服用非甾体抗炎药患者胃黏膜白三烯B4合成增强。
Enhanced gastric mucosal leukotriene B4 synthesis in patients taking non-steroidal anti-inflammatory drugs.
作者信息
Hudson N, Balsitis M, Everitt S, Hawkey C J
机构信息
Department of Medicine, University Hospital, Nottingham.
出版信息
Gut. 1993 Jun;34(6):742-7. doi: 10.1136/gut.34.6.742.
The effects of longstanding non-steroidal anti-inflammatory drug (NSAID) treatment on gastric mucosal synthesis of leukotriene B4 (LTB4), leukotriene C4 (LTC4), and prostaglandin E2 (PGE2) was studied. Gastric antral biopsies in 65 patients with arthritis taking NSAIDs and 23 control patients were taken and eicosanoid concentrations, stimulated by vortex mixing or calcium ionophore, were measured by radioimmunoassay. Median gastric mucosal synthesis of LTB4 was increased in patients taking NSAIDs compared with non-users: (0.9(0.2-2.5) pg/mg v 0 (0-0.6) pg/mg (p < 0.001)). These differences persisted when subgroups of patients were analysed according to Helicobacter pylori colonisation or degree of mucosal injury. Synthesis of LTB4 was strongly associated with the presence of type C (chemical) gastritis. Increased synthesis of LTC4 was associated with Helicobacter pylori colonisation but not NSAID use. Synthesis of PGE2 was decreased in patients taking NSAIDs compared with control patients (p < 0.001). Enhanced gastric mucosal synthesis of LTB4 in patients taking NSAIDs may represent a primary effect of these drugs and could be implicated in the pathogenesis of gastritis and ulceration associated with NSAIDs.
研究了长期使用非甾体抗炎药（NSAID）治疗对胃黏膜白三烯B4（LTB4）、白三烯C4（LTC4）和前列腺素E2（PGE2）合成的影响。对65例服用NSAIDs的关节炎患者和23例对照患者进行胃窦活检，并通过放射免疫分析法测量经涡旋混合或钙离子载体刺激后的类花生酸浓度。与未服用NSAIDs的患者相比，服用NSAIDs的患者胃黏膜LTB4的中位合成量增加：（0.9（0.2 - 2.5）pg/mg对0（0 - 0.6）pg/mg（p < 0.001））。根据幽门螺杆菌定植情况或黏膜损伤程度对患者亚组进行分析时，这些差异仍然存在。LTB4的合成与C型（化学性）胃炎的存在密切相关。LTC4合成增加与幽门螺杆菌定植有关，但与NSAID使用无关。与对照患者相比，服用NSAIDs的患者PGE2的合成减少（p < 0.001）。服用NSAIDs的患者胃黏膜LTB4合成增强可能代表了这些药物的主要作用，并且可能与NSAIDs相关的胃炎和溃疡的发病机制有关。
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