1. Introduction
Gastric cancer remains a major global health challenge, ranking as the fifth-most commonly diagnosed cancer worldwide and the third leading cause of cancer-related deaths [
1]. Despite advances in early detection and treatment, prognosis remains poor, especially in developing regions where diagnoses often occur at advanced stages [
2]. In the Middle East, the incidence of gastric cancer varies across countries due to multiple contributing factors, including
Helicobacter pylori (
H. pylori) infection, dietary habits, smoking, and genetic predisposition, all of which contribute to regional disparities in disease burden [
3]. Among the primary risk factors,
H. pylori infection stands as the most well-established risk factor driving gastric carcinogenesis [
4].
H. pylori is a Gram-negative, spiral-shaped, acid-resistant bacterium primarily colonizing the stomach’s pyloric region. The literature demonstrates its critical role in the development of gastric cancer, peptic ulcer disease, chronic gastritis, and mucosa-associated lymphoid tissue (MALT) lymphoma [
5]. This infection can be spread by oral–oral or fecal–oral pathways and is commonly associated with poor sanitation, overcrowding, and the intake of contaminated food or water [
6]. Although a significant number of carriers are asymptomatic, chronic infection provokes persistent gastric inflammation, causing mucosal damage, atrophic gastritis, and ultimately intestinal metaplasia, a recognized precursor for gastric cancer development [
7]. The bacterium’s virulence factors interfere with host cellular signaling, promote epithelial cell proliferation, and inhibit apoptosis, thereby accelerating malignant transformation [
8]. Additionally, alterations in the host immune response and gut microbiota composition have been implicated in
H. pylori-induced carcinogenesis, underscoring the complexity of its pathogenic mechanisms [
9]. These complications are associated with high morbidity and mortality, warranting its classification as a Group 1 carcinogen by the World Health Organization (WHO) [
10].
Despite improvements in medical research and public health initiatives,
H. pylori remains one of the most common chronic bacterial illnesses, posing a substantial challenge to healthcare systems [
11]. Globally, the prevalence of
H. pylori is estimated at 48.5%, with the highest rates reported in developing regions such as Africa (70.1%) and South America (69.4%). In the Middle East and North Africa (MENA) region, prevalence among adults ranges widely from 36.8 to 94%. In contrast, substantially lower prevalence rates are observed in developed areas like North America (37.1%) and Oceania (24.4%), largely influenced by factors such as socioeconomic conditions, hygiene practices, and healthcare accessibility [
11,
12]. In Lebanon, a reported prevalence of 52.4% has been observed in a single hospital-based investigation among symptomatic patients [
13].
Given the high global burden of
H. pylori, accurate and timely diagnosis is essential to prevent and manage associated diseases. There are several diagnostic techniques that range from non-invasive to invasive. Non-invasive methods such as serology, stool antigen tests, and the Carbon-13 (13C) urea breath test are commonly employed for initial screening [
14]. However, invasive procedures like gastroscopy and biopsy remain the diagnostic gold standard, offering valuable information about the infection’s histological effects [
10]. However, the effectiveness of eradication programs varies based on antibiotic resistance patterns, host factors, and regional prevalence, emphasizing the need for localized epidemiological studies [
2].
Demographic factors and lifestyle habits, including smoking and alcohol consumption, have been shown to influence the colonization and persistence of
H. pylori [
15,
16]. Notably, gender disparities have been observed, with some research suggesting that females may be more susceptible to the infection [
16]. Age also appears to influence infection patterns, as the bacterium is typically acquired during childhood and can persist throughout life if left untreated [
10]. A positive family history of gastric cancer has been identified as another potential risk factor, likely due to shared living environments and utensils that facilitate bacterial transmission [
17,
18]. Furthermore, the use of proton-pump inhibitors (PPIs) has been linked to lower infection rates, possibly because PPIs help suppress gastric acid secretion, thereby promoting mucosal healing and assisting in
H. pylori eradication [
19].
Therefore, understanding how H. pylori interacts with these risk factors is crucial for developing targeted diagnostics and personalized treatment strategies.
In Lebanon, both the prevalence and the associations between demographic characteristics, lifestyle habits, and H. pylori infection remain underexplored. Given the scarcity of data in the Lebanese population, this study seeks to address several key questions. Therefore, the objectives of this study are to: (1) assess the prevalence of H. pylori infection in patients presenting with gastrointestinal (GI) complaints who underwent gastroscopy at a tertiary care center in Lebanon; (2) explore associations between H. pylori infection and various demographic, lifestyle, and clinical factors; and (3) evaluate the occurrence and patterns of gastritis, duodenitis and intestinal metaplasia in relation to the bacterial infection.
4. Discussion
This retrospective analysis of 786 patients who underwent upper gastrointestinal endoscopy at a tertiary care center in Lebanon offers updated insights into the prevalence and characteristics of
H. pylori. Based on histopathological biopsy results, the prevalence was 29.6%, which is notably lower than rates reported in previous Lebanese studies. For instance, a study by [
14] reported an
H. pylori prevalence ranging from 61.6% to 68.3% among adolescent and adult Lebanese individuals. The prevalence observed in our study also appears lower than that reported by [
4], who found a prevalence of 52% in Tripoli, North of Lebanon. In contrast, the prevalence identified in our cohort was higher than that reported in a recent study by [
21], which was conducted in another healthcare facility in Beirut. Compared to broader MENA region data, our results indicate a lower prevalence of
H. pylori in Lebanon than that reported by [
12], who observed prevalence rates ranging from 36.8% to 94% in adults. These discrepancies may be attributed to differences in study design, population characteristics including age distribution and variations in hygiene and socioeconomic status, diagnostic methods, temporal trends in infection rates [
22].
Invasive procedures such as gastroscopy and biopsy remain the diagnostic gold standard for
H. pylori detection, offering valuable insights into the infection’s histological impact—particularly in patients with atypical symptoms or elevated malignancy risk. Moreover,
H. pylori eradication has emerged as a cornerstone of gastric cancer prevention strategies [
10].
H. pylori has been strongly linked to conditions like non-ulcer dyspepsia, peptic ulcer disease, and chronic gastritis, all of which can manifest as epigastric discomfort or reflux-like symptoms [
23]. However, in our study, despite a significant proportion of patients experiencing epigastric pain, only 29.6% tested positive for
H. pylori infection. This suggests that epigastric pain is not specific to the infection and may be caused by other factors such as NSAID use, unhealthy eating habits, bile reflux, or functional dyspepsia [
24,
25]. Furthermore, non-invasive diagnostic methods, like serological testing, showed minimal use and very low detection (0.3%), suggesting a diagnostic pattern that favors invasive confirmation via endoscopy, similar to trends in some developed healthcare systems [
26,
27].
In terms of associated risk factors, our results revealed some unexpected patterns. Dyslipidemia was less common among
H. pylori-positive individuals, possibly indicating a link between chronic infection and altered lipid metabolism through inflammatory or hormonal pathways [
28,
29,
30]. It is noteworthy that a significant relationship was found between the year of the procedure and
H. pylori positivity, suggesting potential temporal trends in infection rates or testing practices over the study period. Additionally, unlike prior studies, we found no significant associations with gender, older age, or high BMI [
31,
32,
33], possibly due to variations in population demographics or lifestyle factors.
Proton-pump inhibitor (PPI) use has been linked to lower
H. pylori infection rates, likely due to its ability to suppress gastric acid secretion, promote mucosal healing, and assist in bacterial eradication. However, excessive or prolonged PPI use may alter gastric pH, leading to complications such as vitamin deficiencies and increased risks of esophageal and gastric cancers [
19]. Similarly, elevated body mass index (BMI) has been associated with increased susceptibility to
H. pylori infection, potentially due to hormonal changes affecting metabolism and immune regulation [
18].
The present study also examined
H. pylori’s role in upper gastrointestinal disease. Duodenitis (21.5%), gastric ulcers (15.4%), and duodenal ulcers (6.4%) were among the notable findings. These results reaffirm the bacterium’s pathogenic role in disrupting mucosal defenses and increased gastric acid secretion [
34]. Nonetheless, gastroscopy findings revealed a remarkably high prevalence of gastritis cases, affecting 91.5% of patients. However, only about one-third of those patients tested positive for
H. pylori infection, suggesting multifactorial causes of mucosal inflammation. The discrepancy between the high rate of endoscopic gastritis (91.5%) and the lower histological
H. pylori detection (29.6%) highlights the importance of biopsy in distinguishing infectious, autoimmune, and chemical causes of gastric inflammation. This dissociation also supports earlier findings that endoscopic features alone cannot reliably identify
H. pylori infection [
35]. Our results reinforce existing guidelines that recommend testing and eradicating
H. pylori in patients with chronic inflammatory changes.
Histologically, nearly 45% of patients showed mild inflammation, and 47% had severe inflammation, consistent with the typical pattern of chronic
H. pylori gastritis and mucosal immune activation reported in the literature [
36]. As illustrated in
Figure 4, the severity of lamina propria inflammation was significantly higher among
H. pylori-positive individuals, reinforcing the bacterium’s role in driving mucosal immune response. This histological grading provides important clinical insight: patients with moderate to severe inflammation may be at increased risk for epithelial damage, atrophy, or progression to more serious gastric pathology. Thus,
Figure 4 supports the use of biopsy not only for diagnosis but also for risk stratification and therapeutic planning. Atrophic gastritis was rare (1.9%) and not significantly associated with infection. Given that
H. pylori is known to contribute to gastric atrophy through chronic inflammation and mucosal damage [
37], other mechanisms such as autoimmune responses may play a role here [
38]. This notion is supported by the association found between atrophic gastritis and immune-related diseases, consistent with previous studies linking autoimmune gastritis to systemic immune disorders [
39,
40]. It is also plausible that eradication therapy prevented progression to mucosal atrophy in previously infected individuals [
41]. The low rates of metaplasia and absence of malignancy suggest limited short-term gastric cancer risk. Nonetheless, surveillance remains important, especially for those with metaplastic or atrophic changes. Erosive gastritis, present in nearly half the patients, was closely linked to
H. pylori infection. Similar associations were found with mosaic gastritis and both forms of duodenitis. These reinforce the bacterium’s role in epithelial injury [
42], consistent with the literature showing that
H. pylori virulence factors like CagA and VacA (Cytotoxin-associated gene A and Vacuolating cytotoxin A) drive mucosal damage, inflammation, and impaired healing [
43,
44]. While other contributors like hormonal influences, NSAIDs, alcohol, and bile reflux remain relevant [
45], our findings emphasize
H. pylori’s prominent effect on erosive disease in this population. Interestingly, nodular gastritis, a relatively rare endoscopic finding, was associated with dyslipidemia and hypertension but not with
H. pylori, which contrasts with the findings of [
46]. Previous studies have indicated that metabolic syndrome can influence gastric mucosal changes through chronic low-grade inflammation, altered microcirculation, and immune dysregulation [
47]. This suggests that in adults, nodularity may be more influenced by systemic metabolic or vascular factors. Among our patients, 39.3% had non-erosive gastritis. These individuals were generally younger, more often female, and more likely to be underweight, which aligns with the literature associating this gastritis type with functional GI symptoms and metabolic influences [
48,
49]. Notably,
H. pylori was significantly less common in non-erosive cases, suggesting underlying mechanisms compared to erosive forms and supporting the need for individualized diagnosis and management.
One of the strengths of our study is the use of biopsy-based histological examination as the gold standard for diagnosing
H. pylori, offering higher diagnostic accuracy compared to non-invasive methods [
50]. Additionally, the presence of infection was confirmed through direct identification of the organism within gastric crypts and by grading the extent of colonization, in line with international diagnostic standards [
51]. Despite these strengths, the study has limitations. As a retrospective, single-center study, it may suffer from selection bias and reduced generalizability. Efforts were made however to ensure that the inclusion criteria were highly specific, focusing on patients with biopsy-confirmed diagnoses and complete clinical records. Additionally, missing data led to the exclusion of certain files, including some
H. pylori-positive cases, possibly underestimating the true prevalence. Lastly, while smoking and alcohol consumption were recorded and analyzed, other relevant clinical variables such as dietary habits were not consistently documented and therefore could not be assessed. This limitation prevented us from exploring associations with
H. pylori infection as thoroughly as previous studies have done.