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Journal of the American Academy of Dermatology
Volume 36, n° 6
pages 938-944 (juin 1997)
Doi : 10.1016/S0190-9622(97)80277-0
accepted : 4 January 1997
Brief communication

High-dose UVA1 radiation therapy for localized scleroderma
 

Helger Stege a, Mark Berneburg a, Stefanie Humke a, Michaela Klammer a, Markus Grewe a, Susanne Grether-Beck a, Rolf Boedeker b, Thomas Diepgen c, Karsten Dierks a, Günter Goerz a, Thomas Ruzicka a, Jean Krutmann a,
a Clinical and Experimental Photodermatology, Department of Dermatology, Heinrich-Heine-University, Düsseldorf, Germany 
b Department of Biomathematics, University of Giessen, Giessen, Germany 
c Department of Dermatology, University of Erlangen, Erlangen, Germany 

*Reprint requests: Jean Krutmann, MD, Professor of Dermatology, Clinical and Experimental Photodermatology, Department of Dermatology, Heinrich-Heine-University, Moorenstr. 5, D-40225 Düs-seldorf, Germany.
Abstract
Background:

Fibrotic skin lesions in patients with localized scleroderma can cause muscle atrophy, disfigurement, and flexion contractures. There is no effective therapy for this disease. Skin fibrosis is thought to be caused by decreased collagenase activity. Collagenase activity can be induced in dermal fibroblasts by UVA1 irradiation.

Objective:

Our purpose was to assess whether UVA1 radiation therapy is effective for patients with localized scleroderma.

Methods:

Patients with localized scleroderma (n = 17) were exposed 30 times to 130 J/cm2 UVA1 (high-dose UVA1 therapy; n = 10) or 20 J/cm2 UVA1 (low-dose UVA1 therapy; n = 7). Therapeutic effectiveness was assessed by evaluation of (1) clinical features, (2) thickness of sclerotic plaques, and (3) cutaneous elastometry. Sequential biopsy specimens from treated lesions were analyzed for collagenase I messenger RNA (mRNA) expression by semiquantitative reverse transcriptase-polymerase chain reaction.

Results:

In all patients, high-dose UVA1 therapy softened sclerotic plaques, and complete clearance was observed in four of 10 patients. High-dose UVA1 therapy significantly reduced thickness and increased elasticity of plaques. These changes could not be detected in unirradiated control plaques and were still present in 9 of 10 patients 3 months after cessation of therapy. For all factors assessed, high-dose UVA1 was superior to low-dose UVA1 therapy (p = 0.001). High-dose UVA1 therapy increased collagenase I mRNA expression about 20-fold in treated plaques.

Conclusion:

High-dose UVA1 therapy is effective in the treatment of localized scleroderma. Effectiveness is UVA1 dose dependent and is associated with induction of collagenase I expression.

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