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他克莫司可降低特应性皮炎中黏附分子的表达,但丁酸氢化可的松则无此作用:一项随机免疫组织化学研究。

Expression of adhesion molecules in atopic dermatitis is reduced by tacrolimus, but not by hydrocortisone butyrate: a randomized immunohistochemical study.

作者信息

Caproni M, Torchia D, Antiga E, Volpi W, Fabbri P

机构信息

Department of Dermatological Sciences, University of Florence, Florence, Italy.

出版信息

Clin Exp Dermatol. 2006 Nov;31(6):813-7. doi: 10.1111/j.1365-2230.2006.02214.x.

DOI:10.1111/j.1365-2230.2006.02214.x
PMID:17040264
Abstract

Topical tacrolimus represents an effective and well-tolerated treatment for atopic dermatitis (AD). Its known effects include reduced production of proinflammatory cytokines and reduced chemokine gradient. We performed lesional skin biopsies on adult patients affected by moderate-to-severe AD. Then, patients were randomized to receive local treatment with tacrolimus ointment 0.1% and hydrocortisone butyrate ointment 1%. On the 21st day of treatment, another skin specimen was taken. Nine patients treated with tacrolimus and seven treated with hydrocortisone successfully concluded the trial. By immunohistochemistry (alkaline phosphatase/antialkaline phosphatase method), we demonstrated that endothelial leucocyte adhesion molecule (ELAM)-1, vascular cell adhesion molecule (VCAM)-1 and intercellular adhesion molecule (ICAM)-1 showed different intensities and patterns of expression in untreated AD lesions. Tacrolimus-treated specimens featured a significant reduction of the expression of ELAM-1, VCAM-1 and ICAM-1, while hydrocortisone-treated lesions did not. Inhibition of adhesion molecule expression may represent another selective mechanism of action of topical tacrolimus in AD.

摘要

外用他克莫司是治疗特应性皮炎(AD)的一种有效且耐受性良好的方法。其已知作用包括减少促炎细胞因子的产生和降低趋化因子梯度。我们对患有中度至重度AD的成年患者进行了皮损活检。然后,将患者随机分组,分别接受0.1%他克莫司软膏和1%丁酸氢化可的松软膏的局部治疗。在治疗的第21天,采集另一皮肤样本。9例接受他克莫司治疗的患者和7例接受氢化可的松治疗的患者成功完成试验。通过免疫组织化学(碱性磷酸酶/抗碱性磷酸酶法),我们证明内皮白细胞黏附分子(ELAM)-1、血管细胞黏附分子(VCAM)-1和细胞间黏附分子(ICAM)-1在未经治疗的AD皮损中表现出不同强度和表达模式。他克莫司治疗的样本中ELAM-1、VCAM-1和ICAM-1的表达显著降低,而氢化可的松治疗的皮损则没有。黏附分子表达的抑制可能代表外用他克莫司在AD中的另一种选择性作用机制。

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