European Journal of Cardiovascular Medicine

Dyspepsia is a common gastrointestinal disorder, affecting nearly 30% of the adult population worldwide, and presents with symptoms such as epigastric discomfort, bloating, early satiety, and nausea. Among its multiple etiologies, Helicobacter pylori (H. pylori) infection stands out as one of the most significant and potentially modifiable factors [3]. This gram-negative, spiral-shaped bacterium colonizes the gastric mucosa and plays a pivotal role in the pathogenesis of chronic gastritis, peptic ulcer disease, mucosa-associated lymphoid tissue (MALT) lymphoma, and gastric carcinoma [4].

The effect of H. pylori on gastric acid secretion is highly variable and depends on the distribution and severity of gastritis. Antral-predominant colonization typically leads to hypergastrinemia and acid hypersecretion, often associated with duodenal ulceration. In contrast, corpus-predominant or pangastritis is linked to parietal cell loss, glandular atrophy, and reduced acid output, resulting in hypochlorhydria or achlorhydria [2,5]. These physiological changes have important clinical consequences, particularly in modifying dyspeptic symptom profiles and increasing the risk for intestinal metaplasia and gastric cancer [6].

Furthermore, elevated gastric juice pH and increased ammonia levels have been observed in infected individuals, suggesting a direct impact of H. pylori on intragastric milieu [1]. Despite a wealth of global data, regional studies examining the interplay between H. pylori infection, gastric acid dynamics, and dyspeptic subtypes remain scarce. Understanding these associations is essential for refining diagnostic approaches and guiding tailored therapeutic interventions [2,3]. Therefore, this study aims to explore the relationship between H. pylori infection, gastric pH, and acid secretion patterns among dyspeptic patients in a tertiary care setting.

Study Design and Setting:
This was a hospital-based, cross-sectional observational study conducted in the Department of General Medicine, Nimra Medical College and Hospital, Vijayawada, Andhra Pradesh. The study was carried out over a five-month period from January 2024 to May 2024.

Study Population:
The study included adult patients aged 18–65 years presenting with symptoms of dyspepsia such as epigastric pain, bloating, postprandial fullness, or early satiety, and referred for upper gastrointestinal endoscopy. Patients with previous eradication therapy for H. pylori, those on proton pump inhibitors or antibiotics within two weeks prior to endoscopy, and those with known malignancy, gastrointestinal bleeding, or major systemic illness were excluded.

Sample Size and Sampling Technique:
A total of 100 dyspeptic patients who met the inclusion criteria were enrolled using consecutive sampling during the study period.

Data Collection Procedures:
After obtaining written informed consent, all participants underwent upper gastrointestinal endoscopy. Two antral biopsies were collected for histopathological examination and rapid urease testing to determine H. pylori infection status. Fasting gastric juice was aspirated for pH measurement using a calibrated digital pH meter.

Gastric acid secretion was assessed in a subset of cooperative patients (n = 100) using standard methodology:

Basal Acid Output (BAO): Measured over one hour in fasting state via nasogastric aspiration.

Maximal Acid Output (MAO): Measured after pentagastrin stimulation (6 μg/kg subcutaneously), collecting four 15-minute samples.

Classification of Dyspepsia:
Based on symptom profile, patients were classified into functional, ulcer-like, or reflux-like dyspepsia, using validated clinical criteria.

Statistical Analysis:
Data were analyzed using SPSS version 26.0. Continuous variables were expressed as mean ± standard deviation and compared using the independent t-test. Categorical variables were analyzed using Chi-square test. A p-value <0.05 was considered statistically significant.

Ethical Considerations:
The study was approved by the Institutional Ethics Committee of Nimra Medical College, Vijayawada. All procedures were conducted in accordance with the Declaration of Helsinki. Confidentiality and voluntary participation were ensured throughout the study.

Out of the 100 dyspeptic patients enrolled in the study, Helicobacter pylori (H. pylori) infection was detected in 58% of individuals, while the remaining 42% tested negative, as shown in Table 1.

Table 1: Distribution of H. pylori Infection Status Among Dyspeptic Patients (N = 100)

Figure1. Distribution of H. pylori Infection Status Among Dyspeptic Patients

Analysis of fasting gastric pH revealed a significant difference between the two groups. Patients with H. pylori infection exhibited a higher mean gastric pH (4.1 ± 1.3) compared to those without infection (2.6 ± 0.9), indicating reduced gastric acidity in the infected group. This difference was statistically significant (p < 0.001) (Table 2).

Table 2: Comparison of Mean Gastric pH Levels Between Groups

Figure 2: Comparison of Mean Gastric pH Levels Between Groups

Evaluation of gastric acid secretion parameters demonstrated that both basal acid output (BAO) and maximal acid output (MAO) were significantly lower in H. pylori-positive patients compared to uninfected individuals. The mean BAO in the infected group was 2.8 mEq/hour, in contrast to 5.2 mEq/hour in the non-infected group. Similarly, MAO values were 12.1 mEq/hour and 18.7 mEq/hour in the infected and uninfected groups, respectively (Table 3). These differences were statistically significant (p < 0.001 for both comparisons).

Table 3: Gastric Acid Secretion Parameters (mEq/hour)

Figure 3. Gastric Acid Secretion Parameters Between H.Pylori Groups

Among the 58 H. pylori-positive patients, functional dyspepsia was the most common presentation (65.5%), followed by ulcer-like dyspepsia (24.1%) and reflux-like symptoms (10.4%), as summarized in Table 4.

Table 4: Dyspepsia Subtypes Among H. Pylori Positive Patients (n = 58)

Figure 4.Dyspepsia Subtypes Among H. pylori Positive Patients

This study highlights a significant association between Helicobacter pylori infection and altered gastric acid physiology in dyspeptic patients. The observed prevalence of infection (58%) reflects the ongoing high burden of H. pylori among symptomatic populations, with known regional and host-related variations [9]. Our findings confirm that H. pylori infection correlates with a notable increase in fasting gastric pH and a marked reduction in both basal and maximal acid outputs, indicating hypochlorhydria.

These results are in line with earlier studies which suggest that chronic infection, particularly with corpus-predominant or pangastritis, leads to parietal cell atrophy, decreased acid secretion, and sustained elevation of intragastric pH [13]. Mechanistically, H. pylori alters the secretion and activity of gastrointestinal hormones such as somatostatin and gastrin, contributing to acid suppression and mucosal injury [7]. Furthermore, infection has been shown to potentiate the inhibitory effects of proton pump inhibitors, indicating its significant role in modulating acid dynamics [8].

Functional dyspepsia emerged as the most frequent subtype among infected patients in our study, consistent with literature suggesting that H. pylori-associated dyspepsia overlaps with functional variants and may not always respond to acid-suppressive therapy alone [12]. This supports the hypothesis that altered gastric sensory perception and motility, rather than hyperacidity, often drive symptoms in these patients [11].

Additionally, our findings reinforce the broader pathogenic spectrum of H. pylori, with chronic hypochlorhydria predisposing to atrophic gastritis, intestinal metaplasia, and gastric malignancy if left untreated [9]. Emerging data also highlight the role of host genetic factors, including ABO and Lewis blood group antigens, in susceptibility to infection and its clinical expression [10].

However, this study has certain limitations. Being cross-sectional, causal inference is restricted. Gastric acid measurements required significant patient cooperation, and advanced histological assessments (e.g., grading of atrophy or presence of cagA/vacA virulence genes) were not performed. Nevertheless, our findings underscore the clinical importance of evaluating acid output and H. pylori status in dyspeptic patients, particularly those with persistent symptoms despite empirical therapy.

This study establishes a significant association between Helicobacter pylori infection and altered gastric acid physiology in dyspeptic patients. Infected individuals demonstrated elevated gastric pH and markedly reduced basal and maximal acid outputs, indicative of hypochlorhydria. Functional dyspepsia emerged as the predominant clinical presentation among the H. pylori-positive group, highlighting the infection’s role in symptom variability. These findings reinforce the need for targeted evaluation and management of H. pylori in dyspeptic populations, especially in regions with high prevalence. Early detection and eradication may not only improve symptom control but also reduce long-term complications such as atrophic gastritis and gastric carcinoma linked to chronic hypochlorhydria.

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