Pantoprazole treatment does not invoke anti-inflammatory properties in vivo

Proton pump inhibitors (PPIs) are antiulcer agents that have gastric antisecretory and mucosal protective actions. The antisecretory effect of these agents derives from the inhibition of gastric parietal cell proton pump H+/K+ ATPase. The exact mechanism of PPI-induced gastric mucosal protection is not known though. It has been suggested that PPI may accumulate, modulating the functions of neutrophils and, thus, may be useful in reducing the gastric mucosal injury caused by these cells. However, these same mechanisms may not be desirable when PPIs are prescribed in prophylaxis and pre-operatively for ill or immunodepressed patients. The present study was designed to examine a possible anti-neutrophil activity of pantoprazole in vivo. A short study with omeprazole and lanzoprazole was also performed.

Dosages of PPIs able to inhibit basal acid secretion (10 and 100 mg kg(-1)) were administered intraperitoneally (i.p.) to rats for 7 or 28 days. Cimetidine (100 mg kg(-1)) and dexamethasone (0.75 mg kg(-1)) were used as controls for antisecretory and anti-inflammatory activity, respectively. Air pouches were then developed in these animals, and Helicobacter pylori suspension or carrageenan was used as inflammatory stimulus. Exudate formation and leukocyte migration to air pouches were assessed.

Neither short nor long treatment with pantoprazole modified the ability of neutrophils to migrate in response to carrageenan or H. pylori. The same results were obtained when omeprazole or lanzoprazole was used. Dexamethasone, alone, a potent anti-inflammatory drug, was able to reduce polymorphonuclear and mononuclear cell migration.

Based on these observations, pantoprazole and other PPIs seem to have no anti-inflammatory properties in vivo.