Rachmilewitz D, Ligumsky M, Fich A, Goldin E, Eliakim A, Karmeli F
Gastroenterology. 1986 Apr;90(4):963-9. doi: 10.1016/0016-5085(86)90874-7.
Synthesis of prostaglandin E2 and 6-keto prostaglandin F1 alpha by cultured antral and fundic gastric mucosa obtained from 86 patients with active duodenal ulcer who were not receiving medication was 50% lower (p less than 0.01) than their respective synthesis by cultured gastric mucosa in normal subjects. Antral and fundic prostanoid synthesis in patients receiving chronic therapy with nonsteroidal antiinflammatory drugs was almost completely inhibited. The decreased synthesis of antral and fundic prostaglandin E2 and 6-keto prostaglandin F1 alpha in duodenal ulcer patients was not affected following ulcer healing achieved after 4 wk of therapy with placebo, arbacet, misoprostol, sucralfate, and pirenzepine. In contrast, following 4 wk of therapy with ranitidine, both antral and fundic prostaglandin E2 synthesis were significantly increased when compared with their respective synthesis before therapy. These results confirm that gastric prostanoid synthesis is decreased in patients with active duodenal ulcer and in subjects treated with nonsteroidal antiinflammatory drugs, suggesting that decreased endogenous prostanoid synthesis may contribute to the pathogenesis of mucosal damage. The induction of endogenous prostanoids by ranitidine may contribute to its therapeutic effect.
从86例未接受药物治疗的活动性十二指肠溃疡患者获取的胃窦和胃底黏膜培养物中，前列腺素E2和6-酮-前列腺素F1α的合成量比正常受试者胃黏膜培养物中的各自合成量低50%（p<0.01）。接受非甾体抗炎药长期治疗的患者，其胃窦和胃底前列腺素合成几乎完全受到抑制。十二指肠溃疡患者胃窦和胃底前列腺素E2及6-酮-前列腺素F1α合成减少，在接受安慰剂、阿巴卡韦、米索前列醇、硫糖铝和哌仑西平治疗4周后溃疡愈合，这一情况未受影响。相比之下，雷尼替丁治疗4周后，与治疗前各自的合成量相比，胃窦和胃底前列腺素E2的合成均显著增加。这些结果证实，活动性十二指肠溃疡患者和接受非甾体抗炎药治疗的受试者胃前列腺素合成减少，提示内源性前列腺素合成减少可能促成黏膜损伤的发病机制。雷尼替丁诱导内源性前列腺素的生成可能有助于其治疗效果。
