ERYTHROMYCIN INDUCES SUPRANORMAL GALL-BLADDER CONTRACTION IN DIABETICAUTONOMIC NEUROPATHY

Gall bladder motor function is impaired in some patients with diabetes . It has been suggested that the abnormalities of gall bladder motilit y are confined to those patients with autonomic neuropathy. Erythromyc in, a motilin receptor agonist, causes gall bladder contraction in bot h normal subjects and patients with gall stones with impaired gall bla dder emptying. The effect of erythromycin on gall bladder motility in seven patients with diabetes with an autonomic neuropathy, six patient s with diabetes without autonomic neuropathy, and 17 normal subjects w as studied using ultrasound. There was no significant difference in ga ll bladder fasting volume between the three groups, but the patients w ith diabetes with autonomic neuropathy had impaired postprandial gall bladder emptying compared with normal subjects (percentage emptied (SE M) 40 (10.3)% v 64 (2.8)%, p<0.01) and those with autonomic neuropathy (48 (7.7)%, NS). Erythromycin produced a dramatic reduction in gall b ladder fasting volume in patients with diabetes with an autonomic neur opathy, compared with either normal subjects or patients with diabetes without autonomic neuropathy (percentage reduction 62 (4.6)% in patie nts with autonomic neuropathy, v 37 (17.6)% in those without autonomic neuropathy, and 26 (7.3)% in the normal subjects, (p<0.02) and return ed gall bladder emptying to normal in all patients with impaired empty ing. The pronounced effect of erythromycin in diabetic autonomic neuro pathy suggests denervation supersensitivity and that the action of ery thromycin on the gall bladder is neurally modulated.