Plasma pentraxin 3 levels are associated with carotid IMT in type 1 diabetic patients
Abstract Aims Pentraxin3 (PTX3), a recently discovered inflammatory mediator, is produced abundantly in various cells in atherosclerotic lesions, and therefore, its plasma level could reflect local inflammation at the site of atherosclerotic lesion. The present study evaluated whether plasma PTX3 le...
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Veröffentlicht in: | Diabetes research and clinical practice 2013-02, Vol.99 (2), p.185-191 |
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Sprache: | eng |
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Zusammenfassung: | Abstract Aims Pentraxin3 (PTX3), a recently discovered inflammatory mediator, is produced abundantly in various cells in atherosclerotic lesions, and therefore, its plasma level could reflect local inflammation at the site of atherosclerotic lesion. The present study evaluated whether plasma PTX3 levels are associated with subclinical atherosclerosis in young subjects with type 1 diabetes. Methods Plasma PTX3 levels, urinary albumin excretion, diabetic retinopathy, and carotid intima-media thickness (IMT) were examined in 78 Japanese type 1 diabetic patients (30 men and 48 women, aged 28.5 ± 5.3 years (±SD), duration of diabetes 19.7 ± 6.5 years). Results There was statistically significant association between plasma PTX3 levels and Max-IMT ( r = 0.363, p = 0.001). A stepwise multivariate regression analysis including conventional coronary risk factors as independent variables revealed that plasma PTX3 levels ( β = 0.389, p < 0.001), duration of diabetes ( β = 0.256, p = 0.035), and serum triglyceride levels ( β = 0.371, p < 0.001) were independent determinants of Max-IMT. In addition, plasma PTX3 levels was an independent determinant of urinary albumin excretion, an indicator of diabetic nephropathy ( β = 0.258, p = 0.018). However, there was no significant association between plasma PTX3 levels and diabetic retinopathy. Conclusions Increased levels of plasma PTX3 are associated with accelerated atherosclerotic change and increased albuminuria in young patients with type 1 diabetes. |
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ISSN: | 0168-8227 1872-8227 |
DOI: | 10.1016/j.diabres.2012.11.020 |