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Hp eradication decreased the expression level of PG II in patients of Hp negative with gastric intestinal metaplasia: a retrospective cross-sectional study

Journal of Health, Population and Nutrition volume 44, Article number: 20 (2025) Cite this article

Abstract

Aims

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.

Methods

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.

Results

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).

Conclusion

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.

Introduction

Globally, gastric cancer (GC) remains a leading cause of mortality [1]. Gastric mucosal intestinal metaplasia (GIM), a preliminary precancerous state impacting the stomach lining, has been associated with an increased likelihood of developing GC. The literature indicates that detecting and closely monitoring individuals with precancerous conditions, such as GIM, can improve GC outcomes in low-incidence countries [2]. It also advocates for utilizing the Operative Link for Gastritis Intestinal Metaplasia (OLGIM) staging system to assess the risk of developing GC [3].The development of this condition results from chronic inflammation of the stomach cells, which occurs due to the interaction between bacterial components and the body’s immune response mechanisms [4]. Continuous exposure to inflammation results in the disappearance of gastric glands, which is then followed by the replacement of gastric mucosa with intestinal epithelium. Chronic injury and inflammation perpetuate a cycle of cellular reprogramming and metaplasia, increasing GC risk [5]. Currently, the diagnosis of GIM is exclusively based on a combination of gastroscopy examination and pathological analysis [6]. It is of utmost importance to detect in vitro markers that can ascertain the existence or nonexistence of GIM.

Pepsinogen(PG), including PGI and PG II, is secreted by different cells; PGI is secreted by gastric chief cells and mucosal cells, while PG II is secreted by the entire stomach and proximal duodenum. In other words, PGI represents the secretory function of body of gastric mucosa, while PG II can reflect the secretory capacity of a broader region of the gastric mucosa [7]. Gastrin(G)-17, on the other hand, is a hormone released by G cells located in the antrum, exerting multiple physiological effects. Its levels provide insight into the quantity and secretory activity of antral mucosal cells [8].The synthesis and release of PG and G17 occur in glands situated within various regions of the gastric mucosa [9]. PG has the capability to provide insights into levels of gastric acidity and may potentially indicate an overgrowth of bacteria in the small intestine [10]. Serum PGs are regarded as indicators of gastric mucosal injury and have been associated with the development of atherosclerosis [11]. G17 plays a vital role in the regulation of gastric function by stimulating the synthesis of stomach acid (especially when acidity levels are insufficient) and contributing to the equilibrium of the gastric mucosa [12]. Some individuals diagnosed with GIM may not manifest any symptoms related to the upper gastrointestinal tract, and these patients are frequently recognized in the general population [13]. Currently, serum markers such as PGI, PG II, and G 17 are being employed to conduct screenings for GC in asymptomatic populations. These screenings have shown positive results [14]. To forecast the performance of the OLGIM III-IV nomogram model, factors such as age, gender, PG, and G17 were employed [15]. In the population of Western Mexico, a PGI/PG II ratio of less than 3 is considered a notable risk marker for GIM among this group [16]. The most prevalent treatment for Hp infection has been eradication therapy, which is impacting an increasing number of individuals [17, 18]. However, the impact of Hp eradication therapy on GIM, especially on serum PG and G17 in GIM patients, is not yet fully understood. Thus, it is crucial for GIM patients to undergo appropriate tests and to promptly assess the condition of their gastric mucosa.

Therefore, the purpose of this retrospective cross-sectional analysis is to investigate the serum expression levels of PGI, PG II, and G 17 in patients diagnosed with GIM and their correlation with the general characteristics of the participants. The objective is to determine whether PG and G17 have potential as indicators for identifying GIM.

Methods

Study design

The present investigation is a retrospective cross-sectional study conducted in Xuzhou, a city located in the northern part of Jiangsu Province, China. The study adhered to the principles stated in the Declaration of Helsinki, which emphasizes ethical considerations in medical research involving human subjects. To ensure that ethical standards were upheld to the highest degree, this study followed the ethical guidelines for medical and health research involving human subjects in China. These guidelines prioritize patient safety, protection of privacy, and obtaining informed consent. Prior to enrolling patients, approval for the study protocol was obtained from institutional review boards at each participating institution after receiving clearance from the Ethics Committee at Affiliated Hospital of Xuzhou Medical University. Additionally, this study was registered with Affiliated Hospital of Xuzhou Medical University under registration number XYFY2020-KL045-01. All participants were initially enrolled between 1 July 2020 and 1 July 2022 after providing written consent with full understanding of the information provided. The data used in this analysis were collected and finalized prior to conducting any statistical analyses.

Study population

The study included patients aged 18 to 80 years who had undergone gastroscopy. Patients with any of the following conditions were not eligible for participation: (1) previous removal of tissue through endoscopy; (2) history or plan of stomach removal surgery; (3) history or plan of chemotherapy for cancer treatment; (4) history or plan of surgery, chemotherapy, or radiation therapy for cancer treatment; (5) pregnant or breastfeeding women; (6) individuals with severe mental illness; (7) those planning to undergo hormone therapy, chemotherapy, or radiation at the time of enrollment; (8) individuals with ulcers in the stomach and/or duodenum; and finally, (9) participants deemed unsuitable for enrollment by the researcher. All participants met the inclusion and exclusion criteria and signed written informed consent. This study was conducted with the approval of the ethics committee at the Affiliated Hospital of Xuzhou Medical University (Approval no. XYFY2020-KL045-01).

Data collection

The participants underwent measurements for their height and weight. And they were asked to complete questionnaires regarding their dietary habits, specifically focusing on salt intake (considered high if it exceeded 20 g/day), frequency of consuming spicy food (considered frequent if more than 3 times/week), consumption of pickled foods (considered regular if greater than 3 times/week), alcohol consumption patterns (considered excessive if exceeding 50 g/day), frequency of consuming leftover food (considered frequent if more than 3 times/week), and smoking habits (defined as smoking more than one cigarette per day). They were then asked about their previous testing for Hp, and if they had tested positive, whether they had received treatment with Hp eradication therapy.

Fluorescence immunochromatography [13

The blood sample was analyzed to measure the levels of serum PGI, PG II, and G17. The participants were given 4 ml of fasting blood in the morning, which was then centrifuged at a speed of 3000 rpm/min for 5 min. Subsequently, 80µL serum were collected and carefully added into the sampling hole on the detection card in a vertical manner. Following a waiting period of 15 min, the detection card was inserted into the HIT-91 A fluorescence immunoanalyzer’s card slot for testing purposes. Immunofluorescence chromatography represents an innovative membrane-based detection method that leverages antigen-specific immune responses. In this technique, antibodies are labeled with fluorescent markers to identify the presence and location of antigens. The incorporation of fluorescence enhances the sensitivity of detection. Compared to alternative immunoassay methods, IFC stands out due to its superior accuracy and sensitivity, making it particularly suitable for precise quantitative analyses [19, 20].The test reagents and instruments utilized in this study were provided by Bioghan Biotechnology (Hefei) Co., LTD.

13-carbon breath test

All participants underwent a 13-carbon breath examination using the Shenzhen Hedway device. The specific procedure involved patients exhaling into an empty stomach, filling the first bag with air. Subsequently, they ingested 75 mg of 13-carbon carbon and waited for 30 min before exhaling into the second bag. The HCBT-01 breath test instrument was utilized to analyze the exhaled air from both bags. A positive result for Hp was indicated if DOB ≥ 4. In the diagnosis of H. pylori infection using a 13-carbon breath test, a 25 mg dose of urea results in a sensitivity of 98.85% and specificity of 99.13%. Within 20 min after consuming urea, both these values can exceed 98% [21].Before conducting the examination, we excluded individuals who were unsuitable for participation. This included those who did not meet the fasting requirements, had used acid suppressants within the past two weeks, or had taken antibiotics, antibacterial traditional Chinese medicine preparations, and bismuth agents within the last four weeks. We also excluded participants who had recently experienced gastrointestinal bleeding, undergone major gastrectomy, suffered from severe chronic atrophic gastritis, or had complex ulcers. As a result, the remaining participants were deemed suitable, ensuring that the examination results were relatively reliable [22].

Endoscopic examination

All participants underwent gastroscopy and were subsequently given the results. Individuals in the NC group are identified as those with chronic non-atrophic gastritis. Individuals in the GIM group are characterized by the replacement of original gastric glands and concave epithelium with intestinal epithelial cells. The biopsy tissue obtained after gastroscopy for pathological examination is considered as the benchmark for diagnosing GIM.

Statistical analyses

An independent statistician (T.N.) utilized IBM Corp.‘s SPSS version 27.0 for Windows software in conducting all statistical analyses. A significance level of p < 0.05 was considered statistically significant. The data presented in this article covers information until July 1, 2022. Categorical variables were reported as frequencies and proportions, while continuous variables were described using the median and interquartile range. Statistical comparisons between these variables were performed using various tests such as the Chi-square test, Fisher’s exact test, or Wilcoxon rank-sum test. To assess the risk for GIM, a logistic regression model was employed. All variables assessed in the univariate analysis were included in the multivariate model to explore factors associated with GIM prevalence. Figures were generated using Grasp Prism 7 software. An interaction test was conducted to examine if there were consistent odds ratios (ORs) across stratified groups.

Results

Baseline characteristics

A total of 487 participants, comprising 247 individuals without gastric intestinal metaplasia (NC) and 240 with GIM, were enrolled in this study. The average age of the participants was 54.31 ± 9.86 years for the NC group and 56.06 ± 10.34 years for the GIM group, ranging from 18 to 80 years old. In comparison to the NC group, there was a decrease in the expression level of PG II in the GIM group [10.71(6.40,16.89) VS 9.21(6.14,14.55), p = 0.010]. The prevalence of Hp infection was found to be approximately 66.80% in the NC group and 62.50% in the GIM group, with around14.98% and23.75% of individuals from each respective group having received Hp eradication treatment(p = 0 0.014). Table 1.

Table 1 Characteristics of the study participants
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Demographic data and risk factors for the development of GIM

The binary analyses revealed significant connections between lower levels of PG II (OR 0.976, 95%CI 0.957–0.996, p = 0.019), and prior eradication treatment for Hp (OR 1.695, 95%CI l.068-2690, p = 0 0.025) with the development of GIM.

The median level of PG II was calculated for all 487 participants, and all participants were divided into a low PG II group (243 cases) and a high PG II group (244 cases) according to the median. A higher incidence rate of GIM was observed within the low PG II group compared to the high PG II group (54.10% VS 44.44%, p = 0.020, Fig. 1) Table 2.

Table 2 Binary regression analysis of characteristics of all participants
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Fig. 1
figure 1

The Incidence of GIM in different level of PG II

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Effect of Hp infection on the general characteristics of GIM

Hp infection promotes GIM. Among the GIM patients, 150 were Hp-positive (Hp+) and 90 were Hp-negative (Hp−). Compared to the Hp + group, the expression level of PGI and PG II was decreased in the 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]. Table 3.

Table 3 Effect of Hp infection on the general characteristics of GIM
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Effect of Hp infection on the general characteristics of GIM patients with different expression levels of PG II

The GIM patients in the HP + group were divided into 2 groups: 77 patients with low PGII levels and 73 patients with high PGII levels. Compared to the high PGII group, the low PGII group had decreased levels of PGI [104.17(83.62, 128.82) VS 178.66(127.63, 243.83), p < 0.001] and increased levels of PGR[16.06(11.66, 21.04) VS 10.78(7.25, 13.99), p < 0.001]. There was no difference in Hp sterilization history between the two groups.

The GIM patients in the HP- group were divided into 2 groups: 58 patients with low PGII levels and 32 patients with high PGII levels. Compared to the high PGII group, the low PGII group had decreased levels of PGI [96.91(86.65, 118.55) VS 160.16(112.98, 230.22), p < 0.001], increased levels of PGR[16.91(13.29, 25.78) VS 10.95(9.14, 13.35), p < 0.001] and decreased levels of G17[3.86(2.00, 8.02) VS 10.08(3.32, 50.46), p = 0.002]. Compared to the high PGII group, a higher proportion of patients with low PGII had a history of Hp sterilization (29.31% VS 3.13%, p = 0.003) Table 4.

Table 4 Effect of Hp infection on the general characteristics of GIM patients with different expression levels of PG II
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The expression level of PG II in GIM people of Hp- with and without a history of Hp sterilization

GIM patients in the HP- group were divided into 2 subgroups: 1 with a history of Hp sterilization (18 cases) and one without (72 cases). Compared to the subgroup without Hp sterilization, the expression level of PG II was decreased in the subgroup with Hp sterilization. Table 5; Figure 2.

Table 5 The expression level of PG II in people of Hp- with and without a history of Hp sterilization
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Fig. 2
figure 2

The expression level of PG II in people of Hp- with and without a history of Hp sterilization. * means p < 0.05

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Discussion

More than 10 years ago, GC was identified as the 2nd most common cause of cancer-related fatalities globally and had a high incidence rate in Eastern Asia [23]. Nevertheless, notable changes have occurred in the epidemiological features of GC over the past few years [24]. Despite remaining a significant global concern, there has been an observable decrease in its prevalence [25]. GC currently holds the 5th position in terms of occurrence and 3rd in mortality rates worldwide [26]. Interestingly enough, specific populations are witnessing an upward trend in incidence rates among individuals below the age of 50 [27]. The occurrence and development of GC, especially in young populations, still have a long way to go for study.

The development of GC (intestinal) in the gastrointestinal tract involves a series of stages including inflammation, atrophy, GIM, dysplasia, and ultimately the formation of carcinoma. The presence of GIM as a direct precursor to cancerous lesions [28]. In this study, patients in GIM group only exhibited low levels of PG II. This could be attributed to the fact that patients in the NC group also experienced stomach inflammation, which results in no difference in PGI, PGR and G17 between GIM patients and the control group [29],while overall secretion levels are reduced in GIM patients. In this study, patients in the GIM group exhibited only low levels of PG II. This could be attributed to the fact that many GIM patients are predominantly in the early stages of the condition, where the gastric body shows signs of inflammation rather than extensive atrophy. Additionally, GIM patients tend to be older, which may lead to an overall reduction in the secretory capacity of the entire gastric mucosa. Consequently, this results in lower PG II levels [30].

In China, the decline in GC incidence and mortality rates can be attributed to changes in individual lifestyles and the persistent efforts of governments at all levels to prevent this disease [14]. Consequently, it is crucial to implement specific preventive measures, such as eradicating Hp and implementing screening projects for GC, considering its risk factors. Numerous studies have provided substantial evidence supporting the advantages of Hp eradication, including reduced recurrence rates for peptic ulcers, successful treatment outcomes for most gastric mucosa-associated lymphoid tissue lymphomas, and approximately a 50% decrease in the occurrence of gastric adenocarcinoma [31]. In a population-based community with significant diversity, the administration of Hp eradication therapy resulted in a notable decrease in the occurrence of noncardia gastric adenocarcinoma after an 8-year period when compared to individuals who did not receive any treatment [32]. The proportion of patients with GIM who had a history of Hp eradication increased in this study, and it was identified as an independent risk factor for GIM. This suggests that Hp eradication may have a certain effect on the gastric mucosa. The normal gastric microbiota exhibits a diverse composition. Following Hp infection, the balance between the host’s gastric microbiota and mucosal-related factors is disrupted, interfering with the intricate mechanisms of gastric homeostasis. This leads to inflammatory changes and ecological disturbances, allowing oral and intestinal pathogenic microbial strains to become predominant [33]. Even after Hp eradication treatment, these bacterial imbalances persist in the short term. Moreover, most patients with Hp infection experience an unfavorable gastric environment, which continues to harm the gastric mucosa even after Hp clearance due to the presence of irritants. Consequently, damaged gastric mucosa cells may progress toward GIM over a certain period.

Gastric mucosal inflammation caused by Hp infection leads to increased expression of serum PGI, especially PG II, which can also be observed in GIM patients [34]. On the other hand, the expression level of serum PGI, especially PG II, is decreased in Hp-negative patients compared with Hp+ patients. This phenomenon is also observed in GIM patients.The fact is widely acknowledged, Hp infection promotes the occurrence of GIM. In the Hp+ group, there was no difference in the proportion of individuals with a history of Hp eradication among different expression levels of PG II. However, in the Hp− group, the proportion of individuals with a history of Hp eradication increased in the low PG II group. Hp infection can foster an environment that promotes the proliferation of other bacteria. In cases of atrophic gastritis resulting from Hp infection, the loss of parietal cells leads to an increase in stomach pH, creating a hypochloric milieu. This condition facilitates bacterial overgrowth, which in turn boosts nitrite production and the accumulation of carcinogenic N-nitroso compounds [35]. However, therapies aimed at eradicating Hp can help restore the gut’s homeostatic symbiotic microbiome, although they may also have adverse effects due to their properties [36]. Consequently, after Hp is eliminated, cell proliferation and damage decrease [37], but there might be disruption in the gastrointestinal bacterial community. This disruption can be long-lasting and may impair barrier function, disrupt nutrient metabolism, and affect the processing of drug toxins. Additionally, since PG II secreting mucosal cells are more widely distributed, the reduction in PG II levels may be more pronounced.

Hp infection, decreased PGI levels, and a decreased PGI/PG II ratio are key indicators for gastric cancer screening in asymptomatic populations [38]. In our previous study, we also found reduced serum PG II levels in healthy subjects with Hp infection among those with metabolic syndrome [39]. In women ≤ 50 years of age, high levels of PG II are associated with a higher risk of anxiety [40]. In this study, GIM patients in the Hp-negative group, compared to the subgroup without Hp eradication, the expression level of PG II was decreased in the subgroup with Hp eradication. This may be related to cell proliferation and damage caused by Hp infection and further imbalance of gastrointestinal bacteria after Hp eradication treatment. Therefore, the history of Hp eradication may lead to decreased PG II expression in GIM patients of Hp-negative.

It has been documented that serum PG II levels decrease significantly in patients 1 to 2 months after completion of Hp eradication therapy [9]. This view is consistent with this study, that is, after the eradication of Hp, gastric acid secretion increases, while the mucosal barrier has not been repaired at this time, leading to an increase in the loss of gastric mucosal epithelial cells. Since the range of cells secreting PG II is broader, the expression level of PG II may be reduced in patients after Hp eradication. In addition, patients with GIM may display less favorable lifestyle and dietary habits, such as a preference for highly processed foods, increased consumption of red meat, and advanced age [41]. These factors can cause more significant and severe damage to the gastric mucosa, consequently leading to reduced expression levels of PG II. If in patients treated with Hp, drinking multi-strain fermented milk can induce a modest but significant faster recovery of microbiota composition (beta-diversity) and short-chain fatty acid production, and limit the increase of potentially pathogenic bacteria [42]. In addition, polyphenols, which are abundant in the plant kingdom, have been shown to alleviate HP-dependent pathology, including even inhibiting tumorigenesis [43]. Therefore, in the practice of GC screening, the new gastric cancer scoring system that includes gender and age has improved the screening rate of GC compared with the traditional ABC screening method that only focuses on PGI, P GII, PGR and G17 [44, 45].

This study presents three clinical implications. Firstly, a significant association exists between decreased levels of PG II and the occurrence of GIM. Previous research has already established a strong connection between the presence of GIM and digestive symptoms [31]. The level of PG II serves as an indicator for the overall secretory function of gastric mucosa, with lower levels indicating reduced secretory function. As GIM progresses, the primary cells responsible for pepsinogen secretion undergo acute reprogramming and transform into mucus-secreting cells involved in wound healing [32]. Consequently, there is a decrease in the number of acid-producing cells within the gastric mucosa of individuals with GIM. When considering serum gastric function as part of a screening protocol for gastric cancer, it becomes crucial to account for the role played by PG II in the assessment system. Some studies have indicated that individuals with higher PGI levels (above 127.20 ng/mL) are more likely to exhibit signs of GIM compared to those with higher PG II levels [46]. This disparity may be attributed to several factors: including outpatients in this study where even individuals from the NC group displayed some degree of gastritis; hence, patients with GIM might present low PG II levels. Secondly, there is a notable correlation between Hp eradication history and the incidence rate of GIM; however, detailed investigations on this topic remain scarce. Lastly, Hp eradication history leads to diminished expression levels of PG II among Hp-GIM patients. This appears to be another unfavorable consequence resulting from Hp eradication - namely long-term inhibition on gastric mucosal secretory function among HP-IM patients after undergoing Hp eradication.

The strength of our study lies in its extensive population-based analysis, which identified predictors for GIM. Moreover, it indicated that low PG II contributed to GIM. Additionally, Hp eradication history increased the prevalence of GIM, and Hp eradication history decreased the expression level of PG II in HP- IM patients. However, this retrospective cross-sectional investigation encountered certain limitations. Firstly, incomplete data in some patients prevented us from conducting severity grading of GIM using the OLGIM system. Secondly, as this study was conducted at a single center, its robustness may be slightly diminished compared to multi-center studies. Future prospective longitudinal studies will be conducted to verify these results. In addition, taking into account cultural differences, we hope that these results can be used for reference by people outside of China.

In conclusion, 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- IM patients.

Disclosure statement

The authors affirm that they do not possess any financial or proprietary interest in any material or method mentioned. The authors bear full responsibility for the content and composition of the paper.

Data Availability

The corresponding authors are able to provide all the necessary data supporting the findings of this investigation upon a reasonable request.

Data availability

No datasets were generated or analysed during the current study.

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Acknowledgements

This cross-sectional observational study was approved by the ethics committee of the Affiliated Hospital of Xuzhou Medical University (Approval no. XYFY2020-KL045-01), and written informed consent was obtained from all participants.

Funding

This work was supported by the Key Development Project of Science and Technology Bureau in Xuzhou (Social development) [grant number KC22233]; the Key Laboratory of Jiangsu Province Open project [grant number XZSYSKF2021029], the Project supported by the Affiliated Hospital of Xuzhou Medical University [grant number 2023ZL19] and the Provincial Graduate Research and Practice Innovation Program of Jiangsu Province [SJCX24-1543] .

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  1. Yanhong Wang and Xixiang Cao contributed equally to this work.

Authors and Affiliations

  1. Department of Gastroenterology, The Affiliated Hospital of Xuzhou Medical University, Huaihai West Road, Xuzhou, Jiang Su, 221004, China

    Yanhong Wang, Sujuan Fei & Xunlei Pang

  2. Graduate school, Xuzhou Medical University, Xuzhou, 221009, China

    Xixiang Cao, Baodong Shan, Song Chen & Shengnan Li

  3. College of Pharmacy, Jiangsu Key Laboratory of New Drug Research and Clinical Pharmacy, Xuzhou, 221009, China

    Xunlei Pang

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Contributions

W.Y. and C.X. wrote the main manuscript text and S.B. prepared Figs. 1 and 2. C.X., S.B., C.S. and L.S. gathered datas. P.X. and F.S. wrote and reviewed the main manuscript text.All authors reviewed the manuscript.

Corresponding authors

Correspondence to Sujuan Fei or Xunlei Pang.

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Ethics approval and consent to participate

This study was conducted with the approval of the ethics committee at the Affiliated Hospital of Xuzhou Medical University (Approval no. XYFY2020-KL045-01). All participants were included in the study after providing written informed consent. The methods employed strictly adhered to relevant guidelines and regulations as stated in the declaration of Helsinki.

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The authors declare no competing interests.

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Wang, Y., Cao, X., Shan, B. et al. Hp eradication decreased the expression level of PG II in patients of Hp negative with gastric intestinal metaplasia: a retrospective cross-sectional study. J Health Popul Nutr 44, 20 (2025). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s41043-025-00756-y

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Journal of Health, Population and Nutrition

ISSN: 2072-1315

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