Abstract
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. 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" (> or =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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