Famotidine and Omeprazole Both Induce Gastric Transmucosal Leak

ABSTRACT

Our group has recently published that proton pump inhibitors (PPIs) induce transmucosal, paracellular, bidirectional leakage in the gastric corpus epithelium to a wide range of molecules.

This study was undertaken to determine if H-2 blocker medications also induce such leakage, or whether it is a result of specific inhibition of H+, K+-ATPase.

At the beginning and end of a dosage regimen of omeprazole or famotidine, healthy volunteers with no history of gastrointestinal disease consumed a (probe) solution of 100 gms of sucrose in 200 cc of water. Subsequently an 8 hr urine specimen was collected. The sucrose concentration in the urine specimen (mg/ml) multiplied by the total urine volume equaled the amount of sucrose (mg) which leaked from the gastric lumen into the bloodstream.

Like omeprazole, famotidine was also able to induce significant transmucosal leakage across the mucosal barrier of the upper gastrointestinal tract. Famotidine-induced leakage exhibited a narrower time course than was observed with omeprazole.

Conclusions: The fact that both classes of acid suppressive medications induce leak implies that leak results not from direct inhibition of the H+, K+-ATPase, or from a side effect of omeprazole-like molecules, but is more generally related to the overall inhibition of acid secretion. The medical significance of such gastric leak is discussed.