Chronic atrophic gastritis: an update on diagnosis

Background and aim. Atrophic gastritis is a precancerous gastric lesion, therefore its early detection is a priority in preventing gastric cancer. The aim of the present paper is to develop a narrative synthesis of the present knowledge on diagnostic methods of chronic atrophic gastritis. Methods. A literature search was carried out on main databases: PubMed, Hinari, SpringerLink and Scopus (Elsevier) for the period 2000-2020. The searched keywords were: chronic atrophic gastritis, intestinal metaplasia and dysplasia + diagnosis. Inclusion criteria were focused on the articles about the invasive and non-invasive diagnosis of chronic atrophic gastritis and of precancerous gastric lesions, intestinal metaplasia and dysplasia; exclusion criteria were articles published before 2000 and those that did not include the proposed theme. Results. The search returned 575 papers addressing the topic of precancerous lesions. From these, 60 articles were qualified representative for the materials published on the topic of this synthesis article, being those that met the inclusion criteria. The data emphasize the need to use upper digestive endoscopy with biopsies for the diagnosis of chronic atrophic gastritis. However serological diagnosis is available as alternative mainly recommended in follow up. Conclusions. There are two main methodological approaches for the evaluation of chronic atrophic gastritis as a precancerous gastric lesions: invasive examination, which requires histological analysis of biopsy samples taken during upper digestive endoscopy, being the "gold standard" for diagnosis, and non-invasive serological examination using markers of gastric function.

Precancerous Gastric Lesions with Helicobacter pylori vacA+/babA2+/oipA+ Genotype Increase the Risk of Gastric Cancer

Objective. The clinical outcomes of gastric diseases such as chronic gastritis, peptic ulcer, and gastric cancer have been attributed to the interplay of virulence factors of Helicobacter pylori (H. pylori), host genetic susceptibility, and host immune responses. This study investigated the presence of cagA, vacA, iceA2, babA2, and oipA genes and their association with clinical outcomes. Methods. Chronic gastritis, atrophic gastritis, and intestinal metaplasia specimens were obtained from patients who underwent endoscopy and surgical resection between January 2017 and December 2018; specimens from gastric cancer patients treated between January 2014 and December 2018 were also added. H. pylori infection and virulence genes (cagA, vacA, iceA2, babA2, and oipA) were determined using real-time PCR. The association between H. pylori genotypes and clinical outcomes were evaluated using multivariate regression model analysis. The overall survival of gastric cancer patients was compared between genotype combinations. Results. H. pylori was positive in 166 patients with chronic gastritis, precancerous gastric lesions, and gastric cancer. The genes vacA, babA2, and oipA were most prevalent in chronic gastritis (73%), precancerous gastric lesions (62%), and gastric cancer (91%), respectively. The vacA, babA2, and oipA genes were associated with increased risk of gastric cancer (OR = 1.23; 95% CI = 1.13–3.32; P=0.033, OR = 2.64; 95% CI = 1.44–4.82, P=0.024, and OR = 2.79; 95% CI = 1.58–5.41; P=0.031, respectively). Interestingly, H. pylori vacA+/babA2+/oipA+ genotype infection was associated with increased risk of gastric cancer (OR = 3.85, 95% CI = 1.67–5.77, P=0.014). Conclusion. In this present study, we reported on the virulence genes of H. pylori infection to reveal their association with increased risk of chronic gastritis, precancerous gastric lesions, and gastric cancer. Precancerous gastric lesions with H. pylori vacA+/babA2+/oipA+ genotype increased the risk of gastric cancer.

A Review of Therapeutic Effects and the Pharmacological Molecular Mechanisms of Chinese Medicine Weifuchun in Treating Precancerous Gastric Conditions

Patients with precancerous gastric conditions are at a high risk for gastric carcinoma. The Chinese medicine Weifuchun (WFC) is used in treating chronic superficial gastritis and in postoperative adjuvant treatment of gastric cancer. Both monotherapy and combination therapy of WFC with other drugs can result in a favorable therapeutic outcome. WFC can dramatically improve clinical outcomes in patients with gastric precancerous lesions by targeting multiple pathways including pathways involved in the pharmacological action of Radix Ginseng Rubra (red ginseng), Rabdosia amethystoides, and fried Fructus Aurantii, including regulation of NF-κB, RUNX3/TGF-beta/Smad, Hedgehog (Hh) and Wnt signaling pathways, modulation of the expression of oncogenes and tumor suppressor genes, and indirect inhibition of Helicobacter pylori (Hp) by maintaining gastric microbial ecosystem. In this review, we will discuss the clinical efficacy and therapeutic regimen of WFC for gastric precancerous lesions and the molecular mechanisms involved. This review will highlight WFC-based therapeutic strategies in disrupting progress to gastric cancer and provide more information on the pharmacological mechanisms of WFC and its clinical application for the treatment of precancerous gastric lesions.

Regulatory role of programmed cell death 4 in precancerous gastric lesions and early gastric cancer

Background Programmed cell death 4 (PDCD4) as a newly identified tumor suppressor is involved in inhibiting tumorigenesis and tumor progression. Epithelial mesenchymal Transition (EMT) is also associated with tumorgenesis of gastric cancer. However, few studies have elucidated the role of PDCD4 in regulation of EMT during precancerous gastric lesions (PLGC) and early gastric cancer. Methods In this study, the expression of PDCD4 and EMT-associated proteins in PLGC and early gastric cancer tissues were detected by immunohistochemistry. The relationship between the expression of PDCD4 and EMT-associated proteins and clinical and pathological parameters were analyzed. The PDCD4 high-expressed SGC-7901 cell line was also used to evaluate the function of PDCD4 in vitro and in vivo. Results PDCD4 and EMT associated proteins expression were significantly altered in PLGC and early gastric cancer tissues. After transfection with the PDCD4 gene, the expression of E-cadherin was significantly increased, the expression of N-cadherin and Vimentin were also remarkably inhibited. PDCD4 high-expressed also inhibited tumor growth and pathological features in nude mice xenograft model. Conclusion This study elucidates a regulatory role of PDCD4 in PLGC and early gastric cancer and provide insights into EMT-associated target which may provide novel therapeutic recourse.