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Expression of adhesion molecules in atopic dermatitis is reduced by tacrolimus, but not by hydrocortisone butyrate: a randomized immunohistochemical study
Author(s) -
Caproni M.,
Torchia D.,
Antiga E.,
Volpi W.,
Fabbri P.
Publication year - 2006
Publication title -
clinical and experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.587
H-Index - 78
eISSN - 1365-2230
pISSN - 0307-6938
DOI - 10.1111/j.1365-2230.2006.02214.x
Subject(s) - tacrolimus , atopic dermatitis , cell adhesion molecule , medicine , proinflammatory cytokine , intercellular adhesion molecule 1 , chemokine , alkaline phosphatase , immunology , pharmacology , gastroenterology , pathology , inflammation , chemistry , biochemistry , transplantation , enzyme
Summary 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.