Document Type

Conference Paper

Publication Date

2006

Abstract

Aims: Investigation of inflammation in Australian adolescents with features similar to the metabolic syndrome. Study design, Subjects and Outcome measures: A prospective longitudinal pregnancy cohort was followed up at 13 years. 1377 children underwent anthropometric, fasting lipid, insulin, inflammatory markers, liver function tests and blood pressure measurements. Cluster analysis defined a group at risk withfeatures akin to adult metabolic syndrome. One way ANOVA defined differences in hsCRP, uric acid, ALT and GGT in the cluster groups.

Results: The high risk group had higher BMI (x = 27.9, SD = 5.1 vs x = 20.2, SD = 2.6, p < 0.001), SBP (x = 120.1, SD = 12.0 vs x = 112.1, SD = 10.4, p < 0.001), insulin (x = 24.6, SD = 15.7 vs x = 10.2, SD = 4.6, p < 0.001), triglycerides (x = 1.5, SD = 1.0 vs x = 0.9, SD = 0.3, p < 0.001) and lower HDL (x = 1.2, SD = 0.3 vs x = 1.4, SD = 0.3, p < 0.001). Markers of inflammation and liver function were higher in the at risk group; hsCRP (x = 2.15, SD = 4.7 vs x = 0.7, SD = 2.7, p < 0.001), uric acid (x = 0.34, SD = 0.08 vs x = 0.29, SD = 0.06, p < 0.001), ALT (x = 21.23, SD = 9.7 vs x16.21, SD = 7.23, p < 0.001) and GGT (x14.6, SD = 5.9 vs x11.0, SD = 4.0, p < 0.001). The highest hsCRP levels were only present in children within the cluster who were also overweight.

Conclusions: This suggests that inflammation exists in at risk children as early as 13 years, preceding overt atherosclerosis. It provides clues to the pathogenesis of inflammation in cardiovascular disease by showing that neither being overweight or within the metabolic syndrome cluster alone is associated with raised CRP, but requires the combination of both. It supports early intervention for preventing childhood obesity and subsequent cardiovascular disease.


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