Elevated tumour necrosis factor‐alpha was associated with intima thickening in obese children. (27th January 2017)

• Record Type: Journal Article
• Authors: Bo, Luo; Yi‐Can, Yang; Qing, Zhou; Xiao‐Hui, Wu; Ke, Huang; Chao‐Chun, Zou
• Is Part Of: Acta pædiatrica. Volume 106:Number 4(2017)
• Page Start: 627
• Page End: 633
• Publication Date: 2017-01-27
• Subjects: Carotid intima‐media thickness -- Immune parameters -- Obese children -- Tumour necrosis factor‐alpha; Pediatrics -- Periodicals; Pediatrics; 618.92
• DOI: 10.1111/apa.13737
• Languages: English
• ISSNs: 0803-5253

Abstract

Abstract: Aim: This study investigated the relationship between intima‐media thickness (IMT) and immune parameters in obese children from five to 16 years of age. Methods: We enrolled 185 obese children with a mean age of 10.65 ± 2.10 years and 211 controls with a mean age of 10.32 ± 1.81 years. Glycometabolism, lipid metabolism, sex hormones, immune indices and carotid IMT were measured. Results: Serum interleukin (IL)‐6, IL‐10, tumour necrosis factor (TNF)‐alpha, white blood cells and common and internal carotid artery IMTs in the obese group were higher than those in the control group (p < 0.05, respectively). Bivariate correlation analysis showed that the common carotid arterial IMT was positively correlated with alanine aminotransferase, triglyceride, uric acid, apolipoprotein B, IL‐6, IL‐10, TNF‐alpha, follicle‐stimulating hormone and testosterone. Internal carotid artery IMT was positively correlated with alanine aminotransferase and follicle‐stimulating hormone. Both common and internal carotid artery IMTs were inversely correlated with apolipoprotein A1 (p < 0.05, respectively). Stepwise multiple regression analysis showed that testosterone, alanine aminotransferase and TNF‐alpha were the independent determinants of common carotid arterial IMT. Conclusion: Tumour necrosis factor‐alpha, alanine aminotransferase and testosterone were associated with intima thickening in the early life in obese children and may increase later risks of premature atherogenicity and adult cardio‐cerebrovascular diseases.