Miederer S E
Fortschr Med. 1989 Mar 30;107(10):63-4, 67-8.
By the mechanism of the inhibition of the endogenous prostaglandin synthesis by NSAIDs, and thus the attenuation of the protective factors in the gastrointestinal mucosa, gastric lesions frequently develop, and the healing of existing peptic ulcers is appreciably slowed. The combination of several risk factors increases the probability of peptic ulcers or ulcer complications developing under NSAID treatment. In such at-risk patients, treatment with NSAIDs should be accompanied by prophylactic measures. The use of various anti-ulcer drugs has shown that for the treatment of NSAID-induced gastropathies the prostaglandin analog, misoprostol is equally as good as the other anti-ulcer drugs, for the prevention of NSAID-induced lesions however it is superior to H2-receptor antagonists (cimetidine, ranitidine), antacids and sucralfate.
通过非甾体抗炎药抑制内源性前列腺素合成的机制，进而削弱胃肠道黏膜中的保护因子，胃部病变经常发生，并且现有的消化性溃疡愈合明显减慢。多种风险因素共同作用会增加在非甾体抗炎药治疗下发生消化性溃疡或溃疡并发症的可能性。在这类高危患者中，使用非甾体抗炎药治疗时应采取预防措施。使用各种抗溃疡药物的结果表明，对于治疗非甾体抗炎药引起的胃病，前列腺素类似物米索前列醇与其他抗溃疡药物效果相当，但在预防非甾体抗炎药引起的病变方面，它优于H2受体拮抗剂（西咪替丁、雷尼替丁）、抗酸剂和硫糖铝。
