Literatür Detay Bilgisi
Lipoprotein-associated phospholipase A2 (Lp-PLA2) and tumor necrosis factor-alpha (TNF-α) and their relation to premature atherosclerosis in β-thalassemia children

Yazarlar : Ragab S, Safan M, Obeid O et al

Yayın : Hematology

Yayın Yılı : 2014

Pubmed Linki :

Konu : Talasemi

Literatür İçeriği :  Background/Objectives Beta (β)-thalassemia adults are prone to premature atherosclerosis but data about this complication among thalassemia children are few. Lipoprotein-associated phospholipase A2 (Lp-PLA2) and tumor necrosis factor-α (TNF-α) are inflammatory markers that could be implicated in atherosclerotic process. We investigated Lp-PLA2 and TNF-α levels in β-thalassemia children and their relation to subclinical atherosclerosis. Methods Twenty-two β-thalassemia major (TM), 20 β-thalassemia intermedia children, and 30 age- and sex-matched healthy controls were included. Lipid profile (by colorimetric assay), serum ferritin, TNF-α, and plasma Lp-PLA2 levels (by enzyme-linked immunosorbent assay technique) were estimated. Carotid intima-media thickness (cIMT) was measured by high-resolution ultrasound. Results Both patient groups exhibited anti-atherogenic lipid profile except increased serum triglycerides. They had significantly higher plasma Lp-PLA2 and serum TNF-α compared to the controls (P < 0.001). Elevated cIMT was documented in 57% of the thalassemia children and was higher among hepatitis C (HCV) positive patients. Serum ferritin, TNF-α, and plasma Lp-PLA2 levels were significantly higher in patients with premature atherosclerosis. cIMT correlated significantly with serum ferritin, TNF-α, and plasma Lp-PLA2 in both patient groups. Among TM children, serum ferritin had significant positive correlation with serum TNF-α and plasma Lp-PLA2. The elevation of both markers was not related to HCV infection. Conclusions Premature atherosclerosis is common among young thalassemia children. Lp-PLA2 and TNF-α are significantly increased in thalassemia children and show strong correlations with cIMT, suggesting that both of them may be appreciated as modulating factors in carotid atherosclerosis pathophysiological process among these children.

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