Background Sleep disturbances (SD) are reported to be common in SLE, but relatively few studies have addressed the issue. We examined the frequency and severity of self-reported SD among individuals with SLE and predictors of SD.
Methods Data were from the National Data Bank for Rheumatic Diseases (NDB), for which participants complete questionnaires every 6 months. In one questionnaire, items about the presence of physician-diagnosed obstructive sleep apnea (OSA) and restless-leg syndrome (RLS), symptoms of OSA and RLS, and the Medical Outcomes Study Sleep Scale (MOS-S) were included. The MOS-S yields 5 subscales; results are shown here only for one (Sleep Problems Index I, SPI-I). Frequencies of reports of OSA, RLS, and RLS symptoms were tabulated. Multivariate regression analyses identified independent predictors of OSA and RLS (logistic regression) and SPI-I scores (linear regression). Potential predictors included age, race, education, smoking, Rheumatic Disease Comorbidity Index (RDCI),1 asthma, obesity (BMI ≥30 kg/m2), disease duration, pain, prednisone and other medication use, and disease activity (Systemic Lupus Activity Questionnaire, SLAQ2) and damage (Brief Index of Lupus Damage, BILD3).
Results Subjects (n=362) were mean age 61±13 years and had SLE duration of 26±13 years. 23% reported physician-diagnosed OSA and 20% RLS, compared to ∼2%–4% and ∼10%, respectively, in the general population. 18% and 34% had symptoms of OSA and RLS, respectively. Mean SPI-I was 39.6 (±20.2), >0.5 standard deviation higher (worse) than a population mean. Independent predictors of diagnosed OSA were greater age, obesity, asthma, RDCI, and disease activity (table 1). Predictors of RLS symptoms were RDCI and disease activity (table 1). Worse scores on SPI-I were associated with younger age, low education, higher RDCI, smoking, and greater pain and disease activity (table 1).
Conclusion Both OSA and RLS were more common in SLE than in the population; SPI-I scores were also worse. Some predictors of SDs were similar to predictors in the population (age, obesity), but disease activity was also associated with SD. Research in SLE has linked SDs to worse outcomes. Previous research in other conditions suggests that SDs might also be a cause of increased disease activity through heighted inflammation. Further research is needed to tease out disease-specific causes and effects of SD in SLE.
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