Abstract
BackgroundSystemic lupus erythematosus (SLE) is associated with severe cardiovascular complications. The T50 score is a novel functional blood test quantifying calcification propensity in serum. High calcification propensity (or low T50) is a strong and independent determinant of all-cause mortality in various patient populations.MethodsA total of 168 patients with ≥ 4 American College of Rheumatology (ACR) diagnostic criteria from the Swiss Systemic lupus erythematosus Cohort Study (SSCS) were included in this analysis. Serum calcification propensity was assessed using time-resolved nephelometry.ResultsThe cohort mainly consisted of female (85%), middle-aged (43±14 years) Caucasians (77%). The major determinants of T50 levels included hemoglobin, serum creatinine and serum protein levels explaining 43% of the variation at baseline. Integrating disease activity (SELENA-SLEDAI) into this multivariate model revealed a significant association between disease activity and T50 levels. In a subgroup analysis considering only patients with active disease (SELENA-SLEDAI score ≥4) we found a negative association between T50 and SELENA-SLEDAI score at baseline (Spearman’s rho -0.233, P = 0.02).ConclusionsDisease activity and T50 are closely associated. Moreover, T50 levels identify a subgroup of SLE patients with ongoing systemic inflammation as mirrored by increased disease activity. T50 could be a promising biomarker reflecting SLE disease activity and might offer an earlier detection tool for high-risk patients.
Highlights
Patients with systemic lupus erythematosus (SLE), a chronic inflammatory autoimmune disease, suffer from a dramatically increased cardiovascular morbidity and mortality compared to age- and gender matched individuals [1, 2]
Integrating disease activity (SELENA-SLEDAI) into this multivariate model revealed a significant association between disease activity and T50 levels
T50 levels identify a subgroup of Systemic lupus erythematosus (SLE) patients with ongoing systemic inflammation as mirrored by increased disease activity
Summary
Patients with systemic lupus erythematosus (SLE), a chronic inflammatory autoimmune disease, suffer from a dramatically increased cardiovascular morbidity and mortality compared to age- and gender matched individuals [1, 2]. Non-traditional cardiovascular risk factors reflecting inflammation, disease activity or oxidative stress may contribute to the increased cardiovascular risk in these patients [5,6,7]. Dysregulation of Fetuin-A levels has been associated with increased systemic inflammation and pro-calcifying cytokine production [12]. Pro-inflammatory cytokines are considered important promoters of vascular smooth muscle cell osteochondrocytic transformation and mineralization [13]. Identification of circulating biomarkers for this process and systematic testing of their links with SLE disease activity and subsequent clinical cardiovascular events is of importance for advancing knowledge in this area of clinical research. High calcification propensity (or low T50) is a strong and independent determinant of all-cause mortality in various patient populations
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