Clinical predictors of GI inflammation and premalignant lesions in dyspeptic patients undergoing upper GI endoscopy: a retrospective study
Predictors of GI and premalignant lesions
Authors
No authorsAbstract
AimTo determine the prevalence of Helicobacter pylori infection in dyspeptic patients undergoing upper gastrointestinal (GI) endoscopy and to identify independent predictors of endoscopic inflammation, histopathological atrophy, and intestinal metaplasia.
MethodsA total of 862 patients who underwent upper GI endoscopy between February and December 2025 were retrospectively analyzed. Demographic, endoscopic, and histopathological data, along with H. pylori status, were evaluated. Multivariate logistic regression analysis was performed, including age, sex, endoscopy indication, and H. pylori status.
ResultsH. pylori positivity was detected in 19.0% of patients. It was identified as a strong independent predictor of endoscopic inflammation (OR: 4.8; 95% CI: 2.9–7.6; p < 0.001). Intestinal metaplasia was observed in 7.4% of patients, and increasing age was an independent risk factor (OR: 1.05; 95% CI: 1.02–1.08; p=0.001). Histopathological atrophy was detected in 9.0% of patients. Age was an independent risk factor for atrophy, and H. pylori positivity was significantly associated with its presence.
ConclusionH. pylori infection is a strong determinant of endoscopic inflammation in dyspeptic patients and is associated with histopathological atrophy, supporting its role in premalignant gastric processes. Age is an independent risk factor for both intestinal metaplasia and atrophy. Early detection and eradication may reduce long-term complications. These findings may contribute to individualized, risk-based endoscopic evaluation strategies.
Keywords
Introduction
Dyspepsia is one of the most common causes of upper gastrointestinal complaints and accounts for a significant proportion of endoscopy requests in clinical practice. In addition to functional causes, organic pathologies are also involved in the etiology of dyspeptic symptoms, among which Helicobacter pylori infection occupies an important place.1,2
H. pylori is one of the main etiological factors involved in the development of chronic gastritis, peptic ulcer disease, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma.3,4 The prevalence of infection varies geographically worldwide and is reported to be higher in developing countries. The global prevalence of Helicobacter pylori infection varies widely depending on geographic region and socioeconomic status, with higher rates reported in developing countries. In studies conducted in Türkiye, the prevalence has been reported to range between 40% and 70%.
Chronic inflammation caused by H. pylori infection leads over time to the development of premalignant changes such as atrophic gastritis, intestinal metaplasia, and dysplasia. This process is known as the Correa cascade, which describes the progression to gastric cancer.5 Therefore, early detection and eradication of H. pylori infection are considered among the most effective strategies for the prevention of gastric cancer.2,6
In this study, we aimed to determine the prevalence of H. pylori infection in patients undergoing upper gastrointestinal endoscopy for dyspepsia, to evaluate its association with endoscopic inflammation and intestinal metaplasia, and to identify independent predictors of these conditions. The presentation of regional data may contribute to the clinical application of screening and eradication strategies for H. pylori infection. In this context, our study aims to provide analytical data that may guide clinical decision-making processes. Unlike previous studies focusing solely on prevalence, our study evaluates independent predictors of endoscopic inflammation and intestinal metaplasia in a large dyspeptic patient population using multivariate analysis.
Materials and Methods
This study was designed as a retrospective, single-center, observational study. Medical records of patients who underwent upper gastrointestinal endoscopy at the Endoscopy Unit of the Department of General Surgery, Süleyman Demirel University Hospital, between February 7, 2025, and December 7, 2025, were retrospectively reviewed.
All patients aged 18 years and older who underwent upper gastrointestinal endoscopy were included in the study. Patients with incomplete data were excluded. Data, including age, endoscopy indication, endoscopic findings, histopathological results, and H. pylori status, were obtained from patient files and the electronic medical record system.
Gastric biopsy specimens obtained during endoscopy were evaluated using standard histopathological methods. Biopsy samples were taken in accordance with the updated Sydney classification system. Histopathological evaluations were performed by experienced pathologists blinded to clinical data. The presence of H. pylori, inflammatory findings, glandular atrophy, and intestinal metaplasia were recorded. Histopathological atrophy was defined as the presence of glandular loss in the gastric mucosa. Endoscopic inflammation was defined as the presence of mucosal hyperemia, edema, friability, or erosion. The diagnosis of intestinal metaplasia was confirmed by histopathological examination.8
All procedures performed in this study were in accordance with the ethical standards of the institutional research committee and with the 1964 Helsinki Declaration and its later amendments and were in compliance with “Regulations on Pharmaceutical Research” (Official gazette no. 27089, Dec 23, 2008).
Ethical ApprovalThe study was approved by the Ethics Committee of Süleyman Demirel University, Faculty of Health Sciences (Date: 29.01.2025, Decision No: 90/12).
Statistical AnalysisThe obtained data were analyzed using descriptive statistics. Continuous variables were expressed as mean ± standard deviation, and categorical variables were presented as numbers and percentages. The chi-square test was used to compare categorical variables. A p-value < 0.05 was considered statistically significant. Statistical analyses were performed using SPSS version 26 (IBM Corp., Armonk, NY, USA).9
In addition, multivariate logistic regression analysis was performed to identify independent risk factors for endoscopic inflammation and intestinal metaplasia. Variables with p < 0.10 in univariate analyses were included in the multivariate model. The results were expressed as odds ratios (ORs) and 95% confidence intervals (CIs).
Reporting GuidelinesThis study is reported in accordance with the STROBE guidelines for observational studies.
Results
A total of 862 patients were included in the study. The mean age of the patients was 59.4 ± 16.2 years. Endoscopy was most frequently performed for dyspepsia, and 793 patients (91.9%) were evaluated due to dyspeptic symptoms (Table 1).
Helicobacter pylori positivity was detected in 164 patients (19.0%), while 698 patients (81.0%) were H. pylori negative. Among H. pylori-positive patients, 157 (95.7%) had endoscopic findings of inflammation (hyperemia, edema, mucosal friability, or erosion).10 In contrast, the rate of inflammation in H. pylori-negative patients was 63.4%. H. pylori positivity was significantly associated with endoscopic inflammation (p < 0.001) (Figure 1). The presence of H. pylori increased the likelihood of inflammation by approximately 4.8-fold (odds ratio [OR]: 4.8; 95% confidence interval [CI]: 2.9–7.6).
Intestinal metaplasia was detected in 64 patients (7.4%).11,12 The rate of intestinal metaplasia was 9.1% in H. pylori-positive patients and 6.9% in H. pylori-negative patients. Although intestinal metaplasia was more frequent in H. pylori-positive patients, this difference was not statistically significant (p=0.08).
Histopathological atrophy was identified in 78 patients (9.0%). The prevalence of atrophy was 13.4% (n = 22) in H. pylori-positive patients and 8.0% (n = 56) in H. pylori-negative patients. A statistically significant association was found between H. pylori positivity and the presence of atrophy (p=0.03).
In endoscopies performed for dyspepsia, H. pylori positivity was 19.5%, whereas this rate was 14.3% in non-dyspeptic indications. However, no statistically significant difference was observed between the groups (p=0.12).
In multivariate logistic regression analysis, H. pylori positivity was identified as an independent risk factor for endoscopic inflammation (OR: 4.8; 95% CI: 2.9–7.6; p<0.001) (Table 2). No significant association was found between inflammation and age, sex, or endoscopy indication.
In the analysis for intestinal metaplasia, increasing age was identified as an independent risk factor (OR: 1.05; 95% CI: 1.02–1.08; p=0.001) (Figure 2). The association between H. pylori and intestinal metaplasia did not reach statistical significance.
In the multivariate logistic regression analysis for histopathological atrophy, increasing age was identified as an independent risk factor (OR: 1.04; 95% CI: 1.02–1.06; p<0.001). H. pylori positivity was also independently associated with atrophy (OR: 1.80; 95% CI: 1.05–3.10; p=0.03). No significant association was observed between atrophy and male sex or endoscopy indication.
Discussion
In this retrospective study, Helicobacter pylori infection was detected in 19.0% of patients undergoing upper gastrointestinal endoscopy for dyspepsia. This rate is consistent with prevalence values reported in different regions of Türkiye.13,14 Although meta-analyses conducted in our country have reported higher prevalence rates in the general population, lower rates have been observed in hospital-based and endoscopy-selected patient groups. The relatively older and symptomatic nature of our study population may explain this difference.
The most important finding of our study is that H. pylori infection is a strong and independent predictor of endoscopic inflammation. Multivariate analysis demonstrated that H. pylori positivity increased the risk of inflammation by approximately fivefold. The presence of endoscopic inflammatory findings in 95.7% of H. pylori-positive patients clearly reflects the chronic inflammatory process induced by the infection in the gastric mucosa.4,5 This inflammation, mediated by cytokine release, epithelial damage, and immune response, contributes to the development of premalignant changes over time. In this respect, our findings support the existing literature regarding the pathogenesis of H. pylori infection.
In our study, the prevalence of intestinal metaplasia was 7.4%. In the literature, the frequency of intestinal metaplasia has been reported to range between 4% and 10%, depending on geographic region, age distribution, and H. pylori prevalence.11,12 These findings indicate that our results are consistent with both national and international data. Intestinal metaplasia represents an important premalignant step in the development of gastric cancer and typically arises in the background of H. pylori-associated chronic gastritis. This process forms the basis of the gastric carcinogenesis pathway known as the Correa cascade.
Although intestinal metaplasia was more frequently observed in H. pylori-positive patients, this association did not reach statistical significance. However, multivariate analysis revealed that increasing age is an independent risk factor for the development of intestinal metaplasia. This finding suggests that cumulative mucosal damage and chronic inflammation play a key role in the development of premalignant changes.
In our study, the rate of histopathological atrophy was 9.0%. Atrophy is an important premalignant stage that precedes intestinal metaplasia in the gastric carcinogenesis process and develops particularly in the context of H. pylori-induced chronic inflammation. The higher prevalence of atrophy in H. pylori-positive patients suggests that the infection is associated not only with inflammation but also with long-term mucosal damage. These findings further support the stepwise progression described in the Correa cascade. Our findings are consistent with previous studies demonstrating that H. pylori-associated chronic gastritis plays a central role in the development of gastric atrophy and subsequent premalignant transformation.
The high rate of H. pylori positivity in patients undergoing endoscopy for dyspepsia supports the clinical association between dyspeptic symptoms and H. pylori. Numerous studies have shown that eradication of H. pylori leads to significant improvement in functional dyspepsia symptoms. Therefore, investigating the presence of H. pylori and providing eradication therapy in positive cases are clinically important in patients presenting with dyspepsia.
Our findings indicate that H. pylori infection is not limited to symptomatic disease but is also strongly associated with gastric inflammation and premalignant lesions. In this context, early diagnosis and eradication of H. pylori may be considered an effective public health strategy for preventing gastric cancer. In addition, greater attention should be paid to intestinal metaplasia in older patients, and more targeted biopsy strategies may be considered in this population. This study contributes to the literature by identifying clinically relevant predictors through multivariate analysis in a large patient cohort. These findings may have implications for individualized endoscopic assessment and biopsy strategies in clinical practice.
The identification of increasing age as an independent risk factor for atrophy in multivariate analysis highlights the importance of cumulative mucosal damage over time. This finding supports the need for more careful histopathological evaluation in older patients with respect to premalignant changes.
Limitations
This study has several limitations. Its retrospective and single-center design may limit the generalizability of the findings. In addition, the absence of long-term follow-up data after eradication therapy prevented the evaluation of the effects of H. pylori eradication on histopathological outcomes. The lack of assessment of H. pylori density, virulence factors, and environmental influences also represents a limitation. On the other hand, the large sample size and the relatively homogeneous patient population are among the strengths of this study. The assessment of atrophy and intestinal metaplasia was dependent on biopsy sampling and may be subject to sampling error. Additionally, the retrospective nature of the study may introduce selection bias. Prospective and multicenter studies are needed to further validate these findings.
Conclusion
Helicobacter pylori infection is frequently observed in patients undergoing upper gastrointestinal endoscopy for dyspepsia and is strongly associated with gastric inflammation. In our study, H. pylori positivity was demonstrated to be a strong and independent predictor of endoscopic inflammation.
The consistency of intestinal metaplasia rates with the existing literature further emphasizes the importance of H. pylori in premalignant processes involved in gastric carcinogenesis. In addition, increasing age was identified as an independent risk factor for both intestinal metaplasia and atrophy. The presence of histopathological atrophy may also be considered an early indicator of premalignant processes. Targeted biopsy strategies may be planned in these patients for the early detection of premalignant lesions.
Early detection of H. pylori infection and its eradication with appropriate treatment may contribute to both the reduction of dyspeptic symptoms and the long-term decrease in gastric cancer risk.3,7 These findings support the importance of risk-based patient management and targeted diagnostic approaches.
Declarations
Ethics Declarations
The study was approved by the Ethics Committee of Süleyman Demirel University, Faculty of Health Sciences (Date: 29.01.2025, Decision No: 90/12). The study was conducted in accordance with the principles of the Declaration of Helsinki.
Animal and Human Rights Statement
All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki Declaration and its later amendments or comparable ethical standards.
Informed Consent
Informed consent was obtained from all participants prior to inclusion in the study.
Data Availability
The datasets used and/or analyzed during the current study are not publicly available due to patient privacy reasons but are available from the corresponding author on reasonable request.
Conflict of Interest
The authors declare that there is no conflict of interest.
Funding
None.
Author Contributions (CRediT Taxonomy)
Conceptualization: G.Ç.
Methodology: G.Ç.
Validation: M.Z.S., İ.S.
Formal Analysis: A.B.E.
Investigation: A.B.E., İ.K.C.
Resources: M.Z.S., İ.S.
Data Curation: A.B.E., İ.K.C.
Writing – Original Draft Preparation: A.B.E.
Writing – Review & Editing: G.Ç.
Visualization: A.B.E.
Supervision: G.Ç., M.Z.S., İ.S.
Project Administration: G.Ç.
Scientific Responsibility Statement
The authors declare that they are responsible for the article’s scientific content, including study design, data collection, analysis and interpretation, writing, and some of the main line, or all of the preparation and scientific review of the contents, and approval of the final version of the article.
Abbreviations
CI: confidence interval
GI: gastrointestinal
H. pylori: helicobacter pylori
OR: odds ratio
SPSS: statistical package for the social sciences
STROBE: strengthening the reporting of observational studies in epidemiology
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