Dataset Information

Worsened Fibrostenotic Outcomes in Eosinophilic Esophagitis Patients Due to COVID-19-Related Endoscopy Cancellations.

ABSTRACT:

Background

Indirect consequences of COVID-19 in eosinophilic esophagitis (EoE) are not known.

Aim

To determine the impact of COVID-19-related endoscopy cancellations on outcomes in EoE patients.

Methods

In this retrospective cohort study, we assessed whether adult EoE patients who had routine endoscopy scheduled from mid-March 2020 to May 2020 (pandemic start) were canceled or proceeded, and if canceled, ultimately returned. We extracted clinical, endoscopic, and histologic data for their pre-COVID procedure as well as the next procedure performed, if a patient returned. Outcomes included histologic response (< 15 eos/hpf) and endoscopic severity. Those with delayed care were compared to those who returned as scheduled.

Results

Of 102 patients identified, 75 had procedures canceled, and 20 (27%) never returned. For the 55 who were canceled but returned, mean time between procedures was 1.1 ± 0.7 years with a delay of 0.5 ± 0.3 years. While treatment rates were similar between the pre- and delayed post-COVID EGD, more patients required a dilation after their return (71% vs 58%; p = 0.05) and their esophageal diameter had significantly decreased (16.8 mm to 15.0 mm; p < 0.001). Of 17 individuals who did not have stricture, narrowing, or dilation pre-pandemic, during their next endoscopy 5 (29%) had a stricture, 1 (6%) had a narrowing, and 7 (41%) required dilation.

Conclusion

Of EoE patients with canceled endoscopies during the beginning of the COVID-19 pandemic, > 25% never returned for care, which is a previously unmeasured impact of the pandemic. Those who returned had > 1 year between procedures with progression of fibrotic features and need for esophageal dilation.

SUBMITTER: Ocampo AA

PROVIDER: S-EPMC9255524 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:ObjectivesEosinophilic esophagitis (EoE) is a chronic inflammatory condition that causes esophageal remodeling and stricture formation. We compared the clinical course of symptoms, endoscopic findings, histology, and changes in phenotype over time in EoE patients with inflammatory and fibrostenotic phenotypes.MethodsData were obtained from EoE patients from three medical centers and followed prospectively. Endoscopic features and histology from index and follow-up endoscopies were recorded. Behavior was classified as inflammatory if endoscopic findings demonstrated furrows or white plaques and as fibrostenotic if endoscopic findings included fixed rings or strictures.ResultsTwo hundred and fifty-six EoE patients were included in the analysis. The mean age was 32±18 years, 25% of patients were <18 years, 89% of patients were Caucasians, and 74% of patients were male. The mean duration of symptoms before diagnosis was 6.8±7.2 years with a follow-up of 1.7±1.9 years (maximum follow-up of 12 years). Fifty-four percent of patients presented with fibrostenotic EoE, whereas 46% presented with inflammatory EoE. Patients with inflammatory disease were younger than those with fibrostenotic disease (24±19 vs. 39±15 years, P<0.001). Patients with fibrostenotic disease had a longer duration of symptoms than those with inflammatory disease (8.1±7.7 vs. 5.3±6.3 years, P=0.002). Over the study period, 47 (18%) had remission of inflammatory EoE, 68 (27%) continued to have inflammatory disease, 74 (29%) continued to have fibrostenotic disease, 65 (25%) fibrostenotic patients had regression of fibrosis, and 2 patients (1%) progressed from inflammatory disease to fibrostenotic disease. Patients who had regression from their fibrostenosis were more likely than patients who continued to demonstrate fibrostenosis to have a decrease in proximal (54% vs. 32%, P<0.001) and distal (70% vs. 38%, P<0.001) eosinophilia.ConclusionsMost EoE patients maintained their phenotype or had an improvement with <1% progressing from inflammatory to fibrostenosis. This suggests that early therapeutic strategies aimed at controlling inflammation may interrupt, decrease, or prevent the remodeling fibrosis in EoE.