Atherosclerosis is a chronic inflammatory disorder characterized by immune cell activation, inflammation driven plaque formation and subsequent destabilization. In other disorders of an inflammatory nature, the chronic inflammatory state per se has been linked to acceleration of the atherosclerotic process which is underlined by an increased incidence of cardiovascular disease (CVD) in disorders such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and antiphopholipid (Hughes) syndrome (APS). SLE is an autoimmune disease that may affect any organ. Premature coronary heart disease has emerged as a major cause of morbidity and mortality in SLE. In addition to mortality, cardiovascular morbidity is also markedly increased in these patients, compared with the general population. The increased cardiovascular risk can be explained only partially by an increased prevalence of classical risk factors for cardiovascular disease; it also appears to be related to inflammation. Inflammation is increasingly being considered central to the pathogenesis of atherosclerosis and an important risk factor for vascular disease. Recent epidemiologic and pathogenesis studies have suggested a great deal in common between the pathogenesis of prototypic autoimmune disease such as SLE and that of atherosclerosis. We will review traditional risk factors for CVD in SLE. We will also discuss the role of inflammation in atherosclerosis, as well as possible treatment strategies in these patients.

Objective: To determine the relationship between cognitive impairment and employment in patients with systemic lupus erythematosus (SLE).Methods: A total of 167 consecutive patients with SLE were prospectively evaluated, and underwent standardized neuropsychological tests. Multivariate logistic regression was used to determine the likelihood of being unemployed, adjusting for sociodemographic characteristics, employment status at study entry, disease activity, disease duration, damage scores, and depression.Results: At study entry, 118 (70.7%) of 167 patients were employed. In the multivariate analysis, after adjusting for confounders, unemployment was predicted by the number of cognitive domains impaired (odds ratio [OR] 1.76, 95% confidence interval [95% CI] 1.58–6.72), depression (OR 1.3, 95% CI 1.1–3.1), fewer years of education (OR 0.12, 95% CI 0.02–0.34), and the presence of anticardiolipin antibodies (OR 1.43, 95% CI 1.2–6.1). Complex attention (OR 1.7, 95% CI 1.2–3.6), memory (OR 3.1, 95% CI 1.5–6.2), and executive functions (OR 2.4, 95% CI 1.9–6.1) were predictors of unemployment at study entry. After 3 years, 61 (51.7%) of 118 patients were employed (OR 2.25, 95% CI 1.38–3.68; P = 0.001). The likelihood of being unemployed after 3 years was predicted by the number of cognitive domains impaired (OR 3.8, 95% CI 2.5–7.71), depression (OR 2.31, 95% CI 1.01–5.21), fewer years of education (OR 0.09, 95% CI 0.01–0.42), and the presence of anticardiolipin antibodies (OR 2.1, 95% CI 1.2–4.9). Complex attention (OR 2.2, 95% CI 1.1–3.8), memory (OR 3.6, 95% CI 2.1–6.4), executive functions (OR 1.8, 95% CI 1.2–7.3), and reasoning/problem solving (OR 1.9, 95% CI 1.4–7.2) were associated with unemployment after 3 years.Conclusion: The number of cognitive spheres, and especially attention, memory, and executive functions, are important factors associated with unemployment in patients with SLE.

Tumor necrosis factor alpha (TNF-α) is deeply related to pathogenesis of neurodevelopmental disorders, especially depression. The aim of this study was to explore potential relationships between sera TNF-α levels and mood and anxiety disorders in systemic lupus erythematosus (SLE) patients. We included 153 consecutive SLE patients (women 148; median age 30; range 10–62) and 40 (women 37; mean age 28.5; range 12–59) age- and sex-matched healthy controls. Mood and anxiety disorders were determined through Beck Depression and Beck Anxiety Inventory. SLE patients were further assessed for clinical and laboratory SLE manifestations. TNF-α levels were measured by enzyme-linked immunosorbent assay using commercial kits. Depressive symptoms were identified in 70 (45.7 %) SLE patients and in 10 (25 %) healthy controls (p < 0.001). Anxiety symptoms were identified in 93 (60.7 %) SLE patients and in 16 controls (40 %) (p < 0.001). Sera TNF-α levels were increased in SLE patients with depressive symptoms (p < 0.001) and with anxiety symptoms (p = 0.014). A direct correlation between the severity of depressive symptoms and sera TNF-α levels (r = 0.22; p = 0.003) was observed. TNF-α levels were significantly increased in patients with active disease (p = 0.012). In addition, we observed a correlation between sera TNF-α levels and disease activity (r = 0.28; p = 0.008). In the multivariate analysis, sera TNF-α levels were independently associated with depressive symptoms (t = 3.28; 95 % CI 1.08–2.2; p = 0.002). Sera TNF-α levels are increased in SLE patients with mood and anxiety disorders. In SLE, sera TNF-α levels are independently associated with mood disorders. The etiology of mood disorders is still debated in SLE, but our findings suggest the presence of immunological basis for depression in SLE.

The objective of this study was to determine the frequency of cognitive impairment in patients with rheumatoid arthritis (RA). A cross-sectional study of 40 patients with RA and 40 healthy controls was performed. To assess cognitive impairment, anxiety and depression, the following standardized psychiatric and clinical research methods were used: the Mini-Mental State Examination (MMSE), logic memory tests, short and long memory tests, verbal fluency tests, attention tests, the Brief Psychiatric Rating Scale (BPRS), the Hospital Anxiety and Depression (HAD)/CAGE scale and the Beck Depression Inventory (BDI). Patients and controls with incomplete primary education were excluded from the study. Statistics were performed by chi-square test and by Fisher's exact test. Cognitive impairment was observed in 30% of patients with RA and in 7.5% (p < 0.05) of healthy controls. Patients with RA had a significantly worse outcome in verbal fluency (p < 0.05), logic memory (p < 0.05) and short memory (p < 0.05). No statistical difference was observed among the results obtained in the MMSE, BPRS, HAD/CAGE and BDI. There was no significant relation to the duration of the illness, use of corticotherapy or disability. We observed a high prevalence of cognitive impairment in RA patients. Cognitive impairment was not related to clinical and treatment features or disability. More studies are necessary to determine clinical impact of cognitive impairment in RA.