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Thalidomide in the management of epidermolysis bullosa pruriginosa

Authors

  • S. Ozanic Bulic,

    1. Department of Dermatology, Great Ormond Street Hospital for Children, Great Ormond Street, London WC1N 3JH, U.K.
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  • H. Fassihi,

    1. Genetic Skin Disease Group, St John's Institute of Dermatology, The Guy's, King's College and St Thomas' Hospital Medical School, London, U.K.
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  • J.E. Mellerio,

    1. Department of Dermatology, Great Ormond Street Hospital for Children, Great Ormond Street, London WC1N 3JH, U.K.
    2. Genetic Skin Disease Group, St John's Institute of Dermatology, The Guy's, King's College and St Thomas' Hospital Medical School, London, U.K.
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  • J.A. McGrath,

    1. Genetic Skin Disease Group, St John's Institute of Dermatology, The Guy's, King's College and St Thomas' Hospital Medical School, London, U.K.
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  • D.J. Atherton

    1. Department of Dermatology, Great Ormond Street Hospital for Children, Great Ormond Street, London WC1N 3JH, U.K.
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  • Conflicts of interest: None declared.

D.J. Atherton.
E-mail: ATHERD@gosh.nhs.uk

Summary

Epidermolysis bullosa (EB) pruriginosa is a distinctive clinical subtype of dystrophic EB. We report a patient with dominant dystrophic EB pruriginosa, who had an excellent response to systemic thalidomide treatment. The mechanism of action of thalidomide in the management of pruriginous disorders is not yet completely understood. Most recent studies point towards an immunomodulatory action of thalidomide that may suppress excessive production of tumour necrosis factor-α and may downregulate certain cell surface adhesion molecules involved in leucocyte migration.

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