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The improvement of treatment efficacy of gastropathy associated with the use of nonsteroidal anti-inflammatory drugs in Helicobacter pylori-negative patients with osteoarthritis

机译:幽门螺杆菌阴性骨关节炎患者使用非甾体类抗炎药治疗胃病的疗效改善

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Among the more common side effects of osteoarthritis treatment are NSAID-gastropathy and NSAID-enteropathy. NSAIDs can cause direct injury to colon tissue and also impair synthesis of prostaglandins, reduce mucosal integrity, increase permeability and promote an influx of bacteria and toxins. Alterations in gastrointestinal permeability are considered as an initial step in the development of lesions of the gastric mucosa such as erosions and ulcers. The mechanisms underlying the ability of NSAIDs to cause ulceration in the stomach and proximal duodenum are well understood and this injury can be largely be prevented through suppression of gastric acid secretion. However, our work showed that 28-day administration of the anti-secretory preparation pantoprazole (20 mg 2 times per day) resulted in a statistically significant increase of dysbiosis. Monitoring of patients with osteoarthritis who used NSAIDs for more than three months showed that, in comparison to the situation before the beginning of treatment, changes in colonic microbiota were present. Multiprobiotic “Symbiter~(?) acidophilic concentrated” introduced simultaneously with pantoprazole during 20 days prevented formation of dysbiotic changes and led to the quicker healing of gastric mucous healing, in comparison with patients who used only pantoprazole alone. Moreover, it brought about total healing of the gastric mucosa within 4 weeks from the beginning of treatment.
机译:骨关节炎治疗中最常见的副作用是NSAID胃病和NSAID肠病。非甾体抗炎药可对结肠组织造成直接伤害,还会损害前列腺素的合成,降低粘膜完整性,增加通透性并促进细菌和毒素的流入。胃肠道通透性的改变被认为是胃粘膜病变如糜烂和溃疡发展的第一步。众所周知,NSAID引起胃和十二指肠近端溃疡的能力的机制是可以通过抑制胃酸分泌而大幅度预防的。然而,我们的工作表明抗分泌制剂pan托拉唑(每天20 mg,每天2次)的28天给药导致统计上的营养不良增加。对使用NSAIDs超过三个月的骨关节炎患者进行的监测显示,与开始治疗前的情况相比,结肠菌群有变化。与仅使用pan托拉唑的患者相比,与pan托拉唑同时使用的多益生菌“ Symbiter〜(?)嗜酸浓缩液”在20天之内可防止形成不良生物,并能更快地治愈胃粘膜。而且,从治疗开始起4周之内,胃粘膜完全愈合。

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