Eosinophil cationic protein and phospholipase A2 activity in human gastric juice. With emphasis on Helicobacter pylori status and effects of antacids

• Published in: Scandinavian journal of gastroenterology Vol. 27; no. 12; p. 1011
• Main Authors: Berstad, K, Berstad, Jr, A, Sjödahl, R, Weberg, R, Berstad, A
• Format: Journal Article
• Language: English
• Published: England 01-12-1992
• Subjects: Adult; Aluminum Hydroxide - pharmacology; Antacids - pharmacology; Bile Acids and Salts - metabolism; Blood Proteins - metabolism; Carbonates - pharmacology; Double-Blind Method; Eosinophil Cationic Protein - metabolism; Female; Gastric Acidity Determination; Gastric Juice - metabolism; Helicobacter pylori - isolation & purification; Helicobacter pylori - physiology; Humans; Male; Middle Aged; Phosphatidylcholines - metabolism; Phospholipases A - metabolism; Phospholipases A2 - metabolism; Ribonucleases; Stomach - enzymology; Stomach - microbiology
• ISSN: 0036-5521
• DOI: 10.3109/00365529209028131

To elucidate possible new effects of antacids, gastric juice from 15 volunteers with known Helicobacter pylori status were analysed for eosinophil cationic protein (ECP), phospholipase A2 (PLA2) activity, phosphatidylcholine (PC), and bile acids (BA) before and after administration of one tablet of antacid or placebo in a double blind cross-over design. Geometric mean ECP concentrations were more than 13 times higher in gastric juice from H. pylori-positive (12.9 micrograms/l) than from H. pylori-negative (0.97 micrograms/l) subjects (p = 0.0032). Geometric mean PLA2 activity was 1.31 U/l for the negative subjects and 4.02 U/l for the positive subjects (p = 0.13). There were no differences between positive and negative subjects with regard to either PC or BA concentration. Regardless of H. pylori status, mean PC concentration increased significantly after antacids as compared with placebo (p = 0.024). The effect of antacids did not differ significantly from placebo for ECP, PLA2 activity, or BA concentration. Hence, antacids may not act by binding 'toxic' H. pylori-associated gastric juice components like ECP or PLA2. Increased concentration of PC may indicate an increased protective capacity induced by antacids.