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Frank Wang, MD; Luis A. Garza, MD, PhD; Soyun Cho, MD, PhD; Reza Kafi, MD; Craig Hammerberg, PhD; Taihao Quan, MD, PhD; Ted Hamilton, MS; Maureen Mayes, MD; Voravit Ratanatharathorn, MD; John J. Voorhees, MD; Gary J. Fisher, PhD; Sewon Kang, MD

Arch Dermatol. 2008;144(7):851-858.

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/cm²; n = 12) or medium-dose (65 J/cm²; 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/cm²) and was assessed for antifibrotic responses. A single high-dose exposure (110-150 J/cm²) 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

Author Affiliations: Department of Dermatology, University of Michigan Medical School, Ann Arbor (Drs Wang, Garza, Cho, Kafi, Hammerberg, Quan, Voorhees, Fisher, and Kang and Mr Hamilton); Division of Rheumatology, Department of Internal Medicine, Wayne State University, Detroit, Michigan (Dr Mayes); and Division of Hematology/Oncology, Department of Internal Medicine, Blood and Marrow Stem Cell Transplant Program, University of Michigan, Ann Arbor (Dr Ratanatharathorn). Dr Garza is now with the Department of Dermatology, University of Pennsylvania, Philadelphia. Dr Cho is now with the Department of Dermatology, Seoul National University School of Medicine, Seoul, Korea. Dr Kafi is now with the Department of Dermatology, Stanford University, Palo Alto, California. Dr Mayes is now with the Division of Rheumatology, Department of Internal Medicine, University of Texas Houston Health Science Center. Dr Ratanatharathorn is now with the Barbara Ann Karmanos Cancer Institute, Wayne State University.

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