OBJECTIVES Repeat colonoscopy in 10 years after a normal screening colonoscopy is recommended in an average-risk patient, and it has been proposed by American Gastroenterological Association (AGA), American College of Gastroenterology (ACG), and American Society for Gastrointestinal Endoscopy (ASGE) as a quality measure. However, there are little quantitative data about adherence to this recommendation or factors that may improve adherence. Our study quantifies adherence to this recommendation and the impact of suboptimal bowel preparation on adherence. METHODS In this retrospective database study, endoscopy reports of average-risk individuals ≥50 years old with a normal screening colonoscopy were reviewed. Quality of colon cleansing was recorded using the Aronchick scale as excellent, good, fair, or poor. Main outcome measurements were quality of bowel preparation and recommendation for timing of repeat colonoscopy. Recommendations were considered consistent with guidelines if 10-year follow-up was documented after excellent, good, or fair prep or if ≤1-year follow-up was recommended after poor prep. RESULTS Among 1,387 eligible patients, recommendations for follow-up colonoscopy inconsistent with guidelines were seen in 332 (23.9%) subjects. By bowel preparation quality, 15.3% of excellent/ good, 75% of fair, and 31.6% of poor bowel preparations were assigned recommendations inconsistent with guidelines (P < 0.001). Patients with fair (odds ratio = 18.0; 95% confidence interval 12.0–28.0) were more likely to have recommendations inconsistent with guidelines compared with patients with excellent/good preps. CONCLUSIONS Recommendations inconsistent with guidelines for 10-year intervals after a normal colonoscopy occurred in >20% of patients. Minimizing “fair” bowel preparations may be a helpful intervention to improve adherence to these recommendations.
Although African‐Americans (AAs) have a higher incidence of colorectal cancer (CRC) than White people, the underlying biochemical mechanisms for this increase are poorly understood. The current investigation was undertaken to examine whether differences in self‐renewing cancer stem/stem‐like cells (CSCs) in the colonic mucosa, whose stemness is regulated by certain microRNAs (miRs), could partly be responsible for the racial disparity in CRC. The study contains 53 AAs and 47 White people. We found the number of adenomas and the proportion of CD44+ CD166− CSC phenotype in the colon to be significantly higher in AAs than White people. MicroRNAs profile in CSC‐enriched colonic mucosal cells, expressed as ratio of high‐risk (≥3 adenomas) to low‐risk (no adenoma) CRC patients revealed an 8‐fold increase in miR‐1207‐5p in AAs, compared to a 1.2‐fold increase of the same in White people. This increase in AA was associated with a marked rise in lncRNA PVT1 (plasmacytoma variant translocation 1), a host gene of miR‐1207‐5p. Forced expression of miR‐1207‐5p in normal human colonic epithelial cells HCoEpiC and CCD841 produced an increase in stemness, as evidenced by morphologically elongated epithelial mesenchymal transition( EMT) phenotype and significant increases in CSC markers (CD44, CD166, and CD133) as well as TGF‐β, CTNNB1, MMP2, Slug, Snail, and Vimentin, and reduction in Twist and N‐Cadherin. Our findings suggest that an increase in CSCs, specifically the CD44+ CD166− phenotype in the colon could be a predisposing factor for the increased incidence of CRC among AAs. MicroRNA 1207‐5p appears to play a crucial role in regulating stemness in colonic epithelial cells in AAs.
AIMTo determine whether and to what extent the gut microbiome is involved in regulating racial disparity in colorectal cancer (CRC).METHODSAll patients were recruited and experiments were performed in accordance with the relevant guidelines and regulations by the Institutional Review Boards (IRB), committees of the John D. Dingell VAMC and Wayne State University guidelines. African American (AA) and Caucasian American (CA) patients were scheduled for an outpatient screening for colonoscopy, and no active malignancy volunteer patients were doubly consented, initially by the gastroenterologist and later by the study coordinator, for participation in the study. The gut microbial communities in colonic effluents from AAs and CAs were examined using 16sRNA profiling, and bacterial identifications were validated by performing SYBR-based Real Time PCR. For metagenomic analysis to characterize the microbial communities, multiple software/tools were used, including Metastats and R statistical software.RESULTSIt is generally accepted that the incidence and mortality of CRC is higher in AAs than in CAs. However, the reason for this disparity is not well understood. We hypothesize that the gut microbiome plays a role in regulating this disparity. Indeed, we found significant differences in species richness and diversity between AAs and CAs. Bacteroidetes was more abundant in AAs than in CAs. In particular, the pro-inflammatory bacteria Fusobacterium nucleatum and Enterobacter species were significantly higher in AAs, whereas probiotic Akkermansia muciniphila and Bifidobacterium were higher in CAs. The polyphyletic Clostridia class showed a divergent pattern, with Clostridium XI elevated in AAs, and Clostridium IV, known for its beneficial function, higher in CAs. Lastly, the AA group had decreased microbial diversity overall in comparison to the CA group. In summary, there were significant differences in pro-inflammatory bacteria and microbial diversity between AA and CA, which may help explain the CRC disparity between groups.CONCLUSIONOur current investigation, for the first time, demonstrates microbial dysbiosis between AAs and CAs, which could contribute to the racial disparity of CRC.
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