Short wavelengths of ultraviolet (UV) light are clearly harmful in systemic lupus erythematosus (SLE), but the action of long UV wavelengths in SLE is more enigmatic. In a series of animal and human studies, long-wavelength UV radiation, i.e., radiation in the ultraviolet-A1 (UVA1) range (340-400 nm), has proven effective in the treatment of SLE. Disease amelioration and a marked decrease in mortality followed ultraviolet-A (UVA) radiation (320-400 nm) of the New Zealand White/New Zealand Black mouse model of lupus. A follow-up study in the same animal suggested that the longer wavelengths (UVA1, 340-400 nm) in the UVA wave band were primarily responsible. There followed four human studies. The first three of these provided data indicating that low-dose UVA1 radiation significantly reduced constitutional symptoms, joint pain, rashes, and the systemic lupus activity measures, a validated gauge of disease activity in SLE. The fourth human study showed that the therapeutic action of low-dose UVA1 action persisted or progressed long term, a period averaging 3.4 y. UVA1 effects on DNA repair, cell-mediated immunosuppression, tumor necrosis factor alpha release, and apoptosis contrast markedly with those of ultraviolet B (UVB, 280-320 nm) radiation and afford a possible basis for the salutary action of this modality of treatment. The unique features of UVA1 wavelengths may be suited to further therapeutic use, not only in SLE but also in other immunologic disorders.

Objective. To determine the prevalence of fluorescent light toxicity in patients with systemic lupus erythematosus (SLE).Methods. SLE patients were polled about their symptomatic responses to sunlight and cool white fluorescent light. Photometry was used to determine the levels of ultraviolet (UV) emissions from fluorescent lamps.Results. Thirteen of 30 photosensitive SLE patients described increases in disease activity following exposure to unshielded fluorescent lamps. Photometry indicated that these lamps emit substantial levels of UV-B (280-320 nm) radiation, which is toxic to patients with SLE. Standard acrylic diffusers absorbed this radiation, and their use was associated with almost no patient-reported problems. Conclusion. Fluorescent lamps, emitting UV-Bradiation, induce disease activity in photosensitive SLE patients. Standard acrylic diffusers absorb UV-B radiation and appear to be protective against induction of disease activity with the use of fluorescent lamps.Sunlight is detrimental to systemic lupus erythematosus (SLE) patients (l), and wavelengths in the ultraviolet-B (UV-B) range (280-320 nm) are responsible (2,3). There is a source of UV-B irradiation,

Ultraviolet-A1 (UV-A1) wavelengths have been found effective in mitigating signs and symptoms of disease activity in systemic lupus erythematosus (SLE) but studies have been uncontrolled. To rigorously assess the effectiveness and safety of daily low-dose UV-A1 irradiation as a therapeutic agent in this disorder we enrolled 26 women with SLE in an 18-week two-phase study. During the initial six-week prospective, double-blind, placebo-controlled phase, the patients were divided into two groups; Group A was exposed to 60kJ/m2 of UV-A1 (340-400 nm) irradiation within a sunbed five days a week for three weeks and Group B was exposed for an equal amount of time to visible light of greater than > 430 nm (placebo). Each group was then crossed over for exposure to the other source for three weeks. During the second phase-2 weeks-patients and physicians were unblinded and patients were irradiated with progressively decreasing levels of UV-A1 only. Twenty-five patients completed the six-week placebo-controlled phase of the study and eighteen patients participated for the entire 18 weeks. In Group A the systemic lupus activity measure (SLAM) score improved significantly after three weeks of five-day-a-week UV-A1 irradiation (P < 0.05), regressing to baseline during the three weeks of placebo irradiation. Improvement recurred and progressed with six weeks of three-day-a-week UV-A1 irradiation (P < 0.05). Group B patients responded negligibly to the three weeks of visible light, more sharply to UV-A1, and as with Group A, maximally to the six weeks of three-day-a-week UV-A1 (P < 0.01). With twice- and then once-weekly UV-A1 irradiation the SLAM scores worsened slightly. All patients decreased their drug use. Anti-double-stranded DNA antibodies (anti-dsDNA) decreased significantly (P < 0.05) and anti-nuclear antibodies non-significantly. Side effects were negligible. Visible light had no significant effect. In conclusion, low-dose UV-A1 irradiation effectively, comfortably, and without apparent toxicity diminished signs and symptoms of disease activity in SLE.