Risk Factor For Colorectal Adenoma Research Articles

Interaction of Colorectal Neoplasm Risk Factors and Association with Metabolic Health Status Focusing on Normal Waist-to-Hip Ratio in Adults.

We aimed to evaluate the interaction between colorectal adenoma risks among asymptomatic individuals in terms of metabolic health status and obesity, and examine the normal waist-to-hip ratio (WHR) in adults with colorectal adenoma risk. A cross-sectional, retrospective study was conducted at MacKay Memorial Hospital involving 16,996 participants who underwent bidirectional gastrointestinal endoscopy between 2013 and 2023. The study recorded important clinicopathological characteristics, including age, body mass index and WHR, Framingham Risk Score (FRS), blood glucose level, and Helicobacter pylori (H. pylori) infection status. Multivariate logistic regression analysis demonstrated that elevated hemoglobin A1C (HbA1c), increased FRS, positive H. pylori infection, and WHR ≥ 0.9 are independent risk factors for colorectal adenoma. In examining the interaction between FRS and WHR using multivariate logistic regression to evaluate adenoma risk, the OR for the interaction term was 0.95, indicating a decline in adenoma risk when considering the interaction between these two factors. Incorporating HbA1c into the analysis, evaluating the interaction between FRS and WHR still demonstrated a statistically significant impact on adenoma risk (OR 0.96, p < 0.001). Participants with WHR < 0.9, elevated FRS, positive H. pylori infection, and increased HbA1c levels were associated with a higher risk of colorectal adenoma formation. Remarkably, the increased risk of adenoma due to rising HbA1c levels was statistically significant only for those with a WHR < 0.9. An increase in FRS and HbA1c or a positive H. pylori infection still warrants vigilance for colorectal adenoma risk when WHR is 0.9. These factors interacted with each other and were found to have a minimal decline in adenoma risk when considering the interaction between WHR and FRS.

MAFLD with central obesity is associated with increased risk of colorectal adenoma and high-risk adenoma

ObjectiveTo analyze the risk factors associated with colorectal adenoma and to investigate the associations of metabolism-related fatty liver disease (MAFLD) with obesity, colorectal adenoma and high-risk adenoma.MethodsA total of 1395 subjects were enrolled and divided into a colorectal adenoma group (593 subjects) and a control group (802 subjects) according to the inclusion and exclusion criteria. The characteristics of patients in the colorectal adenoma group and the control group were compared by the chi-square test. Univariate and multivariate logistic analyses were used to analyze independent risk factors and associations with different MAFLD subtypes. Colorectal adenoma characteristics and the proportion of patients with high-risk colorectal adenoma were also compared.ResultsHigh-density lipoprotein (HDL-C) was significantly lower in patients in the colorectal adenoma group than in those in the control group (P < 0.001). Logistic regression analysis revealed that age, obesity status, central obesity status, hypertension status, diabetes status, fatty liver status, smoking history, BMI, waist circumference, triglyceride level, HDL-C level, fasting blood glucose level and degree of hepatic steatosis were all independent risk factors for colorectal adenoma. Notably, MAFLD was associated with a significantly increased risk of colorectal adenoma in patients with central obesity (P < 0.001). In addition, obesity, central obesity, diabetes, fatty liver and degree of hepatic steatosis were all shown to be independent risk factors for high-risk colorectal adenoma. In addition, a greater proportion of MAFLD patients with central obesity than those without central obesity had high-risk colorectal adenoma.ConclusionMAFLD and central obesity are independently associated with the development of colorectal adenoma. MAFLD with central obesity is associated with an increased risk of colorectal adenoma and high-risk adenoma.

Hemorrhoids as a risk factor for colorectal adenomas on colonoscopy

Background and study aims Colorectal premalignant polyps and hemorrhoids are important findings in colonoscopy; however, the association between them is unclear. Therefore, we investigated the association between the presence and severity of hemorrhoids and the detection of precancerous colorectal polyps on colonoscopy. Patients and methods This retrospective, single-center, cross-sectional study enrolled patients who underwent colonoscopy at Toyoshima Endoscopy Clinic between May 2017 and October 2020. The association between hemorrhoids and other outcomes (patient age, sex, withdrawal time for colonoscopy, expert endoscopist, number of adenomas per colonoscopy, detection rates of adenoma, advanced neoplasia, clinically significant serrated polyp, and sessile serrated lesion) was assessed using a binomial logistic regression model. Results A total of 12,408 patients were enrolled in this study. Hemorrhoids were identified in 1,863 patients. Univariable analysis showed that patients with hemorrhoids were older (61.0 vs. 52.5 years, P < 0.001), had a higher number of adenomas per colonoscopy (1.16 vs. 0.756, P < 0.001) than those without hemorrhoids. Multivariable analyses also demonstrated that hemorrhoids were associated with a higher number of adenomas per colonoscopy (odds ratio [OR]: 1.061; P = 0.002), regardless of patient age, sex, and expert endoscopist. Among patients with hemorrhoids, severe hemorrhoids with a mucosal elevation ≥ 10 mm were associated with a higher number of adenomas per colonoscopy than mild hemorrhoids (OR: 1.112, P = 0.044), regardless of patient age, sex, and expert endoscopist. Conclusions Hemorrhoids, especially severe ones, are associated with a high number of adenomas. Complete colonoscopy should be performed in patients with hemorrhoids.

Adult BMI change over time and risk of colorectal adenoma.

68 Background: Obesity and adult weigh gain are established risk factors for colorectal cancer (CRC). Few studies have investigated the association between adult body weight change over time and risk of colorectal adenoma. We hypothesize adult BMI change over time is associated with risk in the development of colorectal adenomas. Methods: We tested this hypothesis in 2,993 patients undergoing screening colonoscopy from 2007–2017. Weight at age 20, 30, 40, and 50 were self-reported via computer assisted personal interviews. Height and weight at recruitment were measured at the time of colonoscopy exam. BMI (kg/m2) change was calculated as the difference of BMI at recruitment from the BMI estimate for each of the age periods. Results: Of the 2,993 patients, 984 had pathologically confirmed diagnosis of colon adenoma. Multivariate logistic regression adjusted for potential confounders and BMI at recruitment showed statistically significant increase of risk of adenoma with increase of BMI since age 30, age 40, and age 50. Compared to those with BMI change of less than 5, the ORs for those with BMI gain of 5-10 and ≥10 were: 1) 1.16 (0.92-1.46) and 1.48 (1.08-2.03) respectively for change from age 30 (ptrend = 0.05); 2) 1.11 (0.87-1.43) and 1.60 (1.09-2.35) respectively for change from age 40 (ptrend = 0.05); and 3) 1.36 (0.95-1.94) and 2.95 (1.33-6.90) respectively for change from age 50 (ptrend = 0.01). Stratified analysis did not reveal noticeable gender differences. Conclusions: Large adult weight gain over time is an independent risk factor for colorectal adenoma. Our results suggest maintaining healthy body weight throughout adulthood is an important preventive measure against the development of early colorectal neoplasia. [Table: see text]

Abstract P009: Plasma concentrations of multiple oxysterols and risk of colorectal adenomas

Abstract Oxysterols are metabolites of cholesterol and intermediates in pathways for primary bile acid synthesis that regulate homeostasis of cholesterol, fatty acids, and glucose by interacting with widely expressed nuclear receptors. These metabolites are generated throughout the body, either enzymatically or from oxidative stress, and are detectable in peripheral circulation at concentrations much lower than total cholesterol. We previously reported that circulating 27-hydroxycholesterol (27-OHC), the most abundant oxysterol in circulation and an endogenous selective estrogen receptor modulator, may be a risk factor for colorectal adenomas. Here, we report on four other circulating oxysterols: 25-hydroxycholesterol (25-OHC), 24(S)-hydroxycholesterol (24(S)-OHC), 7ɑ-hydroxycholesterol (7ɑ-OHC), and 4β-hydroxycholesterol (4β-OHC). We used high-sensitivity liquid chromatography-mass spectrometry to measure oxysterol concentrations in fasting plasma collected at baseline from 1,440 participants of the Vitamin D/Calcium Polyp Prevention Study, a completed randomized clinical trial that enrolled men and women recently diagnosed with colorectal adenomas with follow-up timed to colonoscopic surveillance intervals. Advanced adenomas were defined as tubulovillous or villous lesions, ≥1 cm in diameter, with high-grade dysplasia, or invasive adenocarcinoma. Risk ratios (RR) with 95% confidence intervals (CI) of new colorectal adenomas occurring during follow-up were estimated using repeated-measures log-linear regression for log-transformed circulating oxysterols. Primary analyses adjusted for multiple potential confounding factors and the five circulating oxysterols simultaneously, including 27-OHC. One geometric standard deviation (SD) higher circulating 7ɑ-OHC at the time of initial adenoma diagnosis was associated with 9% and 20% higher subsequent risk of any adenomas and advanced adenomas, respectively (RR of any adenomas per SD circulating 7ɑ-OHC, 1.09; 95% CI, 1.03-1.15 and RR of advanced adenomas, 1.20; 95% CI, 1.04-1.39). The positive association with adenoma risk that we previously reported for circulating 27-OHC persisted controlling for the other oxysterols including 7ɑ-OHC (RR of any adenomas per SD circulating 27-OHC 1.07; 95% CI, 0.99-1.15 and RR of advanced adenomas, 1.23; 95% CI, 1.03-1.48). No statistically significant associations were observed for circulating 25-OHC, 24(S)-OHC, and 4β-OHC. We conclude that circulating 7ɑ-OHC and 27-OHC may be independently associated with colorectal adenoma risk. Given these two oxysterols are the initial products of the classic (neutral) and alternative (acidic) pathways for primary bile acid synthesis, respectively, our findings provide additional evidence in support of a role for bile acids in the development of colorectal neoplasia. Novel colorectal cancer prevention strategies may target oxysterol formation. Citation Format: Michael N. Passarelli, Bonne M. Thompson, Jeffrey G. McDonald, Thomas J. Palys, Judy R. Rees, Elizabeth L. Barry, John A. Baron. Plasma concentrations of multiple oxysterols and risk of colorectal adenomas. [abstract]. In: Proceedings of the AACR Special Conference: Precision Prevention, Early Detection, and Interception of Cancer; 2022 Nov 17-19; Austin, TX. Philadelphia (PA): AACR; Can Prev Res 2023;16(1 Suppl): Abstract nr P009.

Analysis of the correlation between non-alcoholic fatty liver disease and the risk of colorectal neoplasms.

This study aims at assessing the potential association between non-alcoholic fatty liver disease (NAFLD) and colorectal neoplasms (CRN). PubMed, Cochrane Library, and Embase were searched for cohort studies. 14 cohort studies with a total population of 38,761,773 were included for meta-analysis after selection. The results showed that NAFLD is related to an increased risk of CRN (OR = 1.23; 95% CI: 1.14-1.32; I2 = 70.7%, p < 0.001). In the subgroup analysis, NAFLD were found to be the independent risk factor of colorectal adenoma (CRA) (OR = 1.29; 95% CI = 1.15-1.45; I2 = 66.4%) and colorectal cancer (CRC) (OR = 1.13; 95% CI = 1.12-1.15; I2 = 69.4%). There is no close correlation between smoking status of NAFLD patients and CRN. Interestingly, bioinformatics analysis revealed that there were overlap of dysregulated gene sets among NAFLD, CRC, and two recently identified regulated cell death types, ferroptosis and cuproptosis, respectively. Our meta- and bioinformatics analysis shows that NAFLD increases the risk of CRN. Ferroptosis and cuproptosis may be the critical links between NAFLD and CRN, respectively. These findings here support that NAFLD is necessary to be considered as an emerging risk factor for CRN.

S276 Does Hepatitis C Independently Increase the Risk of Colorectal Adenoma?

Introduction: Hepatitis C virus (HCV) infection has been associated with extrahepatic malignancies, one such is colorectal carcinoma (CRC). The majority of CRC arise from adenomatous polyps, it is not known if HCV infection influences the growth of these precancerous lesions. This study evaluates the prevalence of colorectal adenomas in HCV patients compared to the general population and if HCV is an independent risk factor for the detection of colorectal adenomas. Methods: This case-control study included patients who underwent screening colonoscopy at our hospital. Patients were divided into cases (HCV) and controls (non-HCV). Patients with no biopsy reports, hepatitis B, and inflammatory bowel disease were excluded. Colonoscopy findings were stratified on the biopsy results i.e., hyperplastic, adenomatous, CRC or normal mucosa. Continuous variables were analyzed using Mann Whitney U test and categorical variables using Chi-square and Fisher's exact test with p< 0.05 considered statistically significant. After 1:1 propensity score matching (PSM), a matched cohort of cases and controls was generated. A multivariate regression analysis to compute an odds ratio for colorectal adenoma detection rate was done. Results: 415 patients were screened, of which 109 HCV patients and 97 controls were included. Descriptive analysis showed that age (p = 0.03), BMI (p = 0.001), aspirin (p = 0.01), smoking (p = 0.004), alcohol use (p = 0.01) and adenoma detection (p = 0.006) were significantly different between both groups. After propensity matching, multivariate regression analysis showed patients with HCV had odds ratio (OR) = 2.06 (p = 0.03), and aspirin use had OR = 0.38 (p = 0.01) in having colorectal adenoma. (Table) Conclusion: Our study shows a significantly higher rate of adenomas in chronic HCV patients. On multivariate analysis with and without propensity score matching, HCV infection was found to be an independent risk factor for colorectal adenoma. Current guidelines do not recommend earlier screening for CRC for such patients. Prospective studies would be required to assess if treatment of HCV leads to lower adenoma detection rates. Table 1. - Multivariate logistic regression for colorectal adenoma detection Variables p value Odds ratio Lower Limit of 95% CI Upper Limit of 95% CI Age ( >60, median) 0.0295* 1.043 1.034 2.125 Hepatitis C 0.0314* 2.152 1.125 3.810 Family history of CRC 0.220 1.984 0.665 5.922 Aspirin use 0.0116* 0.387 0.253 0.89 Smoking 0.499 1.229 0.677 2.231 Alcohol use 0.293 1.527 0.694 3.359 Female Gender 0.869 1.050 0.586 1.882 Diabetes Mellitus 0.529 1.244 0.630 2.459 HIV 0.895 1.148 0.150 8.806

330P Does hepatitis C independently increase the risk of colorectal adenoma?

Hepatitis C virus (HCV) infection has been associated with extrahepatic malignancies, one such is colorectal carcinoma (CRC). Majority of CRC arise from adenomatous polyps, it is not known if HCV influences the growth of these precancerous lesions. This study evaluates the prevalence of colorectal adenomas in HCV patients and if HCV is an independent risk factor for the detection of colorectal adenomas. This case-control study included patients who underwent colonoscopy. Patients were divided into cases (HCV) and controls (non-HCV). Patients with no biopsy reports, hepatitis B, and inflammatory bowel disease were excluded. Colonoscopy findings were stratified on the biopsy results i.e., hyperplastic, adenomatous, CRC or normal mucosa. Continuous variables were analyzed using Mann Whitney U test and categorical variables using Chi-square with p<0.05 considered statistically significant. After 1:1 propensity score matching (PSM), a matched cohort was generated. A multivariate regression analysis to compute an odds ratio for colorectal adenoma detection rate was done. 415 patients were screened, of which 109 HCV patients and 97 controls were included. Descriptive analysis showed that age, BMI, aspirin use , smoking, alcohol use and adenoma detection were significantly different between both groups (p<0.05). After propensity matching, multivariate regression analysis showed patients with HCV had odds ratio (OR) = 2.06 (p = 0.03), and aspirin use had OR = 0.38 (p = 0.01) in having colorectal adenoma.Table: 330PMultivariate logistic regression for colorectal adenomaVariablesp valueORUpper limit CILower limit of CIMedian age0.0295*1.0431.0342.125HCV0.0314*2.1521.1253.810Familal CRC0.2201.9840.6655.922Aspirin use0.0116*0.3870.2530.89Smoking0.4991.2290.6772.231Alcohol0.2931.5270.6943.359Female gender0.8691.0500.5861.882Diabetes mellitus0.5291.2440.6302.459HIV co-infection0.8951.1480.1508.806 Open table in a new tab Our study shows a significantly higher rate of adenomas in chronic HCV patients. On multivariate analysis, HCV infection was found to be an independent risk factor for colorectal adenoma. Current guidelines do not recommend earlier CRC screening. Prospective studies would be required to assess if treatment of HCV leads to lower adenomas.

Early gastric neoplasms are significant risk factor for colorectal adenoma: A prospective case-control study.

Although gastric cancer patients have a high incidence and risk of colorectal cancer, evidence is lacking regarding whether early gastric neoplasms (EGNs), such as gastric adenomas and early gastric cancer, are risk factors for colorectal adenoma. This study aimed to investigate the incidence of colorectal adenomas in patients with EGN.This prospective study was conducted between January 2015 and December 2016. Of the 307 patients who underwent gastric endoscopic submucosal dissection for EGN, 110 patients were enrolled in the EGN group, and 110 age- and sex-matched healthy persons from the screening population were included in the control group in a 1:1 ratio. Demographic factors and results of colonoscopy, including quality assessment, were collected, and analyzed.No significant differences in the quality of colonoscopy, including bowel preparation, cecal intubation rate, and withdrawal time between the 2 groups, were observed. The incidence of colorectal adenoma was significantly higher in the EGN group than in the control group (55.5% vs 26.4%, P = .001). Multivariate analysis confirmed that old age (odds ratio: 1.04, 95% confidence interval: 1.01–1.08, P = .005) and a history of EGN (odds ratio: 4.99, 95% confidence interval: 2.60–9.57, P = .001) were independent risk factors for colorectal adenoma.This is the first prospective study to reflect the quality indicator of colonoscopy and confirmed that old age and a history of EGN are significant risk factors for colorectal adenomas. Therefore, more stringent colonoscopy surveillance should be considered in elderly patients with EGN.

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.

Osteoporosis Is Associated with an Increased Risk of Colorectal Adenoma and High-Risk Adenoma: A Retrospective, Multicenter, Cross-Sectional, Case-Control Study.

Background/AimsThe protective effects of vitamin D and calcium on colorectal neoplasms are known. Bone mineral density (BMD) may be a reliable biomarker that reflects the long-term anticancer effect of vitamin D and calcium. This study aimed to evaluate the association between BMD and colorectal adenomas including high-risk adenoma.MethodsA multicenter, cross-sectional, case-control study was conducted among participants with average risk of colorectal cancer who underwent BMD and screening colonoscopy between 2015 and 2019. The main outcome was the detection of colorectal neoplasms. The variable under consideration was low BMD (osteopenia/osteoporosis). The logistic regression model included baseline demographics, components of metabolic syndrome, fatty liver disease status, and aspirin and multivitamin use.ResultsA total of 2,109 subjects were enrolled. The mean age was 52.1±10.8 years and 42.6% were male. The adenoma detection rate was 43%. Colorectal adenoma and high-risk adenoma were both more prevalent in subjects with low BMD than those with normal BMD (48.2% vs 38.8% and 12.1% vs 9.1%). In the univariate analysis, old age, male sex, smoking, metabolic components, fatty liver, and osteoporosis were significantly associated with the risk of adenoma and high-risk adenoma. In the multivariate analysis, osteoporosis was independently associated with risk of colorectal adenoma (odds ratio [OR], 1.65; 95% confidence interval [CI], 1.11 to 2.46; p=0.014) and high-risk adenoma (OR, 1.94; 95% CI, 1.14 to 3.29; p=0.014).ConclusionsOsteoporosis is an independent risk factor of colorectal adenoma and high-risk adenoma.

Low serum pancreatic amylase levels as a novel latent risk factor for colorectal adenoma in non-alcohol drinkers.

Obesity, insulin resistance, and metabolic alterations increase the risk of colorectal cancer and adenoma (CRA). Non-alcoholic fatty liver disease (NAFLD) or pancreatic disease (NAFPD) shares many risk factors with CRA that may have significant roles in its development; however, the relationship between CRA and NAFLD/NAFPD remains unclear. This cross-sectional study recruited 712 eligible participants without current drinking who had undergone total colonoscopy as part of a health checkup. These participants were classified into a CRA group (n=236) and a control group (n=439), which consisted of individuals without CRA and a history of polyp resection. NAFLD and NAFPD were diagnosed based on abdominal ultrasonography findings. Non-alcoholic fatty liver disease was observed more frequently in individuals with CRA than in the control group (55.9% vs 41.6%, P<0.01). There was no significant association between NAFPD and CRA; however, serum pancreatic amylase (P-amylase) levels were significantly lower in individuals with CRA. Although NAFLD was one of the factors increasing the presence of CRA (odds ratio [OR], 1.50; 95% confidence interval [CI], 1.07-2.10), low P-amylase levels were significantly associated with the presence of CRA (OR, 1.73; 95% CI, 1.04-2.88) independent of age, sex, current smoking, obesity, metabolic alterations including insulin resistance, and NAFLD. Low serum P-amylase levels were a possible independent risk factor for CRA in the present study. The latent pancreatic exocrine-endocrine-gut relationship was considered a novel pathway involved in obesity-related CRA development, in non-alcoholic individuals.

The clinical significance of vitamin D levels and vitamin D receptor mRNA expression in colorectal neoplasms.

Background/AimThis study aimed to investigate the clinical significance of changes in vitamin D [25(OH)D] levels and vitamin D receptor (VDR) mRNA expression in colorectal adenoma development.MethodsPlasma concentrations of 25(OH)D and mRNA expression of VDR in tissues were determined by enzyme‐linked immunosorbent assay (ELISA) and real‐time fluorescence quantitative polymerase chain reaction (RT‐qPCR), respectively. In addition, the concentration of plasma 25(OH)D and levels of VDR mRNA in tissues were compared among healthy individuals and adenoma and adenocarcinoma patients.ResultsVitamin D receptor expression in colorectal adenocarcinoma tissues was significantly lower than that in para‐cancerous tissues that were >5 cm away from malignant tumor sites (p < 0.01). The level of VDR expression in normal colorectal tissues from healthy individuals was significantly higher than that in colorectal adenomas (p < 0.01) and colorectal adenocarcinomas (p < 0.01); however, the VDR expression was not significantly different between colorectal adenomas and colorectal adenocarcinomas (p = 0.106). The concentration of 25(OH)D in healthy individuals was significantly higher than that in patients with colorectal adenomas (p < 0.01) and colorectal adenocarcinomas (p < 0.01); however, the concentration of 25(OH)D was not significantly different between colorectal adenomas and colorectal adenocarcinomas (p = 0.489). A low concentration of 25(OH)D was considered a risk factor for colorectal adenoma and colorectal adenocarcinoma, with odds ratios of 4.875 and 2.925, respectively.ConclusionsThe 25(OH)D levels and VDR mRNA expression might be associated with the development of colorectal adenoma and its progression to adenocarcinoma.

The Risk of Colorectal Adenoma in Nonalcoholic or Metabolic-Associated Fatty Liver Disease.

Nonalcoholic fatty liver disease (NAFLD) is the most common cause of liver disease associated with various metabolic disorders. Metabolic dysfunction-associated fatty liver disease (MAFLD) emphasizes metabolic dysfunction in NAFLD. Although the relationship between NAFLD and colorectal adenomas has been suggested, the effect of MAFLD on colorectal adenoma has yet to be investigated. In this study, we examined the relationship between NAFLD/MAFLD and colorectal adenoma in comparison with other metabolic factors. Methods: Examinees who underwent colonoscopy and abdominal ultrasonography on the same day from January 2012 to December 2012 were included. NAFLD was diagnosed according to the findings of ultrasonography. The Fibrosis-4 (FIB-4) index was used as a surrogate marker for advanced hepatic fibrosis. A logistic regression model was used to analyze the risk of NAFLD/MAFLD for colorectal adenoma. Results: The prevalence of NAFLD and MAFLD was 37.5% and 32.8%, respectively. In the multivariate analysis, male sex, older age, diabetes, and smoking increased the risk of colorectal adenoma. NAFLD and MAFLD were the most important risk factors for colorectal adenoma only in females [adjusted odds ratio (OR) 1.43 and 95% confidence interval (CI) 1.01–2.03, and OR 1.55, 95% CI 1.09–2.20, respectively]. NAFLD and MAFLD with an advanced fibrosis index were significantly associated with an increased risk of colorectal adenoma. (NAFLD: OR 1.38, 95% CI, 1.04–1.83, p = 0.027; MAFLD: OR 1.45, 95% CI, 1.13–1.96, p = 0.004, respectively). Conclusion: NAFLD and MAFLD were significantly associated with a higher risk of colorectal adenomas, especially in females. NAFLD and MAFLD with advanced fibrosis were associated with an increased risk of colorectal adenoma. Colonoscopic examinations may be emphasized for patients with NAFLD/MAFLD, for women, or patients with the presence of hepatic fibrosis.

Association between body mass index and colorectal adenomas: Findings from a case-control study in Vietnam.

Colorectal cancer is a leading cancer worldwide and in Vietnam. Adenomas (adenomatous polyps) is an important precursor of colorectal cancer. There is currently no study to determine the modifiable risk factors for colorectal adenomas, including body mass index (BMI) in Vietnam. We conducted an individually matched case-control study of 1149 colorectal adenomas and 1145 controls in a large-scale colorectal screening program involving 103 542 individuals aged 40-75 years old in Hanoi, Vietnam. Conditional logistic regression was used to evaluate the association between BMI and colorectal adenomas prevalence, after controlling for potential confounders. Overall, comparing to normal weight (ie, 18.5-22.9kg/m2 ), underweight (ie, BMI < 18.5) was associated with a non-statistically significant increased prevalence of colorectal adenomas (odd ratio [OR]=1.29 and 95% confident interval [CI]: 0.88-1.87). This association became significant among male (OR=1.98, 95% CI: 1.20-3.27), male who were ever smokers (OR=2.59, 95% CI: 1.33-5.03), nonregular exercise (OR=2.44, 95% CI: 1.26-4.73) and individuals with cardiometabolic disorders (OR=3.46, 95% CI: 1.19-10.00). The association between underweight and colorectal adenomas did not vary by smoking status, drinking status, family history of cancer, adenomas types or cardiometabolic disorders. No association was observed among obese individuals (BMI ≥ 25). In the population with low prevalence of obesity, we found that the association between BMI and colorectal adenomas followed a reversed J-shape that underweight was associated with increased prevalence. Further studies are, therefore, warranted to replicate our results and to investigate the biologic mechanism the effect of underweight on colorectal adenomas prevalence.

Associations of Human Colorectal Adenoma with Serum Biomarkers of Body Iron Stores, Inflammation and Antioxidant Protein Thiols.

Red and processed meat consumption and obesity are established risk factors for colorectal adenoma (CRA). Adverse changes in biomarkers of body iron stores (total serum iron, ferritin, transferrin and transferrin saturation), inflammation (high-sensitivity C-reactive protein [hs-CRP]) and anti-oxidative capacity (total of thiol groups (-S-H) of proteins [SHP]) might reflect underlying mechanisms that could explain the association of red/processed meat consumption and obesity with CRA. Overall, 100 CRA cases (including 71 advanced cases) and 100 CRA-free controls were frequency-matched on age and sex and were selected from a colonoscopy screening cohort. Odds ratios (OR) and 95% confidence intervals (95%CI) for comparisons of top and bottom biomarker tertiles were derived from multivariable logistic regression models. Ferritin levels were significantly positively associated with red/processed meat consumption and hs-CRP levels with obesity. SHP levels were significantly inversely associated with obesity. Transferrin saturation was strongly positively associated with overall and advanced CRA (ORs [95%CIs]: 3.05 [1.30–7.19] and 2.71 [1.03–7.13], respectively). Due to the high correlation with transferrin saturation, results for total serum iron concentration were similar (but not statistically significant). Furthermore, SHP concentration was significantly inversely associated with advanced CRA (OR [95%CI]: 0.29 [0.10–0.84]) but not with overall CRA (OR [95%CI]: 0.65 [0.27–1.56]). Ferritin, transferrin, and hs-CRP levels were not associated with CRA. High transferrin saturation as a sign of iron overload and a low SHP concentration as a sign of redox imbalance in obese patients might reflect underlying mechanisms that could in part explain the associations of iron overload and obesity with CRA.

ID: 3525491 ALCOHOL CONSUMPTION AND COLORECTAL ADENOMA - A DOSE-DEPENDENT RELATIONSHIP

Although several lifestyle factors such as obesity, factors of the metabolic syndrome, physical activity, smoking, and consumption of red meat have been identified as modifiable risk factors for colorectal adenoma and colorectal cancer, the role of alcohol consumption remains controversial. Specifically, low or moderate levels have been considered “safe” due to inconclusive results from published studies. We therefore aimed to clarify the role of alcohol consumption on the prevalence of colorectal lesions.

Circulating 27-hydroxycholesterol and Risk of Colorectal Adenomas and Serrated Polyps.

The oxysterol 27-hydroxycholesterol (27-OHC) is an endogenous selective estrogen receptor modulator implicated in breast cancer etiology. It is unknown whether circulating 27-OHC is associated with colorectal neoplasia risk. Circulating 27-OHC was measured using LC/MS in fasting plasma collected at baseline from participants of the Vitamin D/Calcium Polyp Prevention Study, a completed randomized clinical trial. Participants were between 45 and 75 years old, recently diagnosed with ≥1 colorectal adenoma, and followed for new colorectal polyps during colonoscopic surveillance. Adjusted risk ratios (RR) with 95% confidence intervals (CI) of new colorectal polyps were estimated for quartiles of circulating 27-OHC using log-linear regression for repeated outcomes. Polyp phenotypes included any adenomas, advanced adenomas, hyperplastic polyps, and sessile serrated adenomas/polyps. Circulating 27-OHC was measured at baseline for 1,246 participants. Compared with participants with circulating 27-OHC below the first quartile (<138 ng/mL), those with circulating 27-OHC at or above the fourth quartile (≥201 ng/mL) had 24% higher risk of adenomas (RR, 1.24; 95% CI, 1.05-1.47) and 89% higher risk of advanced adenomas (RR, 1.89; 95% CI, 1.17-3.06). Stronger associations were observed among participants with advanced adenomas at baseline. Circulating 27-OHC was not associated with risk of hyperplastic polyps (RR, 0.90; 95% CI, 0.66-1.22) or sessile serrated adenomas/polyps (RR, 1.02; 95% CI, 0.50-2.07). Circulating 27-OHC may be a risk factor for colorectal adenomas but not serrated polyps. PREVENTION RELEVANCE: This study found that plasma concentration of 27-hydroxycholesterol, a metabolite of cholesterol that regulates lipid metabolism and acts as a selective estrogen receptor modulator, is associated with the risk of developing precursor lesions for colorectal cancer.

Helicobacter pylori infection with atrophic gastritis: An independent risk factor for colorectal adenomas.

BACKGROUNDThe significance of Helicobacter pylori (H. pylori) infection and atrophic gastritis (AG) in the prevalence of colorectal adenomas has been examined in a limited number of studies. However, these studies reported disputed conclusions.AIMTo investigate whether H. pylori infection, AG, and H. pylori-related AG increase the risk of colorectal adenomas.METHODSThis retrospective cross-sectional study included 6018 health-check individuals. The relevant data for physical examination, laboratory testing, 13C-urea breath testing, gastroscopy, colonoscopy and histopathological examination of gastric and colorectal biopsies were recorded. Univariate and multivariate logistic regression analyses were performed to determine the association between H. pylori-related AG and colorectal adenomas.RESULTSOverall, 1012 subjects (16.8%) were diagnosed with colorectal adenomas, of whom 143 (2.4%) had advanced adenomas. Among the enrolled patients, the prevalence of H. pylori infection and AG was observed as 49.5% (2981/6018) and 10.0% (602/6018), respectively. Subjects with H. pylori infection had an elevated risk of colorectal adenomas (adjusted odds ratio [OR] of 1.220, 95% confidence interval (CI): 1.053-1.413, P = 0.008) but no increased risk of advance adenomas (adjusted OR = 1.303, 95%CI: 0.922-1.842, P = 0.134). AG was significantly correlated to an increased risk of colorectal adenomas (unadjusted OR = 1.668, 95%CI: 1.352-2.059, P < 0.001; adjusted OR = 1.237, 95%CI: 0.988-1.549, P = 0.064). H. pylori infection accompanied by AG was significantly associated with an increased risk of adenomas (adjusted OR = 1.491, 95%CI: 1.103-2.015, P = 0.009) and advanced adenomas (adjusted OR = 1.910, 95%CI: 1.022-3.572, P = 0.043).CONCLUSIONH. pylori-related AG was associated with a high risk of colorectal adenomas and advanced adenomas in Chinese individuals.

Leisure-Time Physical Activity Versus Sedentary Behaviour in Relation to Colorectal Adenoma and Cancer: Are these Two Distinct Risk Factors?

This literature review provides an up-to-date overview of the evidence relating to the associations of leisure-time physical activity and sedentary behaviour with the risk of colorectal adenoma and cancer. A summary of possible biological mechanisms underpinning these associations is also presented. Leisure-time physical activity and sedentary behaviour are often conceptualised as independent risk factors for colorectal adenoma and cancer. Regular leisure-time physical activity is associated with a 20%–25% reduction in colorectal cancer risk and an estimated 16% reduction in colonic adenoma. The risk estimates are similar for males and females, and for proximal and distal colon cancers. In contrast, the evidence linking physical inactivity to rectal cancer is inconsistent. Epidemiological evidence suggests that television viewing time and occupational sitting are associated with a 54% and 24% increased risk of colon cancer, respectively. Prolonged TV viewing (a commonly measured type of sedentary behaviour) is associated with a 9–16% increased risk of colorectal adenoma, independent of leisure-time physical activity. There is convincing evidence that higher leisure-physical activity is associated with a lower risk of colorectal adenoma and proximal and distal colon cancer; no consistent association emerges for rectal cancer. There is emerging evidence linking sedentary behaviour to risk of colorectal cancer and adenoma. Epidemiological evidence suggests that there may be an interaction between leisure-time physical activity and sedentary behaviour. While it is possible that both exposures contribute to carcinogenesis through similar biological mechanisms, further mechanistic research is required to discern whether there are different biological pathways operating in response to physical activity versus sedentary behaviour.