This study aimed to investigate the diagnostic potential of serum CXC chemokine ligand 5 (CXCL5) in patients with chronic atrophic gastritis (CAG) and to establish a prediction model for better diagnosis of CAG.

A retrospective analysis was conducted, encompassing 570 cases of CAG patients admitted to the Department of Gastroenterology of the Second Affiliated Hospital of Anhui University of Traditional Chinese Medicine, who underwent gastroscopy and received pathologically confirmed diagnoses between June 2018 and June 2023. Additionally, 570 cases without CAG who underwent health checkups were included and classified into the control group. Single-factor and multi-factorial logistic regression analyses were employed to identify risk factors of CAG, and a prediction model for diagnosing CAG was developed using R software. The predictive performance of the constructed model was verified and evaluated through ROC analysis, decision curve analysis (DCA), and prediction efficacy curve.

Multi-factorial logistic regression analysis revealed that history of smoking, family history of tumurs, Pepsinogen I (PG I), Gastrin 17 (G-17), Helicobacter pylori infection, D-dimer, and CXCL5 were independent risk factors in CAG patients. A nomogram for the diagnosis of CAG was constructed using R software. The ROC curve demonstrated that CXCL5 showed the best predictive efficacy as a single indicator, with an AUC of 0.897, a sensitivity of 0.789, and a specificity of 0.999. Furthermore, the nomogram exhibited an AUC of 0.992, a sensitivity of 0.958, and a specificity of 0.970. Calibration and DCA curves indicated that the predicted values of the nomogram were highly concordant with the observed values, thus demonstrating a high predictive value.

In this study, we found a correlation between serum CXCL5 level and CAG, and developed a prediction model to assist the clinical diagnosis of CAG.

New markers are needed to improve the effectiveness of serological screening for atrophic gastritis.

To develop a cost-effective method for serological screening of atrophic gastritis with a high level of sensitivity.

Of the 169 patients with atrophic gastritis, selected by the visual endoscopic Kimura-Takemoto method, 165 showed histological mucosal atrophy using the updated Kimura-Takemoto method. All 169 patients were examined for postprandial levels of gastrin-17 (G17) and pepsinogen-1 (PG1) using GastroPanel® (Biohit Plc, Helsinki, Finland).

We used the histological standard of five biopsies of the gastric mucosa, in accordance with the Kimura-Takemoto classification system to assess the sensitivity of G17 in detecting gastric mucosal atrophy. We also compared the morpho-functional relationships between the detected histological degree of gastric mucosal atrophy and the serological levels of G17 and PG1, as the markers of atrophic gastritis. The sensitivity of postprandial G17 was 62.2% for serological levels of G17 (range: 0-4 pmol/L) and 100% for serological G17 (range: 0-10 pmol/L) for the detection of monofocal severe atrophic gastritis. No strong correlation was found between the levels of PG1 and degree of histological atrophy determined by the Kimura-Takemoto classification system to identify the severity of mucosal atrophy of the gastric corpus. In the presented clinical case of a 63-year-old man with multifocal atrophic gastritis, there is a pronounced positive long-term dynamics of the serological marker of atrophy - postprandial G17, after five months of rennet replacement therapy.

Serological screening of multifocal atrophic gastritis by assessment of postprandial G17 is a cost-effective method with high sensitivity. Postprandial G17 is an earlier marker of regression of atrophic gastritis than a morphological examination of a gastric biopsy in accordance with the Sydney system. Therefore, postprandial G17 is recommended for dynamic monitoring of atrophic gastritis after treatment.

The noninvasive serum markers pepsinogen I (PGI), pepsinogen II (PGII), gastrin-17 (G17), and PGI:PGII ratio (PGR) have recently been proposed as a new tool for predicting various gastric pathologies.

A total of 83 gastritis patients confirmed by gastroscopy were enrolled, with 78 undergoing concurrent colonoscopies. The control group included 99 healthy subjects. Enzyme-linked immunosorbent assay was used to detect PGI, PGII, G17, and PGR. The performance of serological analysis for detecting gastritis pathology was evaluated using receiver operating characteristic (ROC) curves.

The G17 and PGII levels increased significantly (P < .001), whereas PGR levels decreased (P = .001) in the gastritis group. The ROC analysis revealed that PGR had a sensitivity and specificity of 70.83% and 86.67%, respectively, in predicting Helicobacter pylori-infected gastritis and a sensitivity and specificity of 88% and 65.52%, respectively, in predicting active gastritis. The G17 levels were significantly elevated in gastritis patients undergoing concurrent colonoscopies (P < .05).

Pepsinogen I:pepsinogen II ratio was found to be a useful predictor of active gastritis and H pylori-infected gastritis. Furthermore, G17 was found to be closely related to pathological conditions found by colonoscopy and may provide recommendations for whether gastritis patients should undergo a concurrent colonoscopy.

Gastric cancer (GC) is still one of the most prevalent cancers worldwide, with a high mortality rate, despite improvements in diagnostic and therapeutic strategies. To diminish the GC burden, a modification of the current diagnostic paradigm, and especially endoscopic diagnosis of symptomatic individuals, is necessary. In this review article, we present a broad review and the current knowledge status on serum biomarkers, including pepsinogens, gastrin, Gastropanel®, autoantibodies, and novel biomarkers, allowing us to estimate the risk of gastric precancerous conditions (GPC)-atrophic gastritis and gastric intestinal metaplasia. The aim of the article is to emphasize the role of non-invasive testing in GC prevention. This comprehensive review describes the pathophysiological background of investigated biomarkers, their status and performance based on available data, as well as their clinical applicability. We point out future perspectives of non-invasive testing and possible new biomarkers opportunities.

To explore the potential pathogenic genes of intestinal metaplasia.

Twenty-one patients with intestinal metaplasia admitted to the Department of Gastroenterology at the Second Affiliated Hospital of Anhui University of Chinese Medicine from January, 2022 to June, 2022, and 21 healthy subjects undergoing gastroscopic examination during the same period were enrolled in this study. All the participants underwent gastroscopy and pathological examination, and gastric tissue samples were collected for transcriptome sequencing to screen for differentially expressed genes (DEGs). The biological functions of the DEGs were analyzed using bioinformatics analysis, and qRT-PCR was used to validate the results.

Transcriptomic sequencing identified a total of 1373 DEGs, including 827 upregulated and 546 downregulated ones. The top 6 upregulated genes (AGMAT, CCL25, FABP1, CDX1, SPINK4, and MUC2), ranked based on their significance and average expression level, were selected for validation, and qRT-PCR showed significant upregulation of their mRNAs in the gastric tissues of patients with intestinal metaplasia (P < 0.05).

AGMAT, CCL25, FABP1, CDX1, SPINK4, and MUC2 participate in the occurrence and development of intestinal metaplasia, and may serve as potential biomarkers for diagnosing intestinal metaplasia.

The lack of specific symptoms of gastric cancer (GC) causes great challenges in its early diagnosis. Thus it is essential to identify the risk factors for early diagnosis and treatment of GC and to improve the survival rates.

To assist physicians in identifying changes in the output of publications and research hotspots related to risk factors for GC, constructing a list of key risk factors, and providing a reference for early identification of patients at high risk for GC.

Research articles on risk factors for GC were searched in the Web of Science core collection, and relevant information was extracted after screening. The literature was analyzed using Microsoft Excel 2019, CiteSpace V, and VOSviewer 1.6.18.

A total of 2514 papers from 72 countries and 2507 research institutions were retrieved. China (n = 1061), National Cancer Center (n = 138), and Shoichiro Tsugane (n = 36) were the most productive country, institution, or author, respectively. The research hotspots in the study of risk factors for GC are summarized in four areas, namely: Helicobacter pylori (H. pylori) infection, single nucleotide polymorphism, bio-diagnostic markers, and GC risk prediction models.

In this study, we found that H. pylori infection is the most significant risk factor for GC; single-nucleotide polymorphism (SNP) is the most dominant genetic factor for GC; bio-diagnostic markers are the most promising diagnostic modality for GC. GC risk prediction models are the latest current research hotspot. We conclude that the most important risk factors for the development of GC are H. pylori infection, SNP, smoking, diet, and alcohol.

Chronic atrophic gastritis (CAG) is an important stage of precancerous lesions of gastric cancer, and also a key period of drug intervention. However, there is still a lack of drugs to maintain the treatment of CAG until the advent of moluodan.

This study was conducted to assess the clinical efficacy of moluodan in the treatment of CAG by meta-analysis and trial sequential analysis.

China National Knowledge Infrastructure, China Biology Medicine, VIP, Wanfang, Embase, PubMed, the Cochrane Library, and Web of Science databases were searched, all with the time limit from database establishment to July 2022. The published randomized controlled trials of moluodan for CAG were conducted for meta-analysis and trial sequential analysis.

7 studies with a total sample size of 1143 cases were included. Compared to folic acid/vitamins, moluodan alone significantly increased the effective rate of pathological detection (relative risk [RR] = 1.73, 95% confidence interval [95%CI] = [1.48,2.02], P < .00001), and moluodan in combination with folic acid/vitamins significantly increased the effective rates of pathological detection (RR = 1.37, 95%CI = [1.23,1.52], P < .00001), gastroscopy (RR = 1.37, 95%CI = [1.18,1.60], P < .0001) and symptoms (RR = 1.25, 95%CI = [1.13,1.38], P < .0001). Harbord regression showed no publication bias (P = .22). Quality of evidence evaluation demonstrated moderate quality of evidence for all indicators.

Moluodan can improve the effective rates of pathological examination, gastroscopy and symptoms in patients with CAG, and play a role in slowing down the disease progression and reducing clinical symptoms. It may be a potential drug for the treatment of CAG and has the value of further exploration.