UVA1 Phototherapy

A Concise and Practical Review

Soodabeh Zandi, MD; Sunil Kalia, MD, FRCPC; Harvey Lui, MD, FRCPC

Disclosures

Skin Therapy Letter. 2012;17(1):1-3. 

In This Article

Abstract and Introduction

Abstract

High intensity long-wavelength ultraviolet A (340–400 nm; UVA1) lamps were initially developed as skin research tools; over time they have proven to be useful for treating a number of chronic dermatoses. UVA1 units and dosimetry are strikingly different from conventional UV phototherapy. The therapeutic effect of UVA1 is related to the fact that its long wavelength penetrates the dermis more deeply than UVB. UVA1 radiation induces collagenase (matrix metalloproteinase-1) expression, T-cell apoptosis, and depletes Langerhans and mast cells in the dermis. UVA1 exposure stimulates endothelial cells to undergo neovascularization. Ultraviolet A1 exerts significant therapeutic effects in atopic dermatitis and morphea; there is also evidence for its use in other skin diseases, including cutaneous T-cell lymphoma and mastocytosis.

Introduction

The roots of ultraviolet A1 (UVA1) phototherapy can be traced to the development of a relatively "pure", high-intensity UVA light source that was originally meant to be used for studying the physiologic cutaneous effects of UVA alone. UVA photons are approximately 1000 times less potent than UVB photons in eliciting photobiological responses, and thus, the technological challenge was to develop an artificial lamp that could deliver a biologically relevant UVA dose within a practical time frame and a sufficiently large irradiation field.[1] Using a specially filtered metal halide lamp, the spectral output was weighted towards longer, more penetrating UVA wavelengths (340–400 nm), and was distinctly different from that of fluorescent UVA tubes used for psoralen + UVA (PUVA) therapy. Over time UVA1 came to be used diagnostically for photoprovocation of conditions such as polymorphous light eruption and then as a novel treatment modality for certain inflammatory dermatoses.

UVA1 induces T-cell apoptosis, which is one of its proposed mechanisms for improving atopic dermatitis (AD), mycosis fungoides (MF), and localized scleroderma.[2] Consistent efficacious results with UVA1 have been observed with a variety of inflammatory, sclerosing, and neoplastic skin diseases that are characterized by dermal infiltrates rich in T lymphocytes.[3] UVA1 is one of the most recent advances in phototherapy for localized scleroderma and systemic sclerosis, and has been used more extensively in Europe than North America or Asia.

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