[show abstract][hide abstract] ABSTRACT: To determine if the observed paracellular sucrose leak in Barrett's esophagus patients is due to their proton pump inhibitor (PPI) use.
The in vivo sucrose permeability test was administered to healthy controls, to Barrett's patients and to non-Barrett's patients on continuous PPI therapy. Degree of leak was tested for correlation with presence of Barrett's, use of PPIs, and length of Barrett's segment and duration of PPI use.
Barrett's patients manifested a near 3-fold greater, upper gastrointestinal sucrose leak than healthy controls. A decrease of sucrose leak was observed in Barrett's patients who ceased PPI use for 7 d. Although initial introduction of PPI use (in a PPI-naïve population) results in dramatic increase in sucrose leak, long-term, continuous PPI use manifested a slow spontaneous decline in leak. The sucrose leak observed in Barrett's patients showed no correlation to the amount of Barrett's tissue present in the esophagus.
Although future research is needed to determine the degree of paracellular leak in actual Barrett's mucosa, the relatively high degree of leak observed with in vivo sucrose permeability measurement of Barrett's patients reflects their PPI use and not their Barrett's tissue per se.
World Journal of Gastroenterology 06/2012; 18(22):2793-7. · 2.55 Impact Factor
[show abstract][hide abstract] ABSTRACT: Despite their remarkable safety profile and lack of clinical side effects, proton pump inhibitors (PPIs) induce a transmucosal
gastric leak to non-electrolyte probes of various sizes. The exvivo addition of PPIs to isolated rat gastric corpus increases
transmucosal permeability in a dose-dependent manner, which corresponds with PPIs’ dose-dependent inhibition of acid secretion.
Upon the addition of omeprazole, lansoprazole, or esomeprazole, a small decrease in transepithelial resistance and the concomitant
stimulation of short circuit current was observed. Additionally, transepithelial flux of 14C-[d]-mannitol (MW 182.17) across the gastric mucosa increased by a mean of 68% immediately following the addition of 200μM omeprazole.
This flux increase was bidirectional. Omeprazole also increased the paracellular permeability to larger radiolabeled probes,
including 14C-sucrose (MW 342.3) and 14C-polyethylene glycol (MW 4,000) by 118% and 350%, respectively. However, the flux of still larger probes, 10,000 and 70,000MW
dextrans, was not increased. Because PPIs are so widely used and are assumed to be innocuous, this transmucosal gastric leak
must be further investigated, as it may carry considerable biomedical implications.
Digestive Diseases and Sciences 04/2012; 54(7):1408-1417. · 2.26 Impact Factor