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Official Journal of the Italian Society of Dermatology and Sexually Transmitted Diseases
Indexed/Abstracted in: EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,014
Online ISSN 1827-1820
Capezzera R., Zane C., Calzavara-Pinton P. G. and GIFDE*
Department of Dermatology II University of Brescia, Brescia, Italy
Non ionizing radiations with wavelengths ranging from 340 to 400 nm (UVA1 waveband) have peculiar photophysical, photobiological and phototherapeutical effects. UVA1 penetrates deeply into the skin and modulates the biological and immunological activity of both dermal and epidermal circulating as well as resident cells. Unlike UVB (260-320 nm) and UVA2 (320-340 nm), UVA1 photobiological effects are mediated exclusively by oxidative photochemical processes leading to the formation of singlet oxygen and other reactive oxygen species (ROS). The main targets of ROS are cell membranes and cytoplasmic organelles, particularly mitochondria, that are rich of structural molecules with several double bonds, e.g. lipids and aminoacids. UVA1 phototerapy proved to be an effective and well tolerated therapeutic option in the treatment of atopic dermatitis, localized scleroderma, mastocytosis, systemic lupus erythematosus, mycosis fungoides, chronic graft versus host disease and a growing number of other skin diseases, characterized by dermo-epidermal infiltrates of normal as well as neoplastic lymphocytes, mastocytes and/or eosinophils as well as alterated metabolism of collagen. There is no general agreement on the optimal treatment protocol. UVA1 is delivered at fixed doses without progressive dose adjustments. However, protocols differ in the UVA1 dosage, the number of weekly exposures, and total number of exposures. UVA1 therapy is always well tolerated and episodes of erythemogenic reaction are rare. Long term adverse effects are unknown but the hazard of skin carcinogenicity seems negligible because UVA1 does not damage directly DNA.