Danion J M, Schmidt M, Welsch M, Imbs J L, Singer L
Clinique Psychiatrique, CHRU, Hôpital Civil, Strasbourg.
Encephale. 1987 Jul-Aug;13(4):255-60.
Since the first observation in 1978, it has been clearly established that the non-steroidal anti-inflammatory drugs (NSAIDs) interfere with the pharmacokinetics of lithium: by reducing urinary clearance of the metal, they can raise the plasma lithium level and thus lead to intoxication. Among the NSAIDs available in France, this interaction has been reported with phenylbutazone (Butazolidine, Carudol), diclofenac (Voltarène), indomethacin (Indocid) and its antalgic derivative clomethacin (Dupéran), ketoprofen (Profenid), mefenamic acid (Ponstyl), niflumic acid (Nifluril) and piroxicam (Feldène). This interaction does not occur with aspirin; this exception suggests that the inhibition of prostaglandins synthesis is not the mechanism responsible for the decrease in the urinary elimination of lithium linked with an increase in its tubular reabsorption. In practice, in view of the growing diffusion of NSAIDs, it is necessary to inform all patients under lithium treatment of the risk of interaction resulting from their use.
自1978年首次观察到以来，已明确证实非甾体抗炎药（NSAIDs）会干扰锂的药代动力学：通过降低金属的尿清除率，它们可提高血浆锂水平，从而导致中毒。在法国可用的非甾体抗炎药中，已报道与保泰松（布他唑立丁、卡鲁多）、双氯芬酸（扶他林）、吲哚美辛（消炎痛）及其止痛衍生物氯甲灭酸（杜佩兰）、酮洛芬（优洛芬）、甲芬那酸（扑湿痛）、氟尼酸（氟尼辛）和吡罗昔康（ Feldene）存在这种相互作用。阿司匹林不会发生这种相互作用；这一例外情况表明，前列腺素合成的抑制不是导致锂的尿排泄减少并伴有其肾小管重吸收增加的机制。在实际应用中，鉴于非甾体抗炎药的使用日益广泛，有必要告知所有接受锂治疗的患者使用此类药物可能产生相互作用的风险。
