BACKGROUND: Gastrin has a cholecystokinetic action on gallbladder motility, and cholecystokinin and gastrin act directly on the smooth muscle of the gallbladder. The aim of this study was to investigate the effect of endogenous hypergastrinemia on gallbladder motility in patients with autoimmune gastritis. METHODS: Forty-one patients (29 females, 12 males; mean age, 46 years) with autoimmune gastritis and 29 healthy subjects (17 females, 12 males; mean age, 44.8 years) were enrolled in the study. Fasting and postprandial gallbladder volumes were measured ultrasonographically with the ellipsoid technique and the ejection fraction of the gallbladder was calculated from fasting and postprandial volumes. All subjects were investigated after 12 hours of fasting and 30 minutes after a standard test meal. RESULTS: The gallbladder ejection fraction (%) of the patients with autoimmune gastritis was lower than that of the control group (46.06±18.28% vs 55.03±14.67%, P=0.032). There was no difference between patients with autoimmune gastritis and the control group in terms of the mean fasting gallbladder volume (30.38±12.85 vs 29.27±9.91 cm 3 , P=0.189) and the mean postprandial gallbladder volume (15.67±8.32 vs 13.44±7.69 cm 3 , P=0.258). Logistic regression analysis of baseline parameters revealed that “abdominal bloating” was a risk factor for the low gallbladder ejection fraction in autoimmune gastritis patients (P=0.045, F=4.40). In addition, logistic regression analysis of baseline parameters revealed that smoking (n=5, P=0.025, F=5.44) is a predictor of low gallbladder ejection fraction in patients with autoimmune gastritis.CONCLUSIONS: Patients with endogenous hypergastrinemia have a low gallbladder ejection fraction compared with healthy controls. This study shows that at least part of upper gastrointestinal symptoms observed in this patient population may be due to altered gallbladder motility. BACKGROUND: Gastrin has a cholecystokinetic action on gallbladder motility, and cholecystokinin and gastrin act directly on the smooth muscle of the gallbladder. The aim of this study was to investigate the effect of endogenous hypergastrinemia on gallbladder motility in patients with autoimmune gastritis. METHODS: Forty -one patients (29 females, 12 males; mean age, 46 years) with autoimmune gastritis and 29 healthy subjects (17 females, 12 males; mean age, 44.8 years) were enrolled in the study. Fasting and postprandial gallbladder volumes were measured ultrasonographically with the ellipsoid technique and the ejection fraction of the gallbladder was calculated from fasting and postprandial volumes. All subjects were investigated after 12 hours of fasting and 30 minutes after a standard test meal. RESULTS: The gallbladder ejection fraction (%) of the patients with autoimmune gastritis was lower than that of the control group (46.06 ± 18.28% vs 55.03 ± 14.67%, P = 0.032). There was no diff erence between patients with autoimmune gastritis and the control group in terms of the mean fasting gallbladder volume (30.38 ± 12.85 vs 29.27 ± 9.91 cm 3, P = 0.189) and the mean postprandial gallbladder volume (15.67 ± 8.32 vs 13.44 ± 7.69 cm 3, P = 0.258). Logistic regression analysis of baseline parameters revealed that “abdominal bloating ” was a risk factor for the low gallbladder ejection fraction in autoimmune gastritis patients (P = 0.045, F = 4.40) baseline parameters revealed that smoking (n = 5, P = 0.025, F = 5.44) is a predictor of low gallbladder ejection fraction in patients with autoimmune gastritis. CONCLUSIONS: Patients with endogenous hypergastrinemia have a low gallbladder ejection fraction compared with healthy controls. This study shows that at least part of upper gastrointestinal symptoms observed in this patient population may be due to altered gallbladder motility.