Mucosal barrier defects in gastric intestinal metaplasia: in vivo evaluation by confocal endomicroscopy

Helicobacter pylori infection and intestinal metaplasia (IM) are associated with gastric cancer. An impaired gastric mucosal barrier could be involved in this carcinogenesis.

To evaluate laser confocal laser endomicroscopy (CLE) for in vivo functional imaging of mucosal barrier defects in patients with IM.

Prospective, controlled study.

A tertiary-care academic center.

This study involved patients with IM of the gastric mucosa who underwent CLE for surveillance.

Specific IM mucosa and non-IM mucosa in patients were identified by CLE, and targeted biopsy samples were taken for histopathology and electron microscopy.

Post-CLE assessment of paracellular fluorescein leakage was devised and validated by electron microscopy. We also evaluated the effect of H pylori eradication on the mucosal barrier.

Forty-two patients were included. Of non-IM samples, the paracellular permeability was significantly increased in H pylori-positive samples compared with H pylori-negative controls (54 ± 31% vs 3 ± 6%, P < .05). Of IM samples, the permeability was significantly increased in both H pylori-negative and H pylori-positive samples (67 ± 34% and 72 ± 28% vs 3 ± 6%, both P < .05). The results of post-CLE assessment correlated well with the electron microscopy findings (R(2) 0.834, P < .0001). After the eradication of H pylori, the paracellular barrier dysfunction of non-IM mucosa was significantly improved as shown by electron microscopy and CLE (both P < .001). However, there was no significant change in IM mucosa.

Single-center study.

CLE allows functional imaging of mucosal barrier defects. Gastric IM is associated with an impaired paracellular barrier irrespective of H pylori eradication.