EFFICACY OF TAURINE IN THE TREATMENT OF GASTRIC-MUCOSAL LESIONS ASSOCIATED WITH HELICOBACTER-PYLORI

Objective: We have reported that monochloramine, a neutrophil-derived oxidant, was responsible for the experimental injury to gastric mucosa l cells induced by Helicobacter pylori, and that taurine, a scavenger of the oxidant, reduced the injury. The objective of the present study was to endoscopically, histologically and microbiologically examine t he effect of taurine on the human gastric mucosal lesions associated w ith H. pylori. Design and methods: We studied nine patients with H. py lori-associated intractable gastric ulcers who had shown no endoscopic improvement for at least 4 weeks (a control period) before the admini stration of taurine and 12 patients with gastritis alone. In the patie nts with gastric ulceration, taurine (6.0 g) was administered orally t hree times after meals for 4 weeks with the same H2-receptor antagonis t that had been taken by these patients before the trial began. Among the patients with gastritis only, 3.0 g cetraxate hydrochloride was gi ven orally to six patients with taurine and six patients without tauri ne. Endoscopies and biopsies of the stomach and cultures of biopsy spe cimens for H. pylori were performed before and after the administratio n of taurine or cetraxate hydrochloride in each patient. The number of neutrophils in biopsied mucosa stained with periodic acid-Schiff reag ent was counted. Results: After taurine treatment, mucosal reddening a round the gastric ulcers subsided significantly (56%) compared with sa mples taken before the treatment (0%; P < 0.05), although the diameter of the ulcers did not change. Reddening (100%) and edematous changes (100%) caused by the gastritis subsided or disappeared (33%, 50%, resp ectively) after taurine treatment (P < 0.05 versus before treatment fo r both). Neutrophils in the mucosa decreased significantly (P < 0.05) after taurine treatment in the patients with gastric ulceration (20.6 +/- 2.3 to 9.8 +/- 2.0 cells/high power field) and in the patients wit h gastritis (14.2 +/- 6.4 to 6.0 +/- 2.0 cells/high power field). H. p ylori was not observed in 22% of the gastric ulcer patients after taur ine treatment, but no significant differences in the prevalence of H. pylori were seen between gastritis patients treated with taurine (50% H. pylori-negative) and without taurine (17% H. pylori-negative). Conc lusions: Taurine treatment suppresses the inflammatory changes in gast ric mucosal lesions, possibly through inhibition of neutrophil accumul ation and scavenging of monochloramine produced by activated neutrophi ls.