Invasive techniques for diagnosis of Helicobacter pylori (H. pylori) infection require an endoscopic examination which is expensive and inconvenient and may cause complications. Stool cultures for H. pylori or a direct detection of H. pylori antigen in stools by PCR are expensive, tedious, and have a low sensitivity. We recently used an enzyme immunoassay (EIA) to detect H. pylori antigen in stool specimens. A total of 41 patients were seen at Inha University Hospital, Inchon, Korea between September and October 1998. There were 26 men and 15 women who had an average age of 37.6 years which ranged from 5 to 71 years in the present study. All of these patients came to the hospital complaining of an upper abdominal discomfort and were subjected to endoscopy and biopsies. Fifteen had a gastric ulcer, 13 had a duodenal ulcer, 1 had an early gastric cancer, and there were 12 chronic gastritis patients as shown by endoscopy. The biopsy specimens were examined by histology, CLO test, and cultures and these results were used as gold standards. Stool specimens were tested for the H. pylori antigen by EIA. A dual wavelength cut-off of 0.100 that was recommended by the manufacturer gave a good performance (87.1% sensitivity, 100% specificity, 100% positive predictive value, 71.4% negative predictive value, and a 90.2% efficiency). But the adjusted cut-off value using the receiver operating characteristic curve improved the performance of the test (using the cut-off value of 0.024, the sensitivity, specificity, PPV, NPV, and efficiency were 100%, 90.0%, 96.9%, 100%, and 97.6% respectively). Re-evaluation of the cut-off value may be needed for Korean patients. This technique is non-invasive, rapid, easy-to-use, and shows good performance characteristics for diagnosis of H. pylori infections. Therefore, this technique may be a substitute for gastric endoscopy especially in children and some patients who are unable to tolerate an endoscopic examination and it may be substituted for a serologic test in epidemiological research.

Eosinophilic colitis is a relatively rare complication of hypereosinophilic syndrome which is characterized by abdominal pain and bloody diarrhea and is usually treated with steroids and hydroxyurea. However, no standard regimen exists in cases of intractable disease despite several treatment attempts with Interferon-alpha, cyclosporin, etoposide, and vincristine, etc. We here report a case of a 43-year-old woman with recurrent eosinophilic colitis as a complication of hypereosinophilic syndrome who was successfully treated with cyclophosphamide.

Background and Aims ras Gene and its product (p21) have been reported to be associated with vascular endothelial growth factor (VEGF), which is one of the most important angiogenic factors, and tumor‐associated angiogenesis. We tried to evaluate the correlation between the expression of c‐H‐ras gene product p21 and angiogenesis in advanced gastric carcinoma. Methods Immunohistochemical expression of c‐H‐ras p21 and VEGF was examined in 49 advanced gastric adenocarcinomas. In addition, double immunohistochemical staining was performed using anti‐CD34 and anti‐Ki‐67 antibodies, and the intratumoral microvessel densities and their endothelial proliferative labeling indices were then counted to evaluate the degree of angiogenesis. Results The expression of c‐H‐ras p21 was demonstrated in 43 out of 49 gastric adenocarcinomas (87.8%). It did not correlate with histologic type, depth of invasion or metastasis. However, the degree of c‐H‐ras p21 expression was correlated with VEGF. In addition, the degree of c‐H‐ras p21 expression was correlated with increased intratumoral microvascular density and endothelial proliferative activity. Conclusions We suggest that c‐H‐ras oncogene product p21 contributes to the upregulation of tumor‐associated angiogenesis by the increased production of VEGF in advanced gastric carcinomas. Therefore, treatment involving the targeting of ras oncogene could inhibit solid tumor growth by suppressing tumor‐associated angiogenesis.

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Most GIST have traditionally been classified as submucosal origin by upper gastrointestinal series (UGIS) or endoscopy. However, we experienced a gastrointestinal mesenchymal origin tumor expressed by polypoid mass with a long stalk. The gastric outlet was obstructed by the polypoid mass on the duodenum. The microscopic findings of the resected mass showed a stromal cell component by immunohistochemical stain. We experienced gastric stromal tumor found as a polypoid mass with long stalk which was easily detected by endoscopy. It would not have been suspected as a stromal tumor as a result of endoscopic findings only.