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Background: Opioid treatment often causes debilitating constipation. However, it is not well described how opioids affect colonic motility and whether opioid‐induced constipation is due to either a decrease of powerful peristaltic contractions or "uncoordinated" peristalsis. The present study aims to investigate the effect of oxycodone on parameters of colonic motility and to determine whether motility is normalized by the opioid antagonist naloxegol. Methods: In two randomized, double‐blind crossover trials, oxycodone or placebo was administered to 25 healthy males (Trial A), while another 24 healthy males were administered oxycodone with naloxegol or placebo (Trial B). Colonic motility was assessed by tracking the progression of an electromagnetic capsule throughout the large intestine. Segmental colonic transit times and capsule movements were calculated using displacement distance and velocity. Key Results: In Trial A, colonic transit time increased during oxycodone treatment compared with placebo (39 vs 18 hours, P <.01). Displacement during long fast antegrade movements was shorter during oxycodone treatment than with placebo (10 vs 20 cm, P =.03). In Trial B, colonic transit time was faster during oxycodone + naloxegol than during oxycodone + placebo (40 vs 55 hours, P =.049), mainly caused by an increase of the percentwise fraction of distance covered by fast movements in the left colon (P =.001). Conclusion & Inferences: Oxycodone treatment impaired colonic motility, manifested as increased transit time, specifically decreased long fast antegrade movements, and addition of naloxegol improved motility dynamics. In humans, the increased transit time during opioid treatment is caused by a decrease in long fast movements rather than uncoordinated peristalsis. [ABSTRACT FROM AUTHOR]

Abdominal pain, nausea, vomiting, diarrhoea, constipation, and faecal incontinence are common symptoms of diabetic gastroenteropathy and often have a major impact on quality of life. The symptoms are usually caused by widespread dysfunction of the gastrointestinal tract. Hence, diagnosis requires panenteric assessment. The general principles of management are glycaemic control, diet, prokinetics, laxatives, and in selected cases, gastric electrical stimulation, which is summarised in this review.

Gastroparesis is defined as impaired gastric emptying without mechanical obstruction and cardinal symptoms including vomiting, nausea, early satiety, and upper abdominal pain. Most cases of gastroparesis are diabetic, idiopathic or post-operative. The correlation between symptoms and objective measures of gastroparesis is poor. Basic treatment includes dietary advices and prokinetics. Selected patients not responding to basic treatment can be offered gastric electrical stimulation. In many cases, gastroparesis is present in combination with other motility disorders, especially constipation.