European Journal of Cardiovascular Medicine

Helicobacter pylori (H. pylori) is a gram-negative, microaerophilic bacterium that colonizes the gastric mucosa and is considered one of the most common chronic bacterial infections worldwide (1). It plays a central role in the pathogenesis of chronic gastritis, peptic ulcer disease, gastric adenocarcinoma, and mucosa-associated lymphoid tissue (MALT) lymphoma (2). The infection is typically acquired during childhood and persists for decades if left untreated, leading to progressive mucosal damage through a cascade of inflammatory responses (3).

The histopathological evaluation of gastric biopsies remains a cornerstone in diagnosing H. pylori-associated gastritis. It not only confirms the presence of the organism but also allows the grading of gastritis based on inflammatory activity, glandular atrophy, and intestinal metaplasia, which are crucial indicators for risk stratification in gastric carcinogenesis (4). The Updated Sydney System offers a standardized approach for reporting gastric biopsy findings and enhances diagnostic reproducibility among pathologists (5).

Despite advancements in non-invasive diagnostic modalities such as urea breath tests and stool antigen assays, histological analysis remains invaluable in assessing the severity of mucosal injury and detecting pre-neoplastic changes. This study aims to analyze the histopathological spectrum of gastric mucosal alterations associated with H. pylori infection in patients presenting with chronic gastritis at a tertiary care center.

A total of 150 gastric biopsy samples were included from patients who presented with symptoms of chronic dyspepsia and underwent upper gastrointestinal endoscopy. Inclusion criteria encompassed biopsy specimens with adequate tissue for histological assessment and a clinical indication of gastritis. Biopsies showing malignancy or with inadequate tissue were excluded.

All specimens were fixed in 10% buffered formalin, routinely processed, and embedded in paraffin. Sections of 4–5 microns were cut and stained using Hematoxylin and Eosin (H&E) to assess general histopathological features. Modified Giemsa stain was employed for the specific detection of H. pylori organisms.

Histological features were evaluated according to the Updated Sydney System, focusing on parameters such as chronic inflammation (mononuclear cell infiltration), activity (neutrophilic infiltration), glandular atrophy, intestinal metaplasia, and the presence of lymphoid aggregates or follicles. Each feature was graded on a scale from mild to severe.

Data were recorded and statistically analyzed using SPSS software version 25.0. The chi-square test was applied to assess the association between H. pylori infection and various histological parameters. A p-value < 0.05 was considered statistically significant.

Out of the 150 gastric biopsy specimens evaluated, Helicobacter pylori was identified in 93 cases (62%) using modified Giemsa staining. The remaining 57 cases (38%) tested negative for H. pylori.

Histopathological Features
Chronic inflammation was the most common finding, observed in 135 cases (90%), followed by neutrophilic activity in 78 cases (52%), glandular atrophy in 36 cases (24%), intestinal metaplasia in 21 cases (14%), and lymphoid aggregates in 60 cases (40%). A summary of these findings is presented in Table 1.

Table 1: Distribution of Histopathological Features in Gastric Biopsies (n=150)

Among the 93 H. pylori-positive cases, 79 (85%) showed moderate to severe chronic inflammation, 65 (70%) had active inflammation with neutrophilic infiltration, 30 (32%) exhibited glandular atrophy, and 18 (19%) demonstrated intestinal metaplasia. In contrast, H. pylori-negative cases exhibited significantly lower frequencies of these changes. The comparative distribution is shown in Table 2.

Table 2: Comparison of Histological Features Between H. pylori-Positive and -Negative Cases

A statistically significant association was found between H. pylori infection and the presence of neutrophilic activity, glandular atrophy, intestinal metaplasia, and lymphoid aggregates (p < 0.05), as indicated in Table 2. These findings highlight the pathogenic impact of H. pylori on the gastric mucosa.

The present study evaluated the histopathological features of chronic gastritis and their correlation with Helicobacter pylori infection in a tertiary care setting. The detection rate of H. pylori in our study was 62%, which is consistent with previous studies conducted in similar geographic and clinical settings (1,2). The variation in detection rates globally can be attributed to differences in socioeconomic status, sanitation, and diagnostic techniques (3).

Chronic inflammation was observed in 90% of cases, and 85% of H. pylori-positive cases showed moderate to severe inflammation. These findings are in agreement with the established role of H. pylori in eliciting a chronic inflammatory response due to persistent antigenic stimulation (4,5). The presence of dense mononuclear cell infiltration, mainly lymphocytes and plasma cells, is a hallmark of chronic gastritis associated with H. pylori (6).

Neutrophilic activity, representing acute inflammation or "activity" in the Sydney classification, was significantly higher in H. pylori-positive cases (70%) than in negative cases (23%), supporting the organism's ability to provoke an active inflammatory process (7,8). Similar results were reported by Ranjan et al. and Sharma et al., who noted a strong association between H. pylori colonization and mucosal damage (9,10).

Glandular atrophy and intestinal metaplasia were significantly more common in H. pylori-positive cases (32% and 19%, respectively), aligning with the multistep Correa cascade that describes the progression from chronic gastritis to atrophy, metaplasia, dysplasia, and eventually gastric carcinoma (11,12). These findings emphasize the importance of early detection and eradication of H. pylori to prevent long-term complications (13).

Lymphoid aggregates were identified in 40% of cases, with a significantly higher prevalence among H. pylori-infected patients. This supports the hypothesis that H. pylori infection can lead to the development of organized lymphoid tissue in the gastric mucosa, which in rare cases may evolve into MALT lymphoma (14,15).

The use of modified Giemsa staining for the identification of H. pylori in histological sections is both cost-effective and reliable, particularly in resource-limited settings. However, limitations of our study include its retrospective design and reliance on histology alone without serological or molecular confirmation. Further multicentric studies with larger cohorts and integrated diagnostic approaches are recommended to strengthen these findings.

In conclusion, the histopathological spectrum observed in this study underscores the pivotal role of H. pylori in gastric mucosal damage. The significant associations with active inflammation, atrophy, metaplasia, and lymphoid aggregates highlight the need for routine biopsy and targeted eradication strategies in patients presenting with dyspeptic symptoms.

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