Case series report symptom reductions after pyloric botulinum toxin injection in gastroparesis, but small controlled trials show no benefit. Factors that enhance response to therapy are undefined. A retrospective analysis of 179 gastroparetics undergoing pyloric botulinum toxin injection from 2001 to 2007 assessed responses relating to drug dosing, demographic factors, comorbidities, and gastric function. Overall, there was a decrease in gastroparetic symptoms 1-4 months after pyloric botulinum toxin injection in 92 patients (51.4%). Increasing the botulinum toxin dose significantly improved clinical responses of patients who provided information on symptoms after therapy (100 units: 54.2%; 200 units: 76.7%; P=0.02). Other factors that improved response to botulinum toxin included female gender, age <50 years, and nondiabetic nonpostsurgical etiology (all P<0.05). Eighty-seven patients received 307 follow-up injections. A clinical response to a second injection was observed in 73.4% of evaluable patients. In conclusion, responses to pyloric botulinum toxin depended on dose and were maintained on repeat injection. Subgroup analyses defined subgroups likely to benefit. These findings provide the foundation for large, controlled trials of high-dose botulinum toxin in selected gastroparesis subsets.

BACKGROUND & AIMS: Many patients with gastroparesis are prescribed opioids for pain control, but indications for opioid prescriptions and the relationship of opioid use to gastroparesis manifestations are undefined. We characterized associations of use of potent vs weaker opioids and presentations of diabetic and idiopathic gastroparesis. METHODS: We collected data on symptoms, gastric emptying, quality of life, and health care resource use from 583 patients with gastroparesis (>10% 4-h scintigraphic retention) from the National Institute of Diabetes and Digestive and Kidney Diseases Gastroparesis Consortium, from January 2007 through November 2016. Patients completed medical questionnaires that included questions about opioid use. The opioid(s) were categorized for potency relative to oral morphine.

Acute hyperglycaemia in healthy humans disrupts slow wave rhythm similar to that observed in diabetic gastropathy, but hyperglycaemic effects on regional dysrhythmias, power, coupling and propagation are unexplored. Using mucosal mapping, we aimed to demonstrate that hyperglycaemia elicits region-specific tachygastria and evokes slow wave uncoupling between adjacent regions. Catheters with bipolar electrodes were affixed 10.5, 6 and 2 cm from the pylorus during endoscopy with midazolam in 10 healthy humans. Recordings were obtained for 1 h under basal conditions and for 1 h with hyperglycaemic clamping to 250 mg dL(-1). In basal recordings, proximal and distal slow wave frequencies were similar [2.91 +/- 0.05 vs 2.81 +/- 0.09 cycles per minute (cpm)]. Tachygastria (>3.6 cpm) was present 1.7 +/- 1.1% of the time proximally and 3.3 +/- 1.8% distally and localized to one lead 67% of the time. Proximal to distal gradients in signal power and power variability were observed. Coupling between adjacent sites was 78 +/- 2% with propagation velocities of 1.3 +/- 0.1 cm s(-1). 2 +/- 1% of segments showed >50% uncoupling. Hyperglycaemic clamping increased mean proximal (3.18 +/- 0.11 cpm) and distal (3.50 +/- 0.12 cpm) frequencies and proximal (15 +/- 6%) and distal (32 +/- 9%) tachygastria (all P < 0.01) that localized to one lead 80% of the time. During periods of normal frequency, coupling decreased proximally (54 +/- 6%) and distally (47 +/- 4%) (P < 0.01). 55 +/- 8% of segments showed >50% uncoupling (P < 0.01). In conclusion, gastric slow waves show stable, highly coupled rhythms under basal conditions. Hyperglycaemia elicits isolated tachygastrias and uncoupling of normal slow waves that are most prominent distally. These findings provide a foundation for studying slow wave conduction defects in diabetic gastropathy.

Gastric food retention has obstructive and non-obstructive causes, and is found in one-quarter of gastroparesis, especially postsurgical cases. Gastric emptying delays correlate with amounts of retained food on endoscopy. Retention is influenced by opiates, but not other medications. These analyses delineate pathogenic factors promoting gastric food retention.