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ORIGINAL ARTICLE
Year : 2011  |  Volume : 6  |  Issue : 4  |  Page : 178-184

Study of endothelial dysfunction and its correlation with disease activity in systemic lupus erythematosus patients without conventional cardiovascular risk factors


1 Senior Resident, Department of Medicine, Calcutta Medical College, Kolkata, India
2 Junior Resident, Department of Medicine, Calcutta Medical College, Kolkata, India
3 Associate Professor, Department of Medicine, Calcutta Medical College, Kolkata, India
4 Professor, Department of Medicine; Head, Rheumatology Division, Calcutta Medical College, Kolkata, India
5 Assistant Professor, Department of Radiology, Calcutta Medical College, Kolkata, India

Correspondence Address:
Rathindra Nath Sarkar
Professor, Department of Medicine; Head, Rheumatology Division, Calcutta Medical College, Kolkata
India
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Source of Support: None, Conflict of Interest: None


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Background: Endothelial dysfunction is an important cause of cardiovascular morbidity and mortality in patients of systemic lupus erythematosus (SLE), causing atherosclerosis and its related complications, even in the absence of conventional cardiovascular risk factors. Objective: The present study was aimed at finding the prevalence of endothelial dysfunction in SLE and its relation with disease activity. Methods: Fifty SLE patients without traditional cardiovascular risk factors, and equal number of age and sex matched controls were chosen. Endothelial function was assessed by flow mediated vasodilatation (FMV) on brachial artery, using B-mode ultrasonography. Results: Mean age of SLE patients was 26.06 ± 6.231 years. Thirty-seven (74%) of the patients were having severe disease activity, defined as systemic lupus erythematosus disease activity index (SLEDAI) > 8. We found signifi- cantly lower levels of basal brachial artery diameter in SLE patients (0.3499 ± 0.075 cm) compared to controls (0.3826 ± 0.0002 cm), as also impaired FMV (2.57 ± 2.32% and 8.7082 ± 1.5776%, respectively). Flow mediated vasodilatation significantly correlated with SLEDAI (r = −0.52) and complement (C3) levels (r = 0.33). Conclusion: Endothelial dysfunction in SLE correlates with disease activity.


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