Gastric dysfunction in patients with chronic nausea and vomiting syndromes defined by a noninvasive gastric mapping device

Author:

Gharibans Armen A.123ORCID,Calder Stefan12ORCID,Varghese Chris1ORCID,Waite Stephen2,Schamberg Gabriel2ORCID,Daker Charlotte4ORCID,Du Peng23,Alighaleh Saeed2ORCID,Carson Daniel1ORCID,Woodhead Jonathan2,Farrugia Gianrico5ORCID,Windsor John A.1,Andrews Christopher N.6,O’Grady Greg123ORCID

Affiliation:

1. Surgical and Translational Research Centre, University of Auckland, Auckland 1023, New Zealand.

2. Alimetry Ltd., Auckland 1010, New Zealand.

3. Auckland Bioengineering Institute, University of Auckland, Auckland 1010, New Zealand.

4. Department of Gastroenterology, North Shore Hospital, Auckland 0620, New Zealand.

5. Mayo Clinic, Rochester, MN 55902, USA.

6. Division of Gastroenterology, Cumming School of Medicine, University of Calgary, Calgary, AB T2N 4N1, Canada.

Abstract

Chronic nausea and vomiting syndromes (NVSs) are prevalent and debilitating disorders. Putative mechanisms include gastric neuromuscular disease and dysregulation of brain-gut interaction, but clinical tests for objectively defining gastric motor function are lacking. A medical device enabling noninvasive body surface gastric mapping (BSGM) was developed and applied to evaluate NVS pathophysiology. BSGM was performed in 43 patients with NVS and 43 matched controls using Gastric Alimetry (Alimetry), a conformable high-resolution array (8 × 8 electrodes; 20-mm interelectrode spacing), wearable reader, and validated symptom-logging app. Continuous measurement encompassed a fasting baseline (30 minutes), 482-kilocalorie meal, and 4-hour postprandial recording, followed by spectral and spatial biomarker analyses. Meal responses were impaired in NVS, with reduced amplitudes compared to controls (median, 23.3 microvolts versus 38.0 microvolts, P < 0.001), impaired fed-fasting power ratios (1.1 versus 1.6, P = 0.02), and disorganized slow waves (spatial frequency stability, 13.6 versus 49.5; P < 0.001). Two distinct NVS subgroups were evident with indistinguishable symptoms (all P > 0.05). Most patients (62%) had normal BSGM studies with increased psychological comorbidities (43.5% versus 7.7%; P = 0.03) and anxiety scores (median, 16.5 versus 13.0; P = 0.035). A smaller subgroup (31%) had markedly abnormal BSGM, with biomarkers correlating with symptoms (nausea, pain, excessive fullness, early satiety, and bloating; all r > 0.35, P < 0.05). Patients with NVS share overlapping symptoms but comprise distinct underlying phenotypes as revealed by a BSGM device. These phenotypes correlate with symptoms, which should inform clinical management and therapeutic trial design.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine

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