Authors: Noah Scheinfeld; Vincent A Deleo

Source: Photodermatology Photoimmunology & Photomedicine, Volume 20, Number 5, October 2004 , pp. 272-279(8)

Publisher: Wiley-Blackwell

Abstract:

Background:

Lupus erythematosus is a systemic disease process that may manifest with a variety of internal and cutaneous findings. Photosensitivity is one the most common manifestations of lupus erythematosus. In patients with lupus erythematosus, there is a relationship between exposure to ultraviolet light, autoantibodies, genetics and other factors in the development of photosensitivity. Methods:

Literature was reviewed on the topics of lupus erythematosus and photosensitivity discussed together and separately. The suggested mechanisms for their relationship were reviewed and analyzed. Results:

Photosensitivity's relationship to and influence on the systemic manifestations of lupus remain to be defined. Mechanisms for photosensitivity might include: modulation of autoantibody location, cytotoxic effects, apoptosis induction with autoantigens in apoptotic blebs, upregulation of adhesion molecules and cytokines, induction of nitric oxide sythase expression and ultraviolet-generated antigenic DNA. Tumor necrosis factor also seems to play a role in the development of photosensitivity. Conclusion:

The basis for photosensitivity in lupus has yet to be fully defined. It is more commonly associated with subacute and tumid lupus erythematosus than with other variants. Anti-Ro antibodies appear to relate to photosensitivity. Tumor necrosis factor polymorphisms appear to be important in some variants of lupus with photosensitivity. There is no sin que non antibody or mutation of photosensitivity in lupus. In patients with lupus, more work needs to be done to define the mechanisms of photosensitivity.

Keywords: anti-Ro antibody; photosensitivity; sub-actute lupus erythematosus; systemic lupus erythematosus; ultraviolet light

Document Type: Research article

DOI: http://dx.doi.org/10.1111/j.1600-0781.2004.00094.x

Publication date: 2004-10-01

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