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Implications for Optimizing Patient Selection and Management

Alexander Kreuter, MD; Thilo Gambichler, MD

Arch Dermatol. 2008;144(7):912-916.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Phototherapy is among our most powerful weapons for fighting against chronic inflammatory skin diseases. Since the middle of the past century, numerous controlled studies of broadband UV-B, narrowband UV-B, and psoralen plus UV-A have demonstrated that phototherapy is highly effective in treating cutaneous diseases, such as psoriasis and atopic dermatitis. In 1981, the development of a new lamp that emits radiation predominantly between 340 and 400 nm was described, introducing the era of UV-A1 phototherapy.¹ Three different dosage regimens of UV-A1 are distinguished: high-, medium-, and low-dose UV-A1, emitting 90 to 130, 30 to 89, and less than 30 J/cm², respectively. In contrast to UV-B, which penetrates into the papillary dermis only, longer wavelengths in the UV-A region can reach the subcutis as well. In 1992, UV-A1 was first introduced as a highly potent treatment option for acute atopic dermatitis.² Three years later, . . . [Full Text of this Article]

INDICATIONS FOR TREATMENT AND UV-A1 DOSAGE


MECHANISM OF ACTION AND TREATMENT SCHEDULE FOR UV-A1

EVALUATION OF TREATMENT RESPONSE

LIMITATIONS OF UV-A1 IN SCLEROTIC SKIN DISEASES

AUTHOR INFORMATION


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