S-Space College of Medicine/School of Medicine (의과대학/대학원) Dermatology (피부과학전공) Journal Papers (저널논문_피부과학전공)
Effect of increased pigmentation on the antifibrotic response of human skin to UV-A1 phototherapy
- 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
- American Medical Association
- Arch Dermatol. 2008;144(7):851-858
- Collagen Type I/genetics/metabolism; Collagen Type III/genetics/metabolism; Dose-Response Relationship, Radiation; Hyperpigmentation/*etiology/pathology; Matrix Metalloproteinases/genetics/metabolism; Polymerase Chain Reaction; RNA, Messenger/analysis; Radiation Dosage; Scleroderma, Localized/pathology/*radiotherapy; Severity of Illness Index; Skin/*radiation effects; Treatment Outcome; Ultraviolet Rays; Ultraviolet Therapy/*adverse effects
- 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.
- 1538-3652 (Electronic)
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