Genetic Contribution to Carotid Vascular Disease in Patients with Systemic Lupus Erythematosus

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We investigated whether stromelysin, a candidate gene in atherogenesis, plays a role in atherogenesis of systemic lupus erythematosus (SLE), a leading cause of mortality in SLE.

Patients and Methods

A genetic study using polymorphism located in the promoter region of stromelysin was performed in 55 Italian patients with SLE. Carotid intimal-medial thickness (IMT) was evaluated by B mode ultrasonography.


All patients with an “abnormal” (≥0.9 mm) IMT carried at least one 6A allele, and the degree of IMT was significantly greater in patients carrying at least one 6A allele (0.63±0.22 vs 0.43±0.04 mm, 5A/6A + 6A/6A vs 5A/5A, p=0.018).


Our data show that polymorphism of stromelysin promoter may be relevant for SLE-related cardiovascular disease.

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