Article Text
Abstract
Objectives Lupus systemic erythematosus is characterised by an increasing risk of premature cardiovascular disease (CVD). CVD is one of the most common causes of death in SLE. Subclinical atherosclerosis in comparison to general population is also more prevalent, especially the presence of plaques at the carotid level, as well as thickening of the carotid intima.
The aetiology of atherosclerotic disease is completely unknown. It involves: traditional risk factors (age, male gender, smoking, diabetes, hypertension, dyslipidemia, obesity) as well as risk factors related to the disease itself and the treatments used.
Methods A cross-sectional study was carried out from March to November 2015 in 119 patients. Patients were recruited from consultation at the Systemic Autoimmune Diseases Unit for a routine medical check. Clinical data on the disease (from diagnosis to the time of inclusion in the study) were obtained by reviewing the medical history.
The population was divided into two groups: patients with lupus and endothelial dysfunction and patients with lupus without endothelial dysfunction. The existence of endothelial dysfunction was explained by the presence of plaques at the carotid and/or intimate mean thickness >0.8 in a doppler ultrasonography.
Results There is no association with taking antimalarials, immunosuppressants, corticosteroids prior to high doses.
As for the classification criteria there is no relation with the presence of malar rash, Photosensitivity, Oral ulcers, Arthritis, Serositis, Nephropathy, Cytopenias and DNA.
No significant differences were detected in the determination of antibodies or complement levels.
No differences were found with SLEDAI. Since lupus is a disease that occurs in outbreaks, finding no differences may be due to the fact that at the time of inclusion patients had a low activity.
The presence of hypertension and dyslipidemia favours the existence of endothelial dysfunction. Hypertensive patients have a five-fold increased risk of developing endothelial dysfunction (5,593, 95% CI: 2340 to 14,015) as well as patients with dyslipidemia with a nearly 3-fold increased risk (2,976 CI: 1191 to 7,591).
Conclusions Hypertension and dyslipidemia remain the classic risk factors associated with increased endothelial dysfunction. Strict control of them is imperative.