Volume 113, Issue 1 pp. 107-115
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Mechanism of anthralin inflammation I. Dissociation of response to clobetasol and indomethacin

C.M. LAWRENCE

Corresponding Author

C.M. LAWRENCE

University Department of Dermatology, Royal Victoria Infirmary, Newcastle upon Tyne, U.K.

Dr C.M.Lawrence, Dermatology Dept., North Staffordshire Hospital Centre, Hartshill Road, Stoke on Trent, Staff, U.K.Search for more papers by this author
S. SHUSTER

S. SHUSTER

University Department of Dermatology, Royal Victoria Infirmary, Newcastle upon Tyne, U.K.

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First published: July 1985
Citations: 27

SUMMARY

The effect of topical clobetasol propionate and a 1% topical indomethacin gel which could inhibit UV erythema was measured on anthralin inflammation by change in skin-fold thickness and erythema. The time course of the inflammatory oedema and erythema were different, as was their response to the drugs studies. The oedema of anthralin inflammation was completely inhibited by clobetasol propionate but the erythemal response showed a small and non-significant reduction. Indomethacin had no effect on anthralin oedema but produced a small but significant reduction in erythema in the first 24 h after anthralin application. These results suggest that either anthralin inflammation is not due to production of prostenoids, or that if it is, it occurs by other than the classical enzymic pathway.

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