Correlation between reflux burden, peristaltic function, and mucosal integrity in GERD patients.


Journal

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

Informations de publication

Date de publication:
03 2020
Historique:
received: 17 08 2019
revised: 14 09 2019
accepted: 07 10 2019
pubmed: 2 11 2019
medline: 11 2 2021
entrez: 1 11 2019
Statut: ppublish

Résumé

Mean nocturnal baseline impedance (MNBI) augments the diagnostic yield of multichannel intraluminal impedance-pH (MII-pH) monitoring. While acid exposure time (AET) correlates with MNBI, it remains unclear whether esophageal motility affects MNBI values. The present study was aimed at evaluating the respective roles of esophageal motor function and AET on MNBI. High-resolution manometry (HRM) studies and ambulatory 24-hour MII-pH monitoring tracings were retrospectively analyzed from consecutive endoscopy-negative GERD patients with typical symptoms responsive to previous acid-suppressive therapy from three tertiary care centers. Univariate and multivariate analyses were performed to determine predictors of pathologic MNBI values at 3 cm and 5 cm above the lower esophageal sphincter (LES). Patients with pathological AET displayed lower MNBI values at 3 cm and 5 cm (P < .01) compared to patients with non-pathological AET. Similarly, significantly lower MNBI values were also noted at both sites with type 3 EGJ compared to type 1 EGJ (P ≤ .02 for each comparison), and with absent contractility compared to normal peristalsis (P ≤ .02 for each comparison). On multivariate analysis, the presence of type 2 or 3 EGJ and absent contractility were associated with a significantly higher probability of pathological MNBI values at 3 cm and 5 cm above the LES. Disruption of the EGJ and absent contractility on HRM are both associated with lower MNBI values. HRM findings complement reflux testing using MII-pH monitoring.

Sections du résumé

BACKGROUND
Mean nocturnal baseline impedance (MNBI) augments the diagnostic yield of multichannel intraluminal impedance-pH (MII-pH) monitoring. While acid exposure time (AET) correlates with MNBI, it remains unclear whether esophageal motility affects MNBI values. The present study was aimed at evaluating the respective roles of esophageal motor function and AET on MNBI.
METHODS
High-resolution manometry (HRM) studies and ambulatory 24-hour MII-pH monitoring tracings were retrospectively analyzed from consecutive endoscopy-negative GERD patients with typical symptoms responsive to previous acid-suppressive therapy from three tertiary care centers. Univariate and multivariate analyses were performed to determine predictors of pathologic MNBI values at 3 cm and 5 cm above the lower esophageal sphincter (LES).
KEY RESULTS
Patients with pathological AET displayed lower MNBI values at 3 cm and 5 cm (P < .01) compared to patients with non-pathological AET. Similarly, significantly lower MNBI values were also noted at both sites with type 3 EGJ compared to type 1 EGJ (P ≤ .02 for each comparison), and with absent contractility compared to normal peristalsis (P ≤ .02 for each comparison). On multivariate analysis, the presence of type 2 or 3 EGJ and absent contractility were associated with a significantly higher probability of pathological MNBI values at 3 cm and 5 cm above the LES.
CONCLUSIONS AND INFERENCES
Disruption of the EGJ and absent contractility on HRM are both associated with lower MNBI values. HRM findings complement reflux testing using MII-pH monitoring.

Identifiants

pubmed: 31670453
doi: 10.1111/nmo.13752
doi:

Types de publication

Journal Article Multicenter Study Observational Study

Langues

eng

Sous-ensembles de citation

IM

Pagination

e13752

Informations de copyright

© 2019 John Wiley & Sons Ltd.

Références

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Auteurs

Mentore Ribolsi (M)

Unit of Gastroenterology, Campus Bio Medico University, Rome, Italy.

Chandra Prakash Gyawali (CP)

Department of Medicine, Division of Gastroenterology, Washington University School of Medicine, St. Louis, Missouri.

Edoardo Savarino (E)

Division of Gastroenterology, Department of Surgical, Oncological and Gastroenterological Sciences, University of Padua, Padua, Italy.

Benjamin Rogers (B)

Department of Medicine, Division of Gastroenterology, Washington University School of Medicine, St. Louis, Missouri.

Arvind Rengarajan (A)

Department of Medicine, Division of Gastroenterology, Washington University School of Medicine, St. Louis, Missouri.

Marco Della Coletta (M)

Division of Gastroenterology, Department of Surgical, Oncological and Gastroenterological Sciences, University of Padua, Padua, Italy.

Matteo Ghisa (M)

Division of Gastroenterology, Department of Surgical, Oncological and Gastroenterological Sciences, University of Padua, Padua, Italy.

Michele Cicala (M)

Unit of Gastroenterology, Campus Bio Medico University, Rome, Italy.

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