Abstract

In a clinical setting, diabetic autonomic complications (cardiac, gastrointestinal, urogenital, etc.) are often handled as separate entities. We investigated rectal sensitivity to heat, mechanical distension, and electrical stimulations in 20 patients with diabetes and symptoms of gastroparesis, to evaluate the extent of visceral neuronal damage. Furthermore, to evaluate the relation between the nervous structures we examined gastric emptying and cardiac autonomic function with the hypothesis being an association between these. We found that 60% of patients had delayed gastric empting. Rectal hyposensitivity was a general finding as they tolerated 67% higher thermal, 42% more mechanical, and 33% higher electrical current intensity compared to healthy controls. In patients, most heart rate variability parameters were reduced; they reported significantly more gastrointestinal symptoms and a reduced quality of life in all SF-36 domains. Shortened RR interval correlated with reduced rectal temperature sensitivity, and gastric retention rate was negatively associated with symptoms of nausea and vomiting. To conclude, in these patients with signs and symptoms of diabetic gastroparesis, rectal sensitivity was reduced, and heart rate variability was impaired. Thus, we suggest regarding diabetic autonomic neuropathy as a diffuse disorder. Symptoms of widespread autonomic dysfunction and sensory disorders should be expected and treated in these patients.

Highlights

  • Gastrointestinal (GI) complaints are more common in all types of diabetes mellitus (DM) patients compared to the general population [1, 2]

  • We only investigated the associations in line with our hypothesis

  • Type 1 diabetes mellitus (DM) patients have been shown to be more prone to vomiting, whereas type 2 patients have relatively more

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Summary

Introduction

Gastrointestinal (GI) complaints are more common in all types of diabetes mellitus (DM) patients compared to the general population [1, 2]. Other mechanisms include altered elasticity of the GI wall, enterohormonal changes, anxiety/depression, exocrine pancreatic insufficiency, bacterial imbalance, autoimmunity, Journal of Diabetes Research loss of interstitial cells of Cajal, and the direct effects of hyperglycemia on GI motility [8,9,10]. In line with this complex pathophysiology, the association between upper GI symptoms and gastric emptying is modest. Gastric emptying rate cannot explain the range of upper GI symptoms experienced, neither in DM patients nor in the case of idiopathic gastroparesis [11,12,13,14]

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