This study aims to assess the serum levels of pepsinogen (PG)I, PG II, and gastrin (G17) in patients with gastric intestinal metaplasia (GIM) and evaluate their correlation with demographic characteristics.

A total of 247 normal controls (NC) and 240 patients diagnosed with GIM were enrolled in this study. All participants underwent a gastroscopy procedure followed by pathological examination for diagnosis confirmation. The expression level of PGI, PG II, and G 17 was detected by fluorescence immunochromatography and Hp infection was detected by 13-carbon breath test. The demographic characteristics of the subjects were obtained through questionnaires.

Compared to the NC group, the GIM group showed a reduction in PG II expression level [10.71(6.40,16.89) VS 9.21(6.14,14.55), p = 0.010]. GIM patients had a higher prevalence of previous Hp eradication history (14.98% VS 23.75%, p = 0.014). The low PG II group exhibited a higher incidence rate of GIM compared to the high PG II group (54.10% VS 44.44%, p = 0 0.020). In the Hp-negative(Hp-) group, there was a decrease in both PGI and PG II expression levels when compared to the Hp-positive(Hp+) group [146.73 ± 78.53 VS 125.61 ± 68.75 and 10.19(7.27, 16.58) VS 7.36(5.62,12.53), p = 0.036 and p < 0.001]. Among patients without Hp eradication history, those with low PG II levels had a higher proportion of individuals with a history of Hp eradication than those with high PG II levels (29.31% VS 3.13%, p = 0.003). Additionally, within the subgroup that underwent Hp eradication, there was a decrease in PG II expression level compared to the subgroup without Hp eradication (6.16(5.13, 7.52) VS 8.73(5.67, 13.35), p = 0.041).

The prevalence of GIM was significantly associated with low levels of PG II. There was a significant association between HP eradication history and the prevalence of GIM. Hp eradication history resulted in reduced expression levels of PG II in Hp- GIM patients.

We aimed to investigate whether individuals with low pepsinogen I levels differed from those with normal pepsinogen I levels in terms of proton pump inhibitors (PPIs) use, referral to gastroscopy, and findings on gastroscopy.

Serum pepsinogen I was measured in 518 persons (mean age 51.6, SD 8.8; 49% women). A medical chart review focused on PPI prescriptions and gastroscopic findings in the follow-up period.

Patients with serological atrophic gastritis (pepsinogen I < 28 μg/L) had higher body mass index (27.5 vs 26.2 kg/m2; P = 0.007), were less likely to be current smokers (8% vs 17%; P = 0.025), and had higher prevalence of Helicobacter pylori seropositivity (57% vs 36%; P < 0.001) compared with those without. During follow-up (mean 21.4 years, SD 6.5 years), the patients with serological atrophic gastritis had more often findings of atrophic gastritis or gastric polyps on gastroscopy (20% vs 8%; P < 0.001), despite no differences in the mean number of gastroscopies per 1000 person-years (33 vs 23; P = 0.19) and the mean prescribed PPI dose (omeprazole equivalents) per year (1064 mg vs 1046 mg; P = 0.95). Persons with serological atrophic gastritis had lower odds of being prescribed PPIs at least once (odds ratio [95% confidence interval]: 0.58 [0.35-0.96]), but there was no significant difference in the chance of being referred to gastroscopy at least once (1.15 [0.70-1.96]).

Persons with serological atrophic gastritis were less likely to be prescribed PPIs. Persons with serological atrophic gastritis had more often gastric polyps and atrophic gastritis when referred to gastroscopy.

Serum pepsinogen (PG) is a good indicator of atrophic changes in the gastric mucosa. Gastric mucosal atrophy is a high-risk factor for gastric cancer. Serological testing for PG combined with endoscopy can help to improve gastric cancer screening. In this study, we established the reference ranges of serum PG-I, PG-II, and the PG-I/II ratio (PGR) in the Chinese population by chemiluminescence immunoassay (CLIA) and enzyme-linked immunosorbent assay (ELISA). Besides, in the real world, doctors are often confused by the results of different testing platforms. Thus, a comparison of methods CLIA and ELISA was performed.

2904 individuals were enrolled from six regions in China as part of the Chinese Adult Digestive Diseases Surveillance (2016) program. The individuals completed questionnaires and volunteered to undergo examinations, including gastroscopy, urea breath test, abdominal ultrasound examination and routine serologic tests. Serum was collected to measure PGs (including PG-I, PG-II and PGR) by CLIA and ELISA. Participants who were found obvious abnormalities or absent from the examinations were excluded. Ultimately, 747 healthy individuals were enrolled in this study. The Kolmogorov-Smirnov test was used to assess the distribution of variables. The Kruskal-Wallis H or Mann-Whitney U-tests were used to compare different sex, age, and geographical groups. The 95% reference ranges of PGs obtained by the two methods were established according to document CLSI-EP28-A3, with covariates of sex, age, and region. Spearman correlation analysis, linear regression analysis and allowable total error (ATE) zone analysis were utilized for comparing the two methods.

On overall, the 95% reference ranges of PG-I, PG-II, and PGR measured by CLIA were 23.00-110.64 ng/mL, 2.50-19.13 ng/mL, and 3.87-13.30, respectively. Meanwhile, the reference ranges of PG-I, PG-II, and PGR measured by ELISA were 36.93-205.06 ng/mL, 1.65-17.96 ng/mL, and 7.50-33.60, respectively. Both PG-I and PG-II levels measured by the two platforms were found to be influenced by sex and age. PGR measured by CLIA was influenced by age but not by sex, while PGR measured by ELISA was not affected by either age or sex. Regional factors did not significantly impact the PG results, except for PG-I detected by ELISA. Ultimately, reference ranges for PGs were established based on age and sex stratification. Additionally, the Spearman correlation analysis revealed that the correlation coefficients for PG-I, PG-II, and PGR detected by the two methods were 0.899, 0.887, and 0.777, respectively, indicating a strong correlation between the two methods. The regression equation for the PG levels detected by two methods was obtained through linear regression analysis. The ATE analysis provided a visual depiction of the consistency between the two methods, clearly indicating the poor agreement between them.

This study established the reference ranges of PGs by strict and intact enrollment standard. In addition, the results indicated a strong linear relationship between the two methods, yet with a clear bias, which was valuable for laboratory interpretation.

At the end of the last century, a far-sighted 'working party' held in Sydney, Australia addressed the clinicopathological issues related to gastric inflammatory diseases. A few years later, an international conference held in Houston, Texas, USA critically updated the seminal Sydney classification. In line with these initiatives, Kyoto Global Consensus Report, flanked by the Maastricht-Florence conferences, added new clinical evidence to the gastritis clinicopathological puzzle.The most relevant topics related to the gastric inflammatory diseases have been addressed by the Real-world Gastritis Initiative (RE.GA.IN.), from disease definitions to the clinical diagnosis and prognosis. This paper reports the conclusions of the RE.GA.IN. consensus process, which culminated in Venice in November 2022 after more than 8 months of intense global scientific deliberations. A forum of gastritis scholars from five continents participated in the multidisciplinary RE.GA.IN. consensus. After lively debates on the most controversial aspects of the gastritis spectrum, the RE.GA.IN. Faculty amalgamated complementary knowledge to distil patient-centred, evidence-based statements to assist health professionals in their real-world clinical practice. The sections of this report focus on: the epidemiology of gastritis; Helicobacter pylori as dominant aetiology of environmental gastritis and as the most important determinant of the gastric oncogenetic field; the evolving knowledge on gastric autoimmunity; the clinicopathological relevance of gastric microbiota; the new diagnostic horizons of endoscopy; and the clinical priority of histologically reporting gastritis in terms of staging. The ultimate goal of RE.GA.IN. was and remains the promotion of further improvement in the clinical management of patients with gastritis.

Background: Treatment of Helicobacter pylori (HP) has been shown to reduce the risk of gastric cancer (GC) development. However, previous studies have focused on patients at high risk of GC. This study aimed to assess the effect of HP treatment on the incidence of GC in the general population. Materials and Methods: Medical records were obtained from the Common Data Model-converted sample Cohort of the National Health Insurance Service of Korea (NHIS-CDM). The target cohort included those who had been prescribed HP treatment and the comparator cohort included those who had not. The association between HP treatment and the risk of GC development was assessed using the Cox proportional hazard model. The incidences of GC according to the period after HP treatment in different age groups were analyzed using proportional trend tests. Results: After large-scale 1:4 propensity score matching, 2735 and 5328 individuals were included in the target and comparator cohorts, respectively. During the median follow-up of 6.5 years, the GC incidence was lower in the HP treatment cohort than in the comparator cohort, but this was statistically insignificant (hazard ratio [HR]: 0.76; 95% confidence interval [CI]: 0.50−1.13; p-value = 0.19). This trend was also observed among the older age (≥65 years, HR: 0.87; 95% CI: 0.44−1.68; p-value = 0.69) and male cohorts (HR: 0.82; 95% CI: 0.51−1.27; p-value = 0.38). Among 58,684 individuals who were treated for HP from the whole NHIS-CDM cohort, the incidence of GC consistently decreased over time and showed a marked decrease with increasing age (p for trend < 0.05). Conclusions: In all age groups of the general population, HP treatment could be recommended to reduce the risk of GC.