Post-COVID-19 Dyspepsia Is Not Due to Impairment of Duodenal Barrier Function

Patients with coronavirus disease 2019 (COVID-19) have a higher probability of developing dyspepsia; however, mechanisms are not defined. The study analyzes dyspeptic symptoms during and after COVID-19 and whether mechanisms involved are impaired duodenal barrier function or local inflammatory dysfunction.

Fifty-five patients with COVID-19 were interviewed during hospitalization and 6 months after hospital discharge. Dyspeptic symptoms were assessed using the Rome III questionnaire for functional dyspepsia. Intensity and frequency were assessed using a Likert scale (0-6). Of the recovered patients, 23 underwent upper endoscopy with duodenal biopsies to assess the epithelial barrier function (transepithelial electrical resistance and mucosal fluorescein permeability) and concentration of inflammatory cytokines. These results were compared with those of healthy controls.

When comparing dyspeptic symptoms during and after COVID-19, there was an increase in the intensity of postprandial fullness and epigastric pain/burning (during: 5.5 ± 0.5 vs. after: 7.0 ± 0.6, p = 0.009), but not in early satiety. In contrast, when comparing the frequency of dyspeptic symptoms during COVID-19 and after 6 months of hospital discharge, there were no significant differences. In addition, basal transepithelial electrical resistance and duodenal permeability showed no statistical difference when comparing healthy controls and post-COVID-19 patients with or without dyspepsia. Concentration of pro-inflammatory cytokines was not different among the groups.

The intensity of dyspeptic symptoms increased in the post-COVID-19 period. Furthermore, this event does not seem to be associated with impaired duodenal epithelial barrier.