Z Gastroenterol 2006; 44 - A151
DOI: 10.1055/s-2006-943517

Evaluation of gastric emptying and neuropathy in short- and long-term type-1 diabetes

T Várkonyi 1, É Börcsök 1, R Takács 1, R Róka 1, C Lengyel 1, M Lázár 2, M Papós 2, L Pávics 2, P Kempler 3, J Lonovics 1
  • 11st Dept. of Internal Medicine, University of Szeged
  • 2Dept. of Nuclear Medicine, University of Szeged
  • 31st. Dept. of Internal Medicine, Semmelweis University, Budapest

The aim of this study was to determine the gastric emptying, the autonomic and the sensory neuropathy in diabetic patient groups with different durations. Patients, methods: 17 patients (pts) had shorter, 23 pts had longer type-1 DM. The emptying of the stomach was evaluated by a scintigraphic procedure. Autonomic neuropathy (AN) was assessed by cardiovascular reflex tests. Sensory nerve function was studied with a Neurometer. Results: There was a non-significant tendency of prolonged half-time of gastric emptying (HTE) in longer type-1 DM (93.5±10.1 vs. 67.8±6.7min. p>0.05; long- vs. short-standing DM). The AN score and three reflex tests differed between the groups (AN score: 4.3±0.5 vs. 2.5±0.4, p<0.05; heart rate response to breathing: 12.7±1.5 vs. 19.4±2.2 beats/min. p<0.05; Valsalva ratio: 1.3±0.05 vs. 1.75±0.1, p<0,0001; orthostatic hypotension: 23±3.4 vs. 11±3.7mm Hg, p<0.05). A positive correlation was observed between HTE and the AN score in long-standing DM (r=0.57, p<0.01). The correlations between heart rate response to breathing and HTE (r=–0.57, p<0.01) and between the Valsalva ratio and HTE (r=–0.43, p<0.05) in this group were negative. A positive association was found between the orthostatic hypotension and HTE (r=0.51, p<0.01). The current perception thresholds (CPT) at 2 kHz differed between the groups (CPT at the median nerve: 3.66±0.35 vs. 1.84±0.25 mA, p<0,001; CPT at the peroneal nerve: 5.39±0.71 vs. 3.70±0.68 mA, p<0.05). Conclusions: The impaired gastric emptying was frequently found in pts with long-standing DM and the severe AN exhibited a correlation with the slower gastric motility. These data support the hypothesis, that the most progressive manifestations of neuropathy might be responsible for the development of gastroparesis.