Of the different external factors that have detrimental effects on disease activity, the sun's radiation has been best studied. Already in Cazenave's original description (Cazenave 1881) it was mentioned that outdoor workers were predisposed to the disorder and that exacerbations of the disease were related to environmental factors. Hutchinson (Hutchinson 1888) reported in his Harveian Lectures on Lupus, published in 1888, that patients with LE did not tolerate exposure to the sun. In 1915, Pusey (Pusey 1915) described a young lady with LE that first appeared after some days of extensive golfing in the summertime. The lesions disappeared after strict avoidance of the sun, only to reexacerbate the next summer after a golf tournament. Freund (Freund 1929) evaluated in a study from 1920 to 1927 the admission of patients with LE to the Department of Dermatology in Berlin. He demonstrated an increased prevalence of new LE cases in May and June and concluded that climatic factors were responsible for this climax in the number of new patients with LE.
Shortly after these observations it became clear that artificial light sources were also able to induce LE. Jesionek (Jesionek 1916), a German pioneer of phototherapy,warned clinicians in 1916 not to apply phototherapy in patients with LE. He described two cases in which phototherapy had caused dramatic exacerbation of the disease with induction of systemic multiorgan involvement for previously limited DLE. In 1929, Fuhs (Fuhs 1929) reported a patient with exacerbated "lupus erythematosus subacu-tus" after irradiation with an artificial light source. Possibly, this is the first description of the exquisite light sensitivity of the SCLE subset. The author unsuccessfully tried to determine the action spectra and dosages that led to disease induction.
Epstein (Epstein et al. 1965) was the first investigator to introduce the repeated exposure technique, which enabled him and his coworkers to induce LE lesions in 5 of 25 patients. Baer and Harber (Baer and Harber 1965) also tested a limited number of patients, and Freeman et al. (Freeman et al. 1969) as well as Cripps and Rankin (Cripps and Rankin 1973) performed for the first time studies with monochromatic radiation, because of these studies, the action spectrum of LE was ascribed to the ultraviolet (UV) B range. In 1990, our group (Lehmann et al. 1990) demonstrated that the action spectrum of LE reaches into the long-wave UVA region. In the original study, 128 patients with LE had been tested using a standardized phototest protocol.
This study was extended, and over the ensuing 15 years 405 patients with LE were phototested (Kuhn et al. 2001). Other groups confirmed the published results (Leenu-taphon and Boonchai 1999,Nived et al. 1993,Walchner et al. 1997,Wolska et al. 1989). During these studies, a rare subset of cutaneous LE, namely LE tumidus (LET), turned out to be even more photosensitive than SCLE (Kuhn et al. 2001). LET was first mentioned by Gougerot and Burnier (Gourgerot and Burnier 1930) in 1930,but since then LET has been documented rarely in the literature.
In 1981, Provost and coworkers (Provost 1983, Provost and Reichlin 1981, Provost et al. 1983,1985) described the anti-Ro/SSA autoantibody as a serologic marker for neonatal LE and the association of these autoantibodies with a group of patients with LE and exquisite photosensitivity. Subsequently, Norris and colleagues demonstrated that UV irradiation modulates the expression of Ro/SSA antigens by epidermal ker-atinocytes (LeFeber et al. 1984, Norris and Lee 1985). For the first time, a molecular explanation for photosensitivity of patients with LE was presented. Ten years later, in 1994, Casciola-Rosen et al. (Casciola-Rosen et al. 1994) studied UV-induced apopto-sis of keratinocytes of patients with LE. They demonstrated the compartmentaliza-tion of specific nucleosome constituents to the cytoplasmatic cell surface blebs of apoptotic keratinocytes. This was hypothesized to be a possible first step in the cascade that finally leads to an autoimmune disease.
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