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Journal of the American Academy of Dermatology
Volume 46, n° 2
pages 228-241 (février 2002)
Doi : 10.1067/mjd.2002.120942
Tacrolimus and pimecrolimus: From clever prokaryotes to inhibiting calcineurin and treating atopic dermatitis

Paul Nghiem, MD, PhDa, Greg Pearson, MDb, Richard G. Langley, MDc
Boston, Massachusetts, Columbia, Missouri, and Halifax, Nova Scotia, Canada 
From the Cutaneous Oncology Unit, Dana-Farber Cancer Institute, Harvard Medical School, Bostona; Division of Dermatology, University of Missouri, Columbiab; and the Division of Dermatology, Department of Medicine, Dalhousie University, Halifax.c 


Tacrolimus ointment, a topical inhibitor of the phosphatase calcineurin, has recently been approved in the United States for use in the treatment of atopic dermatitis. It is the first topical immune suppressant that is not one of the hydrocortisone derivatives, important allies in dermatology for nearly 50 years. Although tacrolimus is less able to penetrate thick skin than glucocorticoids, it does not cause dermal atrophy, an important advantage over the hydrocortisone class. Pimecrolimus (ASM 981), a newer calcineurin inhibitor closely related to tacrolimus, is also being developed for atopic dermatitis therapy. Pimecrolimus has an altered skin penetration profile but the same mechanism of action as tacrolimus. In this review we chronicle the discovery of the calcineurin inhibitors, their presumed evolutionary role as a bacterial “smart bomb” against fungi, molecular and cellular mechanisms of action in the immune system, systemic and topical side effects, efficacy in atopic dermatitis, and future applications within the specialty of dermatology. Particular attention is given to the issues of systemic absorption of tacrolimus, the conditions in which absorption can become a concern, efficacy relative to glucocorticoids, and the choice of 0.03% or 0.1% tacrolimus ointment for use in adults and children. (J Am Acad Dermatol 2002;46:228-41.)

The full text of this article is available in PDF format.

 Funding: P. N. was supported by an American Academy of Dermatology Young Investigators Award.
 Disclosure: P. N. and G. P., none. R. G. L., Massachusetts General Hospital, Harvard University, and Dalhousie University received grant support from Fujisawa Corporation and Novartis Pharmaceuticals to conduct research studies.
 Reprint requests: Paul Nghiem, MD, PhD, Dana-Farber Cancer Institute, 44 Binney St, Boston, MA 02115. E-mail:

© 2002  American Academy of Dermatology, Inc. Published by Elsevier Masson SAS@@#104157@@
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