Abstract
A 59-year-old woman visited our hospital with bomplaints of gastric discomfort for along time. The first endoscopy revealed atrophic gastritis, with Helicobacter pylori (Hp) infection. Two months after the completion of Hp eradication therapy with lansoplazoleand clarithromycin, Hp eradication was comfirmed by the method of histology andcultures. A complaint disappeared soon afterward, however, she complained of heartburn8months after the last endoscopic examination. The third endoscopy revealed grade Areflux esophagitis'with an area of linear erythema less than 5 mm long. She was given 30mg of lansoplazole again, and after that, a medical treatment was continued with a halfdosage of H2-receptor antagonist. The fourth endoscopy was done about one year later.Despite of disappearance of a mucosal break, a scar remained on the distal esophagealmucosa. Histological finding of the specimens taken from the middle body on the greatercurvature dernonstrated a decrease of inflammatory cell infiltration. It was uncertainwhether an atrophic change of gastric mcosa improved after therapy. However, there wassignificant rise from a pretreatment value of 1.5 to a posttreatment value of 9.9in serumpepsinogen (PG) I/PGII ratio, which was reported to correlate well with the grade ofgastric mucosal atrophy. Because there was a fall in serum gastrin concentration aftertherapy in addition to a fall of serurn PGI and PGII, it was suspected that lower esophagussphincter pressures decreased after Hp eradication. In conclusion, we should be careful ofreflux esophagitis in'patients whose Hp had been eradicated.
