AIM： To determine if the observed paracellular sucrose leak in Barrett＇s esophagus patients is due to their pro- ton pump inhibitor （PPI） use. METHODS： The in vivo sucrose permeability test was administered to he...AIM： To determine if the observed paracellular sucrose leak in Barrett＇s esophagus patients is due to their pro- ton pump inhibitor （PPI） use. METHODS： The in vivo sucrose permeability test was administered to healthy controls, to Barrett＇s patients and to non-Barrett＇s patients on continuous PPI thera- py. Degree of leak was tested for correlation with pres- ence of Barrett＇s, use of PPIs, and length of Barrett＇s segment and duration of PPI use. RESULTS： Barrett＇s patients manifested a near 3-fold greater, upper gastrointestinal sucrose leak than healthy controls. A decrease of sucrose leak was ob- served in Barrett＇s patients who ceased PPI use for 7 d.Although initial introduction of PPI use （in a PPI-na＇ive population） results in dramatic increase in sucrose leak, long-term, continuous PPI use manifested a slow spon- taneous 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. CONCLUSION： Although future research is needed to determine the degree of paracellular leak in actual Barrett＇s mucosa, the relatively high degree of leak ob- served with in vivo sucrose permeability measurement of Barrett＇s patients reflects their PPI use and not their Barrett＇s tissue perse.展开更多
基金Supported by Sharpe-Strumia Research Foundation of the Bryn Mawr Hospital
文摘AIM： To determine if the observed paracellular sucrose leak in Barrett＇s esophagus patients is due to their pro- ton pump inhibitor （PPI） use. METHODS： The in vivo sucrose permeability test was administered to healthy controls, to Barrett＇s patients and to non-Barrett＇s patients on continuous PPI thera- py. Degree of leak was tested for correlation with pres- ence of Barrett＇s, use of PPIs, and length of Barrett＇s segment and duration of PPI use. RESULTS： Barrett＇s patients manifested a near 3-fold greater, upper gastrointestinal sucrose leak than healthy controls. A decrease of sucrose leak was ob- served in Barrett＇s patients who ceased PPI use for 7 d.Although initial introduction of PPI use （in a PPI-na＇ive population） results in dramatic increase in sucrose leak, long-term, continuous PPI use manifested a slow spon- taneous 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. CONCLUSION： Although future research is needed to determine the degree of paracellular leak in actual Barrett＇s mucosa, the relatively high degree of leak ob- served with in vivo sucrose permeability measurement of Barrett＇s patients reflects their PPI use and not their Barrett＇s tissue perse.
