Patients with systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) have increased risk for atherosclerotic cardiovascular disease. We compared the presence of coronary artery calcium (CAC) in age-and race-matched women with SLE, RA, and healthy controls without diabetes mellitus or history of myocardial infarct, angina pectoris or stroke, and investigated its relation with traditional risk factors, inflammation, and endothelial activation. Study subjects completed cardiovascular risk factor assessment and electron-beam computed tomography that measured CAC. Both female patient groups had similar prevalence and extent of CAC as well as a significant increased odds of having any CAC (odds ratio 1.87, 95% CI 1.09-3.21) and more extensive CAC (odds ratio 4.04, 95% CI 1.42-11.56 for CAC score>100) when compared to healthy controls. After controlling for differences in cardiovascular risk factors, including insulin resistance and hypertension, the results remained statistically significant. After adjustment for differences in levels of C-reactive protein and/or soluble intercellular adhesion molecule-1, however, women with chronic inflammatory diseases no longer had significantly increased odds of having any CAC or more extensive CAC when compared to controls. In conclusion, asymptomatic and non-diabetic women with chronic inflammatory diseases had significantly increased odds of having CAC and more extensive CAC when compared to age-and race-matched healthy controls. The increased odds for coronary artery calcium may in part result from higher levels of inflammation and endothelial activation in these patients.

Women with RA have increased carotid artery diameters compared with healthy women. This may reflect premature vascular aging and may be an early indicator of increased cardiovascular risk.

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Converging lines of evidence support an association between systemic inflammation and depressive symptoms. Neuroimmune pathways may account for the high prevalence of depression in individuals with inflammatory conditions such as rheumatoid arthritis (RA). However, this relationship is complicated by factors linked to both inflammatory disease activity and mood, such as pain and physical disability. The goal of this cross-sectional study was to examine the relationship between C-reactive protein (CRP) and depressive symptoms among 173 women with RA. Somatic symptoms of depression and circulating CRP were significantly associated in regression analyses adjusted for body mass index (β= .19, p < 0.05), but this relationship was attenuated when pain and disability were included as covariates (β= .09, p = 0.24). CRP was not significantly associated with negative mood symptoms of depression. Findings suggest that depression in the context of RA may result from the overlap of somatic depressive and RA symptoms rather than neuroimmune pathways. KeywordsRheumatoid arthritis; Autoimmune disorders; Inflammation; C-reactive protein; Depression In response to infection, cytokines coordinate biological changes to clear the pathogen and promote tissue repair. Peripheral proinflammatory cytokines also act on neural substrates to produce psychiatric symptoms including fatigue, anorexia, impaired learning and memory, and reductions in exploratory, social, and sexual behavior (Dantzer et al., 2008;Maier and Watkins 1998). These "sickness behaviors" are hypothesized to serve evolutionary functions by prioritizing recuperation and allocating metabolic resources to fighting infection. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. et al., 1995;Raison, Capuron, & Miller, 2006). In healthy adults, experimental administration of inflammatory stimuli transiently increases both sickness behaviors and negative mood (Reichenberg et al., 2001;Wright et al., 2005). Community-based studies report a positive correlation between depressed mood and circulating markers of inflammation such as C-reactive protein (CRP;Bremmer et al., 2008;Ford & Erlinger, 2004;Suarez, 2004). These converging lines of evidence support a positive association between systemic inflammation and both somatic and affective depressive symptoms. NIH Public AccessNeuroimmune pathways are postulated to explain the high prevalence of depression in inflammatory conditions such as rheumatoid arthritis (RA; Dantzer et al., 2008;Lorton, Lubahn, Zautra, & Bellinger, 2008). RA is a female-predominant autoimmune disease characterized ...