TY - JOUR
T1 - Effect of increased pigmentation on the antifibrotic response of human skin to UV-A1 phototherapy
AU - Wang, Frank
AU - Garza, Luis A.
AU - Cho, Soyun
AU - Kafi, Reza
AU - Hammerberg, Craig
AU - Quan, Taihao
AU - Hamilton, Ted
AU - Mayes, Maureen
AU - Ratanatharathorn, Voravit
AU - Voorhees, John J.
AU - Fisher, Gary J.
AU - Kang, Sewon
PY - 2008/7
Y1 - 2008/7
N2 - 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 highdose (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 highdose 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. Asingle 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
AB - 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 highdose (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 highdose 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. Asingle 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
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U2 - 10.1001/archderm.144.7.851
DO - 10.1001/archderm.144.7.851
M3 - Article
C2 - 18645136
AN - SCOPUS:47849086393
SN - 0003-987X
VL - 144
SP - 851
EP - 858
JO - Archives of Dermatology
JF - Archives of Dermatology
IS - 7
ER -