Clinical use of proton-pump inhibitors but not H₂-blockers or antacid/alginates raises the serum levels of amidated gastrin-17, pepsinogen I and pepsinogen II in a random adult population

Abstract

Objective. Proton-pump inhibitors (PPIs), H₂ receptor antagonists (H₂RAs) and antacids/alginates reduce intragastric acidity and may thus influence normal gastric physiology. The purpose of this study was to examine the effect of these compounds on serum levels of amidated gastrin-17 (G-17) and pepsinogens (PGI & PGII) in a large, random, adult Swedish population sample with uninfected stomach mucosa. Material and methods. The initial sample subjects (n=1000, mean age 50 years, range 20–80 years) completed a questionnaire on the use of acid inhibitory drugs 1 week and/or 3 months before study entry. All subjects (n=590) with normal gastric mucosa as delineated by serum biomarkers were included. Among them, serum levels of PGI, PGII and G-17 were compared between those who used acid inhibitory drugs and those who did not. Results. The serum levels of G-17 or pepsinogens in the subjects who reported use of H₂RAs (n=18) or antacid/alginates (n=66) during the previous 3 months did not differ from those in non-users (n=471). However, the median levels of G-17 and pepsinogens were significantly (p<0.001) higher among the PPI users (n=35) than among non-users: the levels were approximately doubled. The ratio of PGI/PGII was, however, similar between PPI users and non-users, or those using antacids/alginates or H₂RAs. Among subjects using PPIs, the serum levels of pepsinogens correlated positively (p<0.01) with the serum levels of G-17. Conclusions. PPIs but not antacids/alginates or H₂RAs markedly increase the fasting levels of serum amidated G-17 and pepsinogens among ordinary patients in everyday clinical practice.

• Biological markers
• gastric mucosa/pathology
• gastrins
• omeprazole/analogs & derivatives
• pepsinogens