Abstract

Cardiovascular (CV) morbidity is the major cause of death in patients with Systemic Lupus Erythematosus (SLE). Previous studies on mannose-binding lectin (MBL) gene polymorphisms in SLE patients suggest that low levels of complement MBL are associated with cardiovascular disease (CVD). However, as large studies on MBL deficiency based on resulting MBL plasma concentrations are lacking, the aim of our study was to analyze the association of MBL concentrations with CVD in SLE patients. Plasma MBL levels SLE patients included in the Swiss SLE Cohort Study were quantified by ELISA. Five different CV organ manifestations were documented. Of 373 included patients (85.5% female) 62 patients had at least one CV manifestation. Patients with MBL deficiency (levels below 500 ng/ml or 1000 ng/ml) had no significantly increased frequency of CVD (19.4% vs. 15.2%, P = 0.3 or 17.7% vs. 15.7%, P = 0.7). After adjustment for traditional CV risk factors, MBL levels and positive antiphospholipid serology (APL+) a significant association of CVD with age, hypertension, disease duration and APL+ was demonstrated. In our study of a large cohort of patients with SLE, we could not confirm previous studies suggesting MBL deficiency to be associated with an increased risk for CVD.

Highlights

  • Systemic lupus erythematosus (SLE) is an idiopathic, chronic and highly heterogeneous inflammatory disorder, driven by an immune response against self-antigens

  • Previous studies described deficiency of complement mannose-binding lectin (MBL) to be related to cardiovascular disease (CVD) in the general population[36] and in Systemic Lupus Erythematosus (SLE) patients[54,55]

  • With a focus on patients with SLE, previous studies on MBL gene polymorphisms suggest that low-producing MBL genotypes are associated with increased intima-media thickness[56] and arterial thrombosis, with coronary events[55]

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Summary

Introduction

Systemic lupus erythematosus (SLE) is an idiopathic, chronic and highly heterogeneous inflammatory disorder, driven by an immune response against self-antigens. Associated with the presence of immune complexes, ongoing complement system activation leads to inflammation and consumption of complement proteins[5]. This chronic inflammatory state predisposes SLE patients to premature cardiovascular disease (CVD) and infections. The prevalence of ischemic heart disease in SLE patients is estimated to be between 3.8 and 16%13–18, a 10-fold higher prevalence compared to the general population[19]. Www.nature.com/scientificreports women with SLE has been found to be 50 times higher compared to women of similar age[20] and the risk of stroke was found to be increased by 2–8 fold[19,21,22]

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