Original articleDelayed gastric emptying rate in Type 1 diabetics with cardiac autonomic neuropathy
Introduction
Autonomic neuropathy is a common complication to diabetes mellitus assumed to manifest as, for instance, cardiac vagal denervation, as well as impaired gastric emptying (GE) due to vagal damage. However, several studies indicate no or weak relationship between autonomic nerve function, as assessed by tests of cardiovascular autonomic function and gastric emptying rate (GER) Campbell et al., 1977, Nowak et al., 1995, Scarpello et al., 1976. Therefore, it has been suggested that the gastric and cardiac systems may be affected independently in diabetic autonomic neuropathy (Soler, 1980). Impaired GE in diabetic patients is clinically important, and may be associated with poor glycaemic control and increased risk of postprandial hypoglycaemia, changes in oral drug absorption, and gastrointestinal symptoms (Horowitz & Fraser, 1994). Cross-sectional studies have shown that approximately 30–50% of randomly selected patients with longstanding types 1 or 2 diabetes have delayed GE of solid and/or nutrient liquid meals Horowitz et al., 1989, Horowitz et al., 1991, Keshavarzian et al., 1987, Lyrenas et al., 1997, Wegener et al., 1990. Despite the high prevalence of upper gastrointestinal symptoms in unselected patients with type 1 diabetes, diabetic gastroparesis could be asymptomatic, possibly due to visceral afferent neuropathy (Rathmann et al., 1991). Assuming a true relationship between diabetic gastroparesis and autonomic neuropathy, it should be of importance to measure GE in any diabetic subject showing abnormal results on an autonomic nervous function test, since the correlation between gastrointestinal symptoms and delay in GE is poor Horowitz et al., 1989, Horowitz et al., 1991, Keshavarzian et al., 1987, Wegener et al., 1990. Currently, there is no good method of assessing gastrointestinal autonomic nerve function, making it necessary to use tests of cardiovascular autonomic nerve function as a surrogate marker for gastrointestinal autonomic neuropathy. A variety of different factors could influence the autonomic nervous system, causing reduced autonomic responses not attributable to diabetic autonomic neuropathy, or affecting the gastric motor function by mechanisms beyond the autonomic nervous system. The aim of this study was to evaluate, by avoiding the influence of confounding factors, if any relationship exists between delayed GE and cardiac autonomic neuropathy (CAN) in type 1 diabetics.
Section snippets
Patients
Using a standardized ultrasound technique, GE was studied in 20 type 1 diabetic patients with poor glycaemic control despite good compliance (the mean value of HbA1c for the preceding year was 8% or greater; hence, normal <5.3%) and 10 normal healthy volunteers without symptoms of gastrointestinal disease (Group 1). Diabetic patients were classified into two groups according to the absence (Group 2) or presence (Group 3) of CAN, using the deep breathing test (Sundkvist, Almér, & Lilja, 1979) to
Results
There was no significant difference between the three groups regarding age and BMI. The mean duration of diabetes and the glycaemic control (HbA1c) did not differ significantly between patients with and without signs of CAN (Table 1).
Significantly lower rates of GE were observed in diabetic patients with CAN, in comparisons with diabetic patients without CAN (median GER 16% vs. 54%, P<.01). Also, GER were significantly lower in diabetic patients with CAN compared to the healthy volunteers
Discussion
The first description of the association between delayed GE and diabetes mellitus was made by Rundles (1945). Despite intensive research, the pathogenesis of abnormal gastrointestinal motility in diabetes mellitus is still not fully understood, but has been attributed to vagal nerve dysfunction, occurring as part of a generalized autonomic neuropathy Battle et al., 1980, Buysschaert et al., 1987, Feldman et al., 1979, Fox & Behar, 1980, Horowitz et al., 1985, Keshavarzian et al., 1987,
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