Factors associated with gastric dysrhythmias in patients with type 1 diabetes and without dyspeptic symptoms.

Impairment of gastric function in diabetes has been attributed to autonomic neuropathy (AN). Multichannel electrogastrography (EGG) is a non-invasive method to detect gastric electrical activity (GEA). Type 1 diabetes occurring at early age allows to study GEA abnormalities without interference of aging. Our aims are to study the presence of early GEA disturbances in patients with type I diabetes and to test the correlation between GEA and glycaemia levels, duration of disease and presence of AN. 37 patients with type-1 diabetes (17 m; 23- 54 y), diagnosed from more than 5 years, without dyspeptic symptoms, 34 dyspeptics (15 m, 20-51 y) and 10 healthy volunteers (7 m, 23-37 y) that served as positive and negative controls were studied. After an overnight fasting, all subjects underwent multichannel EGG study 30 min before and after a standard liquid meal (300 kcal). Pre and postprandial percentage and power of normogastria (2-4 cpm), bradygastria, tachygastria and arrhythmias were calculated by running spectral analysis. In diabetics AN was assessed by ECG beat-tobeat variation analysis and lying-to-standing blood pressure variations. Dyspeptic symptoms were assessed by a standardized questionnaire. Data were expressed as mean±SD. Diabetics had a significantly higher rate of gastric arrhythmias than dyspeptics and controls during the fasting phase (27±16%, 18±11 and 20±14, p<0.05) especially at the pace-maker recording site. In a longer history of diabetes (>20 y) percentage of pre-prandial normogastria was lower than in subjects with a history < 10 y (59±15 vs 79±15, p<0,01). Fasting glycaemia > 200 mg/dl correlated with a higher percentage (8,4±5,9 vs 4,2±4,8, p<0,05) and power (44,5±15,8 vs 33,7±15,3, p<0,05) of postprandial bradygastria. Presence of AN correlated with lower fasting normogastria power (22±8 vs 33±17 p<0,05) and postprandial bradygastria percentage (4,1±4,8 vs 10,9±6,5, p<0,001). We confirmed that gastric electric activity is altered in diabetics. Type I diabetics without dyspepsia had gastric arrhythmias and increased power of bradygastria. These events mainly occurred at the gastric pacemaker region and were associated with disease duration, severity of hyperglycaemia and AN. Gastric dysrhytmias precede dyspeptic symptoms appearance and probably represent an early gastric neuromuscolar injury.