Mielants H, Goemaere S, De Vos M, Schelstraete K, Goethals K, Maertens M, Ackerman C, Veys E M
Department of Rheumatology, Gastroenterology and Nuclear Medicine, University Hospital, Ghent, Belgium.
J Rheumatol. 1991 Mar;18(3):389-93.
Using the 51Cr-EDTA resorption test, gut permeability was measured in 129 patients with inflammatory joint diseases and in 97 control patients (42 patients with no inflammatory rheumatic disorders taking antiinflammatory medication and 55 healthy controls). Thirty-two patients (30 arthritis and 2 control patients) taking nonsteroidal antiinflammatory drugs (NSAID) as well as corticosteroids were excluded from statistical analysis. The intake of NSAID significantly increased gut permeability in controls but not in the arthritis groups. The same applied to corticosteroid intake. This could be due to the restricted number of arthritis patients who had never taken antiinflammatory drugs or to a disease related increased permeability. There was no statistically significant difference in altered gut permeability between patients taking NSAID and patients taking corticosteroids. Our findings suggest that drug induced alteration of gut permeability may not only be accounted for by an inhibition of mucosal cyclooxygenase activity, but that other enzymatic pathways in the arachidonic cascade might be implicated.
采用51Cr-乙二胺四乙酸吸收试验,对129例炎性关节病患者和97例对照患者(42例无炎性风湿性疾病但服用抗炎药物的患者及55例健康对照者)的肠道通透性进行了测量。32例同时服用非甾体抗炎药(NSAID)和皮质类固醇的患者(30例关节炎患者和2例对照患者)被排除在统计分析之外。NSAID的摄入显著增加了对照组的肠道通透性,但在关节炎组中未增加。皮质类固醇的摄入情况亦是如此。这可能是由于从未服用过抗炎药物的关节炎患者数量有限,或者是由于疾病相关的通透性增加。服用NSAID的患者与服用皮质类固醇的患者在肠道通透性改变方面无统计学显著差异。我们的研究结果表明,药物诱导的肠道通透性改变可能不仅是由于黏膜环氧化酶活性受到抑制,花生四烯酸级联反应中的其他酶促途径可能也与之有关。