Difference in the distribution pattern of Helicobacter pylori and grade of gastritis in the antrum and in the body between duodenal ulcer and benign gastric ulcer patients

OBJECTIVES: To investigate the relationship between the Helicobacter pylori (H. pylori) colonization and the grade of gastritis in the antrum and in the body of patients with duodenal ulcer (DU) or benign gastric ulcer (BGU). METHODS: This study was performed in H. pylori-positive 220 DU patients and 180 BGU patients. H. pylori density was evaluated by modified Giemsa staining and CLO test, and gastritis grade was graded by H+ACY-E staining in the antrum and in the body. RESULTS: H. pylori grade by Giemsa staining was 1.24 in the antrum and 0.82 in the body for DU group (p +ADw- 0.01), and those of BGU group were slightly reversed, 0.83 and 0.87, respectively, but without statistical significance. Similarly H. pylori grade by CLO test was 3.1 in the antrum and 2.8 in the body for DU group (p +ADw- 0.01), and those of BGU group 2.3 and 2.6 (p +ADw- 0.05), respectively. In contrast, gastritis grade was 1.7 in the antrum and 1.2 in the body for DU group (p +ADw- 0.01), and those of BGU group 1.6 and 1.3 (p +ADw- 0.01), respectively, similar to those of DU. However, there was a correlation between H. pylori grade and gastritis grade in the antrum and in the body, not only in DU but also in BGU group (p +ADw- 0.01). CONCLUSION: In spite of different distribution patterns of H. pylori between DU group and BGU group, gastritis grade of the antrum was significantly higher than that of the body in both DU and BGU. However, gastritis is correlated with H. pylori density not only in DU but also in BGU patients. It looks like the inflammatory reaction to H. pylori is stronger in the antrum than in the body.

A Case of Gastric Mucormycosis Associated with Diabetes Mellitus and Uremia / 대한소화기내시경학회지

Mucormycosis is an infection caused by fungi of the class Zygomycetes, order Mucorales. These are usual ubiquitous saprophytes but occasionally cause opportunistic infection in immunocompromised patients. Typically, these fungi invade blood vessels, and produce thrombosis and tissue infarction, so causing host fatality. These infections can be categorized into rhinocerebral, pulmonary, widely disseminated, gastrointestinal, cutaneous and miscellaneous form. Most of mucormycosis cases reported in Korea were rhinocerebral form except for three cases, which were gastrointestinal mucormycosis, accompanied with hematologic malignancy or immunosuppressing treatment. We experienced a 58-year-old male with gastric mucormycosis, who had diabetes and mild uremia without hematologic malignancy and immunosuppressive treatments. His chief complaints were abdominal pain and melena, and gastroscopy showed a 3 3 cm irregular edged ulcer considering malignancy. Its histological findings showed large, thin-walled, non-septate and right-angled branching fungal hyphae in necrotic tissue, diagnosed as mucormycosis. Finally he was dead due to severe hematemesis.

Effect of eradication of Helicobacter pylori on the benign gastric ulcer recurrence - a 24 month follow-up study

OBJECTIVES: To evaluate the effect of eradication of Helicobacter pylori (H. pylori) on the recurrence of benign gastric ulcer (BGU) in the patients with BGU. METHODS: This study was performed for 40 H. pylori-positive BGU patients cured of BGU and H. pylori eradicated, and for 25 H. pylori-positive patients (non-eradicated group) who were not treated with H. pylori eradication regimen or H. pylori was not eradicated. Four different methods--CLOtest, microscopy of Gram stained mucosal smear, culture and histology of modified Giemsa staining--were taken for identifying colonization of H. pylori before treatment, and 4 weeks after completion of triple therapy. For the control group in which triple therapy was not tried, follow-up gastroscopy was done to confirm the healing of the ulcer. To detect BGU recurrence, the gastroscopy was performed at 6, 12, 18, and 24 months after therapy. RESULTS: In the non-eradicated group, the BGU recurrence rate was 16% within 6 months, 40% within 1 year, 56% within 18 months and 60% within 2 years. The respective recurrence rates in the 40 patients in whom the bacteria had been eradicated were 0%, 7.5%, 10% and 10% (4 patients), respectively. Among the four BGU-recurred patients in whom H. pylori had been eradicated, one patient was found to have BGU recurring with H. pylori positive again in one year, and another two patients had NSAIDs ingestion history. CONCLUSION: The eradication of H. pylori in patients with BGU reduces the recurrence of BGU. In addition, the major causes of BGU recurrence look like NSAIDs ingestion and reinfection of H. pylori.