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Eradication of Helicobacter pylori (HP) has been widely performed, but subsequent upper gastrointestinal lesions associated with HP eradication have been reported. In this study, we investigated the frequency of upper intestinal lesions that developed after successful HP eradication and the course for five years after eradication. Subjects and methods: The subjects were 122 patients with HPpositive gastric ulcer or duodenal ulcer for whom successful eradication therapy with a proton pump inhibitor and antibiotics was performed. Patients did not receive medication after ulcer was healed, and the upper digestive tract was examined by endoscopy 3, 6, and 12 months after eradication and yearly for five years to investigate the development of lesions in the upper digestive tract. Results Duodenal erosion developed in the third month after eradication in 8.6% of the patients. Most of these patients had no subjective symptom and erosion resolved without treatment. Antral stomach erosion was observed in 12% in the third month after eradication. Antral stomach erosion was observed in 8.1% and 4.8% in the second and third year, but not in the fourth and fifth year. Most of these cases were not accompanied by symptoms. The frequency of gastroesophagial reflux disease was only 2.2% one year after eradication, but the frequency remained 2-4% even 2-5 years after eradication. Many cases were accompanied by symptoms. Despite successful eradication, stomach or duodenal ulcer recurred in 10 patients (8.2%) during the period from three months to five years after eradication. Two of 10 patients used NSAID, but the other 8 patients did not. Conclusion Long-term careful observation of ulcer patients is necessary to prevent recurrence of ulceration and development of duodenal erosion, antral gastritis, and gastroesophagial reflux disease, although HP eradication was successful. [ABSTRACT FROM AUTHOR]

The pathogenesis of cap polyposis remains unknown. Here, we report a patient with cap polyposis that developed simultaneously in the colon and stomach, and which regressed after Helicobacter pylori eradication. A 63-year-old man was diagnosed as having cap polyposis with mucoid stool, diarrhea, and bleeding on defecation. Following 5 weeks of total parenteral nutrition, his symptoms and hypoproteinemia improved and he was discharged, although follow-up colonoscopic findings revealed no improvement. Subsequent gastroscopy revealed diffusely erosive polyps with cap-like "fur" from the angle to the antrum of the stomach, similar to the lesions observed in the colon. Because H. pylori infection was demonstrated in the stomach, eradication therapy was administered. After this treatment, his symptoms immediately disappeared, and the polypoid lesions in the colon and stomach had completely disappeared 8 months later. Because there have been no previous reports of a relationship between H. pylori and cap polyposis, this case is of great interest.

Glucocorticoid is an important drug for ulcerative colitis. In this paper, the action mechanism of glucocorticoid, particularly that at molecular level in the cell, was mentioned. Mechanism in anti-inflammatory action, influence on cytokine production, immunosuppressive action and glucocorticoid resistance were reviewed.

Recently, there has been a resurgence in the interest of the role of the appendix in ulcerative colitis. The lesion of appendix in ulcerative colitis is reviewed. Surgical studies were mainly reported in western countries and endoscopic studies were mainly reported in Japan. Epidemiological and experimental studies suggest a central role of the appendix in development of ulcerative colitis. It was considered that understanding of the significance of a skip lesion in the appendix would contribute to the elucidation of the pathogenesis of ulcerative colitis.