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胃酸减少导致的细菌过度生长。

Bacterial overgrowth as a consequence of reduced gastric acidity.

作者信息

Stockbruegger R W

出版信息

Scand J Gastroenterol Suppl. 1985;111:7-16. doi: 10.3109/00365528509093749.

Abstract

Reduction in acid secretion in atrophic gastritis allows bacterial colonization of the stomach, most extremely in achlorhydric patients with pernicious anaemia, in whom overgrowth may cause nitrate reduction and formation of potentially carcinogenic N-nitroso compounds. Subsequent bacterial contamination of the upper small intestine can induce mucosal damage and malabsorption. The situation is similar after gastrectomy. In achlorhydria and after gastrectomy, the risk of gastric cancer is increased. There is controversy as to the risks of long-term treatment with H2-receptor antagonists. Increase in nitrate-reducing bacteria, nitrite and N-nitrosamine have been observed in patients by some investigators but not in volunteers and patients by others. Bacterial concentrations after cimetidine are inversely related to pretreatment acid secretory capacity. Demonstration of increased mutagenicity of gastric juice after H2-receptor antagonists gives grounds for caution. Drastic acid reduction may in future be reserved for short-term and intermittent treatment and mild or moderate reduction for long-term treatment of peptic ulcer and ulcer prevention.

摘要

萎缩性胃炎中胃酸分泌减少会使胃部细菌定植,在患有恶性贫血的无胃酸患者中最为严重,细菌过度生长可能导致硝酸盐还原并形成潜在致癌的N-亚硝基化合物。随后上小肠的细菌污染可引起黏膜损伤和吸收不良。胃切除术后情况类似。在无胃酸状态和胃切除术后,胃癌风险会增加。关于H2受体拮抗剂长期治疗的风险存在争议。一些研究者在患者中观察到了硝酸盐还原菌、亚硝酸盐和N-亚硝胺的增加,但其他研究者在志愿者和患者中未观察到。西咪替丁治疗后细菌浓度与治疗前胃酸分泌能力呈负相关。H2受体拮抗剂治疗后胃液诱变活性增加的证据令人谨慎。未来,剧烈的胃酸减少可能仅用于短期和间歇性治疗,而轻度或中度胃酸减少用于消化性溃疡的长期治疗和溃疡预防。

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