Risk factors for intestinal metaplasia in a southeastern Chinese population: an analysis of 28,745 cases

Jiang, Jianxia; Liu, Qing; Zhao, Bing; Zhang, Haihan; Sang, Huaiming; Djaleel, Soyfoo-Muhammad; Zhang, Guoxin; Xu, Shaofa

doi:10.1007/s00432-016-2299-9

Cited by 36 publications

(27 citation statements)

References 28 publications

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“…The present results indicated that H. pylori infection was positively associated with IM. This is consistent with results from earlier studies, which examined the prevalence of the infection in IM in large cohorts (21,22). Based on this information, H. pylori infection was indicated to be inversely associated with HPs.…”

Section: Discussionsupporting

confidence: 91%

Gastric hyperplastic polyps inversely associated with current Helicobacter�pylori infection

Wang

et al. 2020

Exp Ther Med

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The incidence of gastric hyperplastic polyps (HPs) has been on the rise in recent years. The contribution of Helicobacter pylori infection to this trend has remained to be elucidated. The present study aimed to explore the association between HPs and H. pylori in China, an area with a high infection rate of H. pylori. In order to study trends of HPs and H. pylori infection over the past decades, cases encountered from 2009 to 2018 were assessed and a total of 109,150 consecutive patients who underwent esophagogastroduodenoscopy at Qingdao Municipal Hospital (Qingdao, China) were enrolled. The incidence of HPs and the prevalence of H. pylori were determined and their correlation was explored. Gastric HPs were detected in 1,497 patients (1.6%) who received gastric biopsies. The incidence of HPs exhibited a rising trend, with a ~4-fold increase in the annual detection rate from 2009 to 2018. The prevalence of H. pylori infection was inversely associated with the prevalence of HPs (adjusted odds ratio, 0.66). The prevalence of H. pylori in the examined cohort decreased with time (r=-0.76, P=0.011). The decreasing trend of H. pylori infection was negatively correlated with the rising trend of HPs (r=-0.64, P=0.048), further indicating an inverse association between them. The difference in the prevalence of HPs between H. pylori-negative and-positive patients increased with age (r=0.80, P=0.018). The age-associated increase was slower in H. pylori-infected patients. The decline in H. pylori infection with time appeared to not be associated with the birth cohort effect, suggesting the decline was not caused by exposure to environmental factors during an early period of life. The present results indicated that the incidence of gastric HPs increased with the decline in H. pylori infection, demonstrating an inverse association between the occurrence of HPs and the infection.

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Section: Discussionsupporting

confidence: 91%

Gastric hyperplastic polyps inversely associated with current Helicobacter�pylori infection

Wang

et al. 2020

Exp Ther Med

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“…IM places patients at a higher risk of developing gastric adenocarcinoma than patients without IM (34). In addition, mounting epidemiological evidence has demonstrated that exposure to bile acids can induce IM in the stomach (19). Tatsugami et al reported that grades of atrophy and IM are significantly positively correlated with bile acid concentrations in patients with Helicobacter pylori infections (18).…”

Section: Discussionmentioning

confidence: 99%

“…Clinical and experimental studies have reported that AG and IM are associated with the phenomenon of duodenogastric reflux (DGR) (16,17). Bile acids, which are the primary duodenal components of DGR, are generally considered to be carcinogens in gastric IM formation and gastric tumourigenesis (18,19). Bile acids, particularly CDCA and DCA, have been reported to be associated with the induction of CDX2 and MUC2 expression.…”

Section: Introductionmentioning

confidence: 99%

Bile acids promote gastric intestinal metaplasia by upregulating CDX2 and MUC2 expression via the FXR/NF-κB signalling pathway

Zheng

et al. 2019

Int J Oncol

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Bile acids serve a critical role in the induction of gastric intestinal metaplasia (IM) and gastric carcinogenesis. The present study investigated the effects of bile acids on the induction of gastric IM formation. The results demonstrated that the expression levels of caudal-related homeobox transcription factor 2 (CDX2), mucin 2 (MUC2) and farnesoid X receptor (FXR) were increased in vitro and in vivo following treatment with bile acids, and CDX2 transcriptionally activated MUC2 expression. Furthermore, knockdown of FXR attenuated bile acid-enhanced CDX2 promoter activity and protein expression. Conversely, the FXR agonist GW4064 synergistically enhanced bile acid-induced CDX2 promoter activity. Bile acid treatment led to an increase in nuclear factor (NF)-κB activity and protein expression. Treatment with GW4064 or the FXR antagonist Z-guggulsterone enhanced or attenuated bile acid-induced NF-κB activity, respectively. In addition, quantitative chromatin immunoprecipitation confirmed that bile acids led to enhanced binding of p50 to the CDX2 promoter, whereas this effect was not observed for p65. Treatment with GW4064 or Z-guggulsterone enhanced and attenuated the binding activity of p50 to the CDX2 promoter, respectively. These results indicated that bile acids may activate the FXR/NF-κB signalling pathway, thereby upregulating CDX2 and MUC2 expression in normal gastric epithelial cells.

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“…It is generally believed that chronic environmental stimulation leads to gastric IM, such as Helicobacter pylori (Hp) infection and bile acids (BA) re ux [4,5]. However, whether Hp eradication could prevent the occurrence or further development of gastric cancer is still controversial [6,7], indicating other factors may contribute to the development of IM.…”

Section: Introductionmentioning

confidence: 99%

Bile acids increase intestinal markers via FXR/SNAI2/miR-1 axis in the stomach

Wang

Chen

Zeng

et al. 2020

Preprint

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Background Intestinal metaplasia (IM) is a precancerous lesion that increases risk of subsequent gastric cancer (GC). However, factors governing the transformation from normal gastric epithelial cells to IM remain unclear. Previously, miR-1 turned out to play an essential role in the initiation of bile acids (BA)-induced IM. Here, we investigate the mechanism underlying miR-1 inhibition by BA in gastric cells. Methods We conducted IPA analysis to determine the potential molecular interacting BA with miR-1. The changes of FXR and SNAI2 after BA treatment were detected by western blot and qRT-PCR. IHC was performed to assess the expression level of FXR and SNAI2 in normal and IM tissue microarrays. The transcriptional regulation of SNAI2 or miR-1 was verified by bioinfamatics, luciferase reporter assay and chromatin immunoprecipitation PCR. Results BA treatment caused aberrant expression of FXR and IM markers in gastric cells. Augmented FXR led to the transcriptional activation of SNAI2 which further stimulates the expression of downstream IM markers. Bioinformatics analysis indicated that SNAI2 had miR-1 promoter binding region and we identified that SNAI2 negatively regulated miR-1 transcription. Both FXR and SNAI2 were increased in patients with IM. Conclusions This study demonstrated that FXR might be responsible for a series molecular changes in gastric cells after BA, and FXR/SNAI2/miR-1 axis exert a crucial role in BA-induced IM progression. Blocking the activation of the FXR-oriented axis may provide a promising approach for IM or even GC treatment.

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Risk factors for intestinal metaplasia in a southeastern Chinese population: an analysis of 28,745 cases

Cited by 36 publications

References 28 publications

Gastric hyperplastic polyps inversely associated with current Helicobacter�pylori infection

Gastric hyperplastic polyps inversely associated with current Helicobacter�pylori infection

Bile acids promote gastric intestinal metaplasia by upregulating CDX2 and MUC2 expression via the FXR/NF-κB signalling pathway

Bile acids increase intestinal markers via FXR/SNAI2/miR-1 axis in the stomach

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