Background İmpaired sleep quality negatively influences quality of life, morbidity/mortality, and pain perception. Tumor necrosis factor-alpha (TNF-α), which plays a role in the pathogenesis of rheumatoid arthritis (RA), is also a functional cytokine in sleep regulation (1,2). Anti-TNF-α treatment is effectively used in RA treatment
Objectives The aims of this study were to evaluate sleep quality in RA patients, determine the relationship between sleep disorders and disease activity, and investigate the effects of anti-TNF-α therapy on sleep.
Methods We evaluated 35 RA patients; 22 had a high disease activity and were included in the study group, and 13 were in remission and were included in the control group. The disease activity index-28 (DAS 28) was used to measure disease activity. Patients in the study group were evaluated at the beginning and at week 12 of therapy; control patients were only evaluated at the beginning of the study. The Pittsburgh Sleep Quality Index (PSQI) and polysomnography (PSG) findings (total sleep time, sleep latency, sleep efficiency, number of awakenings after sleep onset, apnea hypopnea index (AHI), periodic leg movements, and snoring) were used to assess sleep quality and disturbance.
Results Sleep quality disturbances, evaluated by the PSQI, were present in 60% of the study participants. The median PSQI value was significantly higher in patients with high disease activity than in patients in the remission group (p=0.026). After treatment with anti-TNF-α, the median PSQI value significantly improved (p=0.012) in the high disease activity patients. In the PSG examination, 82.9% of the study patients demonstrated obstructive sleep apnea syndrome (OSAS), 83% demonstrated snoring, and 45.7% demonstrated periodic leg movements. There were no significant differences in the PSG parameters between the patients with high disease activity and those in remission, or between the before and after treatment measurements in patients receiving anti TNF-α therapy (p>0.05).
Conclusions Sleep quality, as measured by the PSQI, was impaired in the majority of the RA patients. Sleep disorders were more obvious in patients with high disease activity, but improved after anti TNF-α treatment. On PSG, most RA patients demonstrated OSAS, altered lengths of sleep stages, periodic leg movements, and snoring, but these findings were not related to disease activity and remained unchanged after anti TNF-α treatment. These results suggest that PSQI and PSG evaluations measure different sleep properties. However, these results also support a relationship between RA sleep disorders and the cytokines and mediators that play roles in disease pathogenesis rather than disease activity. These data suggest that sleep disorders in RA patients should be evaluated by both clinical and laboratory measurements. In particular, early detection and treatment of OSAS, which contributes to mortality and morbidity, is important in RA.
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Disclosure of Interest None declared