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UVA1 phototherapy promising for sclerotic, fair skin


According to researchers, phototherapy appears to have promising results in lightly pigmented patients who do not tan easily. Treatment has a better chance for good results if patients present with sclerotic skin disease early on.

Key Points

Los Angeles - The challenge of treating sclerotic skin disorders persists, and ultraviolet A1 phototherapy appears to yield promising results in lightly pigmented patients who do not tan easily.

Dr. Wang says the fairly new ultraviolet A1 phototherapy (340 to 400 nm) has been used more frequently in Europe to treat sclerotic skin disorders, and equipment can be obtained from Germany. Dr. Wang says the European literature about UVA1 treatment of sclerotic skin disorders indicated "dramatic results" could be attained, and that the modality had "normalized sclerotic skin in some cases."

He and colleagues initiated the present study after witnessing - over several years - clinical results that were not really as impressive as the European literature had described.

"Patients (treated with UVA1 phototherapy) at our center had some degree of skin softening, but they were not returning to 'normal.'"

To investigate reasons for this, the researchers began their study to test the hypothesis that skin darkening brought on by UVA1 therapy possibly was preventing the penetration of UVA1 radiation into the dermis, where diseases like morphea stimulate collagen deposition. They suspected the pigment darkening brought on by phototherapy was also diminishing the skin's antifibrotic response to phototherapy.

"UVA1 is known to induce pigment, and that pigment may be blocking subsequent effects of UVA1," Dr. Wang explains.

Dr. Wang says, "Indeed, we found that increased pigmentation is a potential limitation of UVA1 phototherapy." Whether increased pigmentation is facultative (induced by UVA1 therapy) or constitutive (pre-existing, darker skin), it appears the antifibrotic effects of UVA1 phototherapy are attenuated.

Given the difficult nature of biopsying sclerotic skin, the researchers studied the biological effects of UVA1 phototherapy on normal skin in 28 subjects. In light, medium and dark skin, they administered UVA1 phototherapy using different doses and schedules, and studied the gene expression of MMP-1 - a matrix metalloproteinase enzyme that breaks down collagen.

Results showed that darker skin had less induction of MMP-1 with any dose of UVA1 exposure. For lighter skin, the antifibrotic response was induced by UVA1 doses ranging from 70 to 150 joules/cm2.

To minimize increases in skin pigmentation during treatment, high doses of UVA1 phototherapy (130 joules/cm2) were given to an additional 10 lighter-skinned normal subjects in weekly intervals, rather than the "conventional" three to five times per week. Results showed that gene expression of MMP-1 was highest after one treatment, but diminished with subsequent weekly treatments.

"MMP-1 expression is a measure of antifibrotic response, and importantly, this enzyme represents a first key step in degrading collagen," Dr. Wang explains. "We want to have the highest MMP-1 induction but also the least amount of tanning as possible during UVA1 phototherapy."

To minimize tanning, Dr. Wang says doses and frequency can be decreased. However, the challenge is to maintain the dose and frequency that also give the greatest antifibrotic response.

"It is a balancing act. It is made more difficult by the fact that every patient is different," Dr. Wang notes.

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