Why the study?
Does ambulatory 24-hour jejunal manometry reveal altered small bowel motility in diabetic patients with cardiac autonomic neuropathy compared to healthy controls?
Does ambulatory 24-hour jejunal manometry reveal altered small bowel motility in diabetic patients with cardiac autonomic neuropathy compared to healthy controls?
Diabetic patients with cardiac autonomic neuropathy exhibit significant disturbances in small bowel motility, including altered circadian variability and postprandial hypomotility.
Altered jejunal motility in diabetic autonomic neuropathy may underlie GI symptoms; hypothesis-generating and should not yet change practice.
Concerning alteration of small bowel motility in diabetic patients with autonomic neuropathy controversial data were obtained with stationary manometry and over a limited period of time. The aim of our study was to examine ambulatory 24 h jejunal motility in 15 diabetic patients with cardiac autonomic neuropathy compared with data obtained in 50 healthy controls. Twenty-four hour motility was recorded in the proximal jejunum with a portable datalogger and tube-mounted miniature pressure sensors. Diurnal and nocturnal fasting motility and the motor response to a standardized evening meal of 600 kcal were evaluated by visual and computer-aided analysis. The following abnormalities were found during fasting motility (n = number of patients): absence of phase III over 24 h (n = 2), retrograde migration or simultaneous occurrence of phase III (n = 5). During postprandial motility irregular bursts with tonic baseline elevation (n = 3) and contraction frequencies below the range of controls (n = 8) occurred. Furthermore patients exhibited an inversion of the normal relationship between phase I and phase II during nocturnal MMC-cycles, and discrete clustered contractions were diminished (P < 0.01) in the fasting and digestive state. All patients showed at least one abnormal manometric finding. We conclude that small bowel motility in diabetic autonomic neuropathy is characterized by disturbances in the generation and aboral migration of phase III, an altered circadian variability of the MMC cycle and by postprandial hypomotility.
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Hackelsberger et al. (1997) studied this question.
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