Literature DB >> 20889234

A phase II placebo-controlled study of photodynamic therapy with topical hypericin and visible light irradiation in the treatment of cutaneous T-cell lymphoma and psoriasis.

Alain H Rook1, Gary S Wood, Madeleine Duvic, Eric C Vonderheid, Alfonso Tobia, Bernard Cabana.   

Abstract

BACKGROUND: Hypericin is a known photodynamic agent that has been demonstrated to induce apoptosis in normal and malignant B and T lymphocytes, and has potential to treat benign and malignant disorders of the skin, including psoriasis and cutaneous T-cell lymphoma.
OBJECTIVE: We wished to test whether topical hypericin was an effective, safe, and well-tolerated therapy for patch or plaque phase mycosis fungoides and for plaque psoriasis.
METHODS: We conducted a phase II placebo-controlled clinical study in patients who had either patch or plaque phase mycosis fungoides or plaque type psoriasis vulgaris. Representative lesions were treated twice weekly for 6 weeks with topically applied hypericin or placebo followed 24 hours later by exposure to visible light at 8 to 20 J/cm(2).
RESULTS: After 6 weeks of twice-weekly therapy, several concentrations of hypericin resulted in the significant improvement of treated skin lesions among the majority of patients with cutaneous T-cell lymphoma and psoriasis whereas the placebo vehicle was ineffective. LIMITATIONS: The clinical trial involved a small number of patients.
CONCLUSIONS: Overall, the data from this study support the conclusion that topical hypericin/visible light photodynamic therapy is an effective and well-tolerated alternative to standard psoralen plus ultraviolet A treatment of these disorders.
Copyright © 2010 American Academy of Dermatology, Inc. Published by Mosby, Inc. All rights reserved.

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Year:  2010        PMID: 20889234     DOI: 10.1016/j.jaad.2010.02.039

Source DB:  PubMed          Journal:  J Am Acad Dermatol        ISSN: 0190-9622            Impact factor:   11.527


  16 in total

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10.  Hypericin-mediated photodynamic therapy induces apoptosis in K562 human leukemia cells through JNK pathway modulation.

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