Sunlight-Induced Pathogenesis in Systemic Lupus Erythematosus

Enhanced membrane binding of autoantibodies to cultured keratinocytes of systemic lupus erythematosus patients after ultraviolet B/ultraviolet A irradiation.

“…2). These findings, as well as those described above, may have bearing on the unresolved debate regarding the formation of the lupus band, which is present in both the damaged and apparently healthy skin ofSLE patients (5,27,28). This linear band at the dermoepidermal junction is thought by some investigators to be the result of deposition of immune complexes formed in circulation, whereas others have suggested that they are produced locally in the areas of UV-damaged skin (6,8,(29)(30)(31).…”

“…Exposure to solar radiation is known to induce skin lesions and may also exacerbate systemic disease activity (2). Although cutaneous lesions in sun-sensitive patients have been elicited by ultraviolet radiation (UVR) under controlled experimental conditions (3,4), the exact mechanisms are not fully understood (5). In SLE patients, immunoreactants are mainly deposited at the dermoepidermal junction of sun-exposed skin (6).…”

Trends in the incidence and mortality of systemic lupus erythematosus, 1950-1992

“…On the other hand, the percentages of neurologic and hematologic manifestations were similar in the 2 cohorts (Table 1), which suggests that SLE may not, in fact, have been more benign in the 1980-1992 cohort compared with the earlier cohort. Other possible explanations for an increase in incidence of SLE over time include an increased exposure to hormones such as oral contraceptives (6) and estrogen replacement therapy (7), exposure to ultraviolet light (8,9), and smoking (10). The increased utilization of the ANA test as a screening tool may have contributed to the increased ascertainment of SLE.…”

Ciclosporin in the Treatment of Lupus Nephritis

“…The classical approach, using a double blind study comparing two homogenous groups of pa tients, one receiving placebo, the other the drug under investigation, is not applicable for two reasons, (a) It has been proved in SLE that present treatments, although causing severe side effects, significantly prolong the sur vival of both the kidney and the patient [10]. (b) It is impossible to establish two homogenous groups in a dis ease where uncontrollable factors, such as heredity and environment, can change the course of the disease in an unpredictable fashion [11][12][13]. Thus, the only acceptable procedure is to take a group of patients who are resistant to a well-known drug regimen or who developed intoler able side effects, and to replace one or more drugs of the previous schedule by the new medication.…”