Goodwin J S
Am J Med. 1984 Jul 13;77(1A):57-64. doi: 10.1016/s0002-9343(84)80020-0.
Recent data from several laboratories, which suggest that generally accepted concepts relating to the mechanism of action of nonsteroidal, anti-inflammatory drugs (NSAIDs) in rheumatoid arthritis may be incorrect, are reviewed. Over the past decade, most researchers have espoused the idea that NSAIDs act by inhibiting cyclooxygenase, thereby removing prostaglandins, which are thought to be responsible for pain and inflammation. Recent studies demonstrating that prostaglandins have important immunomodulating properties and that NSAIDs actually provide partial correction of several immunoregulatory dysfunctions in patients with rheumatoid arthritis are described. In addition, some NSAIDs inhibit migration along with other monocyte and polymorphonuclear leukocyte functions. Data suggest that these actions are not related to inhibition of cyclooxygenase.
来自多个实验室的近期数据表明,与非甾体抗炎药(NSAIDs)在类风湿性关节炎中的作用机制相关的普遍接受的概念可能是错误的,本文对此进行了综述。在过去十年中,大多数研究人员支持这样的观点,即NSAIDs通过抑制环氧化酶起作用,从而去除被认为是疼痛和炎症原因的前列腺素。本文描述了近期的研究,这些研究表明前列腺素具有重要的免疫调节特性,并且NSAIDs实际上可部分纠正类风湿性关节炎患者的几种免疫调节功能障碍。此外,一些NSAIDs会抑制迁移以及其他单核细胞和多形核白细胞的功能。数据表明,这些作用与环氧化酶的抑制无关。