Johansson C
Scand J Gastroenterol Suppl. 1987;128:24-32. doi: 10.3109/00365528709090966.
Nonsteroidal antiinflammatory drugs (NSAID) and steroids are ulcerogenic to the gastroduodenal mucosa in man although the exact incidence of drug-induced lesions is unknown. It is assumed that NSAID are ulcerogenic because they block the biosynthesis of prostaglandins, thereby reducing the mucosal resistance to acid peptic digestion. NSAID inhibit recognized mucosal defense factors, such as bicarbonate transport and mucus glycoprotein production and release; they reduce the thickness of the pH-mucus barrier, interfere with cytoprotection and have antitrophic actions. Prostaglandins reverse the inhibition of defense factors by NSAID and prevent their ulcerogenic actions; they stimulate secretion of bicarbonate and glycoproteins and have trophic and cytoprotective properties. Challenge of the mucosa stimulates defense factors and prostaglandin formation in parallell; pretreatment with NSAID impairs the defensive response and reduces local prostaglandin formation. Mucosal lesions, produced by NSAID may be prevented by agents that neutralize or inhibit gastric acid, such as H2-receptor blockers, antacids and acid antisecretory prostaglandins. Compounds, which stimulate--or simulate--mucosal defense factors are also effective such as sucralfate, colloidal bismuth and prostaglandins devoid of acid antisecretory properties. Of these, several may work by increasing local prostaglandin concentration.
非甾体抗炎药（NSAID）和类固醇对人类胃十二指肠黏膜具有致溃疡作用，尽管药物诱发损伤的确切发生率尚不清楚。据推测，NSAID具有致溃疡作用是因为它们阻断了前列腺素的生物合成，从而降低了黏膜对酸消化的抵抗力。NSAID抑制公认的黏膜防御因子，如碳酸氢盐转运以及黏液糖蛋白的产生和释放；它们会降低pH-黏液屏障的厚度，干扰细胞保护作用并具有抗营养作用。前列腺素可逆转NSAID对防御因子的抑制作用并防止其致溃疡作用；它们刺激碳酸氢盐和糖蛋白的分泌，并具有营养和细胞保护特性。对黏膜的刺激会同时刺激防御因子和前列腺素的形成；用NSAID预处理会损害防御反应并减少局部前列腺素的形成。NSAID产生的黏膜损伤可通过中和或抑制胃酸的药物来预防，如H2受体阻滞剂、抗酸剂和抑制胃酸分泌的前列腺素。刺激或模拟黏膜防御因子的化合物也有效，如硫糖铝、胶体铋和不具有抑制胃酸分泌特性的前列腺素。其中一些可能通过增加局部前列腺素浓度起作用。
