Determination of an Appropriate Endoscopic Monitoring Interval for Patients with Gastric Precancerous Conditions in China.

OBJECTIVE: Gastric precancerous conditions such as atrophic gastritis (AG) and intestinal metaplasia (IM) are considered independent risk factors for gastric cancer (GC). The suitable endoscopic monitoring interval is unclear when we attempt to prevent GC development. This study investigated the appropriate monitoring interval for AG/IM patients. METHODS: Totally, 957 AG/IM patients who satisfied the criteria for evaluation between 2010 and 2020 were included in the study. Univariate and multivariate analyses were used to determine the risk factors for progression to high-grade intraepithelial neoplasia (HGIN)/GC in AG/IM patients, and to determine an appropriate endoscopic monitoring scheme. RESULTS: During follow-up, 28 AG/IM patients developed gastric neoplasia lesions including gastric low-grade intraepithelial neoplasia (LGIN) (0.7%), HGIN (0.9%), and GC (1.3%). Multivariate analysis identified H. pylori infection (P=0.022) and extensive AG/IM lesions (P=0.002) as risk factors for HGIN/GC progression (P=0.025). CONCLUSION: In our study, HGIN/GC was present in 2.2% of AG/IM patients. In AG/IM patients with extensive lesions, a 1-2-year surveillance interval is recommended for early detection of HIGN/GC in AG/IM patients with extensive lesions.

Relationship between endoscopic gastric abnormalities and colorectal polyps: a cross-sectional study based on 33439 Chinese patients.

Background: No study on the relationship between common abnormalities of the upper digestive tract and colorectal polyps (CPs) has been conducted. Methods: 33439 patients were enrolled in this cross-sectional study, of which 7700 had available Helicobacter pylori (H.pylori) information. All participants underwent colonoscopy and esophagogastroduodenoscopy (EGD) simultaneously or within six months at Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology from January 2015 to November 2021. The study assessed whether the risk of CPs was affected by the following gastroesophageal diseases: atrophic gastritis (AG), gastric polyps, Barrett's esophagus and reflux esophagitis, bile reflux, gastric ulcer, gastric mucosal erosion, superficial gastritis, and gastric H.pylori infection. The crude and adjusted odds ratios (ORs) of H.pylori on the occurrence of CPs were computed by logistic regression. Additionally, we also evaluated whether AG had an impact on the relationship between H.pylori infection and CPs. Results: A total of 10600 cases (31.7%) were diagnosed as CPs. Multivariate logistic analysis showed that age, male (OR, 1.80; 95% confidence interval [CI], 1.61 to 2.02), gastric polyps (OR, 1.61; 95% CI, 1.05 to 2.46 for hyperplastic polyps; OR, 1.45; 95% CI, 1.09 to 1.94 for fundic gland polyps), H.pylori infection (OR, 1.21; 95% CI, 1.07 to 1.37) and atrophic gastritis (OR, 1.38; 95% CI, 1.21 to 1.56) were independent risk factors for colorectal polyps. Moreover, the combined effect of H.pylori infection and AG was slightly greater than the sum of their individual effects on the risk of CPs, but there was no additive interaction between them. Conclusions: Gastric conditions including gastric polyps, H.pylori infection, and AG increased the risk of CPs. However, Barrett's esophagus and reflux esophagitis, bile reflux, erosive gastritis, gastric ulcer, and superficial gastritis might not have relationship with CPs occurrence.

Hypertriglyceridemia may contribute to stroke and pancreatitis: A case report and review of the literature.

Hypertriglyceridemia (HTG) is one of the most common clinical dyslipidemia. Nevertheless, stroke and acute pancreatitis co-occurrence due to hypertriglyceridemia are extremely rare. We present a case of hypertriglyceridemia-associated stroke and pancreatitis in a 39-year-old woman. The patient's laboratory tests reported high triglyceride concentrations beyond the instrument's detection range, and radiological examination showed typical signs of cerebral infarction and acute pancreatitis. The patient received combined blood purification therapy, intravenous thrombolysis with urokinase, and conservative treatment of pancreatitis. We discuss the clinical features, pathogenesis, diagnosis, and treatment of hypertriglyceridemic stroke and pancreatitis combined with the relevant literature. We reviewed the mechanisms by which triglycerides contribute to atherosclerosis and acute pancreatitis. We point out the superiority of combined blood purification therapy and caution physicians about the effects of prescribed drugs on blood lipids.

Hepatic HRC induces hepatocyte pyroptosis and HSCs activation via NLRP3/caspase-1 pathway.

The histidine-rich calcium-binding protein (HRC) is a regulator of Ca2 + homeostasis and it plays a significant role in liver fibrosis. Pyroptosis, a specific inflammatory cell death, can lead to hepatic stellate cells (HSCs) activation and liver fibrosis. However, the role of HRC in pyroptosis has not been explored. In this study, we demonstrated that HRC, mainly located in the hepatocyte, was over expressed in fibrotic liver tissues. We further found that enforced expression of HRC in hepatocytes induced pyroptosis and HMGB1 release, and subsequently led to HSCs activation by NLRP3/caspase-1 pathway. In addition, the proliferation and migration of HSCs were also enhanced by HRC overexpression in hepatocytes. Furthermore, NLRP3 inhibitor MCC950 and caspase-1 inhibitor VX-765 alleviated hepatic HRC-mediated hepatocytes pyroptosis and HSCs activation. This study demonstrated that hepatic HRC promoted HSCs activation by inducing hepatocyte pyroptosis, which suggests that HRC may be a promising therapeutic target to prevent liver fibrosis.

Improving the quality of bowel preparation by smartphone education platform prior to colonoscopy: a randomized trail.

OBJECTIVE: Adequate bowel preparation is an essential factor in colonoscopy. Enhanced education on the procedure of bowel preparation is very necessary for patients before colonoscopy. We analysed the influence of a novel education platform on bowel preparation quality before colonoscopy. PATIENTS AND METHODS: The study enrolled outpatients who underwent colonoscopy in the digestive endoscopy centre of Wuhan Tongji Hospital. They were divided into the control group and the intervention group according to different educational ways. The control group patients were provided with the regular colonoscopy preparation leaflet. The intervention group patients were asked to add the education platform. The primary outcome was the rate of adequate bowel preparation. The study was registered at Chinese ClinicalTrials.gov (ChiCTR2100053547, 24/11/2021). RESULTS: A total of 378 patients who underwent colonoscopy were enrolled, including 189 patients in the control group and 189 patients in the intervention group. The Boston bowel preparation score (BBPS) was significantly higher in the intervention group than that in the control group (p < .05). The adequate rate of bowel preparation in the intervention group was significantly improved than that in the control group (p = .000). Compared with the control group, the polyp detection rate (PDR) was significantly higher in the intervention group (p = .006), especially in the left colonic (p = .006). Among constipation patients, the adequate rate of bowel preparation (p = .000) and the PDR (p = .004) were significantly improved than that in the control group. CONCLUSIONS: The smartphone education platform may effectively improve bowel preparation quality, PDR, and patients' compliance.Key messagesThe quality of bowel preparation mainly relies on the patients' compliance with the bowel preparation instructions.The study reveals that the superiority of the smartphone education platform by Mini Program in improving bowel preparation and colorectal polyp detection rate.The smartphone education platform may provide a more effective, convenient, and labour-saving way to provide further improvements to patients prior to colonoscopy.

Epstein-Barr Virus is Associated with Gastric Cancer Precursor: Atrophic Gastritis.

Background: About 10% of gastric cancer (GC) has been described to be Epstein-Barr virus (EBV) positive. Previous researches have described the association between EBV and GC. However, the association of EBV with atrophic gastritis (AG) is underrecognized. Our study aimed to investigate the relationship between EBV and AG and assess the influence of EBV on gastric function. Methods: A total of 468 pathologically-confirmed chronic gastritis patients underwent circulating EBV DNA test, include 271 non-atrophic gastritis (NAG) and 197 AG patients. Results: In this study, H. pylori infection rate was 33.3%, EBV infection rate was 40%, and co-infection rate was 15%. The EBV DNA-positive was significantly associated with AG (P=0.031, OR= 1.509, 95% CI 1.037-2.194), especially in H. pylori-negative subjects (P=0.044, OR=1.619, 95% CI 1.012-2.589). EBV DNA-positive patients had a lower pepsinogen I (PG I) / pepsinogen II (PG II) ratio (PGR) than EBV DNA-negative patients (P=0.0026), especially in the AG subgroup (P=0.0062). There was no significant association between EBV and H. pylori co-infection with increased risk of AG (P>0.05). Conclusion: EBV infection significantly increased the risk of AG, especially in H. pylori-negative patients. The circulating EBV DNA had a potential in predicting the risk of atrophic gastritis.

NSAID-Associated Small Intestinal Injury: An Overview From Animal Model Development to Pathogenesis, Treatment, and Prevention.

With the wide application of non-steroidal anti-inflammatory drugs (NSAIDs), their gastrointestinal side effects are an urgent health burden. There are currently sound preventive measures for upper gastrointestinal injury, however, there is a lack of effective defense against lower gastrointestinal damage. According to a large number of previous animal experiments, a variety of NSAIDs have been demonstrated to induce small intestinal mucosal injury in vivo. This article reviews the descriptive data on the administration dose, administration method, mucosal injury site, and morphological characteristics of inflammatory sites of various NSAIDs. The cells, cytokines, receptors and ligands, pathways, enzyme inhibition, bacteria, enterohepatic circulation, oxidative stress, and other potential pathogenic factors involved in NSAID-associated enteropathy are also reviewed. We point out the limitations of drug modeling at this stage and are also pleased to discover the application prospects of chemically modified NSAIDs, dietary therapy, and many natural products against intestinal mucosal injury.

HRC promotes anoikis resistance and metastasis by suppressing endoplasmic reticulum stress in hepatocellular carcinoma.

Histidine-rich calcium binding protein (HRC) is markedly overexpressed in hepatocellular carcinoma (HCC) and is significantly correlated with metastasis. Anoikis resistance and endoplasmic reticulum (ER) stress may have a critical effect on survival before metastasis. However, the potential functions of HRC in anoikis resistance in HCC remain unknown. Here, we uncovered the clinical value of HRC and its functional significance on anoikis in HCC. The positive expression of HRC was observably correlated with tumor size, tumor encapsulation, and tumor-node-metastasis (TNM) stage. The expression of HRC increased in HCC cells cultured in suspension. HRC enhanced the anoikis resistance of HCC, and promoted the HCC metastasis in vivo. Mechanistically, the anoikis resistance was probably dependent on endoplasmic reticulum stress. Modulating HRC level changed the ERS to affect anoikis resistance by acting protein kinase RNA-like ER kinase (PERK)-eIF2a-ATF4-CHOP signaling axis. In conclusion, we define HRC as a novel candidate oncogene involved in anoikis resistance and HCC metastasis, and provide a new potential therapeutic target for HCC.

SLC7A2 deficiency promotes hepatocellular carcinoma progression by enhancing recruitment of myeloid-derived suppressors cells.

The main reason for poor prognosis in hepatocellular carcinoma (HCC) patients is high metastasis and recurrence. Cancer progression depends on a tumor-supportive microenvironment. Therefore, illustrating the mechanisms of tumor immunity in underlying HCC metastasis is essential. Here, we report a novel role of solute carrier family 7 member 2 (SLC7A2), a member of the solute carrier family, in HCC metastasis. The reduction of SLC7A2 was an independent and significant risk factor for the survival of HCC patients. Upregulation of SLC7A2 decreased HCC invasion and metastasis, whereas downregulation of SLC7A2 promoted HCC invasion and metastasis. We further found that deficient SLC7A2 medicated the upregulation of CXCL1 through PI3K/Akt/NF-kκB pathway to recruit myeloid-derived suppressor cells (MDSCs), exerting tumor immunosuppressive effect. Moreover, we found that G9a-mediated di-methylation of H3K9 (H3K9me2) silenced the expression of SLC7A2 to suppress HCC metastasis and immune escape. In conclusion, G9a-mediated silencing of SLC7A2 exerts unexpected functions in cancer metastasis by fostering a tumor-supportive microenvironment through CXCL1 secretion and MDSCs recruitment. Thus, SLC7A2 may provide new mechanistic insight into the cancer-promoting property of MDSCs.