Sleep Disturbance is Increased in Rheumatoid Arthritis

Sleep Disturbance is Increased in Rheumatoid Arthritis

Sleep quality has a profound affect on pain perception and mood, and poor sleep itself may affect immune function by increasing allostatic load.  All of these effects may relate to the RA disease process.  However, little investigation into sleep disturbance has been undertaken in RA patients.  Here, Wolfe et el investigate self-reported sleep disturbance in RA patients participating in the National Databank for Rheumatic Diseases (NDB).

Methods In 2002, subjects with RA and non-inflammatory disorders (except fibromyalgia) completed two self-reported sleep assessments, the Medical Outcome Study (MOS) sleep questionnaire and a visual analogue sleep disturbance scale (VAS SD), in addition to the annual RA disease related questionnaires completed as part of the NDB.  The MOS sleep questionnaire is a 12 item questionnaire with items relating to quantity and quality of sleep, sleep habits, and waking and daytime symptoms for the past four weeks.

Results 8676 RA subjects were compared to 1364 non-RA subjects.  RA subjects were predominantly White (92.7%) and female (77.4%) with a mean age of 61 years.  The mean HAQ score was approximately 1.0.

Optimal sleep (7 to 8 hours) was found in 51.2% of RA patients.  Compared to normalized values, a greater proportion of RA patients reported sleep problems.  Increased sleep problems were also associated with the number of comorbid conditions and were more often reported in women than men, even though the number of hours of sleep did not differ by gender.

Compared to normalized values, an estimated 24 to 29% of the total sleep disturbance as measured by the MOS sleep questionnaire and 41.8% of the total sleep disturbance as measured by the VAS SD could be attributed to RA.

The degree of sleep disturbance correlated with RA disease related variables: HAQ, global severity, and pain.  In hierarchical modeling, pain and depression accounted for most of the explainable variability in sleep disturbance.  The reported use of TNF inhibitors was not associated with any significant difference in sleep disturbance or daytime sleepiness.  No significant meaningful differences were found in sleep disturbance between RA subjects and those with non-inflammatory disorders (OA/back pain).

Conclusions Sleep disturbance is increased in RA patients, with 24 to 42% of reported sleep disturbance attributable to the RA disease process.  Pain and depression are major contributors to sleep disturbance, with functional limitation as measures with the HAQ contributing little above these.  TNF inhibitor use does not appear to be related to improvements in sleep disturbance.  Patients with non-inflammatory musculoskeletal disorders experience similar levels of sleep disturbance as RA patients.

Editorial Comment Sleep has been understudied in RA, as links between inflammation and sleep patterns have been noted in the general population.  In addition, poor sleep may serve to exaggerate pain symptomatology.  This study adds some valuable new insights.  Particular strengths are the large sample size and the comprehensive nature of the data collection.  However, some important questions remain unanswered.  Disease activity is estimated using subjective measures, and not with objective measures of joint swelling, tenderness, or systemic inflammatory markers.  Without these, it is hard to reach definitive conclusions about the role of disease activity measures.

Recent small scale studies in patients without RA have demonstrated short term improvements in daytime sleepiness with the use of TNF inhibitors.  While no differences in self-reported sleep outcomes according to TNF inhibitor use were found here, more definitive comparisons would require an objective measure, such as polysomnography.  Hypercytokinemia associated with the systemic inflammatory response of RA may have central effects on the CNS that effect sleep.  Thus, improvements in sleep may not be specific to TNF inhibitors, but related to generic improvements in systemic inflammation.

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