消化性溃疡疾病的发病机理和治疗。
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彼得森王
消化性溃疡疾病的发病机理和治疗。
中国新药杂志。1990;12增刊2:S1-6。
- PubMed ID
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1978840 (在PubMed]
- 文摘
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胃和十二指肠的上皮细胞通常受酸和胃蛋白酶的破坏性影响粘膜抵抗的平衡机制。如果出现不平衡,可能会导致消化性溃疡。传统教学强调的重要性,酸和胃蛋白酶失衡的原因;然而,很明显,酸和胃蛋白酶并不是唯一重要的因素在消化性溃疡的发病机制。最近的调查工作已经针对什么是粘膜抵抗和它如何能产生中断,在胃酸的存在,消化性溃疡。损耗的内源性前列腺素和幽门螺杆菌胃炎已成为著名的理论。作为证据来支持和反驳这些理论存在于人类,不能在这个时候任何明确的结论。急性消化性溃疡疾病的管理是针对缓解疼痛,加速溃疡愈合,预防并发症。消化性溃疡与antisecretory代理(即可以愈合。H2-receptor拮抗剂,奥美拉唑)、抗酸药、前列腺素和硫糖铝。 Because they are effective, safe, and convenient, the H2-receptor antagonists are the most widely used agents for the management of peptic ulcer disease. Because the H2-receptor antagonist agents are equally effective in their indicated uses and are equally safe based on scientifically valid data, selection should be based primarily on cost. Omeprazole is the newest antisecretory agent: a single morning dose of 20 mg suppresses acid secretion for 24 h. The agent offers little advantage over H2-receptor antagonists for the majority of patients with peptic ulcer.(ABSTRACT TRUNCATED AT 250 WORDS)