Gastroparesis syndromes: Response to electrical stimulation.


Journal

Neurogastroenterology and motility
ISSN: 1365-2982
Titre abrégé: Neurogastroenterol Motil
Pays: England
ID NLM: 9432572

Informations de publication

Date de publication:
03 2019
Historique:
received: 24 07 2018
revised: 14 11 2018
accepted: 03 12 2018
pubmed: 2 2 2019
medline: 23 1 2020
entrez: 2 2 2019
Statut: ppublish

Résumé

Factors underlying gastroparesis are not well defined, nor is the mechanism of action of gastric electrical stimulation (GES). We hypothesized that GES acts via several mechanisms related to underlying disordered pathophysiology. We studied 43 consecutive eligible patients with gastroparetic symptoms, previously evaluated by two methods in each of five core areas: inflammatory, autonomic, enteric, electrophysiologic, and hormonal; and also categorized by GI symptoms, metabolic status, illness quantification, and gastric physiology. We then studied 41 patients who underwent temporary GES for 5-7 days. Thirty-six of those patients were implanted and 30 were followed up at 6 months after permanent GES. In previous but separately reported work, patients had similar GI symptoms regardless of baseline gastric emptying or diabetic/idiopathic status and all patients demonstrated abnormalities in each of the five areas studied. After GES, patients showed early and late effects of electrical stimulation with changes noted in multiple areas, categorized by improvement status. Patients with symptoms of gastroparesis have multiple abnormalities, including systemic inflammation and disordered hormonal status. GES affects many of these abnormalities. We conclude electrical stimulation improves symptoms and physiology with (a) an early and sustained anti-emetic effect; (b) an early and durable gastric prokinetic effect in delayed emptying patients; (c) an early anti-arrhythmic effect that continues over time; (d) a late autonomic effect; (e) a late hormonal effect; (f) an early anti-inflammatory effect that persists; and (g) an early and sustained improvement in health-related quality of life. This study is registered with Clinicaltrials.gov under study # NCT03178370 (https://clinicaltrials.gov/ct2/show/NCT03178370).

Sections du résumé

BACKGROUND AND AIMS
Factors underlying gastroparesis are not well defined, nor is the mechanism of action of gastric electrical stimulation (GES). We hypothesized that GES acts via several mechanisms related to underlying disordered pathophysiology.
METHODS
We studied 43 consecutive eligible patients with gastroparetic symptoms, previously evaluated by two methods in each of five core areas: inflammatory, autonomic, enteric, electrophysiologic, and hormonal; and also categorized by GI symptoms, metabolic status, illness quantification, and gastric physiology. We then studied 41 patients who underwent temporary GES for 5-7 days. Thirty-six of those patients were implanted and 30 were followed up at 6 months after permanent GES.
RESULTS
In previous but separately reported work, patients had similar GI symptoms regardless of baseline gastric emptying or diabetic/idiopathic status and all patients demonstrated abnormalities in each of the five areas studied. After GES, patients showed early and late effects of electrical stimulation with changes noted in multiple areas, categorized by improvement status.
CONCLUSION
Patients with symptoms of gastroparesis have multiple abnormalities, including systemic inflammation and disordered hormonal status. GES affects many of these abnormalities. We conclude electrical stimulation improves symptoms and physiology with (a) an early and sustained anti-emetic effect; (b) an early and durable gastric prokinetic effect in delayed emptying patients; (c) an early anti-arrhythmic effect that continues over time; (d) a late autonomic effect; (e) a late hormonal effect; (f) an early anti-inflammatory effect that persists; and (g) an early and sustained improvement in health-related quality of life. This study is registered with Clinicaltrials.gov under study # NCT03178370 (https://clinicaltrials.gov/ct2/show/NCT03178370).

Identifiants

pubmed: 30706646
doi: 10.1111/nmo.13534
doi:

Substances chimiques

Cytokines 0
Hormones 0

Banques de données

ClinicalTrials.gov
['NCT03178370']

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

e13534

Subventions

Organisme : NIH Diabetic Complications Consortium
ID : U24DK076169
Pays : International

Informations de copyright

© 2019 John Wiley & Sons Ltd.

Auteurs

Thomas L Abell (TL)

University of Louisville, Louisville, Kentucky.

Archana Kedar (A)

University of Louisville, Louisville, Kentucky.

Abigail Stocker (A)

University of Louisville, Louisville, Kentucky.

Karen Beatty (K)

University of Louisville, Louisville, Kentucky.

Lindsay McElmurray (L)

University of Louisville Physicians, Louisville, Kentucky.

Michael Hughes (M)

University of Louisville, Louisville, Kentucky.

Hani Rashed (H)

Methodist Hospital, Memphis, Tennessee.

William Kennedy (W)

University of Minnesota, Minneapolis, Minnesota.

Gwen Wendelschafer-Crabb (G)

University of Minnesota, Minneapolis, Minnesota.

Xiu Yang (X)

University of Louisville, Louisville, Kentucky.

Mostafa Fraig (M)

University of Louisville, Louisville, Kentucky.

Endashaw Omer (E)

University of Louisville, Louisville, Kentucky.

Ed Miller (E)

University of Louisville, Louisville, Kentucky.

Michael Griswold (M)

University of Mississippi Medical Center, Jackson, Mississippi.

Christina Pinkston (C)

University of Louisville, Louisville, Kentucky.

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Classifications MeSH