Junji Yoshino

Omeprazole, a proton pump inhibitor is known to function not only as a proton pump inhibitor but also as an anti-inflammatory agent, an antioxidant or a stimulator of gastric mucus secretion. We have shown that the pathogenesis of acute gastric mucosal lesions induced by compound 48/80, a mast cell degranulator, in rats involves neutrophil infiltration, lipid peroxidation, and mucin depletion, but not acid secretion, in the gastric mucosal tissue. Therefore, we examined whether omeprazole protects against acute gastric mucosal lesions induced by compound 48/80 in rats. Rats were injected with omeprazole (10 or 50 mg kg(-1), i.p.) at 0.5 h before injection of compound 48/80 (0.75 mg kg(-1), i.p.). Omeprazole prevented gastric mucosal lesion development at 0.5 and 3 h after compound 48/80 injection. Omeprazole attenuated decreased nonprotein sulfhydryl content and increased myeloperoxidase and xanthine oxidase (XO) activities and lipid peroxide (LPO) content in the gastric mucosa at 0.5 h after compound 48/80 injection and increased myeloperoxidase and XO activities and LPO content, but not decreased hexosamine and adherent mucus contents, in the gastric mucosa at 3 h. These results indicate that omeprazole protects against compound 48/80-induced acute gastric mucosal lesions in rats possibly through its anti-inflammatory and antioxidant actions. (C) 2002 Elsevier Science Ltd. All rights reserved.

Omeprazole, a proton pump inhibitor is known to function not only as a proton pump inhibitor but also as an anti-inflammatory agent, an antioxidant or a stimulator of gastric mucus secretion. We have shown that the pathogenesis of acute gastric mucosal lesions induced by compound 48/80, a mast cell degranulator, in rats involves neutrophil infiltration, lipid peroxidation, and mucin depletion, but not acid secretion, in the gastric mucosal tissue. Therefore, we examined whether omeprazole protects against acute gastric mucosal lesions induced by compound 48/80 in rats. Rats were injected with omeprazole (10 or 50 mg kg(-1), i.p.) at 0.5 h before injection of compound 48/80 (0.75 mg kg(-1), i.p.). Omeprazole prevented gastric mucosal lesion development at 0.5 and 3 h after compound 48/80 injection. Omeprazole attenuated decreased nonprotein sulfhydryl content and increased myeloperoxidase and xanthine oxidase (XO) activities and lipid peroxide (LPO) content in the gastric mucosa at 0.5 h after compound 48/80 injection and increased myeloperoxidase and XO activities and LPO content, but not decreased hexosamine and adherent mucus contents, in the gastric mucosa at 3 h. These results indicate that omeprazole protects against compound 48/80-induced acute gastric mucosal lesions in rats possibly through its anti-inflammatory and antioxidant actions. (C) 2002 Elsevier Science Ltd. All rights reserved.

Background: The normal gastric wall has been reported to appear to be a five-layered structure. The structure of the gastric wall using a 30MHz endoscopic ultrasound probe and especially the identification of the muscularis mucosae (MM), has not been analyzed clearly. Methods: In a basic study, 11 sections of normal gastric wall with 26 horizontally inserted nylon sutures were immersed in water. The sections were scanned and the findings correlated using standard histology. In a clinical study, 15 early gastric cancers were examined by a 30 MHz endoscopic ultrasound probe. Results: In a basic study, layers deeper than the lower part of the submucosa could not be seen using ultrasonography. The first to fourth layers represented the mucosal layer except the MM, the fifth layer (high-echo layer) represented the boundary echo and a part of the MM, while the sixth layer (low-echo layer) represented the rest of the MM. The muscularis mucosae was seen clearly in all samples. In a clinical study the layers deeper than the submucosal layer could not be seen and the MM was visible in 87% of cases. The depth of invasion was estimated accurately in 90% of mucosal cancers and in 80% of submucosal cancers. Conclusion: A 30MHz endoscopic ultrasound probe, which cannot image the entire gastric wall, can visualize the MM and may help to confirm the structure of gastric wall layers and improve the ability to determine the depth of invasion in gastric cancer.

Background: This prospective study was designed to clarify the present status and problems inherent in endoscopic treatment of early gastric cancer by endoscopic mucosal resection and other modalities in Japan and to investigate the possibility of extending the indications for endoscopic treatment. Methods: A total of 409 patients with early gastric cancer lesions were enrolled in this study. Of these, 219 lesions (182 in group I and 37 in group II) were evaluated. Results: Histological evaluation in group I showed that complete resection, relatively incomplete resection, and absolutely incomplete resection were carried out for 103 (56.6%), 20 (11.0%), and 59 (32.4%) lesions, respectively. Surgery was performed for two lesions of the absolutely incomplete resection group. The remaining 180 lesions were followed up with endoscopy after endoscopic treatment. Recurrence occurred in 14 of 57 lesions with absolutely incomplete resection receiving additional endoscopic treatment, while no recurrence was noted in the lesions of the complete resection or relatively incomplete resection group. At present, 175 lesions of group I have been followed up with endoscopy. Histological evaluation of 30 lesions with differentiated carcinoma in group II revealed that complete resection was successful in only six (20%) lesions. Thirty lesions, including 24 receiving additional endoscopic treatment for absolutely incomplete resection, were followed up endoscopically. None of the lesions showed recurrence. Conclusion: An interim report of this study is presented herein. Both groups have been followed up over the past 5 years, and in the final report of this study the authors aim to discuss the effectiveness of various kinds of therapeutic modalities and extend the indication of endoscopic treatment for early gastric cancer.