Objective To explore the application value of the sequential colorectal cancer screening program in population completed health check-ups .Methods The healthy individuals were enrolled from November 2013 to July 2014 .Questionnaire survey of risk factors quantity assessment and fecal occult blood test (FOBT) were used for initial screening for colorectal cancer .According to the results of initial screening ,subjects were divided into high-risk group and low-risk group .The detection rates of polyps and cancers of two groups were compared .Chi-square test was performed for statistic alanalysis .Results A total of 525 individuals completed the colonoscopy .There were 187 individuals in high-risk group and 338 individuals in low-risk group .The results of colonscope examination showed that 70 cases of high-risk group were detected with polyps or colorectal cancer ,including 7 (10 .0% ) cases of colorectal cancers , 8(11 .4% ) cases of advanced adenoma ,30(42 .9% ) cases of non-advanced adenoma and 25(35 .7% ) cases of inflammatory polyps . In low-risk group , 63 individuals had polyps or colorectal cancer , including 5(7 .9% ) cases of advanced adenoma ,38(60 .3% ) cases of non-advanced adenoma and 20(31 .7% ) cases of inflammatory polyps .The differences of polyps and colorectal cancer detection rates between two groups were statistically significant (χ2=3 .905 and 10 .136 ,P=0 .048 and 0 .001) .Conclusion The sequential colorectal screening program including colorectal cancer risk factors quantity assessment questionnaire and FOBT seems to be a valuable tool in clinical practice .

Inflammatory bowel disease (IBD) is a non-specific inflammatory disease of the gastrointestinal (GI) tract that is generally accepted to be closely related to intestinal dysbiosis in the host. GI infections contribute a key role in the pathogenesis of IBD; however, although the results of recent clinical studies have revealed an inverse correlation between Helicobacter pylori (H. pylori) infection and IBD, the exact mechanism underlying the development of IBD remains unclear. H. pylori, as a star microorganism, has been a focus for decades, and recent preclinical and real-world studies have demonstrated that H. pylori not only affects the changes in the gastric microbiota and microenvironment but also influences the intestinal microbiota, indicating a potential correlation with IBD. Detailed analysis revealed that H. pylori infection increased the diversity of the intestinal microbiota, reduced the abundance of Bacteroidetes, augmented the abundance of Firmicutes, and produced short-chain fatty acid-producing bacteria such as Akkermansia. All these factors may decrease vulnerability to IBD. Further studies investigating the H. pylori-intestinal microbiota metabolite axis should be performed to understand the mechanism underlying the development of IBD.
Chronic Disease ; Dysbiosis/microbiology* ; Gastrointestinal Microbiome ; Helicobacter Infections ; Helicobacter pylori ; Humans ; Inflammatory Bowel Diseases/microbiology* ; Microbiota

Eosinophilic gastroenteritis (EGE) is a gastrointestinal disorder of unclear etiology that is characterized by eosinophilic infiltration of the stomach and small intestine, and consists of mucosal, muscular, and serosal subtypes. Eosinophilic infiltration of the gastrointestinal tract is a fundamental histopathological characteristic of EGE and is driven by several T-helper type 2 (Th2)-dependent cytokines and induced by food allergy. Due to the lack of a diagnostic gold standard, EGE has a high rate of delayed diagnosis or misdiagnosis. However, several new diagnostic strategies have been developed, such as novel genetic biomarkers and imaging tests. Although dietary therapy and corticosteroids remain the common choices for EGE treatment, recent decades have seen the emergence of novel treatment alternatives, such as biologics that target particular molecules involved in the pathogenic process. Preliminary investigations and clinical trials have demonstrated the efficacy of biologics and provided additional insights for the era of refractory or corticosteroid-dependent EGE biologics.
Humans ; Enteritis/drug therapy* ; Gastritis/drug therapy* ; Eosinophilia/therapy* ; Abdomen ; Adrenal Cortex Hormones