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肥大细胞中除组胺外的介质可诱导特应性皮炎患者瘙痒:一项皮肤微透析研究

Mast cell mediators other than histamine induce pruritus in atopic dermatitis patients: a dermal microdialysis study.

作者信息

Rukwied R, Lischetzki G, McGlone F, Heyer G, Schmelz M

机构信息

Department of Physiology and Experimental Pathophysiology, University of Erlangen/Nürnberg, Universitätsstr. 17, D-91054 Erlangen, Germany.

出版信息

Br J Dermatol. 2000 Jun;142(6):1114-20. doi: 10.1046/j.1365-2133.2000.03535.x.

DOI:10.1046/j.1365-2133.2000.03535.x
PMID:10848733
Abstract

While histamine is the crucial mediator of pruritus in type 1 allergic reactions, its role in atopic dermatitis (AD) is unclear. In this study, the role of mast cell mediators in protein extravasation and pruritus was evaluated using intradermal microdialysis. The microdialysis capillaries were used to apply the mast cell degranulating substance compound 48/80 (C48/80; 0.05%) or histamine (0.01%) and also to deliver H1-blockers (cetirizine, 200 microg mL-1) in nine AD patients and nine controls. Large pore size membranes (3000 kDa) enabled simultaneous analysis of protein extravasation. Itch sensation was measured psychophysically and weal and flare reaction were evaluated planimetrically. Protein extravasation induced by histamine and C48/80 was significantly reduced in AD patients. Blockade of H1-receptors by cetirizine significantly reduced C48/80-induced protein extravasation in AD patients and controls to an identical level. C48/80-induced pruritus was abolished by cetirizine in controls, whereas pruritus in AD patients was unchanged after H1 blockade. We conclude that mast cell mediators others than histamine are involved in C48/80-induced pruritus in AD patients. Whether the reduced capacity of AD patients to induce protein extravasation is of pathophysiological relevance for pruritus remains to be established.

摘要

虽然组胺是1型过敏反应中瘙痒的关键介质,但其在特应性皮炎(AD)中的作用尚不清楚。在本研究中,使用皮内微透析评估肥大细胞介质在蛋白质外渗和瘙痒中的作用。微透析毛细管用于向9名AD患者和9名对照施加肥大细胞脱颗粒物质化合物48/80(C48/80;0.05%)或组胺(0.01%),并给予H1受体阻滞剂(西替利嗪,200μg mL-1)。大孔径膜(3000 kDa)能够同时分析蛋白质外渗情况。通过心理物理学方法测量瘙痒感觉,并通过平面测量法评估风团和潮红反应。组胺和C48/80诱导的蛋白质外渗在AD患者中显著降低。西替利嗪对H1受体的阻断显著降低了AD患者和对照中C48/80诱导的蛋白质外渗至相同水平。在对照中,西替利嗪消除了C48/80诱导的瘙痒,而在AD患者中,H1受体阻断后瘙痒无变化。我们得出结论,除组胺外,肥大细胞介质参与了AD患者中C48/80诱导的瘙痒。AD患者诱导蛋白质外渗能力降低是否与瘙痒的病理生理学相关仍有待确定。

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