Ryu Nishiyama

Endoscope Images of Schönlein-Henoch Purpura

Background/Aims: Schönlein-Henoch purpura (SHP) is a systemic condition characterized by purpura associated with leukocytoclastic vasculitis. SHP diagnosis is more difficult in infrequent cases where gastrointestinal (GI) symptoms precede purpura. This report examines 11 cases of SHP at our hospital with specific regard to the incidences and details of GI symptoms. Methods: The clinical manifestations and endoscopic findings were investigated for their utility in SHP diagnosis. Results: Among the 11 cases, 3 showed GI symptoms prior to other manifestations. In terms of GI symptoms, abdominal pain was reported in all 11 cases, diarrhea in 4 cases, and bloody stools in 3 cases. Endoscopic findings were seen in the stomach in 7/10 cases, in the small intestine including the duodenum in 10/11 cases, and in the large intestine in 6/10 cases. The frequency of ulcer formation was significantly higher in the small intestine (including the duodenum) than in the stomach. Multiple specific erythematosus lesions were observed in the stomach and large intestine. Conclusion: Familiarity with characteristic endoscopic findings and careful observation of all GI findings are essential for diagnosing SHP in cases in which GI tract symptoms precede cutaneous findings.

The expression of IGF-1R in Helicobacter pylori-infected intestinal metaplasia and gastric cancer.

Overexpression of IGF-1R has been demonstrated in gastrointestinal cancers, and its expression is reported as the result of the loss of tumor suppressors. IL-16 is involved in the pathophysiological process of chronic inflammatory diseases. The aim of this study is to determine the changes in the expression of IGF-1R in intestinal metaplasia (IM) and gastric cancer (GC) as well as the effect of Helicobacter pylori (H. pylori) and IL-16 on cell proliferation and IGF-1R expression in gastric cells. AGS cells were incubated with combinations of IL-16 and H. pylori. Gastric cell proliferation was studied by BrdU uptake. In H. pylori infected mucosa, IGF-1R was significantly higher in IM than chronic gastritis (CG), and also higher in GC than CG and IM. H. pylori significantly decreased BrdU uptake. IL-16 increased BrdU uptake and IGF-1R on AGS cells which had been decreased by H. pylori. Co-incubation with IL-16 increased the expression of IGF-1R mRNA in H. pylori infected cells. We conclude that the expression of IGF-1R in H. pylori infected gastric mucosa may indicate an early stage of carcinogenesis. The IL-16 secretion by H. pylori can be a trigger for the expression of IGF-1R, and it may also be a factor for gastric carcinogenesis.

Diagnostic Value of Open Biopsy for Malignant T-Cell Lymphoma of the Liver

A 62-year-old man was referred to our hospital because of pain in the right upper quadrant. Laboratory tests revealed normal levels of tumor markers. Abdominal ultrasonography showed a hypoechoic mass of approximately 9 cm in diameter in the right lobe of the liver. Computed tomography revealed a low-density mass with peripheral enhancement in the posterior segment of the right lobe. Magnetic resonance imaging showed a low-intensity mass on T(1)-weighted images and a high-intensity mass on T(2)-weighted images. Abdominal angiography showed enhanced staining only at the periphery of the tumor. An open biopsy was performed and intraoperative examination of frozen sections indicated malignant lymphoma. The histopathologic diagnosis was malignant T-cell lymphoma. After combined chemotherapy, the tumor shrank to 4 cm in diameter. To our knowledge, only 15 cases of malignant T-cell lymphoma have been reported previously. Diagnosis is particularly challenging because this type of tumor has no distinctive imaging characteristics or signs or symptoms. This case emphasizes the need to include malignant T-cell lymphoma in the differential diagnosis and demonstrates the importance of open biopsy in patients with a suspected liver tumor.

Green tea polyphenols reduce gastric epithelial cell proliferation and apoptosis stimulated by Helicobacter pylori infection

Helicobacter pylori (H. pylori) infection in the human stomach is associated with increased epithelial proliferation, and the increased proliferation is one of the risk factors for developing gastric carcinoma. Recently, cells undergoing apoptosis were found to be increased in human gastric mucosa in persons carrying H. pylori. Green tea polyphenols (polyphenols) have been reported to show a variety of biological activities against various foodborne pathological bacteria. Therefore, we studied the effect of polyphenols on gastric epithelial proliferation and apoptosis in H. pylori infected mice. Methods: We challenged Balb/C mice with I08cfu/mouse of the H. pylori (NCTC 11637) strain for 18 weeks. After this challenge, mice were treated with 0.5% polyphenols dairy in drinking water for 2 weeks, and given 5 mg/kg bromodeoxyuridine (BrdU) by introperitoneal injection, I hour before sacrify. Gastric epithelial cell proliferation was evaluated by immunohistochemical anti-BrdU labeling. Apoptosis was examined by using the Tunel method on tissue sections. Results: The number of BrdUlabeled cells in was significantly increased on the H. pylori challenged mice compared with control. The increased proliferation was reduced by polyphenols administration. The number of apoptosis cells also was increased in H. pylori challenged mice. The increased apoptosis was reduced by polyphenols administration. Conclusions: Green tea polyphenols reduced the gastric epithelial cell proliferation and apoptosis caused by H. pylori infection. Administration of green tea polyphenols may reduce gastric carcinogenesis induced by H. pylori infection. 2803