E0256 - Different Duodenal pH Profiles Relating to Individual Dyspeptic Symptoms Measured by Wireless Motility Capsules in Suspected Gastroparesis: Evidence for Delayed Neutralization in Patients With Greater Epigastric Pain
Introduction: Increased duodenal acid exposure is proposed as a mechanism of symptoms in functional dyspepsia but is rarely measured. Wireless motility capsules (WMC) measure transit in suspected dysmotility but also quantify small bowel (SB) pH. WMC SB pH has not been related to dyspepsia severity. We compared SB pH to severity of epigastric pain and nausea/vomiting (NV) in patients with suspected gastroparesis and devised an estimate of delayed duodenal neutralization as a marker of possible increased duodenal acid exposure.
Methods: 91 patients with symptoms suspicious for gastroparesis from a parent study of concurrent WMC and gastric scintigraphy had interpretable WMC SB pH tracings from gastric emptying (GE) to ileocecal junction (ICJ) passage. Nausea/vomiting (NV) scores from GCSI surveys and epigastric pain scores from PAGI-SYM surveys (0=no symptoms, 5=very severe) were related to SB pH. Delayed duodenal neutralization was defined when mean SB pH over the first 30 minutes after GE remained below pH values in the first 15 minutes after GE.
Results: GE was detected by WMC pH increases >2 units. Most tracings showed initial rapid duodenal pH decreases followed by increases progressing to ICJ passage (Fig 1A). Others showed delayed pH decreases then slower increases, perhaps reflecting delayed duodenal neutralization (Fig 1B). Duodenal pH profiles were similar in patients with epigastric pain scores above and below median severity (Table). However patients with NV scores above median severity showed higher duodenal pH than with NV scores below median. 18/30 patients (60%) with pain scores above median showed delayed duodenal neutralization (lower pH in the 30 vs. 15 minutes after GE) compared to 20/61 (33%) with pain scores below median (P=0.02). Conversely, 16/36 (44%) with NV scores above median and 22/55 (40%) with NV below median showed delayed neutralization (P=0.83).
Discussion: Duodenal pH profiles in suspected gastroparesis relate to symptom severity and vary depending on the symptom measured. Compared to milder symptoms, severe nausea/vomiting is associated with increased duodenal pH and little delay in duodenal neutralization while increased overall duodenal pH is not seen with severe epigastric pain. Rather, a subset of patients with severe pain exhibits delayed initial duodenal pH decreases followed by slow neutralization. These findings support possible increased duodenal acid exposure relating to dyspeptic pain severity in some patients.