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Correlation Between Gastric and Gallbladder Helicobacter pylori Infection in South Indian Patients Undergoing
Abheesh Hegde1, Sajal Gupta1,2, Syed F Ahamed3
1Urology, Father Muller Medical College, Mangalore, IND.
Background:
Helicobacter pylori has been established as an etiological agent in gastric adenocarcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma in the stomach. Recent reports have implicated this bacterium in the causation of benign and malignant gallbladder disease. We investigated the correlation between gallbladder and gastric mucosal H. pylori in patients with symptomatic cholelithiasis.
Aims:
To estimate the prevalence of H. pylori colonization in the gallbladder and assess its correlation with gastric H. pylori in South Indian patients undergoing cholecystectomy.
Methods:
A cross-sectional prevalence study was conducted at a tertiary care center in South India. A total of 49 consecutive patients undergoing cholecystectomy with clinical indications for preoperative gastroscopy were enrolled. Gastric mucosal biopsies were assessed using culture, rapid urease test, and DNA polymerase chain reaction (PCR). Gallbladder tissue was evaluated via culture, PCR, histology (modified Giemsa), and rapid urease test. Concordance between gastric and gallbladder positivity was analyzed.
Results:
Out of 49 patients undergoing cholecystectomy, 12 (24.5%) were in the age group of 51-60 years. Females comprised 64.89% of the study population. Laparoscopic cholecystectomy was performed in 40 (81.91%) of the cases, and chronic cholecystitis was diagnosed in 43 (88%) patients. Among the 49 gastric specimens analyzed for H. pylori, all tested negative by rapid urease test and culture; however, 10 samples were positive for H. pylori by DNA PCR (10/49 gastric PCR positive; 20.4%, 95% CI: 10.2-33.7%). In contrast, all 49 gallbladder samples were negative for H. pylori by DNA PCR, culture, histopathology, and rapid urease test.
Conclusion:
H. pylori was not detected in gallbladder tissue among South Indian patients despite a 20.4% prevalence in the gastric mucosa. These findings suggest no correlation between gastric and gallbladder H. pylori colonization in this cohort. Further multicentric studies are needed to evaluate regional microbiological and pathological variations.
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