Cross-sectional studies of patients with systemic lupus erythematosus (SLE) have demonstrated an association between activation of type I interferon (IFN) pathway and disease activity. This study examined longitudinal changes in IFN-regulated gene expression in peripheral blood using microarrays. A cross-section of 66 patients from the Autoimmune Biomarkers Collaborative Network SLE archive was evaluated. We also examined paired samples from a 15 patient subset collected during a period of low disease activity (Baseline) and at a subsequent flare event, and baseline scores of 29 patients who maintained low disease activity. IFN response (IFNr) scores were calculated from three IFN-regulated genes. Overall, higher IFNr scores were associated with increased disease activity. However, IFNr scores were not significantly different between the paired Baseline and Flare samples. An extended longitudinal analysis in 11 patients indicated little change in IFNr scores over time, even during dynamic disease activity. In patients with low disease activity, IFNr scores were not different between patients who experienced a subsequent flare and those who maintained low disease activity. In summary, although higher IFNr scores were associated with greater disease activity, IFNr scores of individual patients did not correlate with changes in disease severity or flare risk.

The organ system distribution of A and B flares is very different, with A flares more common in renal and mucocutaneous, and B flares more common in hematologic and renal systems. A or 2B flares are significantly more common in African Americans and in patients with abnormal serologies (low C3, low C4, or high anti-dsDNA). If flare is an outcome in an SLE clinical trial, these factors must be balanced by taking them into account at baseline in terms of randomization, or by statistical adjustment in final analyses.

Purpose:To evaluate the relationships of right ventricular (RV) and left ventricular (LV) myocardial perfusion reserves with ventricular function and pulmonary hemodynamics in patients with pulmonary arterial hypertension (PAH) by using adenosine stress perfusion cardiac magnetic resonance (MR) imaging. Materials and Methods:This HIPAA-compliant study was institutional review board approved. Twenty-fi ve patients known or suspected to have PAH underwent right heart catheterization and adenosine stress MR imaging on the same day. Sixteen matched healthy control subjects underwent cardiac MR imaging only. RV and LV perfusion values at rest and at adenosine-induced stress were calculated by using the Fermi function model. The MR imaging-derived RV and LV functional data were calculated by using dedicated software. Statistical testing included KruskalWallis tests for continuous data, Spearman rank correlation tests, and multiple linear regression analyses. Results:Seventeen of the 25 patients had PAH: 11 with sclerodermaassociated PAH, and six with idiopathic PAH. The remaining eight patients had scleroderma without PAH. groups. There were signifi cant correlations between biventricular MPRI and both mean pulmonary arterial pressure (mPAP) (RV MPRI: r = 2 0.59, Bonferroni P = .036; LV MPRI: r = 2 0.79, Bonferroni P , .002) and RV stroke work index (RV MPRI: r = 2 0.63, Bonferroni P = .01; LV MPRI: r = 2 0.75, Bonferroni P , .002). In linear regression analysis, mPAP and RV ejection fraction were independent predictors of RV MPRI. mPAP was an independent predictor of LV MPRI. Conclusion:Biventricular vasoreactivity is signifi cantly reduced with PAH and inversely correlated with RV workload and ejection fraction, suggesting that reduced myocardial perfusion reserve may contribute to RV dysfunction in patients with PAH.q RSNA, 2010

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Objective-C-reactive protein (CRP) may play an anti-inflammatory role during the acute phase of inflammation, and is also used as a marker of inflammation associated with cardiovascular disease. In the present study, we investigated the association between high-sensitivity CRP (hsCRP) and systemic lupus erythematosus (SLE) manifestations, autoantibodies, and organ damage.Methods-In this cross-sectional study, 610 SLE patients from a prospective cohort had more than one hsCRP measurement. Organ damage was assessed using the Systemic Lupus International Collaborating Clinics (SLICC)/American College of Rheumatology (ACR) Damage Index. Multiple linear regression models were used to adjust for age, gender, ethnicity, disease duration, body mass index, education, disease activity, current prednisone dose, statin use, and estrogen use.Results-After adjusting for confounders, hsCRP was associated with myocarditis, cardiac murmur, interstitial pulmonary fibrosis, pulmonary hypertension, gastrointestinal lupus manifestations, and anemia. Anti-dsDNA antibodies and lupus anticoagulant were associated with hsCRP in unadjusted models, and these associations remained significant after adjustment for confounders. hsCRP levels were significantly higher in patients with pulmonary, musculoskeletal, and endocrine damage, and a total SLICC Damage Index score ≥1. After adjustment, hsCRP was associated with pulmonary, musculoskeletal, and total damage, but no longer with endocrine damage.Conclusions-hsCRP is associated with a broad range of clinical features and organ damage in SLE, particularly in the pulmonary and musculoskeletal systems. This association holds true independent of sociodemographic, disease activity, and treatment factors, and may be useful to identify high-risk SLE patients who would benefit from additional screening and surveillance studies.