BACKGROUND/AIMS: To investigate whether diabetics have altered gallbladder motility, and whether cisapride has any effect on gallbladder motility in these patients. The factors associated with abnormal gallbladder contractility, and with the effects of cisapride on gallbladder contractility in diabetics were also evaluated. METHODOLOGY: The gallbladder contractility parameters of 20 diabetics and 20 controls were assessed by real time ultrasonography. The same measurements were made after cisapride treatment in diabetics. RESULTS: Fasting gallbladder volume and residual gallbladder volume were statistically higher in the diabetic group than in the controls (P = 0.018 and P = 0.022, respectively). Multivariate analysis also showed a significant association between fasting gallbladder volume and existing diabetes (P = 0.0002). There was a significant positive correlation between level of hemoglobin A1c and fasting gallbladder volume (r = 0.48, P = 0.031). Responders to cisapride treatment had significantly higher hemoglobin A1c levels than nonresponders (6.6 +/- 1.3 vs. 9.1 +/- 1.8, respectively; P = 0.004). Logistic multiple regression analysis revealed that hemoglobin A1c level was the only independent factor that was predictive for efficacy of cisapride treatment. CONCLUSIONS: This study demonstrates that diabetics have impaired gallbladder contractility, and that control of diabetes is predictive for gallbladder contractility and response to cisapride therapy in these patients.
BACKGROUND/AIMS: To investigate whether diabetics have altered gallbladder motility, and whether cisapride has any effect on gallbladder motility in these patients. The factors associated with abnormal gallbladder contractility, and with the effects of cisapride on gallbladder contractility in diabetics were also evaluated. METHODOLOGY: The gallbladder contractility parameters of 20 diabetics and 20 controls were assessed by real time ultrasonography. The same measurements were made after cisapride treatment in diabetics. RESULTS: Fasting gallbladder volume and residual gallbladder volume were statistically higher in the diabetic group than in the controls (P = 0.018 and P = 0.022, respectively). Multivariate analysis also showed a significant association between fasting gallbladder volume and existing diabetes (P = 0.0002). There was a significant positive correlation between level of hemoglobin A1c and fasting gallbladder volume (r = 0.48, P = 0.031). Responders to cisapride treatment had significantly higher hemoglobin A1c levels than nonresponders (6.6 +/- 1.3 vs. 9.1 +/- 1.8, respectively; P = 0.004). Logistic multiple regression analysis revealed that hemoglobin A1c level was the only independent factor that was predictive for efficacy of cisapride treatment. CONCLUSIONS: This study demonstrates that diabetics have impaired gallbladder contractility, and that control of diabetes is predictive for gallbladder contractility and response to cisapride therapy in these patients.