Resolution of gastritis induced by Helicobacter pylori 4-5 weeks after successful eradication of infection using a triple therapy regimen of pantoprazole, amoxycillin and clarithromycin for one week

This open-label study was designed to determine the extent of histological resolution of gastritis induced by Helicobacter pylori infection 4-5 weeks after successful eradication of the infection. Eradication was achieved usi ng a triple therapy regimen consisting of a twice daily dose of pantoprazol e 40 mg, clarithromycin 500 mg, and amoxicillin 1,000 mg taken for 1 week o nly. No other medications were given thereafter. Four biopsies were process ed for histological examination of each patient, two from the antral and tw o from the corporeal mucosa, fi rst at the sta rt of the study and then aga in 4 weeks after cessation of the medication trial. Scoring for H. pylori c olonization and the severity of gastritis was determined for each patient a ccording to the Sydney system. 53 of 57 patients in this study had their H. pylori infection successfully eradicated by the regimen mentioned and coul d be histologically evaluated. According to the severity of gastritis in th e antral mucosa, patients were studied in 3 groups: mild, moderate and seve re gastritis. 17 of 19 cases with mild gastritis showed complete resolution of the inflammation, with residual inflammatory changes persisting in 2 ca ses only. 22 of the 26 cases with moderate gastritis showed almost complete recovery except for minor residual inflammatory changes as judged by irreg ularity of intracytoplasmic mucine storage. Persistent residual inflammator y changes in the lamina propria were detected in 4 cases. Of the 8 cases wi th severe gastritis 5 showed subsidence of the inflammatory changes, but th e mucosa in these cases revealed some scarring, distortion of the glandular epithelium and atrophy. In 3 cases residual inflammation persisted. Conclu sion: One-week therapy with a twice daily dose of pantoprazole 40 mg, clari thromycin 500 mg and amoxicillin 1,000 mg, used to eradicate H. pylori caus ing active inflammation of the gastric mucosa, has led to subsidence of the acute inflammatory changes in all the cases with residual inflammation per sisting in 17%. Severe gastritis may cause irreparable damage to the gastri c mucosa. The density of H. pylori colonization does not appear to be relat ed to the severity of gastritis, nor to the successful eradication achieved .