BackgroundChronic widespread pain (CWP) has been suggested as a risk for mortality in especially cardiovascular diseases and malignancies (1, 2). Most studies are based on the CWP definition that is part of ACR1990 criteria for fibromyalgia (3). The ACR1990 definition has been criticized for being too including, and recently a more stringent definition, the WP2019, has been suggested (4). It is yet to be investigated how the more stringent WP2019 definition compares to the ACR1990 definition regarding excessed mortality and certain causes of death.ObjectivesTo study if overall mortality and common causes of death are increased among people with CWP in a 25 year follow up of a cohort from the general population. Additionally, to study if the definition of CWP, according to ACR1990 or WP2019, influences these outcomes.MethodsA 25-year follow up of the EPIPAIN cohort study that in 1995 included 2425 person from the general population (5). They were at baseline divided into three pain groups: CWP, chronic regional pain (CRP) and no chronic pain (NCP). CWP was defined according to both the ACR1990 (CWPACR1990) and the more stringent WP2019 (CWPWP2019) criteria. Deaths and causes of death were derived from the official national Swedish register. Mortality, adjusted for age, sex, socioeconomic status, and smoking habits, was analyzed with Cox regression and presented as Hazard Ratios (HR).ResultsAn overall increased mortality was predicted by CWPWP2019 (HR 1.32, p = 0.033), but not by CWPACR1990 (HR 1.08, p = 0.484), compared to NCP. An increased mortality in diseases of the circulatory system was predicted by CWPWP2019 (HR 1.70, p= 0.016), but not by CWPACR1990 (HR 1.35, p=0.128). Neither definition of CWP, CWPWP2019 (HR 1.35, p= 0.176) or CWPACR1990 (HR 1.21, p=0.327) predicted a significantly increased mortality for neoplastic diseases overall.ConclusionThe WP2019 definition of CWP enhanced the association between CWP and increased mortality, and especially mortality in diseases of the circulatory system. This suggests that the CWPWP2019 definition captures a more vulnerable subset of the population that should be assessed for other cardiovascular risk factors in the clinic.References[1]Da Silva JAP, Geenen R, Jacobs JWG. Chronic widespread pain and increased mortality: biopsychosocial interconnections. Ann Rheum Dis. 2018;77(6):790-2.[2]Macfarlane GJ, Barnish MS, Jones GT. Persons with chronic widespread pain experience excess mortality: longitudinal results from UK Biobank and meta-analysis. Ann Rheum Dis. 2017;76(11):1815-22.[3]Wolfe F, Smythe HA, Yunus MB, Bennett RM, Bombardier C, Goldenberg DL, et al. The American College of Rheumatology 1990 Criteria for the Classification of Fibromyalgia. Report of the Multicenter Criteria Committee. Arthritis Rheum. 1990;33(2):160-72.[4]Wolfe F, Butler SH, Fitzcharles M, Häuser W, Katz RL, Mease PJ, et al. Revised chronic widespread pain criteria: development from and integration with fibromyalgia criteria. Scand J Pain. 2019;20(1):77-86.[5]Bergman S, Herrström P, Jacobsson LT, Petersson IF. Chronic widespread pain: a three year of pain distribution and risk factors. J Rheumatol. 2002;29(4):818-25.Disclosure of InterestsNone declared
BackgroundPrevious studies have reported associations between obesity, chronic pain and increased pain sensitivity. The adipokine leptin has been suggested to be involved in the osteoarthritis process as well as in pain sensitisation.ObjectivesThe aim was to study associations between chronic widespread pain, pain sensitivity and leptin in individuals with knee pain.MethodsIn all, 306 individuals with knee pain were included in the Halland osteoarthritis cohort, ClinicalTrials.gov NCT04928170. Of those, 265 were included in this cross-sectional baseline study. The mean age (sd) was 51.6 (8.8) years, and 71% was women. The participants marked their painful areas on a pain figure with 18 predefined areas. They were categorised in three different pain groups according to the modified WP2019 definition (1), with knees excluded (due to highest goodness of fit): Chronic widespread pain (CWP), chronic regional pain (ChRP) if CWP was not met, and no chronic pain (NCP). The group with CWP were compared with those reporting no CWP (ChRP and NCP). The pressure pain thresholds (PPT) were measured using a computerised pressure algometry (AlgoMed, Medoc) on eight predefined tender points (trapezius (bilateral), right second rib, right lateral epicondyle, knees, gluteal (bilateral)) (2). Increased pain sensitivity was defined as having PPT in the lowest third in all tender points. Obesity was measured via waistline measurement and a bioimpedance (InBody 770) measuring BMI and visceral fat area (VFA). Serum-Leptin were analysed with an ELISA method (Alpco). Knee Injury and Osteoarthritis Outcome Score (KOOS) was used to describe the groups.ResultsIn this baseline study, 16% reported CWP, and 15% had low pain pressure thresholds at baseline in the study. Those fulfilling CWP were more often women, had higher BMI, VFA, and increased leptin levels and worse KOOS in four of five subscores, see Table 1A. The age and gender-adjusted leptin levels were 21.6 ng/ml (95% CI 18.2-25.0) in the group with no CWP vs. 35.5 ng/ml (95% CI 27.6-43.4) in the CWP group, p=0.002. In a logistic regression adjusting for age and gender, leptin was associated with reporting CWP OR 1.015 (95% CI 1.004-1.027, p= 0.008).Table 1.A Comparisons between those without CWP and those fulfilling CWP and table 1B comparisons between those not having low PPT and those with low PPT.ABNo CWPMean (sd)CWPMean (sd)p-valueNot Low PPTMean (sd)Low PPTMean (sd)p-valuen2104022639Age51.8 (8.7)52.8 (7.6)0.46552.1 (8.5)48.8 (9.9)0.030Gender, female n(%)67900.00472670.524BMI (kg/m2)26.2 (4.6)28.0 (5.0)0.02226.4 (4.9)27.5 (4.3)0.213VFA (cm2)107 (50)137 (56)0.001110 (54)127 (49)0.088Leptin (ng/ml)21.0 (23.9)39.0 (36.6)<0.00123.0 (26.0)31.8 (31.6)0.061CRP (mg/L)1.9 (2.7)2.2 (2.3)0.6022.0 (2.7)1.9 (1.8)0.825KOOSPain (0-100, worst to best)74 (15)61 (17)<0.00173 (15)65 (18)0.002Symptom (0-100, worst to best)72 (17)64 (18)0.01671 (17)67 (19)0.188ADL (0-100, worst to best)84 (13)69 (19)<0.00184 (14)72 (21)<0.001Sport/rec (0-100, worst to best)49 (26)34 (27)0.00149 (26)36 (25)0.009QoL (0-100, worst to best)53 (18)46 (20)0.05053 (18)45 (21)0.017BMI, body mass index; VFA, visceral fat area; CRP, C-reactive protein; KOOS, knee injury and osteoarthritis outcome score; ADL; function in daily living; sport/Rec, Function in sport and recreation; QOL, knee-related Quality of lifeThe participants with low PPT were younger and had a mean (sd) leptin 31.8 ng/ml (31.6) vs 23.0 (26.0), p=0.061 in the group not having low PPT, Table 1B. In a logistic regression adjusting for age and gender, leptin was associated with low PPT OR 1.016 (95% CI 1.004-1.029, p= 0.012).ConclusionThe pathophysiological mechanism causing widespread pain is probably multifactorial, involving both biological and physical factors. The adipokine leptin could be involved in some of these mechanisms, but longitudinal studies are needed to be able to study causal relationships.References[1]Wolfe F, et al. Scand J Pain. 2019;20:77-86.[2]Wolfe F, et al. Arthritis and rheumatism. 1990;33:160-72.Disclosure of InterestsNone declared
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