Gallbladder motility in diabetic patients with and without cardiovascular neuropathy

• Published in: Zeitschrift für Gastroenterologie Vol. 30; no. 8; p. 519
• Main Authors: Wedmann, B, Dröge, C, Amoiridis, G, Schmidt-Heinevetter, G, Wegener, M, Ricken, D
• Format: Journal Article
• Language: German
• Published: Germany 01.08.1992
• Subjects: Adult; Aged; Aged, 80 and over; Autonomic Nervous System - physiopathology; Autonomic Nervous System Diseases - diagnosis; Autonomic Nervous System Diseases - physiopathology; Blood Pressure - physiology; Cholelithiasis - diagnosis; Cholelithiasis - physiopathology; Diabetes Mellitus, Type 1 - diagnosis; Diabetes Mellitus, Type 1 - physiopathology; Diabetes Mellitus, Type 2 - diagnosis; Diabetes Mellitus, Type 2 - physiopathology; Diabetic Neuropathies - diagnosis; Diabetic Neuropathies - physiopathology; Female; Gallbladder - innervation; Gallbladder Emptying - physiology; Heart Rate - physiology; Humans; Male; Middle Aged; Risk Factors
• ISSN: 0044-2771

In 50 diabetic patients without gallstones, including 26 patients with cardiovascular autonomic dysfunction, and 60 normal volunteers the fasting volume and volume reduction of the gallbladder after a liquid fatty meal were determined ultrasonically in intervals of ten minutes up to one hour. Simultaneously the gastric emptying of the liquid meal was followed by ultrasound imaging. Despite an association of other complications of diabetic disease (peripheral neuropathy, retinopathy) with autonomic cardiovascular dysfunction, an altered gallbladder resting volume or impaired fat-induced volume reduction was not evident in this group of patients when compared the diabetics without cardiovascular dysfunction or controls. The time to reach the minimal residual gallbladder volume was only tendentiously prolonged in diabetics with autonomic cardiovascular dysfunction. The residual volume of the stomach showed no significant difference between the three study groups using a liquid test meal. In conclusion neuropathic dysfunction of the gallbladder is unlikely to play a major pathogenetic role in the development of gallstones in diabetic patients.