Ohara Tadashi, Kanoh Yuhsaku, Higuchi Kazuhide, Arakawa Tetsuo, Morisita Testsuo
Department of Internal Medicine, Chiba Hospital, Tokyo Dental College, Ichikawa General Hospital, Chiba, Japan.
Hepatogastroenterology. 2003 May-Jun;50(51):607-9.
BACKGROUND/AIMS: A possibility that the eradication therapy not only eliminates Helicobacter pylori (H. pylori) but also influences some factors regulating pathological changes in the gastric mucosa should be taken into consideration from some phenomena. Such as non-recurrent cases of peptic ulcer long-term in spite of unsuccessful anti-H. pylori eradication therapy and the effectiveness of eradication therapy for mucosa-associated lymphoid tissue with a low-grade malignancy except stomach. We hypothesized and investigated that antibiotic treatment for elimination of H. pylori might directly affect inflammatory cells to induce apoptosis in them and protect against pathological changes of gastric mucosa.
Subjects consisted of twenty-one patients with chronic gastritis. All were H. pylori positive and we investigated the effects of eradication therapy of H. pylori on inflammation-related immunocytes in the gastric mucosa of patients with chronic gastritis caused by H. pylori isolated mononuclear leukocytes which were taken from the patients and were examined for apoptosis-related morphological changes and DNA fragmentation before and after the therapy. Eradication therapy of H. pylori was performed by lansoprazole 30 mg/day, amoxicillin 1500 mg/day and clarithromycin 400 mg/day for one week.
After the H. pylori eradication therapy, regardless of its effect on H. pylori status, marked vacuolation and degeneration were observed in mononuclear leukocytes in the gastric mucosa with a concomitant enhancement of nuclear DNA fragmentation.
This observation suggests that H. pylori eradication therapy itself induces apoptosis in mononuclear leukocytes in the gastric mucosa.
背景/目的:从某些现象来看,应考虑根除治疗不仅能消除幽门螺杆菌(H. pylori),还可能影响一些调节胃黏膜病理变化的因素。例如,尽管抗H. pylori根除治疗未成功,但消化性溃疡长期不复发的病例,以及根除治疗对胃外低级别恶性黏膜相关淋巴组织的有效性。我们假设并研究了消除H. pylori的抗生素治疗可能直接影响炎症细胞,诱导其凋亡,并预防胃黏膜的病理变化。
研究对象为21例慢性胃炎患者。所有患者H. pylori均呈阳性,我们研究了根除H. pylori治疗对由H. pylori引起的慢性胃炎患者胃黏膜中炎症相关免疫细胞的影响。从患者体内采集分离的单核白细胞,在治疗前后检查其凋亡相关的形态变化和DNA片段化情况。H. pylori根除治疗采用兰索拉唑30毫克/天、阿莫西林1500毫克/天和克拉霉素400毫克/天,持续一周。
H. pylori根除治疗后,无论其对H. pylori状态的影响如何,胃黏膜中的单核白细胞均出现明显的空泡化和变性,同时核DNA片段化增强。
这一观察结果表明,H. pylori根除治疗本身可诱导胃黏膜中单核白细胞凋亡。