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Abstract Number: 352

Remaining Pain in Spite of Suppressed Inflammation in Early Rheumatoid Arthritis – Long-Term Strongly Increased Risk for Widespread Pain and Fatigue

Maria E.C. Sandberg1, Saedis Saevarsdottir2, Reem Altawil3, Lars Klareskog4, Lars Alfredsson1 and Jon Lampa3, 1The Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden, 2Rheumatology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden, 3Rheumatology Unit, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden, 4Department of Medicine, Rheumatology Unit, Karolinska Institute, Stockholm, Sweden

Meeting: 2014 ACR/ARHP Annual Meeting

Keywords: Arthritis and pain

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Session Information

Title: Rheumatoid Arthritis - Clinical Aspects: Novel Biomarkers and Other Measurements of Disease Activity

Session Type: Abstract Submissions (ACR)

Background/Purpose: Pain is common in rheumatoid arthritis (RA), even after adequate inflammatory disease control. Important long-term health effects of RA are fatigue, sleeping disturbances and a significant portion of patients also develop generalized pain, often leading to decreased quality of life. The aim of the present study was to investigate the distribution of remaining pain dimension in RA, which patients that may be at increased risk, and whether it is a risk factor for long-term generalized (widespread) pain and fatigue.

Methods: We used the cases (incident RA patients aged 18-70 recruited 1996-2009) from the Swedish population-based case-control study; EIRA, linked to the Swedish Rheumatology Quality Register (N=1633). Three years after diagnosis an additional questionnaire was sent out, assessing fatigue, pain outside joints and sleeping problems (N=186). Remaining pain was defined as pain on visual-analog scale (VAS) ≥20 mm and CRP <10 g/L at the 12 month follow-up visit. Logistic regression was used both to calculate the odds ratio (OR) of baseline clinical parameters as possible predictors of remaining pain, adjusted for sex, age and period and also OR of widespread pain (WSP; pain outside joints in all four quadrants)/any pain outside joints/sleeping problems/fatigue, as an effect of remaining pain.

Results: 35% of the patients had remaining pain at 12 months after diagnosis. Several factors at diagnosis significantly and independently increased the risk for remaining pain at 12 months: higher HAQ (ORs per additional unit; OR=1.28 [95%CI: 1.02 – 1.60]), tender joint count (OR=1.04 [95%CI: 1.02 – 1.06]) and patient global assessment (OR=1.25 [95%CI: 1.12 – 1.38] per 20 units). A higher CRP, ESR and swollen joint count all significantly and independently decreased the risk for remaining pain. (OR=0.84 [95%CI: 0.76 – 0.92] per 10 units), (OR=0.89 [95%CI: 0.80 – 0.99] per 10 units), (OR=0.97 [95%CI: 0.94 – 1.00] per joint); respectively. After 3 years; 7% had WSP, 36% had any pain outside joints, 17% had sleeping problems (defined as quite big/very big problem by the patient) and 26% had significant fatigue (VAS ≥40). Regarding the effect of remaining pain at 12 months on WSP/any pain outside joints/sleeping problems/fatigue we, despite our somewhat few observations, found strongly increased risk for these conditions after 3 years in those with remaining pain after 12 months: OR: WSP=3.48 [95%CI: 1.24-9.73], any pain outside joints= 2.67 [95%CI:1.44-4.94], sleeping problems=3.82 [95%CI:1.61-9.06], fatigue=2.43 [95%CI:1.25-4.72]. All these ORs remained after adjustment for very high baseline pain levels (VAS > 70), indicating that presence of WSP/fibromyalgia at diagnosis had no major impact on the results.

Conclusion: More than a third of all RA-patients have remaining pain despite satisfactory inflammation control 12 months after diagnosis. This condition is a very strong predictor for development of widespread pain 3 years after diagnosis. Moreover, we found strong associations with long-term non-joint-related pain, sleeping problems and fatigue. These observations stress the importance to acknowledge and optimize pain treatment also in patients with adequate inflammation control early in RA.


Disclosure:

M. E. C. Sandberg,
None;

S. Saevarsdottir,
None;

R. Altawil,
None;

L. Klareskog,
None;

L. Alfredsson,
None;

J. Lampa,
None.

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