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Histologic Regression of Barrett's Esophagus After Antireflux Surgery: Incidence and Predictive Factors
Journal article   Open access   Peer reviewed

Histologic Regression of Barrett's Esophagus After Antireflux Surgery: Incidence and Predictive Factors

Wyatt Rodan, Sven E Eriksson, Vineeth Sadda, Michelle Bojalad, Ping Zheng and Shahin Ayazi
Annals of surgery, Forthcoming
01 Apr 2026
PMID: 41917730
Featured in Collection :   Drexel's Newest Publications
url
https://doi.org/10.1097/SLA.0000000000007059View
Published, Version of Record (VoR) Open

Abstract

Fundoplication magnetic sphincter augmentation barrett's esophagus intestinal metaplasia Antireflux Surgery Regression
To evaluate the rate of Barrett's esophagus (BE) regression after antireflux surgery (ARS) and identify predictors of regression. The impact of ARS on BE regression remains unclear. Defining the likelihood of intestinal metaplasia regression and identifying patients most likely to benefit may help guide postoperative surveillance. Patients with biopsy proven BE undergoing fundoplication or magnetic sphincter augmentation (MSA) between 2013 and 2023 with ≥1-year endoscopic and histologic follow-up were included. Preoperative demographics, esophageal physiology, and endoscopic findings were compared between postoperative histologic regression and persistent BE using univariable and multivariable analyses. A total of 234 patients were included (163 fundoplication, 71 MSA). Histologic regression occurred in 53.4% overall, including 68.9% in ultrashort, 51.2% in short, and 0% in long-segment BE (P<0.001). Rates were similar between fundoplication and MSA (51.5% vs. 57.7%, P=0.396) but higher with an anatomically intact repair (64.2% vs. 38.8%, P<0.001). Independent predictors of regression were intact repair (OR 2.57, P=0.004), absence of severe esophagitis (OR 3.31, P=0.002), and shorter BE length (P<0.001). Patients without regression had a more severe reflux phenotype, including larger hiatal hernia, severe esophagitis, higher DeMeester score, and lower LES resting pressure (all P<0.05). Histologic regression of BE occurred in 53% of patients after ARS, confined to ultrashort and short segments, with no regression in long-segment BE. Intact repair was associated with regression, whereas disrupted repair was associated with segment lengthening. Regression appears to depend on restoration of an effective reflux barrier and underlying disease severity.

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