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Abstract: Objectives: To describe the evolution of valve involvement and myocardial dysfunction over time in patients with systemic lupus erythematosus (SLE) with or without antiphospholipid antibodies (aPL) and/or antiphospholipid syndrome (APS). Methods: From an initial cohort of 150 patients assessed by transthoracic echocardiography 10 years ago, 17 patients with primary APS (PAPS), 23 with SLE-associated APS (SLE/APS), 19 with SLE positive for aPL without APS, and 23 with SLE negative for aPL were re-evaluated in the present echocardiography study. Results: Valvulopathy was detected in 65% of PAPS and 62% of SLE patients with or without aPL. Disease duration [odds ratio (OR), 1.63; 95% confidence interval (CI), 1.13–2.36; p = 0.009 for every 5 years of increase] and presence of SLE/APS (OR, 3.51; 95% CI, 1.27–9.67; p = 0.015) were the only factors associated with the progression of valvular disease in univariate and multivariate analyses. Left ventricular diastolic dysfunction similarly progressed over time, with deceleration time (DT) and isovolumic relaxation time (IVRT) being equally prolonged in each of the four groups (p < 0.05). Right ventricular DT was significantly prolonged in each of the three SLE patient groups (p < 0.001), whereas IVRT increased only in SLE/APS patients (p = 0.040). Conclusions: Among patients with APS and SLE (with or without aPL), SLE/APS and disease duration were independent factors for valvular disease progression in the present 10-year follow-up echocardiography study. Anticoagulation did not arrest valvular disease progression. Ventricular diastolic dysfunction, primarily of the left ventricle, also progressed over the 10-year period. [Copyright &y& Elsevier]

Atherosclerosis has been considered an inflammatory disease based on the finding that atherosclerotic lesion contains activated T lymphocytes reacting with oxidized low-density lipoproteins (oxLDL) and heat shock proteins (HSP); it also contains autoantigens like β2GPI, a target of antibodies occurring in an immune-mediated thrombophilia called antiphospholipid syndrome (APS). Further support to this hypothesis comes from the cross-reactivity, which occurs between antiphospholipid antibodies (aPL) and antibodies to oxLDL. Animal experiments have shown that aPL are associated with atheroma. In addition, accelerated atherosclerosis has been detected in patients with a prototype systemic autoimmune disease, such as systemic lupus erythematosus (SLE). However, the association of APS or aPL with atherosclerosis is a matter of debate due to the small numbers of patients studied, and the fact that traditional risk factors for atherosclerosis coexist. The prevalence of APS ranges from 1.7% to 6%, and that of aPL reaches to 14% among patients with peripheral vascular disease defined on the basis of clinical outcomes. On the other hand, the prevalence of asymptomatic atherosclerosis, defined in terms of plaques in ultrasonography, reaches to 15% of patients with APS compared to 9% of SLE patients and 3% of normal controls. Among SLE patients with aPL, the prevalence of plaques ranges from 6% in premenopausal women to 31% in unselected patients. Less than 10% of APS patients express premature atherosclerosis in the absence of other risk factors. Which APS patient will develop atherosclerosis is unpredictable. [Copyright &y& Elsevier]

Abstract Objectives This study aimed to investigate whether positive serum autoantibodies (AAbs) have any impact on survival and time evolution of radiological findings and pulmonary function indices in patients with interstitial lung disease (ILD). Patients and methods Ninety four patients with regular clinical, functional and high resolution computed tomography (HRCT) imaging follow-up for at least 12 consecutive months and complete testing for a panel of AAbs most commonly associated with ILD were enrolled in this retrospective two-center study. Eligible patients were divided into two groups based on the presence [ILD/AAb(+)] (n = 69) or absence [ILD/AAb(−)] (n = 25) of positive serum AAbs. All-cause mortality and longitudinal indicators of ILD progression such as a sustained decrease from baseline in absolute measurements of forced vital capacity (FVC) of ≥10% or single-breath diffusion capacity (DLCO SB) of ≥15% were the primary study endpoints. DLCO SB < 40% predicted on at least two consecutive measurements and progression of HRCT findings were our secondary endpoints. Kaplan–Meier (K-M) survival analysis and multivariate Cox proportional-hazards (PH) model were used to evaluate the prognostic significance of positive AAbs in the outcome of patients with ILD. Results ILD/AAb(+) patients were predominantly female (71% vs 32%), were significantly younger (54.8 ± 14.6 vs 66.8 ± 10.1 years), and had longer duration of follow-up (78.1 ± 53.1 vs 41.6 ± 26.7 months), compared with ILD/AAb(−) patients (p <.01 for each comparison). Baseline measurements of FVC (% pred.) and DLCO SB (% pred.) did not differ significantly between the two groups. At the end of follow-up, mortality rates and the percentage of patients with a sustained FVC decrease were lower in the ILD/AAb(+) group (p <.05 for each comparison). With the exception of DLCO SB < 40% pred., ILD/AAb(+) patients had a longer median time-to-event for each of the other studied outcomes (p <.01 for each K-M analysis). In addition, Cox PH models adjusted for age, smoking status, baseline pulmonary function tests and morphological pattern of ILD remained statistically significant in favor of the ILD/AAb(+) group (p <.05 for each comparison). Conclusions AAb(+) patients with ILD seem to have a more favorable prognosis regarding all-cause mortality, long-term deterioration in lung function parameters and progression of HRCT findings than their AAb (−) counterparts. Highlights • Long-term, clinically meaningful decrease of FVC or DLCO SB was observed in >50% of patients with ILD. • AAb positivity in patients with ILD is associated with lower mortality rates and prolonged survival. • PFTs and HRCT findings deteriorate less rapidly in ILD/AAb(+) than ILD/AAb(−) patients. [ABSTRACT FROM AUTHOR]

Abstract: We report a case of septic arthritis due to Roseomonas mucosa in a rheumatoid arthritis patient receiving infliximab therapy. This is the first report of septic arthritis due to R. mucosa, and infliximab therapy might be a predisposing factor because this infection was never reported in the pre–anti-tumor necrosis factor α therapy period. [Copyright &y& Elsevier]