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Case Reports
. 2011 Jun;147(6):719-23.
doi: 10.1001/archdermatol.2011.13. Epub 2011 Feb 21.

Progression of toxic epidermal necrolysis after tanning bed exposure

Affiliations
Case Reports

Progression of toxic epidermal necrolysis after tanning bed exposure

Na Tosha Gatson et al. Arch Dermatol. 2011 Jun.

Abstract

Background: In addition to recreational tanning bed use, UV radiation exposures are sometimes sought to self-treat skin conditions. The ability of tanning bed radiation exposure to trigger toxic epidermal necrolysis has not been reported.

Observations: A young woman attempted to treat a self-limiting drug hypersensitivity reaction via tanning bed radiation exposure, which resulted in a systemic toxic epidermal necrolysis-like reaction. Studies with cultured keratinocytes and an epithelial cell line reveal that UV-A radiation can synergize with other stimuli such as phorbol esters or interleukin 1 to produce large amounts of tumor necrosis factor, providing a potential mechanism for this exaggerated reaction.

Conclusion: In addition to inducing photodamage and skin cancer, tanning bed radiation exposure can trigger a toxic epidermal necrolysis-like reaction, possibly via the exaggerated production of keratinocyte cytokines such as tumor necrosis factor.

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Figures

Figure 1
Figure 1. Clinical Photographs Demonstrating Photo-accentuation of Blistering Skin Eruption and Biopsy Specimen of Skin Showing Epidermal Necrosis and Increased TNF-α Immunoreactivity
A,B-clinical pictures of patient demonstrating blisters in areas of tanning bed exposure and residua of mild morbilliform eruption on covered skin (breasts). C-. Histology of skin biopsy specimen demonstrating necrotic keratinocytes (100×). D,E- Immunohistochemical studies demonstrating increased cytoplasmic TNF-α immunoreactivity in patient (D) over control tissue (E); (200×)
Figure 2
Figure 2. UVA Irradiation Augments TNF-α Production in Human Keratinocytes and KB cell line
Primary cultures of human keratinocytes or KB cell line were treated with vehicle control, 1 ng/ml IL-1α, or 10 nM PMA, followed 30 min later by treatment with sham, 5 or 20 kJ/m2 UVA. The TNF-α released into the supernatants was measured 6 h following UVA treatment by EIA. The data depicted are mean +/− SD from triplicate samples of a representative experiment from at least four with similar results.

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