Hideharu Tsuji

Helicobacter pylori-negative gastric and duodenal ulcers.

Abstract: It is unclear whether Helicobacter pylori infection is essential to the development of peptic ulcers. In this study, we examined the rates of H. pylori-negativity among patients with peptic ulcers. We also attempted to clarify the characteristics of H. pylori-negative peptic ulcers to throw light on the pathogenesis of peptic ulcers. The study included 215 consecutive patients with gastric ulcers (GUs) and 120 consecutive patients with duodenal ulcers (DUs). After routine endoscopic examination and phenol red dye endoscopy, forceps biopsies were performed for culture, histology, and the rapid urease test. A patient was considered H. pylori-negative when the serum anti-H. pylori IgG and the three tests on biopsied specimens were all negative. H. pylori-negative rates were 3.2% in the patients with GUs and 1.7% in the patients with DUs. Lack of atrophy of the gastric mucosa was significantly more common in the H. pylori-negative patients with GUs. A history of ulcer disease was less common and antral ulcers were more common in H. pylori-negative GU patients, but not significantly so. As the urea breath test had not been performed, the possibility of a false-negative result cannot be completely ruled out, but we believe that the H. pylori-negative rate in our study is more reliable than these rates in previous reports, because we visualized H. pylori distribution by phenol red dye endoscopy to avoid false-negative results in biopsies, and we used both biopsy and serum anti-H. pylori IgG findings to establish an H. pylori-negative diagnosis. Since H. pylori-negative peptic ulcers certainly exist, H. pylori infection is thought not to be essential to the development of peptic ulcers. There were few differences between the characteristics of H. pylori-negative and H. pylori-positive peptic ulcers in our study. A large-scale study is required to clarify the characteristics of H. pylori-negative peptic ulcers.

Healing Process of Experimental Esophageal Ulcers Induced by Acetic Acid in Rats

We studied the healing of acetic acid-induced esophageal ulcers in rats with respect to the cellular kinetics. Esophageal ulcers were induced by topical application of acetic acid to the serosal surface. Well-demarcated circular or elliptical ulcers had developed by day 3 after the acid treatment. These ulcers began to decrease in size from day 7 and had healed by day 14. Histological and cellular kinetic findings, with bromodeoxyuridine (BrdU), were degeneration of the esophageal mucosa on day 1 and ulcer formation on day 3, with an increase in the number of BrdU-labeled cells in the esophageal mucosa around the ulcer. On day 7, regenerated epithelium was found to extend towards the ulcer base and the regenerated epithelium had become thicker, with papilla formation, by day 10. On day 14, the ulcer base was covered with thickened regenerated mucosa, with a decrease in the number of BrdU-labeled cells. Marked proliferative activity of the regenerated mucosa and thickening of the esophageal mucosa, with papilla formation, were observed during the healing process.