Souvik Seal, Tami L. Crawford, Todd A. MacKenzie, Elizabeth L. Barry, Jessica E. Thaxton, Martha J. Shrubsole, Benjamin Vincent, John A. Baron, Alexander V. Alekseyenko, Kristin Wallace. Impact of BMI on immune pathways in preinvasive colorectal lesions [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 7324.

P188 Cumulative inflammatory burden as a risk factor for colorectal neoplasia in inflammatory bowel disease patients with primary sclerosing cholangitis: a multi-center case-control study

Abstract Background Inflammatory bowel disease (IBD) patients with concomitant primary sclerosing cholangitis (PSC-IBD) have a 25-year cumulative risk of up to 50% to develop colorectal neoplasia (CRN). Mucosal inflammation is an important driver of CRN, but it is unknown whether this also applies to PSC-IBD patients. We aimed to assess the impact of chronic mucosal inflammation per colonic segment on CRN risk in PSC-IBD patients. Methods This is a multi-center case-control study including cases with PSC-IBD and CRN and controls with PSC-IBD without CRN. Subjects were included from 8 medical centers in Canada and the Netherlands. Exclusion criteria were a CRN diagnosis prior to IBD or PSC diagnosis, familial CRC syndromes, and <2 available colonoscopy reports. Data was collected on demographics, IBD and PSC disease characteristics, CRN lesions, and endoscopy reports between 1977 and 2023. Pan-colonic and segmental (right colon, transverse colon, left colon, rectum) endoscopic cumulative inflammatory burden scores were calculated as the sum of (mean) endoscopic inflammation severity between colonoscopies x length of the surveillance interval until index procedure. The index procedure was the colonoscopy during which CRN was detected (cases) or randomly selected and matched for disease duration (controls). The primary outcome was a CRN diagnosis, secondary outcomes were CRN grade and location, time to CRN (Kaplan-Meier curve), pan-colonic cumulative inflammatory burden, cumulative inflammatory burden per colonic segment harboring CRN, and colonic surgery. Results We included 335 PSC-IBD patients (224 UC, 101 CD) with a median follow-up of 8 years (IQR: 5.0-14.0) and 6 endoscopies (IQR: 4.0-8.0). Median disease duration was 19.5 years for IBD (IQR: 11.0-26.0) and 13 years for PSC (IQR: 7.0-19.0). Advanced neoplasia (HGD or CRC) was found in 35 out of 102 cases (34%). Fifty-six (55%) cases were diagnosed with > 1 lesion, and 43 (42%) had ≥ 1 right-sided lesion. Median time to index CRN was 17 years (IQR: 8.0-24.0). Sixty-six patients underwent (sub)total colectomy or proctocolectomy, including 49 (74%) due to CRN diagnosis. There was no difference in pan-colonic cumulative inflammatory burden scores (mean scores: 4.7 (cases) and 3.7 (controls); P=0.21, 95%-CI: -2.52-.56) and segmental scores (mean scores: 4.9 (cases) and 4.1 (controls); P=0.27, 95%-CI: -2.29-.65) between cases and controls. Mortality was 13% (n=45.) Conclusion In this large multi-center cohort study, the risk for CRN-associated colectomy in PSC-IBD was high, while pan-colonic and segmental cumulative inflammatory burden scores were not associated with CRN risk.

Risk and incidence of colorectal stricture progressing to colorectal neoplasia in patients with inflammatory bowel disease: a systematic review and meta-analysis.

This study aims to assess the risk of colorectal stricture progressing to colorectal neoplasia (CRN) in patients with inflammatory bowel disease (IBD). The literature from PubMed, Embase, Web of Science, and Cochrane Library databases was searched from the date of databases' creation to 5 November 2022. The Newcastle-Ottawa Scale was used to evaluate the quality of the included literature. Meta-analysis was conducted using the Stata 15 software and R 4.04 software. Two case-control studies and 12 cohort studies were eventually included. Colorectal stricture in patients with IBD increased the risk of progressing to CRN [odds ratio (OR): 1.52, 95% confidence interval (CI): 1.02-2.29, P = 0.042], but was irrelevant to the risk of progressing to ACRN (OR: 3.56, 95% CI 0.56-22.70, P = 0.180). The risk of CRN were further distinguished in patients with ulcerative colitis (UC) and Crohn's disease (CD) Our findings showed that colorectal stricture may increase the risk of progressing to CRN in patients with UC (OR = 3.53, 95%CI 1.62-7.68, P = 0.001), but was irrelevant to the risk of progressing to CRN in patients with CD (OR = 1.09, 95% CI 0.54-2.21, P = 0.811). In conclusion, colorectal stricture in patients with IBD can be used as a risk factor for predicting CRN but cannot be used as a risk factor for predicting ACRN. Stricture is a risk factor for CRN in patients with UC but not in patients with CD. More prospective, multi-center studies with large samples are expected to confirm our findings.

Colorectal Cancer Risk and Recommendations for Colorectal Cancer Surveillance in Adult Survivors of Childhood Cancer.

While many organizations have published guidance on the approach to colorectal cancer (CRC) screening in average-risk and certain high-risk groups, adult survivors of childhood cancer (ASCC) who have a heightened risk of CRC are rarely included as a target group for enhanced CRC surveillance. The population of ASCC continues to grow due to increasingly effective cancer therapies and improved survival. With this increased survival comes an increased risk for subsequent malignant neoplasms, including CRC. Since there is little published guidance for CRC surveillance in ASCC and limited awareness of increased CRC risk among both physicians and patients, the objectives of our paper are to review the incidence of and risk factors for colorectal neoplasia in ASCC, describe the clinical phenotypes of colorectal neoplasia in ASCC, review published surveillance strategies based on consensus-based survivorship guidelines, and outline areas for future research to optimize surveillance strategies.

Risk of colorectal neoplasia according to histologic disease activity in patients with inflammatory bowel disease and colonic post-inflammatory polyps.

While post-inflammatory polyps (PIPs) have historically been a risk factor for colorectal neoplasia (CRN), histologic activity may explain this association. We aimed to assess the impact of histologic activity on CRN occurrence in IBD patients with colonic PIPs. Patients with PIPs on surveillance colonoscopy at Saint-Antoine hospital between 1 January 1996 and 31 December 2020 were included and subsequent colonoscopies were assessed. Histologic IBD activity was assessed by the Nancy histologic index. Survival and Cox regression analysis were performed to assess the strength of the association of PIPs and other patient variables with progression to CRN. A total of 173 patients with at least two surveillance colonoscopies with PIPs at index colonoscopy were compared to a similar group of 252 patients without PIPs. In survival analysis, the presence or PIPs at index colonoscopy did not impact the risk of CRN in patients with histological inflammation (p = 0.83) and in patients without histological inflammation (p = 0.98). The risk of CRN was associated with increasing Nancy index score of 3 or 4 (HR: 4.16; 95% CI 1.50-11.52 and HR: 3.44; 95% CI 1.63-7.24), age (HR per 10-year increase: 1.37; 95% CI 1.13-1.66) and first-degree family history of colorectal cancer (HR: 5.87; v 1.31-26.26), but not PIPs (HR: 1.17; 95% CI 0.63-2.17). After controlling for histologic activity, PIPs do not increase the risk of CRN in IBD patients. Histologic activity rather than PIPs should be considered in the risk assessment of CRN.

Inflammation in the proximal colon is a risk factor for the development of colorectal neoplasia in inflammatory bowel disease patients with primary sclerosing cholangitis.

Patients with primary sclerosing cholangitis (PSC) and inflammatory bowel disease (IBD) have an increased risk of developing colorectal neoplasia (CRN) in the proximal colon. To evaluate whether duration and severity of inflammation are linked to the development of CRN in this population. Retrospective, case-control chart review of patients with PSC and IBD at a tertiary care center. Disease activity was scored per colonic segment at each colonoscopy prior to the first instance of observed CRN using a modified Mayo endoscopic sub-score and histologic assessment. Patients in the CRN-positive group were compared to controls that did not. In all, 72 PSC-IBD patients with no history of CRN were identified, 13 of whom developed CRN after at least one colonoscopy at our institution. Patients in the CRN-positive group had significantly more endoscopic (p < 0.01) and histologic (p < 0.01) inflammation in the right compared to the control group prior to the development of dysplasia. There was significantly greater endoscopic inflammation in the segment of the colon with a dysplastic lesion than other segments of the colon (p = 0.018). Patients with moderate/severe lifetime endoscopic (p = 0.02) or histologic inflammation (p = 0.04) score had a lower probability of remaining free of dysplasia during follow-up. Nearly half of the patients with dysplasia had invisible lesions found on random biopsy. Endoscopic and histologic inflammation in the proximal colon are risk factors for CRN in patients with PSC-IBD. PSC-IBD patients frequently have subclinical inflammation, and these findings support the practice of regular assessment of disease activity and random biopsy of inflamed and uninflamed areas in patients with PSC with the goal of reducing inflammation to prevent the development of CRN.

The relationship between colorectal cancer and gastric histopathology: case-control study

Aim: The aim of this study was to investigate the gastric histopathological findings (Helicobacter pylori (H. pylori), intestinal metaplasia (IM), atrophic gastritis (AG), and dysplasia) in the patients with and without colorectal cancer (CRC). Material and Method: Two hundred ninety five patients (160 CRC patients and 135 control individuals) were included in the study. Gastric histopathological findings of the patients who underwent upper gastrointestinal (GI) endoscopy were analyzed retrospectively. Results: H. pylori positivity and IM rates in the CRC patient group were significantly higher than the control group (58.8%&amp;amp;27.8% and 33.1%&amp;amp;19.5%, p&amp;lt;0.001 and p&amp;lt;0.012, respectively). In addition, AG, lymphoplasmocytic infiltration, and dysplasia rates were also higher in the CRC patients compared to the control group. But, they were not statistically significant (p=0.462, p=0.103, and p=0.195, respectively). Conclusion: In our study, the frequency of H. pylori and IM in patients with CRC was higher than in the control group. Since the prevalence of H. pylori infection is high in Turkey and H. pylori-related gastric diseases may be potential risk factors for colorectal neoplasia, it is recommended that individuals in the high-risk group to be screened for colonoscopy. Also, upper GI endoscopic examination should be performed to screen for gastric premaling lesions in patients with CRC.

Prevalence and risk of colorectal polyps among the Korean population under 50 years.

Colorectal cancer is a common cancer; generally, adults aged ≥ 50 years are screened using stool occult blood tests and colonoscopy. However, colorectal adenoma and cancer have been found in patients under the aged of 50, and studies on characteristics and risk factors in young patients are lacking. We evaluated the prevalence and risk factors of colorectal adenoma and cancer in young adults aged under 50 years.We retrospectively analyzed 570 individuals aged under 50 years who underwent colonoscopy at the Haeundae Paik Hospital, Korea, from January to June 2018. Logistic regression model was used to identify the risk factors for colorectal adenoma and colorectal cancer.The prevalence of colorectal adenoma in group of 19–29 years was 3.2% (1 of 31), 30–39 years was 13.8% (30 of 217) and in the group of 40–49 years was 21.1% (68 of 322) (P = .009). In multivariable analysis, age over 45 years (adjusted odds ratio [OR], 1.941; 95% confidence interval [CI], 1.187–3.172; P = .008) and male sex (adjusted OR, 1.711; 95% CI, 1.044–2.806; P = .033) were independent risk factors for colorectal neoplasia including cancer.The prevalence of colorectal adenoma increases as the age increased in young adults under 50 years of age, especially after the age of 45 years, the risk of colorectal neoplasia increases; hence, early screening should be considered before the age of 50 years.

Antibiotic Therapy and Risk of Early-Onset Colorectal Cancer: A National Case-Control Study.

INTRODUCTION:Antibiotic use has emerged as a risk factor for colorectal neoplasia and is hypothesized as a contributor to the rising incidence of colorectal cancer under age 50 years or early-onset colorectal cancer (EOCRC). However, the impact of antibiotic use and risk of EOCRC is unknown.METHODS:We conducted a population-based case-control study of CRC among individuals aged ≥18 years in the Epidemiology Strengthened by histoPathology Reports in Sweden (ESPRESSO) cohort (2006–2016). The primary outcome was EOCRC. A secondary outcome was CRC at any age. Incident CRC was pathologically confirmed, and for each, up to 5 population-based controls were matched on age, sex, county of residence, and calendar year. We assessed prescriptions until 6 months before CRC diagnosis. Conditional logistic regression was used to estimate adjusted odds ratios (aORs) and 95% confidence intervals (CIs).RESULTS:We identified 54,804 cases of CRC (2,557 EOCRCs) and 261,089 controls. Compared with none, previous antibiotic use was not associated with EOCRC risk after adjustment for potential confounders (aOR 1.06, 95% CI: 0.96, 1.17) with similarly null findings when stratified by anatomic tumor site. In contrast, previous antibiotic use was weakly associated with elevated risk for CRC at any age (aOR 1.05, 95% CI: 1.02, 1.07). A potential but modest link between broad-spectrum antibiotic use and EOCRC was observed (aOR 1.13, 95% CI: 1.02, 1.26).DISCUSSION:We found no conclusive evidence that antibiotics are associated with EOCRC risk. Although antibiotic use was weakly associated with risk of CRC at any age, the magnitude of association was modest, and the study period was relatively short.

Prevalence and associated risk of advanced colorectal neoplasia in adults with sarcopenia.

Background/AimsAlthough several studies have shown that sarcopenia is associated with poor outcomes in colorectal cancer patients, the impact of sarcopenia on the development of colorectal neoplasia remains unclear. We aimed to evaluate the prevalence and association of colorectal neoplasia, especially advanced colorectal neoplasia, in adults with sarcopenia.MethodsWe retrospectively analyzed the data for 10,676 adults who underwent first-time colonoscopy and bioelectrical impedance analysis (BIA) on the same day in a health screening program at a single center. Sarcopenia was diagnosed using established BIA-based criteria as adjusted appendicular skeletal muscle mass (ASM) divided by body mass index (BMI) (ASM/BMI), height (ASM/height2), or weight (ASM/weight). Prevalence of overall and advanced colorectal neoplasia and their association with sarcopenia, as established by the aforementioned diagnostic criteria, were evaluated.ResultsAmong 10,676 subjects, 583 were diagnosed with sarcopenia using ASM/BMI. Subjects with sarcopenia had a higher prevalence of colorectal neoplasia than those without. In the multivariate analysis after adjusting for confounding factors, sarcopenia was an independent risk factor for any colorectal neoplasia (odds ratio [OR], 1.31; 95% confidence interval [CI], 1.09 to 1.56) and advanced colorectal neoplasia (OR, 1.97; 95% CI, 1.27 to 3.06). The association between sarcopenia and advanced colorectal neoplasia remained significant for all sarcopenia measures including ASM/height2 (OR, 2.19; 95% CI, 1.24 to 3.85) and ASM/weight (OR, 2.41; 95% CI, 1.54 to 3.77).ConclusionsPrevalence of overall and advanced colorectal neoplasia was higher in subjects with sarcopenia than in those without. Sarcopenia was a significant risk factor for colorectal neoplasia, especially for advanced colorectal neoplasia.

CIGARETTE SMOKE INCREASES RISK FOR COLORECTAL NEOPLASIA IN INFLAMMATORY BOWEL DISEASE

Patients with inflammatory bowel disease are at increased risk of colorectal neoplasia (CRN) due to mucosal inflammation. As current surveillance guidelines form a burden on patients and healthcare costs, stratification of high-risk patients is crucial. Cigarette smoke reduces inflammation in ulcerative colitis (UC) but not Crohn’s disease (CD) and forms a known risk factor for CRN in the general population. Due to this divergent association, the effect of smoking on CRN in IBD is unclear and subject of this study.

CIGARETTE SMOKE INCREASES RISK FOR COLORECTAL NEOPLASIA IN INFLAMMATORY BOWEL DISEASE

Abstract Objective Patients with inflammatory bowel disease are at increased risk of colorectal neoplasia (CRN) due to mucosal inflammation. As current surveillance guidelines form a burden on patients and healthcare costs, stratification of high-risk patients is crucial. Cigarette smoke reduces inflammation in ulcerative colitis (UC) but not Crohn’s disease (CD) and forms a known risk factor for CRN in the general population. Due to this divergent association, the effect of smoking on CRN in IBD is unclear and subject of this study. Design In this retrospective cohort study, 1,386 IBD patients with previous biopsies analyzed and reported in the PALGA register, were screened for development of CRN. Clinical factors and cigarette smoke were evaluated. Patients were stratified for guideline-based risk of CRN. Cox-regression modeling was used to estimate the effect of cigarette smoke and its additive effect within the current risk stratification for prediction of CRN. Results 151 (11.0%) patients developed CRN. Previously described risk factors, i.e. first-degree family member with CRN in CD (p-value=0.001), presence of post-inflammatory polyps in UC (p-value=0.004), were replicated. Former smoking increased risk of CRN in UC (HR1.72;1.04–2.84), whereas passive smoke exposure yielded no effect. For CD, active smoking (2.52; 1.14–5.58) and passive smoke exposure (1.88;1.10–3.21) significantly increased CRN risk. Addition of cigarette smoking to the current risk-stratification model significantly improved model fit for CD. Conclusion This study is the first to describe the important role of cigarette smoke in CRN development in IBD patients. Adding this risk factor improves the current risk stratification for CRN surveillance strategies.

Cigarette Smoke Increases Risk for Colorectal Neoplasia in Inflammatory Bowel Disease

Patients with inflammatory bowel disease are at increased risk of colorectal neoplasia (CRN) due to mucosal inflammation. As current surveillance guidelines form a burden on patients and healthcare costs, stratification of high-risk patients is crucial. Cigarette smoke reduces inflammation in ulcerative colitis (UC) but not Crohn's disease (CD) and forms a known risk factor for CRN in the general population. Due to this divergent association, the effect of smoking on CRN in IBD is unclear and subject of this study. In this retrospective cohort study, 1,386 IBD patients with previous biopsies analyzed and reported in the PALGA register were screened for development of CRN. Clinical factors and cigarette smoke were evaluated. Patients were stratified for guideline-based risk of CRN. Cox-regression modeling was used to estimate the effect of cigarette smoke and its additive effect within the current risk stratification for prediction of CRN. 153 (11.5%) patients developed CRN. Previously described risk factors, i.e. first-degree family member with CRN in CD (p-value=.001), presence of post-inflammatory polyps in UC (p-value=.005), were replicated. Former smoking increased risk of CRN in UC (HR 1.73; 1.05-2.85), whereas passive smoke exposure yielded no effect. For CD, active smoking (2.20; 1.02-4.76) and passive smoke exposure (1.87; 1.09-3.20) significantly increased CRN risk. Addition of smoke exposure to the current risk-stratification model significantly improved model fit for CD. This study is the first to describe the important role of cigarette smoke in CRN development in IBD patients. Adding this risk factor improves the current risk stratification for CRN surveillance strategies.

Meat intake, meat cooking methods, and meat-derived mutagen exposure and risk of sessile serrated lesions

Red and processed meat, recognized carcinogens, are risk factors for colorectal neoplasia, including polyps, the precursor for colorectal cancer. The mechanism is unclear. One possible explanation is the mutagenic activity of these foods, perhaps due to generation during cooking [e.g., heterocyclic amine (HCA) intake]. Few studies have evaluated meat intake and sessile serrated lesion (SSL) risk, a recently recognized precursor, and no study has evaluated meat cooking methods and meat-derived mutagens with SSL risk. We evaluated intakes of meat, meat cooking methods, and inferred meat mutagens with SSL risk and in comparison to risk of other polyps. Meat, well-done meat, and inferred meat mutagen intakes were evaluated. Polytomous logistic regression models were used to estimate ORs and 95% CIs among cases (556 hyperplastic polyp, 1753 adenoma, and 208 SSL) and controls (3804) in the large colonoscopy-based, case-control study, the Tennessee Colorectal Polyp Study. The highest quartile intakes of red meat (OR: 2.38; 95% CI: 1.44, 3.93), processed meat (OR: 2.03; 95% CI: 1.30, 3.17), well-done red meat (OR: 2.19; 95% CI: 1.34, 3.60), and the HCA 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQX; OR: 2.48; 95% CI: 1.49, 4.16) were associated with increased risk of SSLs in comparison to the lowest quartile intake. High intakes of red and processed meats are strongly and especially associated with SSL risk and part of the association may be due to HCA intake. Future studies should evaluate other mechanism(s) and the potential for primary prevention.

193 Decreased Levels of High-Molecular-Weight Adiponectin Is Associated With Colorectal Neoplasia in Japan

INTRODUCTION: In Japan, the incidence and mortality rate of colorectal cancer (CRC) has been increased and CRC is considered to be one of obesity-related malignancies. Adiponectin is an adipocyte-specific adipokine, which possesses pleiotropic properties on various disease including atherosclerotic diseases, cardiovascular diseases, inflammatory diseases and tumors. In addition, recent studies have demonstrated that high-molecular-weight (HMW) form of adiponectin is active form of this adipokine. The objective of the present study was to investigate whether HMW adiponectin was a risk factor for colorectal neoplasia (CRN; adenomatous polyp ≥5 mm in size and cancer) using comprehensive health checkup data. METHODS: We conducted a retrospective analysis in clinical practice at a single center. Among 10138 subjects who took comprehensive health checkup at our hospital between in August 2012 and December 2016, 315 subjects who underwent screening both colonoscopy and optional metabolic syndrome course were enrolled. HMW adiponectin was measured using commercially available ELISA kit. We evaluated demographic characteristics, anthropometric measurements, visceral fat area (VFA) measured by CT, hematological metabolic parameters, degree of liver fat evaluated by ultrasonography, and current smoking and drinking habits as variables. Association between variables and CRN was evaluated by univariate analysis using t-test, χ2 test, Mann-Whitney test, and then by multivariate analysis using multiple logistic regression model. A P value &lt;0.05 was considered statistically significant. RESULTS: Of 315 subjects (men: 228, women: 87) analyzed, 97 subjects were diagnosed as MetS (30.8%) and 33 subjects had CRN (10.5%). Subjects with MetS had more CRN (12 subjects, 12.4%) compared with those without MetS (21 subjects, 9.6%) (n.s.). Univariate analysis identified significant association of sex, age, VFA, systolic blood pressure, current smoking habits, drinking habits and ≥10 kg weight gain compared with the body weight at the age of twenty with CRN prevalence. Moreover, HMW adiponectin level was inversely corelated with CRN prevalence (P = 0.003). Logistic regression analysis revealed that age, systolic blood pressure, current smoking, and HMW adiponectin level were independent factors associated with CRN prevalence (Table 1). CONCLUSION: The present study demonstrated that decreased levels of HMW adiponectin is a risk factor for colorectal neoplasia in Japan.

Increased Prevalence of Colorectal Adenomas in Patients with Nonalcoholic Fatty Liver Disease: A Cross-Sectional Study

Background: Nonalcoholic fatty liver disease (NAFLD) is the most common liver disorder worldwide. Previous studies have suggested an association between colorectal adenomas and NAFLD but are limited by a lack of biopsy-proven NAFLD or comparison with matched controls. Objectives: We aimed to determine whether histologically demonstrated NAFLD is an independent risk factor for colorectal adenomas. Methods: Patients who underwent liver biopsy showing steatosis who had also undergone screening or surveillance colonoscopy in 2007–2017 were retrospectively studied by manual chart review, excluding patients with liver disease other than NAFLD. Adenoma detection rates and characteristics such as location, histologic type, and size were compared in the resulting 123 NAFLD patients against controls without liver disease matched by age, gender, and endoscopist. Results: Adenoma prevalence was significantly higher in the NAFLD group at 40.7 versus 28.1% in controls (OR 1.87, 95% CI 1.15–3.03, p = 0.01) and remained significant on multivariable analysis controlling for rates of hyperlipidemia, diabetes, and obesity (OR 1.74, 95% CI 1.05–2.88, p = 0.032). Comparing NAFLD patients with advanced fibrosis to those with simple steatosis, there was a trend toward higher adenoma prevalence in advanced fibrosis (50.0 vs. 36.8%; OR 1.84, 95% CI 0.50–6.70, p = 0.36). Conclusions: Patients with histologically demonstrated NAFLD had a significantly higher adenoma prevalence on colonoscopy compared to matched controls, which remained significant after adjusting for rates of diabetes, obesity, and hyperlipidemia. NAFLD should be investigated further as an independent risk factor for colorectal neoplasia.

Overweight as an Additional Risk Factor for Colorectal Neoplasia in Lean Population

Background:Overweight in Thailand is not as common as in Western countries. We sought to evaluate overweight as the additional risk factor that can increase the prediction of colorectal neoplasia (CRN) detection in Thais apart from the Asia-Pacific Colorectal Screening (APCS) score.Methods:We prospectively enrolled asymptomatic 338 subjects who underwent screening colonoscopy between November 2016 and September 2017. All risk factors according to APCS, BMI and the presence of metabolic syndrome were collected. Overweight was defined as BMI ≥23 kg/m2. By APCS score, subjects were categorized into 1) high-risk and 2) average-risk. Using the combination of APCS score and overweight, subjects were stratified into 4 groups; high-risk with overweight (G1), average-risk with overweight (G2), high-risk with normal weight (G3) average-risk and with normal weight (G4). Logistic regression analysis was used to estimate the risk of detecting CRN.Results:The prevalence of CRN in the high-risk subjects was higher than that of in the average-risk subjects (49%vs.32%; OR, 2.00; 95%CI, 1.17-3.41). After adjustment for APCS risk factors and metabolic syndrome, overweight significantly increased the risk of detecting CRN (OR, 2.52; 95%CI, 1.57-4.05). Among the 4 groups, the detection rates of CRN were significantly different (G1=64%, G2=40%, G3=32% and G4=21%, p<0.01). The relative risk of detecting CRN increased when G1 (OR 6.49; 95%CI, 2.87-14.67), and G2 (2.42; 1.39-4.21) were compared with G4.Conclusions:In addition to the APCS score, overweight is an independent risk factor for detecting CRN. In Thai population, combining overweight and APCS score may be useful to improve the prediction for CRN.

Risk factors for colorectal neoplasia in patients with underlying inflammatory bowel disease: a multicenter study.

BackgroundThis study sought to evaluate the risk factors for the development of colitis-associated neoplasia (CAN) in Chinese patients with inflammatory bowel disease (IBD).MethodsIBD patients who developed CAN between 1999 and 2016 were identified from eight medical centers. In addition to initial pathology evaluation, a CAN diagnosis was confirmed by two expert pathologists. Patients with CAN (n = 29) were compared with non-CAN controls (n = 87). Matching was performed for gender and IBD type with a ratio of three controls to one subject.ResultsOf the 29 patients with CAN, 8 (27.6%) had colorectal cancer (CRC), 20 (69.0%) had a final diagnosis of low-grade dysplasia and 1 (3.4%) had high-grade dysplasia. Multivariate analysis revealed that an older age at the time of IBD diagnosis and a longer IBD duration were independent risk factors for the development of CAN, with odds ratios of 1.09 [95% confidence interval (CI): 1.04–1.14, P < 0.001] and 1.14 (95% CI: 1.03–1.27, P = 0.013), respectively. Comparison between IBD patients with CRC and those with dysplasia indicated that the former were older at the time of IBD diagnosis (P = 0.012) and had longer IBD durations (P = 0.019).ConclusionsOlder age at the time of IBD diagnosis and longer IBD duration were found to be associated with the development of CAN in IBD patients.

Increased Prevalence of Colorectal Adenomas in Patients With Non-Alcoholic Fatty Liver Disease: A Cross-Sectional Study

Introduction: Non-alcoholic fatty liver disease (NAFLD) is the most common liver disorder worldwide. Previous studies have suggested an association between colonic adenomas and NAFLD. In this study we aimed to determine whether patients with biopsy-proven NAFLD have an increased colorectal adenoma prevalence on screening and surveillance colonoscopies compared to matched controls. Methods: We identified 254 patients at Columbia University Medical Center who underwent liver biopsy with steatosis in 2006-2018 and had also undergone screening or surveillance colonoscopy during the same period. Patients with a history of alcoholic liver disease or viral hepatitis were excluded, as were patients with inadequate bowel preparation, leaving 168 patients with NAFLD as the study group. Each patient was matched with 2 controls by age, gender, and endoscopist. The adenoma prevalence was then determined for each group, and compared using conditional logistic regression. Results: The mean age at time of colonoscopy was 60.8 years in the NAFLD group and 60.5 years in the control group (p=0.72). 49.4% of patients were male. Screening colonoscopies made up 68.5% of the NAFLD group vs. 69.4% of the controls, with the remainder surveillance colonoscopies (p=0.84). The adenoma prevalence was 33.9% in the NAFLD group vs. 25.9% in the control group (OR 1.55, p=0.047). On multivariable analysis comparing the subset of NAFLD patients with moderate or high-grade steatosis vs. mild steatosis, controlling for age, gender, colonoscopy indication, and endoscopist, there was a trend towards higher adenoma prevalence in the high-grade steatosis group (OR 2.26, p=0.053). Conclusion: Patients with biopsy-proven NAFLD have a significantly higher adenoma prevalence on screening and surveillance colonoscopies compared to matched controls. Patients with more severe NAFLD were noted to have a higher ADR than those with mild disease, although this did not reach statistical significance. NAFLD should undergo further investigation as a potential risk factor for colorectal neoplasia.276_A Figure 1 No Caption available.276_B Figure 2 No Caption available.276_C Figure 3 No Caption available.

Influence of Obesity and Metabolic Abnormalities on the Risk of Developing Colorectal Neoplasia.

Obesity and metabolic syndrome are risk factors for colorectal neoplasia (CRN). However, the association between metabolically healthy obese (MHO) or metabolically unhealthy non-obese (MUNO) status and the risk of CRN remains unclear. We aimed to elucidate the association between MHO or MUNO status and the risk of CRN. A total of 139,023 asymptomatic subjects who underwent a primary screening colonoscopy were categorized into 4 groups according to obesity and metabolic status: metabolically healthy non-obese (MHNO), MHO, MUNO, and metabolically unhealthy obese (MUO). Mean participant age was 41.0years, and the proportion of men was 65.3%. Among men, the risk of overall CRN increased in MHO (adjusted odds ratio [AOR] 1.22, 95% confidence intervals [CI] 1.12-1.33), MUNO (AOR 1.25, 95% CI 1.18-1.31), and MUO groups (AOR 1.47, 95% CI 1.40-1.54) compared with the MHNO group, whereas the risk of advanced CRN (ACRN) increased in MUNO (AOR 1.16, 95% CI 1.002-1.33) and MUO groups (AOR 1.49, 95% CI 1.31-1.70), but not in the MHO group (AOR 0.92, 95% CI 0.70-1.21). Moreover, among non-obese men, the risk of overall CRN and ACRN linearly increased with an increasing number of metabolic abnormalities. However, among women, only the MUO group had an increased risk of overall CRN (AOR 1.34, 95% CI 1.21-1.47) and no other significant associations were observed. Poor metabolic health, regardless of obesity, is an independent risk factor for CRN in men. Our results suggest that men with metabolic abnormalities should be considered as a high-risk group for colorectal cancer, even if they are not obese.