101 research outputs found

    The role of Kyoto classification in the diagnosis of Helicobacter pylori infection and histologic gastritis among young subjects in Japan

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     BACKGROUND AND AIM: Helicobacter pylori (H. pylori) infection induces inflammation of the gastric mucosa and leads to erosions, gastro-duodenal mucosa atrophy, and intestinal metaplasia. The Kyoto classification diagnoses H. pylori infection via endoscopic findings. We aimed to clarify the role of the Kyoto classification in diagnosing H. pylori infection and histologic gastritis in young Japanese individuals. METHODS: From1031 consecutive subjects aged ≤29 years who underwent esophagogastroduodenal endoscopy at our two hospitals from 2010 to 2017, 220 were selected for participation in the present study. Endoscopic biopsy specimens from the antrum and corpus were used to investigate H. pylori infection and histology. Endoscopic and histological interpretations were based on the Kyoto classification and updated Sydney System. H. pylori infection was confirmed by histology and Giemsa or Gimenez staining. RESULTS: Endoscopic findings were normal in 103 cases. Atrophy was found in 56 cases; diffuse redness, in 45 cases; nodularity, in 38 cases; and mucosal swelling, in 34 cases. The infection rate was 30.9% (68/220). In total, 67 subjects with H. pylori -positive endoscopic findings and confirmed as H. pylori -positive had histologic gastritis of the antrum and corpus. In contrast, of 153 subjects with H. pylori -negative endoscopic findings only 1 was subsequently confirmed to be H. pylori positive. Among the 67 subjects with H. pylori -positive endoscopic findings, 23 (34.3%) presented with histological atrophic gastritis of the corpus and 6 (9.0%) with intestinal metaplasia. CONCLUSIONS: Our findings show that H. pylori infection is strongly associated with endoscopic and histologic gastritis in young subjects and both H. pylori infection and histologic gastritis can be evaluated endoscopically based on the Kyoto classification. Furthermore, prompt H. pylori eradication may prevent gastric cancer development given the high prevalence of atrophic gastritis and intestinal metaplasia in young Japanese individuals

    Effect of Cetraxate, a Mucosal Protective Agent, on Gastric Mucosal Blood Flow and Gastric Clarithromycin Concentration in Nicotine-treated Rats

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    Our previous study demonstrated that combination treatment with cetraxate plus omeprazole, amoxicillin, and clarithromycin is effective for the eradication of Helicobacter pylon in smokers. To evaluate the effect of cetraxate on gastric mucosal blood flow (GMBF) and the gastric concentration of clarithromycin in nicotine-treated rats, 10 rats were divided into two groups given nicotine with or without cetraxate, and GMBF was measured by laser Doppler blood flowmetry. Another 36 rats were divided into three groups (control, nicotine, and nicotine + cetraxate). Clarithromycin was administered intraduodenally and nicotine was administered after 30 minutes, with cetraxate being given 30 minutes later. The gastric mucosal clarithromycin concentration was measured. After cetraxate administration, GMBF increased significantly in the nicotine + cetraxate group compared with the nicotine group (p<0.05). The mucosal clarithromycin concentration increased in the nicotine + cetraxate group compared with the nicotine group, but the difference was not significant. Our results indicate that cetraxate increased GMBF in nicotine-treated rats

    Clinicopathological features of advanced gastric cancer discovered after Helicobacter pylori eradication

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     Helicobacter pylori infection is closely associated with gastric cancer, and its eradication is expected to prevent gastric cancer. However, gastric cancer is often detected discovered after eradication therapy for H. pylori infection. We aimed to investigate the endoscopic and clinical features of advanced gastric cancer after H. pylori eradication. We retrospectively investigated tumor location, macroscopic and histological type, endoscopic gastric mucosal atrophy (using the Kimura-Takemoto classification), and the interval between eradication and detection of gastric cancer. Nine patients (five males; mean age, 65.3 years [range, 44-79 years]), histologically diagnosed with advanced gastric cancer after successful H. pylori eradication between April 2003 and December 2018, were enrolled in this study. In all cases, the cancer was located in the middle-to-upper portion of the stomach. With respect to macroscopic type, six cases were ulcerative, two were scirrhous, and one was polypoid. Histologically, all cancers were poorly or moderately differentiated adenocarcinomas. Endoscopic mucosal atrophy was mild in two cases, moderate in two cases, and severe in five cases. Two cases of scirrhous tumors developed from mild mucosal atrophy. Moreover, the tumor was detected within 36 months after H. pylori eradication in six patients (maximum: 120 months, mean: 38.7 months). Our data demonstrated that post-eradicated advanced gastric cancers were located in the middle-to-upper portion of the stomach and were mainly ulcerative, poorly or moderately differentiated adenocarcinoma. More than half of the patients exhibited severe mucosal atrophy

    A case of synchronous triple cancer of the esophagus, stomach, and colon detected by using gastrointestinal screening endoscopy

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     In recent years, the detected number of multiple primary malignant tumors (MPMTs) in the gastrointestinal tract has been increasing with the advancement of gastrointestinal endoscopic equipment and the spread of endoscopic screening. Here, we report a case of synchronous MPMTs of the esophagus, stomach, and colon detected by means of gastrointestinal screening endoscopy. The patient was a 67-year-old man who regularly visited the medical clinic for hypertension. He had a history of alcohol consumption (sake index: 250, with alcohol flushing syndrome) and smoking (Brinkman index: 800), and a family history of cancer (his father had gastric cancer). At the medical clinic, he underwent gastrointestinal endoscopy for screening purposes. Prior observation with linked-color imaging (LCI), a type of image-enhanced endoscopy (IEE), revealed an irregular depressed lesion in the mid-esophagus. Simultaneously, an irregular, highly deformed depressed lesion and a small depressed lesion were detected on the incisura of the lesser curvature and the lesser curvature of the antrum, respectively. The esophageal lesion was identified as squamous cell carcinoma and both gastric lesions were identified as well-differentiated adenocarcinoma. The patient was referred to our hospital for further examination and treatment for esophageal and gastric cancer. Subsequent colonoscopy revealed a well-defined, ulcerative tumor in the transverse colon. First, endoscopic submucosal dissection was performed for the esophageal lesion, followed by laparoscopy-assisted distal gastrectomy with D1+ lymph-node dissection and transverse colectomy with D2 lymph-node dissection for the gastric and colorectal lesions, respectively. Histopathologically, the main gastric and colonic tumors were in advanced stages; fortunately, the esophageal cancer was an early-stage lesion (7 × 5 mm, 0-IIc, pT1a-LPM, INFa, ly0, v0, pCurA), which has a much better prognosis than advanced esophageal cancer. In patients with multiple cancer risk factors (alcohol consumption, smoking, and family history), it is important to consider the possibility of MPMTs. Furthermore, upper gastrointestinal observation combined with IEE, such as LCI, may be useful in the early detection of lesions

    当院で経験したA 型胃炎の4例

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    A 型胃炎は稀な疾患で,悪性貧血や胃癌,胃NET の発生母地として知られている.抗胃壁細胞抗体陽性,高ガストリン血症,さらに胃体部を中心とした萎縮性胃炎が診断基準とされている.今回,過去1年に4例のA 型胃炎を診断した.全例で自覚症状は見られなかったが,内視鏡検査での逆萎縮所見からA 型胃炎を疑い,胃生検の病理所見と血液検査で確診した.A 型胃炎が他の自己免疫性疾患に合併することが多いとされているが,本症例にも高齢発症のBasedow 病が1例あり,A 型胃炎は日本でも決してまれな疾患ではないと考えられた.診断には内視鏡所見からA 型胃炎を疑うことが重要で,胃生検や血清ガストリンと抗胃壁細胞抗体の測定を行うことにより確診できる.Type A gastritis is a rare disease and is known as a cause of various conditions including pernicious anaemia, gastric cancer and gastric NETs (Neuroendocrine tumour). The diagnostic criteria of type A gastritis include positive parietal cell antibody, hypergastrinaemia and the presence of atrophic gastritis mainly corpus predominantly atrophic gastritis. We diagnosed four cases of type A gastritis in the past year in our hospital. Although they were all asymptomatic, type A gastritis was suspected by the endoscopic findings (the reverse atrophy) and all confirmed by pathological examination of biopsy specimens and blood test subsequently. It is well known that the patients with autoimmune disease are frequently associated with type A gastritis and there is a case of late onset of Basedow’s disease in our case report. Our study suggests that type A gastritis is not as rare as initially thought in Japan. In order to diagnose type A gastritis, it is important to have a high index of suspicion with endoscopic findings, and to confirm it with gastric biopsy, serum gastrin level and parietal cell antibody
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