European Journal of Cardiovascular Medicine

Post-cholecystectomy syndrome (PCS) is the recurrence or development of gastrointestinal symptoms following cholecystectomy, including dyspepsia, epigastric pain, bloating, nausea, and alteration of bowel habits. While the pathogenesis of PCS is multifactorial, one of the potential causes increasingly identified is Helicobacter pylori infection, whose expression can be modulated by anatomical and physiological changes following gallbladder removal.

Cholecystectomy alters bile flow physiology, which typically leads to increased duodenogastric reflux and can compromise gastric mucosal defense and cause mucosal damage, gastritis, and metaplastic change (Atak et al., 2012; Kellosalo et al., 1991) [2,7]. Such changes could provide a substrate for H. pylori colonization or increase its pathogenetic activity. Series have reported increased prevalence of infection with H. pylori following cholecystectomy, and this was suggested to reflect an association between altered gastric physiology and bacterial overgrowth (Caldwell et al., 1995; Gad Elhak et al., 2004) [1,3].

In addition, alkaline reflux gastritis and intestinal metaplasia that have developed after cholecystectomy have been risk factors for chronic gastritis and precancerous conditions, particularly with H. pylori infection (Robles-Campos et al., 1993; Rugge et al., 2018) [5,8]. Histopathological demonstration of H. pylori through gastric biopsies with routine staining, special staining, or immunohistochemistry remains essential in definitive diagnosis and follow-up (Benoit et al., 2018) [4].

Furthermore, patients with mucosal integrity defect or systemic illness, such as hemodialysis patients, are at risk of developing gastroduodenal lesions when exposed to H. pylori infection (Al-Mueilo, 2004) [6]. Thus, understanding the interaction between cholecystectomy-induced reflux, mucosal change, and H. pylori infection is crucial in maximizing post-operative care and symptom improvement. The objective of the study is to assess the relationship between H. pylori infection and post-cholecystectomy symptoms and endoscopy and histopathology in a tertiary care hospital.

Study Design and Setting

This was a cross-sectional observational study that took place in the Department of General Surgery and Gastroenterology, Chhatrapati Shivaji Subharti Hospital, Subharti Medical School, Swami Vivekanand Subharti University (SVSU), Meerut. The aim of the study was to establish the relationship between Helicobacter pylori infection and post-cholecystectomy syndrome (PCS) as well as endoscopic presentation in symptomatic patients. The study was ongoing for 12 months, from [****Start Date] to [***** End Date], after institutional ethical clearance.

Study Population

They recruited patients who had undergone laparoscopic cholecystectomy at least 3 months prior and were being discovered with new or recurrent upper gastrointestinal symptoms that were suggestive of PCS. Symptoms were epigastric pain, bloating, nausea, vomiting, heartburn, and indigestion. Exclusion criteria were patients with pre-existing documented peptic ulcer disease, malignancy, history of gastric surgery, or patients who had been on recent proton pump inhibitors or antibiotic therapy within the last 2 weeks of endoscopy.

Clinical and Endoscopic Evaluation

All of the enrolled patients underwent a full clinical evaluation with history, physical exam, and review of surgical charts. Upper endoscopy with a standard video gastroscope was performed to evaluate for mucosal changes such as erythema, erosions, gastritis, bile reflux, or ulceration. Duodenogastric reflux was diagnosed if bile puddling in the stomach in the absence of pyloric obstruction was observed.

Biopsy and Histopathological Examination A number of gastric biopsies were taken from the body and antrum by the Updated Sydney System for detecting H. pylori. The tissue was stained by hematoxylin and eosin (H&E), modified Giemsa, and, if required, immunohistochemistry to diagnose infection with H. pylori (Benoit et al., 2018). Histological evidence of active inflammation, chronic gastritis, atrophy, and intestinal metaplasia was present.

Detection and Grading of H. pylori Infection

The H. pylori infection was scored based on the colonization density, in line with standard pathology criteria. The cases were divided into H. pylori-positive or -negative. OLGA (Operative Link on Gastritis Assessment) staging was employed wherever possible to measure the severity of gastritis and the risk of gastric cancer in the future (Rugge et al., 2018). Data Analysis Data were recorded in Microsoft Excel and statistically examined using SPSS version [Insert Version]. Demographics and clinical characteristics were statistically examined using descriptive statistics. Chi-square or Fisher's exact test were employed to examine the associations among endoscopic findings, H. pylori infection, and PCS symptoms. A p-value of <0.05 was employed as statistically significant.

Demographic and Clinical Characteristics

A total of 120 patients who underwent laparoscopic cholecystectomy later presented with upper gastrointestinal symptoms that were suggestive of post-cholecystectomy syndrome (PCS). The demographics of the age, gender, and distribution are as follows: Mean age 42.6 ± 11.3 years, with 68 (56.7%) females and 52 (43.3%) males. The most common symptoms reported are epigastric pain (65%), bloating (50%), nausea (46%), and heartburn (38%).

Table 1: Demographic and Symptom Profile of Study Population

Endoscopic Findings and H. pylori Status

Endoscopic examination showed bile reflux in 54 patients (45%), and gastritis in 68 patients (56.7%) was seen. Duodenitis (18.3%), gastric erosions (25%), and normal mucosa (15%) were the other findings. H. pylori infection was confirmed by histopathological examination in 61 patients (50.8%).

In the H. pylori-positive group, 76% showed endoscopic signs of gastritis and 59% had bile reflux, with a high probability of an association between mucosal pathology and H. pylori infection in PCS patients.

Table 2: Correlation Between H. pylori Infection and Endoscopic Findings

Histopathological Findings and OLGA Staging

Histological study showed that in H. pylori-positive cases, the most common diagnosis was antral chronic gastritis (83.6%), active inflammation (57.4%), and intestinal metaplasia (18%). Based on the OLGA staging system, stage II or more was observed in 38.5% of infected individuals, whereas just 10.1% of uninfected individuals were in these stages.

Figure 1: Distribution of OLGA Staging in H. pylori Positive vs Negative Patients
Figure 1 comparing OLGA stages 0–IV across H. pylori positive and negative groups.

Symptom Correlation with H. pylori

1. pylori-infected patients were significantly more likely to complain of chronic epigastric pain (p = 0.003), bloating (p = 0.02), and nausea (p = 0.04), while vomiting and heartburn were not significantly different between the two groups.

Figure 2: Prevalence of Key Symptoms in H. pylori Positive vs Negative Groups
 Figure 2 showing symptom prevalence between two groups.

This research illustrates a strong correlation between Helicobacter pylori infection and post-cholecystectomy syndrome (PCS), specifically with endoscopic evidence such as bile reflux, gastritis, and gastric erosions. Our findings show that more than half of the symptomatic patients after cholecystectomy were positive for H. pylori with increased mucosal pathology versus non-infected controls. These observations lend support to the working hypothesis that H. pylori could worsen gastric mucosal injury in the context of deranged biliary dynamics after cholecystectomy.

Bile reflux was noted in 45% of the cases, and its presence alongside H. pylori infection was strongly associated with intestinal metaplasia and chronic gastritis. This corresponds with the evidence of Agin and Kayar (2019) [9], who showed that duodenogastric bile reflux exacerbates H. pylori-induced gastritis, even among children. Likewise, Vere et al. (2005) [15] noted that bile reflux plays a part in antral inflammation and epithelial progression, along with H. pylori colonization further intensified.

Our histopathological analysis revealed a substantial proportion of H. pylori-positive patients with OLGA stage II or higher, indicating increased risk for gastric atrophy and potentially carcinogenic progression. Tham et al. (1997) [11] noted that H. pylori-associated gastritis tends to persist and evolve histologically over time, especially if not eradicated. These chronic changes, especially when combined with bile exposure, likely explain the symptomatic burden seen in our PCS population.

Interestingly, we also found symptom frequency, specifically epigastric pain, bloating, and nausea, were much more prevalent among H. pylori-positive patients. Hurlimann et al. (1998) [12] also noted that H. pylori infection is linked with elevated gastric inflammation and changed acid control, both of which are factors in non-ulcer dyspepsia. Although some sources indicate H. pylori can have a protective action against disease of reflux caused by hypochlorhydria, our results disprove this hypothesis in a post-cholecystectomy population. Indeed, Chen et al. (1998) [13] demonstrated that gastritis induced by H. pylori, especially in the gastric cardia, might simulate or coexist with pathology of reflux, making it more complex clinically.

Unlike fears that eradication of H. pylori would exacerbate reflux symptoms, research such as Tefera et al. (2002) [14] has indicated that severity of reflux does not increase after eradication in mildly to moderately affected patients. This is supporting evidence for the clinical justification for treating H. pylori in symptomatic PCS patients with confirmed gastritis or metaplasia.

In addition, the existence of heterotopic gastric mucosa, as described by Gutierrez et al. (2003) [10], although not evaluated in our study, is still a reservoir for H. pylori and can be a cause of recurrent symptoms in some cases. In conclusion, our findings point to the interaction between bile reflux, gastric mucosal alterations, and H. pylori infection in the pathogenesis of PCS and emphasize the need for focused endoscopic and histologic assessment in the management of such patients.

This paper identifies a strong association between Helicobacter pylori infection and post-cholecystectomy syndrome, specifically in patients showing endoscopic signs of bile reflux and gastritis. The combination of changed biliary physiology and infection with H. pylori is found to contribute to chronic upper gastrointestinal symptoms and mucosal damage in patients after cholecystectomy. Due to the high incidence of H. piloeri in this symptomatic group and with its linkage to histological lesions like chronic gastritis and intestinal metaplasia, routine endoscopic evaluation and targeted eradication therapy can be a key component in enhancing patient outcomes as well as in the prevention of long-term complications. 

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