Relation of gallbladder function and Helicobacter pylori infection to gastric mucosa inflammation in patients with symptomatic cholecystolithiasis

Background. Inflammatory alterations of the gastric mucosa are
commonly caused by Helicobacter pylori (Hp) infection in patients
with symptomatic gallstone disease. However, the additional
pathogenetic role of an impaired gallbladder function leading to an
increased alkaline duodenogastric reflux is controversially
discussed. Aim:To investigate the relation of gallbladder function
and Hp infection to gastric mucosa inflammation in patients with
symptomatic gallstones prior to cholecystectomy. Patients:
Seventy-three patients with symptomatic gallstones were studied by
endoscopy and Hp testing. Methods: Gastritis classification was
performed according to the updated Sydney System and gallbladder
function was determined by total lipid concentration of gallbladder
bile collected during mainly laparoscopic cholecystectomy. Results:
Fifteen patients revealed no, 39 patients mild, and 19 moderate to
marked gastritis. No significant differences for bile salts,
phospholipids, cholesterol, or total lipids in gallbladder bile
were found between these three groups of patients. However, while
only 1 out of 54 (< 2%) patients with mild or no gastritis was
found histologically positive for Hp, this infection could be
detected in 14 (74%) out of 19 patients with moderate to marked
gastritis. Conclusion: Moderate to marked gastric mucosa
inflammation in gallstone patients is mainly caused by Hp
infection, whereas gallbladder function is not related to the
degree of gastritis. Thus, an increased alkaline duodenogastric
reflux in gallstone patients seems to be of limited
pathophysiological relevance. Copyright (c) 2006 S. Karger AG,
Basel.