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To Determine the Association Between Helicobacter Pylori Infection and Gallstone Disease
*Corresponding author: Jayeshkumar B. Bagada, Department of General Surgery, Gujarat Medical Education and Research Society Medical College and Hospital, Himmatnagar, Gujarat, India. jbagada@yahoo.in
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Received: ,
Accepted: ,
How to cite this article: Gohil AA, Dave SR, Bagada JB, Desai JA. To Determine the Association Between Helicobacter Pylori Infection and Gallstone Disease. Int J Recent Surg Med Sci. 2026:12(e001). doi: 10.25259/IJRSMS_71_2025
Abstract
Objectives:
To investigate the potential association between Helicobacter pylori (H. pylori) infection and the occurrence of gallstone disease. To correlate the association between investigations and H. pylori as it is well-known gastric pathogen,has been hypothesized to contribute to gallstone formation through mechanisms such as chronic inflammation,altered bile composition, and direct colonization of the biliary system.
Material and Methods:
A hospital-based observational study was conducted at Shree Krishna Hospital and Pramukh Swami Medical College, Karamsad, a tertiary care center serving a rural population in Gujarat, India. This study included 200 adult patients (aged 18–75 years) presenting with symptoms suggestive of gallstone disease. Diagnosis was confirmed through abdominal ultrasonography (USG). All participants were evaluated for H. pylori infection using serum IgG antibody testing. Data on clinical symptoms, ultrasound findings, and H. pylori status were collected and analyzed.
Results:
Out of the 200 patients studied, 59% were found to have gallstones. A considerable proportion of these patients also tested positive for H. pylori infection. A statistically significant association was observed between H. pylori infection and postprandial upper abdominal heaviness (p = 0.003). Additionally, gallstones were significantly associated with postprandial upper abdominal pain (p = 0.001) and vomiting (p = 0.025). The prevalence of H. pylori was notably higher among patients with gallstones, suggesting a possible pathogenic role.
Conclusion:
The findings of this study indicate a potential link between H. pylori infection and gallstone disease. The observed associations support the hypothesis that H. pylori may play a contributory role in gallstone pathogenesis. These results warrant further research to elucidate the underlying mechanisms and to explore whether eradication of H. pylori could serve as a preventive or therapeutic strategy in gallstone disease management.
Keywords
Gallstone disease
H. pylori
Postprandial abdominal pain
INTRODUCTION
Globally, gallstones are a leading cause of disease and mortality.[1] Gallstones develop within the biliary system or gallbladder. Only gallstones with symptoms or consequences are classified as gallstone disease, even though these stones can be asymptomatic or symptomatic.[2]
The phrase “gallstone disease” describes gallstones that produce symptoms. Gallstone disease (GSD) is a prevalent gastrointestinal illness affecting millions of individuals worldwide. It is distinguished by the development of solid deposits inside the gallbladder, which are mostly made up of calcium salts, bilirubin, and cholesterol.[3] Gallstone disease is a complex aetiology that includes metabolic variables, food, obesity, hormonal impacts, and genetic predisposition. However, recent studies have suggested a possible role of infectious agents, particularly H. pylori, in the development of gallstone disease. About 3.5 microns in length and 0.5 microns wide, H. pylori is a gram-negative, spiral-shaped, microaerophilic bacterium.[4]
Successful isolation and culture of a spiral bacterium species—later identified as H. pylori—from the human stomach was reported by Barry Marshall and Robin Warren.[5] The microaerophilic, gram-negative, urease-producing H. pylori fulfils each of Koch’s postulates. In the normal living form, it is a spiral-shaped bacterium, but the coccoid form can also cause lesions.[6]
The gall bladder is thought to have a connection similar to that between H. pylori and stomach cancer. By inducing chronic cholecystitis from gallstones and then developing dysplasia, metaplasia, and carcinoma. By eliminating H. pylori through medical treatment, it increases the likelihood that this illness may be prevented.[7]
Nonetheless, recent studies suggest that H. pylori may have a role in the emergence of gallstones and other hepatobiliary conditions.[8] The proposed mechanisms linking H. pylori to gallstone disease include chronic inflammation, bile composition alteration, and direct bacterial colonization of the biliary system. Studies have revealed H. pylori DNA in bile samples and gallbladder tissues from cholelithiasis patients, suggesting a potential connection.[9]
Inflammation plays a crucial role in gallstone pathogenesis. Chronic infection with H. pylori triggers systemic inflammation, which may alter cholesterol metabolism, bile acid secretion, and gallbladder motility—factors that contribute to gallstone formation. Further evidence of H. pylori’s involvement in biliary disorders has come from molecular research that found the bacterium’s virulence factors in gallbladder tissues, particularly vacuolating cytotoxin A (vacA) and cytotoxin-associated gene A (cagA).[10]
While some studies have found no direct correlation, others have reported a significant association.[11] To clarify the exact function of H. pylori in gallstone development and to ascertain whether eliminating the infection could be a viable preventive or treatment approach for gallstone disease, more investigation is required. By examining its incidence in gallstone patients and assessing potential harmful processes, this study seeks to determine if H. pylori infection and gallstone disease are related. Gaining knowledge of this link may help develop fresh strategies for managing and preventing gallstone-related disease.
MATERIAL AND METHODS
This study was conducted at the Department of General Surgery, Shree Krishna Hospital, Karamsad, affiliated with Pramukh Swami Medical College, Gujarat, India. The study combines both prospective and retrospective data collection, utilizing patient records. The study duration was from April 2023 to October 2024, with data collection occurring from outpatient and in-hospital records of patients presenting with symptoms of gallstone disease. This hospital serves a diverse population, providing tertiary care services, and is equipped with the necessary diagnostic tools for the investigation of gallstone disease and H. pylori infection.
Inclusion criteria
Male and female patients aged 18-75 years were included with diagnosis of gallstones based on clinical presentation and confirmed by ultrasound or other radiological imaging methods.
Exclusion criteria
Patients older than 75 years were and younger than 18 years were excluded.
All patients were initially evaluated by a general surgeon to assess the symptoms suggestive of gallstone disease, including a detailed history and physical examination. Symptoms like abdominal pain, fullness after meals, and nausea were documented. After the clinical evaluation, patients underwent ultrasonography (USG) of the abdomen and pelvis. This non-invasive imaging technique was used to confirm the presence of gallstones. An ultrasound was chosen as the primary diagnostic tool due to its accuracy, availability, and non-invasive nature. All patients included in the study were tested for H. pylori infection via the IgG antibody blood test. The H. pylori IgG test was performed routinely at the Central Diagnostic Laboratory of Shree Krishna Hospital. A positive result was determined by the presence of IgG antibodies against H. pylori in the patient’s blood. Data was collected from the medical records of the patients, which included clinical details, radiological findings, and results from the H. pylori IgG test. The demographic details of the patients, such as age, sex, and comorbidities, were also recorded. The thesis has been approved by the Institutional Ethics Committee with waiver of patient consent for data collection. Patient privacy was strictly maintained throughout the study. Identifiable information was anonymized. Ethical Approval: Ethical clearance for this study was obtained from the Institutional Ethics Committee of Pramukh Swami Medical College, Karamsad, prior to the commencement of the study.
The data collected was analyzed using appropriate statistical methods to determine the association between H. pylori infection and gallstone disease. Descriptive statistics, including frequencies and percentages, were used to summarize demographic information and the prevalence of H. pylori infection. To assess the relationship between H. pylori infection, symptomatology, and the presence of gallstones, chi-square tests were applied for categorical variables, and t-tests or ANOVA were used for continuous variables. A p-value < 0.05 was considered statistically significant.
RESULTS
The study comprised a total of 200 patients, among whom there were 93 males and 107 females. The majority of individuals fall within the 31–40 years (42 patients) and 41–50 years (41 patients) age groups, indicating a strong representation of middle-aged individuals. The 51–60 years group follows closely with 38 patients. Younger patients, aged 0–20 years, constitute the smallest group among the primary working-age population, with only 11 individuals. Patients aged 21–30 years are moderately represented with 30 individuals. A noticeable decline is observed in the older age groups, with 25 patients in the 61-70 years range, eight patients between 71-80 years, and only five patients above 80 years. This distribution suggests that the study primarily reflects the views and experiences of individuals in the 30-60 years age bracket, providing insights predominantly from the active and professionally engaged segment of the population.
Nausea and upper abdominal pain were the most prevalent symptoms within the study population, indicating a significant burden of gastrointestinal discomfort among the patients [Figure 1]. In the present study, out of the total subjects examined, 118 patients (59%) were found to have gall bladder calculi, whereas 82 patients (41%) did not exhibit any evidence of gall bladder stones. This indicates a relatively high prevalence of gall bladder calculi among the studied population, emphasizing the importance of early detection and management. The findings highlight the need for further investigation into potential risk factors contributing to the development of gall bladder calculus in this group.
- Distribution of symptoms
These findings of Figure 2 suggest a high burden of H. pylori among the individuals assessed, reinforcing its recognized association. The observed prevalence emphasizes the necessity for routine screening, early detection, and appropriate therapeutic interventions to mitigate the potential health impacts attributed to H. pylori infection in the studied cohort.
- Prevalence of H.pylori among the Patients
It was observed that postprandial upper abdominal heaviness was significantly associated with H. pylori positivity (p = 0.003). A higher proportion of patients with H. pylori infection reported experiencing postprandial heaviness compared to those without the infection. This suggests that postprandial heaviness could be an important clinical symptom indicative of H. pylori infection in patients presenting with dyspeptic complaints. On the other hand, other symptoms, including postprandial upper abdominal pain (p = 0.329), nausea (p = 0.280), and vomiting (p = 0.292), did not show statistically significant associations with H. pylori status. Although a majority of patients with H. pylori infection reported nausea and vomiting, the difference was not significant when compared to the H. pylori-negative group. These findings imply that while non-specific gastrointestinal symptoms are common among patients with or without H. pylori infection, postprandial heaviness may serve as a more specific symptom associated with the infection. Further studies with larger sample sizes may help to better clarify the symptom profile associated with H. pylori infection.
Among the symptoms assessed, postprandial upper abdominal pain and vomiting were found to have a statistically significant association with gallstone detection on ultrasonography (p = 0.001 and p = 0.025, respectively). Patients presenting with postprandial pain were more likely to have gallstones compared to those without this symptom. Similarly, vomiting was significantly more common in patients with gallstones. In contrast, postprandial upper abdominal heaviness (p = 0.91) and nausea (p = 0.12) did not show a significant association with gallstone presence. These findings suggest that specific gastrointestinal symptoms, particularly postprandial pain and vomiting, may be important clinical indicators of gallstone disease. The graph demonstrates the association between Helicobacter pylori infection and the presence of gallbladder calculus detected by ultrasonography. In the H. pylori-positive group, a significantly higher number of patients (86 individuals) were found to have gallstones compared to 56 patients who were gallstone-negative [Figure 3]. Conversely, among H. pylori-negative individuals, 32 patients were gallstone-positive, while 26 were gallstone-negative. This distribution indicates a greater prevalence of gallstone disease among patients with H. pylori infection. The visual trend supports the hypothesis that H. pylori infection may be associated with an increased risk of gallstone formation. The analysis accompanying these findings suggests that H. pylori infection could contribute to gallstone pathogenesis, potentially through mechanisms involving chronic inflammation, changes in gallbladder motility, or alteration of bile composition. Further research with a larger sample size may be warranted to elucidate the exact biological pathways linking H. pylori infection to gallstone disease.
- Association between Gallbladder calculus and H.pylori
DISCUSSION
This research explores the possible link between H. pylori infection and gallstone disease, emphasizing the prevalence of gastrointestinal symptoms in individuals affected by both conditions. The results indicate a notable association between H. pylori and gallstone formation, highlighting the importance of clinical symptomatology in the diagnosis of these disorders. The discussion draws from previous research to contextualize these findings and explore their potential implications for clinical practice. Various pathophysiological mechanisms have been suggested to elucidate this observed association. H. pylori infection is known to induce chronic inflammation in the gastric mucosa, and similar inflammatory processes could extend to the gallbladder. Furthermore, H. pylori has been shown to alter bile composition by increasing the secretion of cholesterol and other lipids, which are key contributors to the formation of cholesterol gallstones.[11] Furthermore, impaired gallbladder motility—potentially induced by H. pylori infection—may lead to bile stasis, thereby facilitating gallstone formation.[11] Although not widely recognized, H. pylori infection has been linked to both cholelithiasis and cholecystitis. Several studies have investigated the association between gallstone disease and H. pylori, demonstrating that individuals with H. pylori colonization of the gallbladder have a markedly increased risk of developing gallstones compared to controls. Evidence from large-scale studies conducted by Zhang et al. and Takahashi et al.[12,13] reinforces this association. In Zhang et al.’s[12] study of 15,523 participants, the prevalence of gallstones was significantly lower among individualswho had undergone H. pylori eradication therapy compared to those who remained H. pylori-positive without prior treatment (9.02% vs. 9.47%; p < 0.0001). Similarly, Takahashi et al., analyzing data from 15,551 participants, reported a lower incidence of gallstones in the eradicated group compared to the non-eradicated group (4.73% vs. 6.08%; p < 0.001).[13] These findings underscore the importance of further investigating the potential role of H. pylori eradication in the prevention and management of gallstone disease.
Demographic characteristics and prevalence of gallstones
The demographic profile of our study population revealed that females represented the majority (53.5%), which is consistent with the well-documented higher prevalence of gallstone disease among women, especially those aged 40– 60 years. This pattern of gender distribution is consistent with the observations of Everhart et al., who noted an increased risk of gallstone formation in women, likely influenced by hormonal factors including estrogen and progesterone.[14] In contrast, H. pylori infection did not show a significant gender difference in our cohort, suggesting that the bacterium affects both genders equally, as also reported by Malfertheiner et al.[15]
The age distribution in our study was concentrated in the 31– 60 year age group, reflecting the peak incidence of gallstone disease, which typically occurs in middle-aged adults.[16] This age distribution is corroborated by prior studies, which suggest that gallstones are more prevalent among individuals aged 40 years and older, with a gradual increase in incidence as age progresses.[17] Given the established association between aging and gallstone formation, our results reinforce the clinical observation that gallstones are most commonly diagnosed in middle-aged individuals.
Gastrointestinal symptoms are pivotal in diagnosing gallstone disease and H. pylori infection. In our study population, upper abdominal pain and nausea were the most frequently reported symptoms, affecting 64% and 71% of patients, respectively [Table 1]. These findings are consistent with prior studies indicating that these symptoms are commonly experienced by patients with both conditions.[18,19] The presence of upper abdominal pain as a predominant symptom in patients with gallstones is well-established in the literature and is a hallmark of biliary colic.[20] Nausea, a common symptom in individuals with gallstone disease, may result from impaired biliary motility or complications like obstruction of the biliary tract.[21] The observed link between postprandial upper abdominal discomfort and H. pylori infection in our study (p = 0.003) is noteworthy and merits further consideration. Additionally, studies have suggested that H. pylori infection could exacerbate symptoms such as bloating and heaviness due to alterations in gastric motility and gastric acid secretion.[22] This aligns with our findings, where postprandial heaviness was strongly correlated with H. pylori positivity.
| Symptoms | H. Pylori | P-value | ||
|---|---|---|---|---|
| Positive | Negative | |||
| Post prandial upper abdominal pain | Present | 89 (62.7%) | 39 (67.2%) | 0.329 |
| Absent | 53 (37.3%) | 19 (32.8%) | ||
| Post prandial upper abdominal heaviness | Present | 88 (62.0%) | 23 (39.7%) | 0.003 |
| Absent | 54 (38.0%) | 35 (60.3%) | ||
| Nausea | Present | 103 (72.5%) | 39 (67.2%) | 0.280 |
| Absent | 39 (27.5%) | 19 (32.8%) | ||
| Vomiting | Present | 56 (39.4%) | 26 (44.8%) | 0.292 |
| Absent | 86 (60.6%) | 32 (55.2%) | ||
The p-value level of significance was 0.05
Correlation between symptoms and gallstone disease
The relationship between symptoms and gallstone disease was also explored in this study. In the present study, postprandial upper abdominal pain and vomiting demonstrated statistically significant associations with gallstone disease (p = 0.001 and p = 0.025, respectively) [Table 2]. These findings are in agreement with earlier studies, which have identified postprandial pain as a defining symptom of biliary colic, frequently linked to the presence of gallstones.[14,16] Similarly, vomiting in gallstone patients may indicate more severe complications such as gallstone pancreatitis or gallbladder inflammation, both of which can result from obstructed bile flow.[23] Conversely, nausea and postprandial heaviness did not show a significant association with gallstones, highlighting the specificity of symptoms in diagnosing gallstone disease. The absence of these symptoms in patients with gallstones may suggest that they are more indicative of functional dyspepsia or other non-gallstone-related gastrointestinal conditions.[24]
| Symptoms | Gali stone on USG | P-value | ||
|---|---|---|---|---|
| Positive | Negative | |||
| Post prandial upper abdominal pain | Present | 85 | 43 | 0.001 |
| Absent | 33 | 39 | ||
| Post prandial upper abdominal heaviness | Present | 66 | 45 | 0.91 |
| Absent | 52 | 37 | ||
| Nausea | Present | 89 | 53 | 0.12 |
| Absent | 29 | 29 | ||
| Vomiting | Present | 41 | 41 | 0.025 |
| Absent | 71 | 41 | ||
USG: Ultra sonography, The p-value level of significance was 0.05
Coexistence of H. Pylori infection and gallstones: a potential link explored
A key observation in this study was the statistically significant relationship between H. pylori infection and gallstone presence. Gallstones were detected in 73% of patients with H. pylori infection, compared to 55% among those without the infection. This aligns with prior research proposing that H. pylori may play a role in gallstone pathogenesis through mechanisms such as chronic gallbladder inflammation, modifications in bile composition, and impaired gallbladder motility.[25,26]
Multiple studies have demonstrated a lower prevalence of gallstones among individuals who underwent successful H. pylori eradication, supporting the hypothesis of a potential pathogenic link. Considering that H. pylori infection is highly prevalent and can be effectively treated with standard antibiotic regimens, this association warrants attention, particularly in endemic regions. Early identification and eradication of H. pylori could represent a cost-effective strategy to reduce the burden of gallstone disease, pending confirmation through prospective interventional studies.
Following translocation, Helicobacter species may establish colonization within the biliary tract. In studies involving patients who underwent cholecystectomy for chronic cholecystitis associated with gallstones, bile and gallbladder tissue samples were analyzed. Findings revealed that individuals with gallstones were approximately 3.5 times more likely to have H. pylori present in their bile compared to those in the control group.[27] H. pylori-induced chronic inflammation may play a significant role in gallstone pathogenesis. This persistent inflammatory state can impair gallbladder motility, leading to bile stasis—a key factor in stone formation. Additionally, inflammation may alter bile composition, promoting cholesterol supersaturation and decreasing bile acid solubility, thereby creating conditions favorable for lithogenesis.
Clinical implications
This study emphasizes the importance of considering H. pylori infection in patients presenting with upper abdominal pain and postprandial discomfort, as these symptoms may reflect both gallstone disease and H. pylori infection. Given their overlapping clinical presentations and high prevalence, clinicians should consider H. pylori testing in symptomatic gallstone patients. Timely detection and eradication may not only improve symptoms but also reduce the risk of complications such as cholecystitis and gallstone pancreatitis.
CONCLUSION
This study provides valuable insights into the association between H. pylori infection and gallstone disease, highlighting the potential role of H. pylori in the pathogenesis of gallstones. Our findings suggest a significant correlation between H. pylori infection and the presence of gallstones, particularly in individuals experiencing common gastrointestinal symptoms such as upper abdominal pain, nausea, and postprandial heaviness. The significant overlap of symptoms between H. pylori infection and gallstone disease emphasizes the importance of considering both conditions in the differential diagnosis of gastrointestinal complaints.
The study supports existing literature that proposes several mechanisms through which H. pylori may influence gallstone formation. These include chronic systemic and local inflammation, the production of virulence factors such as CagA and VacA that may directly damage gallbladder tissue, the alteration of bile composition through urease activity, and bile salt deconjugation. Additionally, H. pylori’s potential to act as a nidus for stone formation and its detection in gallbladder tissue and bile samples further strengthen the argument for a causal link. Findings suggest that H. pylori infection could play a role not only in gastrointestinal conditions like gastritis and peptic ulcer disease but also in hepatobiliary disorders such as cholelithiasis. Despite the promising results, further research is needed to confirm the causal relationship between H. pylori infection and gallstone formation, particularly through prospective longitudinal studies.
In conclusion, this study highlights a noteworthy association between H. pylori infection and gallstone disease, suggesting that bacterial infection may be an underrecognized factor in gallstone development. These insights open avenues for further research, including the potential role of H. pylori eradication therapy in the prevention or management of gallstone disease. A better understanding of this relationship may lead to novel diagnostic and therapeutic strategies that could significantly improve patient outcomes.
Ethical approval:
The research/study approved by the Institutional Review Board at PSMC, Bhaikaka University, Karamsad, Gujarat-388325, number IEC/BU/153/Faculty/20/221/2024, dated 07-06-2024.
Declaration of patient consent:
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patients have given their consent for their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Conflicts of interest:
There are no conflicts of interest
Use of artificial intelligence (AI)-assisted technology for manuscript preparation:
The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.
Financial support and sponsorship: Nil
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