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Effect of increased pigmentation on the antifibrotic response of human skin to UV-A1 phototherapy

Cited 33 time in Web of Science Cited 37 time in Scopus
Authors
Wang, Frank; Garza, Luis A; Cho, Soyun; Kafi, Reza; Hammerberg, Craig; Quan, Taihao; Hamilton, Ted; Mayes, Maureen; Ratanatharathorn, Voravit; Voorhees, John J; Fisher, Gary J; Kang, Sewon
Issue Date
2008-07-23
Publisher
American Medical Association
Citation
Arch Dermatol. 2008;144(7):851-858
Keywords
Collagen Type I/genetics/metabolismCollagen Type III/genetics/metabolismDose-Response Relationship, RadiationHyperpigmentation/*etiology/pathologyMatrix Metalloproteinases/genetics/metabolismPolymerase Chain ReactionRNA, Messenger/analysisRadiation DosageScleroderma, Localized/pathology/*radiotherapySeverity of Illness IndexSkin/*radiation effectsTreatment OutcomeUltraviolet RaysUltraviolet Therapy/*adverse effects
Abstract
OBJECTIVE: To investigate the efficacy, potential limitations, and biological mechanisms of UV-A1 phototherapy for skin sclerosis due to collagen deposition disorders. DESIGN: Before-and-after trial of UV-A1 irradiation of sclerotic skin; in vivo biochemical analyses after UV-A1 irradiation of normal skin. SETTING: Academic referral center. PARTICIPANTS: Patients with morphea/scleroderma or sclerodermoid graft-vs-host disease and volunteers without skin disease. Intervention Sclerotic skin was treated with high-dose (130 J/cm(2); n = 12) or medium-dose (65 J/cm(2); n = 6) UV-A1 phototherapy 3 times per week for 14 weeks; normal skin was treated with UV-A1 irradiation at various doses and frequencies, with biopsies performed afterwards. MAIN OUTCOME MEASURES: In sclerotic skin, induration was clinically assessed using a scoring scale. In normal skin, quantitative polymerase chain reaction was used to assess antifibrotic responses, defined as decreased type I and type III procollagen and increased matrix metalloproteinase levels. RESULTS: In patients with sclerotic skin treated with high-dose UV-A1 irradiation, clinical scores for induration modestly decreased. To investigate what factors prevented further improvement (ie, complete clearance), normal skin with light pigmentation was exposed to UV-A1 irradiation (70-150 J/cm(2)) and was assessed for antifibrotic responses. A single high-dose exposure (110-150 J/cm(2)) elicited substantial antifibrotic responses and induced skin darkening. This skin darkening attenuated responses to subsequent UV-A1 exposures and was dose dependent. Thus, to minimize skin darkening, additional patients with sclerotic skin were treated with medium-dose UV-A1 phototherapy, which was no less effective than high-dose therapy. CONCLUSION: Clinical responses of sclerotic skin to UV-A1 phototherapy were modest because of UV-A1-induced skin darkening, which is photoprotective and attenuates antifibrotic responses. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT00129415.
ISSN
1538-3652 (Electronic)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=18645136

http://archderm.ama-assn.org/cgi/reprint/144/7/851.pdf

https://hdl.handle.net/10371/67549
DOI
https://doi.org/10.1001/archderm.144.7.851
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College of Medicine/School of Medicine (의과대학/대학원)Dermatology (피부과학전공)Journal Papers (저널논문_피부과학전공)
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