Genetic contribution to carotid vascular disease in patients with systemic lupus erythematosus.
OBJECTIVE
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.


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.


RESULTS
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).


CONCLUSIONS
Our data show that polymorphism of stromelysin promoter may be relevant for SLE-related cardiovascular disease.
Marasini
Bianca
B
Rheumatology Unit, IRCCS Humanitas Clinical Institute, Rozzano, Milan, Italy.
Massarotti
Marco
M
De Monti
Marco
M
Erario
Maddalena
M
Ghilardi
Giorgio
G
Biondi
Maria Luisa
ML
D000328:Adult; D000368:Aged; D002340:Carotid Artery Diseases / Q000209:etiology / Q000235:genetics* / Q000473:pathology; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000150:complications*; D019278:Matrix Metalloproteinase 3 / Q000235:genetics*; D008875:Middle Aged; D011110:Polymorphism, Genetic; D011401:Promoter Regions, Genetic; D017539:Tunica Intima / Q000378:metabolism / Q000473:pathology
C511768:MMP3 protein, human; D019278:Matrix Metalloproteinase 3